Mike Dewey has a plan to eliminate breast cancer: He's offering $1 billion to the person who discovers the cure. Never mind the fact the 48-year-old Austin consultant has nothing close to that much money. Dewey, whose daughters are at increased risk for the disease because his wife was diagnosed with breast cancer, says he'll come up with the cash. "I get pretty fired up about this because I've got girls in danger," said Dewey, who says he's raised about $22 million in pledges so far and about $90,000 in actual donations through his nonprofit foundation.
"I think that we've cracked the code for a new kind of philanthropy," said Dewey, who says he'd retain the intellectual rights to the cure but put it into the public domain for free. "People always have and people always will respond to economic stimuli." Arthur Caplan, chair of the department of medical ethics at the University of Pennsylvania in Philadelphia, said Dewey's plan seems naive. "I think sometimes there is a belief that if we have the right incentive, anything can be solved," he said. "This isn't a problem of incentive. It's having the right luck, the right breakthrough, the right science to get the problem solved." Margaret "Peg" Mastrianni, deputy director of the Breast Cancer Research Foundation, said in a statement that donors want assurance that their money will go to the "most promising investigations and that progress will be monitored." Dewey isn't alone in feeling some impatience with the pace of research. Dr. David Euhus, a surgical oncologist at the University of Texas Southwestern Medical Center, said he's noticed that those making grants are willing to take bolder steps because they're "getting a little frustrated" by the slow pace of traditional research. While Dewey's idea may make a social statement, Euhus said he doesn't think many people will look at it as realistic. "It's not one disease. It's hundreds of diseases. There are hundreds of ways of getting to the same endpoint — getting from a normal cell to a cancer cell," he said, pointing out that research takes millions of dollars. Stan Cohen, who teaches a medical ethics course at Nova Southeastern University in Fort Lauderdale, Fla., said offering a financial incentive might help considering the slow, bureaucratic pace of funding research. "There's nothing wrong with giving people rewards like that, in my opinion," he said. Dewey said some people think his idea is wacky, but that others are intrigued. Australian businessman and investor Toby Davidson said he has pledged $1 million to the foundation after meeting Dewey last year and provided "working capital" to the foundation but declined to say how much. He said he hopes to be writing a check for $1 million one day. "That's the whole point," he said. "Hopefully sooner rather than later." Dewey, whose wife, Barbara, has been cancer-free since surgery following her diagnosis in 2000, founded his nonprofit Dewey Foundation in 2006. He launched its Web site last year for the foundation, which he says is offering other "Victory Project Awards" worth $1 billion each to anyone who cures diabetes, reduces greenhouse emissions from petroleum-powered automobiles by 95 percent, or creates a car capable of getting 150 miles per gallon. Dewey said he's in the process of assembling panels of experts to judge whether a cure or solution to one of his stated issues has been achieved. If no cure or solution is found within 30 years of the foundation's inception, the foundation will distribute any money raised to traditional charities, Dewey said. |
$1 Billion Reward for Breast Cancer Cure
Skeptics question ‘breast cancer-free’ baby claim
| The headlines were compelling, holding out a promise that seems to answer every parent’s prayer. Through genetic screening and in vitro fertilization, a British couple had conceived a daughter who would be “cancer free.” But the claim, NBC medical editor Dr. Nancy Snyderman told TODAY’s Meredith Vieira Monday, is misleading at best. And the screening that was done does not guarantee the child will not get cancer. “I don’t think ‘guarantee’ is ever smart in medicine,” Snyderman said. She pointed out that the unidentified woman and her husband had used medical science to screen 11 embryos fertilized via the in vitro process for the presence of one gene, called BRCA-1. That gene had triggered breast cancer in the husband’s grandmother, mother, sister and cousin. Women who carry either the BRCA-1 or BRCA-2 gene have a 50 to 80 percent chance of developing breast cancer, usually at a young age.
But, said Snyderman, “There are two problems: You could have [the genes] and never get breast cancer, and there may be other genes that cause breast cancer that she’s not even screened for.” Sword of Damocles “Damocles’ sword is still hanging over her head, as for every woman. She can still get breast cancer — just not this specific kind,” Snyderman told Vieira. There are moral and ethical issues associated with such screening. Some people believe it is not morally acceptable to destroy viable embryos just because they carry a gene that may cause cancer. For years, there has been screening through procedures such as amniocentesis for such birth defects as Down syndrome. Women are given the option of aborting the pregnancy or going ahead with the birth, according to their personal beliefs. Genetic screening is simply the next step in that process, Snyderman said. What we still have to deal with are the destinations to which genetic technology will eventually lead. There is no stopping the science, Snyderman said. “Science will always win. What we have to come to grips with in society is these moral and ethical questions should be in tandem with the science,” she told Vieira. Already, Snyderman said, there are labs around the world that will select embryos for certain characteristics: “The science is available for you to say ‘I only want a boy, and I want a tall boy, and I’d like this eye color.’ ” The future is here Some people may see it as a black-or-white issue. Most, Snyderman said, will see it in shades of gray. “Screening for illness, terminal illness or perhaps terrible neurological problems — some people may say, ‘That’s the gray line for me. I’m willing to go there,’ ” she told Vieira. “Your gray line might be black-and-white to someone else. But the science absolutely will be there.” Where Snyderman has a problem is with the suggestion that screening such as that the British couple underwent “guarantees” a disease-free baby, or even one that will grow up to be a healthy and happy adult. You can screen for everything, but the child can still get hit by a bus. “The guarantee in medicine — I have a real issue with that,” Snyderman concluded. “You cannot guarantee a healthy child no matter what. There’s always going to be something else that might befall one of our children.” |
Liver Cancer Patients Live Longer By Taking Anti Cancer Drug Sorafenib
| Researchers at Mount Sinai School of Medicine in New York have found that sorafenib (Nexavar) helps patients with advanced liver cancer live about 44 percent longer compared with patients who did not receive the anti-cancer drug. The findings, published in the July 23rd, 2008 issue of the New England Journal of Medicine, is a significant advance in the management of liver cancer, which is the third cause of cancer death globally, often resulting in death within a year of diagnosis. |
How to Do a Breast Self-examination
How women feel about their breasts largely determines how they feel about themselves as women. Because of this, breast cancer and with it the thought of losing a breast generates more fear among women that almost any other single disease. This fear keeps the average woman at home for five or six months before she consults her doctor about a lump she has found in her breast. Not every lump, however, has to be a cancer. If fact, very few are. Even so, breast cancer is the most common form of cancer among women. For this reason, it is essential to be especially vigilant - and vigilance begins at home. Early detection depends, first and foremost, on regular monthly self-examinations. The more practiced you get at examining and feeling your breasts and the irregularities between them, the greater your chance of spotting a significant change at the earliest possible opportunity.
Examine your breasts once a month just after your period has finished. Breasts undergo glandular changes through the menstrual cycle and many people find that their breasts are naturally lumpy and tender just before menstruation. If you have been through menopause, you should examine your breasts on the first day of each calendar month. Most breasts are naturally asymmetrical - the shape may be uneven, the nipples may point in different directions or one breast may be significantly higher or lower or larger or smaller than the other. Study your breasts to see whether any of these apply. The key to successful, less anxious breast examination is change, so you must be aware of what is normal for you. What to watch out for: * A lump in the breast. Only a very small proportion of all lumps are cancerous, bit it is impossible to tell by feeling whether a lump in innocent or not. Only a doctor can decide whether or not this is the case. * Any moles that have changed in sized, shape or color. * Dimpling or puckering of the skin, an unusual prominence in the blood veins on either breast, or a retraction (drawing in of the skin tissue). Any of these many indicate the presence of a lump pressing on the ligaments inside the breast, this affecting the contour and appearance. Again only a doctor can decide whether or not this is the case. * Inverted nipples. Some women have naturally inverted nipples, or, more rarely, one nipple may always have been inverted while the other one is not. If your nipples have always been this way, you have no cause for concern. Any situation, however, in which the nipple has recently become inverted, requires further investigation. * A discharge coming from one or both nipples. Check for this by looking inside your bra before carrying out your monthly breast self-examination. Although a discharge is not uncommon when taking or, particularly, when coming off the contraceptive pill, just prior to menstruation, or after breastfeeding, when a small secretion may persist for some months, it should never be ignored, particularly if it is persistent, coming from one nipple only or is bloodstained. So consult your doctor and, in the meantime, do not squeeze or interfere with the nipples in any way. Consult your doctor also, if you have an ulcer or sore on the nipple that does not heal. * Enlarge of inflamed lymph glands. The lymph glands surrounding the breast lie on the outer sides and run up towards the armpit. They are essential for regulating the body's fluid balance and for fighting off infection. Although they may enlarge quite naturally if you have an infection or before menstruation, you should see a doctor if the inflammation has not subsided after three weeks. 1. Start with a visual inspection. * Stand in front of a large mirror with a good light placed to the side, not overhead. Now look at your breasts. If this is the first time you have carried out a breast examination, take the opportunity to note exactly how they look. 2. To help check the differences between the two breasts, place the hands on top of the head. * Turn slowly to the left and the right. The crossways angle of the lighting should help you to spot any irregularities or dimpling in the skin surface. 3. Place you hands on your hips and press firmly down and inwards. * This should tighten the pectoral muscle and help you to spot any dimpling. Then, keeping your hands where they are, lean forwards from the hips so that the breasts fall straight downwards and inspect them head-on. Look particularly for any tautness in the skin tissue, any change in the way the nipple is pointing, and for a nipple that becomes inverted on leaning over but everts itself naturally as you stand up again. 4. Lie down on a firm surface and place a folded towel or pillow beneath the shoulder of the side you examine first. * This is especially important if your breasts are large, as the breast will then sit evenly on the chest wall. Feel each breast in turn with the opposite hand and, to begin with, keep your arm by your side. Feel with the flat surface of your middle three fingers, keeping them straight, but not tense, and the wrist flexible. The amount of pressure you exert should be firm enough for the skin surface to move with your fingers but not so firm that the natural texture becomes hard and lumpy if you press too hard. Press the breast tissue gently but firmly towards the chest wall, starting just above the nipple and tracing small circles radiating outwards in a spiral the whole way round the breast. Be particularly on the look-out for any fixed, hard lump that will not move away easily when you press the breast tissue between your fingers. Make sure that you feel every part of the breast, beneath as well as above. 5. Finally place your arm above your head so that the outer side of the breast is stretched and accessible. * Repeat the examination and pay particular attention to the upper part of the breast which extends up into the armpit. |
Cancer Institute Urges Caution With Cell Phones
A prominent US cancer institute has posted a notice on its website urging cell phone users to take precautions when using cell phones because advice from an international panel of experts says cell phones have not been around long enough for scientists to be sure about their safety.
The National Cancer Institute website says that studies have so far failed to show a link between brain tumours and cell phone use. The US Food and Drug Administration (FDA) says on its website that: "The available scientific evidence does not show that any health problems are associated with using wireless phones. There is no proof, however, that wireless phones are absolutely safe. " In research, there is a saying "absence of evidence is not evidence of absence", which perhaps urges us all to consider this news carefully and make up our own minds. |
Does Too Much Sun Cause Melanoma?
We are continuously bombarded with messages about the dangers of too much sun and the increased risk of melanoma (the less common and deadliest form of skin cancer), but are these dangers real, or is staying out of the sun causing us more harm than good? Sam Shuster, a consultant dermatologist at Norfolk and Norwich University Hospital, says that sun exposure is the major cause of the common forms of skin cancer, which are all virtually benign, but not the rarer, truly malignant melanoma.
There is good evidence that the reported increase in melanoma incidence is an artefact caused by the incorrect classification of benign naevi as malignant melanomas, this, he argues, explains why melanoma mortality has changed little despite the great increase in alleged incidence. He recognises that ultraviolet light causes the common, mainly benign skin cancers and, like smoking, wrinkles the skin. But he says, this is not a good enough reason for a blanket ban and we have to strike a balance with the sun's many other effects on health--from psychological and immunological, to the synthesis of vitamin D essential for bones and apparent protection against many major organ cancers. But Professor Scott Menzies, from the University of Sydney at the Sydney Melanoma Diagnostic Centre, argues that melanoma is far more common on body sites receiving more sun exposure and in people of races who tend to burn rather than tan. According to Menzies, there is considerable evidence that intermittent sun exposure and sunburn are strong independent indicators of the risk of developing melanoma in white populations. He argues that there is a clear association between increasing cases of melanoma and increasing environmental ultraviolet light. Genetic evidence is also supportive, he claims, with the major genes causing melanoma showing ultraviolet light "signature" mutations, while people deficient in repairing ultraviolet light genetic damage have a 1000 times greater risk of developing the disease. He points to data from Australia which shows that cases of melanoma among young adults fell between 1983 and 1996 and this coincided with strong public health messages to use sun protection. When you examine the geographical, sun exposure and genetic evidence together, sun exposure is clearly a major cause of melanoma, he concludes. |
Drug for deadly prostate cancer
| Scientists are hailing a new drug to treat aggressive prostate cancer as potentially the most significant advance in the field for 70 years. Abiraterone could potentially treat up to 80% of patients with a deadly form of the disease resistant to currently available chemotherapy, they say. The drug works by blocking the hormones which fuel the cancer. The Institute of Cancer Research hopes a simple pill form will be available in two to three years. An advanced clinical trial involving 1,200 patients around the world is currently under way, with more trials likely later this year.
It is estimated that up to 10,000 men a year in the UK are diagnosed with the most aggressive - and almost always lethal - form of prostate cancer. It had been assumed that the cancer was driven by sex hormones such as testosterone produced in the testicles. Current treatments work by stopping the testicles from producing testosterone. New action However, experts have now discovered that the cancer can feed on sex hormones from all sources, including supplies of the hormone produced by the tumour itself. Abiraterone works by blocking production of the hormones throughout the body. The latest study, published in the Journal of Clinical Oncology, is based on just 21 patients with advanced, aggressive prostate cancer treated with the drug - but data has been collected on a total of 250 worldwide. It found significant tumour shrinkage, and a drop in tell-tale levels of a key protein produced by the cancer called prostate specific antigen in the majority of patients. Many of the patients, who have been monitored for up to two-and-a-half years, have reported a significant improvement in the quality of their lives. Some were able to stop taking morphine for the relief of pain caused by the spread of the disease to their bones. Real hope Lead researcher Dr Johann de Bono said the findings needed to be confirmed in larger trials. But he said: "We believe we have made a major step forward in the treatment of end-stage prostate cancer patients. "These men have very aggressive prostate cancer which is exceptionally difficult to treat and almost always proves to be fatal. "We hope that abiraterone will eventually offer them real hope of an effective way of managing their condition and prolonging their lives." It is hoped the drug will also aid other cancer patients, including those with breast cancer. Professor David Webb, an expert in clinical pharmacology at the University of Edinburgh, said: "This agent clearly looks promising, but it is still at the early stages of clinical development. "It will be crucial to look carefully at the balance between its benefits and harms, before drawing firm conclusions about the usefulness of this new drug. "Important side effects often only emerge with the larger clinical studies that now need to be done." John Neate, of The Prostate Cancer Charity, said: "This is an exciting development which has been eagerly anticipated." |
Target-seeking Antibodies For Cancer Therapy
The chemist Dario Neri has carried out research for more than 15 years to find antibodies suitable as drug delivery vehicles for selective anti-cancer treatment. In his most recent publication he presents a new marker together with three associated monoclonal antibodies as further promising candidates for cancer therapy. Up to now, monoclonal antibodies have only lived up to their expectations in the chemotherapeutic fight against cancer to a limited extent. Although these therapies are effective in prolonging the lives of patients who have types of cancer with a small chance of survival, for example advanced lung cancer, they cannot cure them. One of the main problems with current antibody chemotherapies is that the medicines lack selectivity. The active ingredients become distributed throughout the whole body and also attack healthy tissues in the liver, lungs or heart as well as the actual tumour that is to be treated. Targeted anti-tumour treatment via the blood supply By using “targeting”, Dario Neri from the Institute of Pharmaceutical Sciences at ETH Zurich has followed a promising path in cancer therapy. “Targeting” employs antibodies as delivery vehicles for medicines to carry their active ingredients through the blood circulation and into the tumour. Blood vessels that grow together with the tumour as a result of what is known as angiogenesis (neo-vascularization) and supply the tumour with nutrients enable drugs to be transported via the body’s own blood circulation and into the centre of the tumour. The researchers use markers to help the antibodies find their way into the diseased cells. These markers can be thought of as a kind of antibody dock to which only proteins with specific characteristics can attach themselves. If the matching proteins are now loaded with an anti-cancer agent, the markers enable the drugs to be positioned highly selectively in the tumour as well as in the metastases, thus protecting the remainder of the healthy body. Among other things, Neri’s group is searching for such markers, i.e. protein characteristics that occur solely in the tumour’s blood circulatory system. Neri’s colleague Luciano Zardi had already found such a marker 21 years ago in the shape of the extra-domain B (EDB) of the protein fibronectin. EDB is a variant of the fibronectin protein that occurs practically exclusively in the blood supply of tumours and their metastases. Today EDB is one of the best characterised markers in cancer research. In the past 10 years Neri and his team have developed two very promising antibodies, F16 und L19, that can “dock on to” tumour blood vessels and can be readily loaded with an anti-cancer active agent. A large number of markers and antibodies is needed for therapy In the “International Journal of Cancer”, Neri has described another marker, the fibronectin extra-domain A (EDA), together with three monoclonal antibodies that bind selectively to EDA. Explaining the relevance of the new results, Neri says, “Because each type of cancer has its own molecular characteristics, it is important that we make various different markers and antibodies available for therapy.” The publication describes the antibody F8 in particular as a promising candidate for this cancer therapy. Tests on laboratory mice have shown that F8 accumulates very selectively in the tumour and in cancerous metastases, while healthy organs remain largely protected against the antibodies. According to Neri, “We believe that the F8 antibody could become an important building block in the development of selective and effective anti-cancer bio-pharmaceuticals.” Up to now, F8 has been tested only on mice. However, in collaboration with two pharmaceutical companies, clinical studies on humans are already taking place for the EDB antibodies F16 and L19, which have been known for longer. Initial results should be published soon, and, according to Neri, these are very promising. Neri says “We have good reason to assume that F8 could soon prove in clinical studies to be just as promising a cancer therapy candidate as F16 and L19.” |
Better Way To Detect Melanoma
University of Rochester Medical Center researchers found a new protein produced excessively in malignant melanoma, a discovery that is particularly relevant as skin cancer rates climb dramatically among young women. |
Using Magnetic Nanoparticles To Combat Cancer
Scientists at Georgia Tech have developed a potential new treatment against cancer that attaches magnetic nanoparticles to cancer cells, allowing them to be captured and carried out of the body. The treatment, which has been tested in the laboratory and will now be looked at in survival studies, is detailed online in the Journal of the American Chemical Society. "We've been able to use magnetic nanoparticles to capture free-floating cancer cells and then take them out of the body," said John McDonald, chair of the School of Biology at Georgia Tech and chief research scientist at the Ovarian Cancer Institute. "This technology may be of special importance in the treatment of ovarian cancer where the malignancy is typically spread by free-floating cancer cells released from the primary tumor into the abdominal cavity."
They began by testing the therapy on mice. After giving the cancer cells in the mice a fluorescent green tag and staining the magnetic nanoparticles red, they were able to apply a magnet and move the green cancer cells to the abdominal region. "If the therapy is able to pass further tests that show it can prevent the cancer from spreading from the original tumor," Scarberry said, "it could be an important tool in cancer treatment." This technology holds more promise than solely using antibodies to fight cancer because there seems to be less potential for the body to develop an immune response due to the unique peptide-targeting strategy, and the composition of the magnetic nanoparticles. "If you modify the nanoparticle and target it directly to the tumor cells using a small peptide, you are less likely to generate an undesirable immune response and more accurately target the cells of interest," said Research Scientist Erin Dickerson. In addition to testing magnetic nanoparticles, the research team is collaborating with other groups at Georgia Tech to determine how peptide-directed gold nanoparticles and nanohydrogels might also be used in fighting cancer. |
Predicting Outcomes For Stomach Cancer Patients
| Researchers at Rhode Island Hospital have identified two potential molecular markers that may predict outcomes for patients with stomach cancer, one of the most common and fatal cancers worldwide. According to the study, published in the July 1 issue of Clinical Cancer Research, patients who had poor outcomes following surgery for stomach cancer also had extremely low amounts of two proteins, known as gastrokine 1 and 2 (GKN1 and GKN2), which are produced by normal stomach cells. The study's findings confirm previous research showing that once stomach cells become cancerous, they manufacture very low amounts of GKN1 and GKN2. However, this is the first known study to link these low protein levels with outcomes following stomach cancer surgery. Researchers say this discovery could eventually help physicians better determine and individualize therapy for stomach cancer, including which patients should be offered chemotherapy and other treatments in addition to surgery.
"Unfortunately, stomach cancer is difficult to cure unless it's discovered early, but because the early stage of the disease has very few symptoms, the cancer is usually advanced by the time it's diagnosed," says lead author Steven Moss, MD, a gastroenterologist with Rhode Island Hospital and an associate professor of medicine at The Warren Alpert Medical School of Brown University. "That's what makes our findings so significant, because if the potential markers identified in our study can help predict a patient's prognosis, we can decide right away which course of action to take and hopefully help patients live longer and more comfortably," he adds. According to the National Cancer Institute, approximately 760,000 cases of stomach cancer are diagnosed worldwide each year. Microscopically, stomach cancers can be subdivided into those which appear "diffuse" (a more aggressive form of cancer that can occur throughout the stomach and is more likely to spread) or "intestinal" (resembling the cells normally found only in the small or large intestines). Stomach cancers of both types are often triggered by a chronic infection brought on by Helicobacter pylori (H. pylori), a common bacterium that causes stomach inflammation and ulcers. Surgery is the most common treatment for stomach cancer and can include partial or full removal of the stomach. The five-year relative survival rate of patients with stomach cancer is 24 percent. Moss, an expert on H.pylori, and colleagues initially set out to learn more about what the bacterium does to normal stomach cells. They focused on GKN1 and GKN2 because these proteins are also suppressed by stomach infections caused by H. pylori. After looking at tissue samples from more than 150 stomach cancer patients who underwent surgery, the researchers discovered a near total suppression of GKN1 and GKN2 in the majority of patients. This was particularly evident in those patients with the diffuse variant of stomach cancer. More than three-quarters of these patients had extremely low levels of GKN1 and 85 percent had nearly nonexistent levels of GKN2. Furthermore, in those patients with the intestinal variant of stomach cancer, very low levels of GKN 1 or GKN 2 at the time of surgery were associated with a significantly worse outcome. The median survival was about two years in these patients compared to a survival of more than 10 years for patients with normal levels of GKN1 or GKN2. Researchers do not yet know the exact function of GKN1 and GKN2. They say further studies are needed to demonstrate the mechanisms responsible for the loss of GKN1 and GKN2 in this patient popoulation as well as the clinical biomarker potential of these two proteins. The study included tissue samples from 155 patients with stomach cancer (81 men and 74 women) who underwent surgery at Rhode Island Hospital and The Miriam Hospital, both in Providence, R.I. The average age at surgery was 72 years. All four stages of cancer were represented in the study, including 37 patients with Stage I, 44 patients with Stage II, 34 patients with Stage III, and 40 patients with Stage IV. More than 61 patients were being treated for the intestinal variant of stomach cancer while 90 patients had the diffuse variant.
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Vitamin A Pushes Breast Cancer To Form Blood Vessel Cells
Researchers at Georgetown University Medical Center have discovered that vitamin A, when applied to breast cancer cells, turns on genes that can push stem cells embedded in a tumor to morph into endothelial cells. These cells can then build blood vessels to link up to the body's blood supply, promoting further tumor growth. They say their findings is a proof of principle of the new -- and controversial -- "vasculogenic mimicry" theory, proposing that, as needed, tumors build their own blood pipelines. This is very different from the well-accepted role of tumor angiogenesis, when tumors send signals to blood vessels to grow toward the cancer.
For example, use of beta-carotene, the most important dietary precursor of vitamin A and the chemical that makes carrots orange, has been found to increase lung cancer progression in a large clinical trial. Additionally, fenretinide, a synthetic retinoid, appears to reduce the risk of second breast cancers in premenopausal women, but increase the risk in postmenopausal women, Byers says. "None of this means that people should avoid foods rich in vitamin A, or should refuse to take their vitamins," he says. "What led us to this study is that previous research on retinoids implied that they may be effective in a preventative setting, but may actually have a negative effect after tumor initiation and during progression." The researchers demonstrated that treating the cells with RA turns on 81 genes that are associated with endothelial cells, such as vascular endothelial (VE) cadherin, which plays a role in binding endothelial cells together into a structure. When they then mixed the treated cancer cells with endothelial cells taken from human umbilical cord blood, structures similar to blood vessels developed within the tumor masses grown in culture. This makes sense, says Byers, because vitamin A is known to be necessary for embryonic development precisely because it helps to "differentiate" stem cells, pushing them to become required tissue. In the same way, taking too much vitamin A can result in birth defects. So, in cancer cells, vitamin A seems to be turning on cancer stem cells, allowing them to form the blood vessel tissue -- needed most as tumors develop. Independent formation of these vessels is what has been proposed in the vasculogenic mimicry theory, developed by Mary Hendrix, , Ph.D., of Northwestern University, Byers says. "Like many scientists, I was not an advocate of this notion because it seemed too far fetched, but now, based on these findings and my years of working on retinoids and breast cancer, I am a believer," he says. "And what this study tells us is that treating stem cells that have retained the ability to become cell types other than breast with differentiating agents such as vitamin A may cause an inappropriate cell to develop - in this case potentially promoting tumor vasculogenesis and growth, which is not a desired effect." While there is much work yet to do to further define the molecular mechanisms by which endothelial cells form within tumors and assemble themselves into blood vessels, Byers says that these findings open a new door to drug development. "Cancer drugs based on stopping host-derived angiogenesis have met with mixed success, and we think there could be new ways to target and halt the ability of tumor cells themselves to contribute to their own blood supply," he says. This research is published in the July 16 online issue of PLoS One. The study was funded by grants from the National Institutes of Health and the Department of Defense. Co-authors include Georgetown University Medical Center researchers Yoshimi Endo, M.D., Ph.D., Kamla Deonauth, Ph.D., and Priya Prahalad BS, (co-first authors of the study) and Yuelin Zhu Ph.D. |
Rare Breast Cancer Recurrence may Be Prevented by Radiation
| Radiation therapy can help prevent cancer recurrence of a rare type of breast cancer in patients, a new study from City of Hope National Medical Centre in Duarte, California has revealed. Phyllodes tumours are rare breast tumours that develop in the connective tissue of the breast, as opposed to more common carcinomas, which develop in the ducts or lobules of the breast Presently, patients with the rare tumours are treated either with a lumpectomy or mastectomy, with only a small fraction receiving radiation therapy.
The adjuvant radiation therapy is recommended for cancer patients with local recurrence risks of 15 percent or greater but the effect have never been studied for phyllodes tumors because they are so rare. Researchers reviewed the records of 478 patients with malignant phyllodes tumors who were treated between March 1964 and August 2005 and found that the risk of local recurrence for phyllodes tumors was related to tumour size and the type of surgery received. "Typically these tumours are treated well by surgery alone. However, local recurrences are not uncommon," said Richard Pezner, M.D., lead author of the study and a radiation oncologist at City of Hope National Medical Center in Duarte, Calif. They determined that adjuvant radiation therapy should be evaluated for phyllodes tumor patients who received lumpectomies for tumours at least 2 centimeters in size or a mastectomy for tumours at least 10 centimetres in size to reduce the risk of recurrence. The study appears in the July issue of the International Journal of Radiation Oncology*Biology*Physics, the official journal of the American Society for Therapeutic Radiology and Oncology. |
Childhood Cancers Vary Depending on Region and Sex
Could your children be more at risk to different types of cancer depending on the region you live in? A government study on just that topic has found there are numerous differences in types of cancer depending on age, race, sex and where in the United States the child lives. It was shown that Caucasian children had the highest incidence of all types of cancers and the children in the Northeast were diagnosed with cancer more often than children in all other parts of the United States. The research also shows that boys are more likely to have a pediatric malignancy than girls, and that adolescents are more likely to have cancer than children of a younger age. The lead author of the study and a member of the intelligence office for the U.S. Centers for Disease Control and Prevention (CDB) in Atlanta, Dr. Juan Li, said "We looked at the childhood cancer incidence rate from 2001 through 2003, and further looked at the data by age, sex, ethnicity and U.S. census region." He also stated, "We identified 36,446 cases of childhood cancer during these three years, which is about 166 per every million." The information for the study, which represents over 90 percent of the population in the United States, was collected from 39 National Program of Cancer Registries and five Surveillance, Epidemiology and End Results (SEER) databases. The results of this study were published in the June issue of the journal Pediatrics.
Overall, the study also shows that boys are much more likely to develop cancer than girls. The cancer incidence rate for boys was 174 per one million, while the rate for girls was 157 per one million. The type of cancer that the different sexes developed also varied. The boys were more likely to develop lymphoid leukemia, hepatoblastoma, Burkitt lymphoma, non-Hodgkin lymphoma, osteosarcomas, and more. The girls were more likely to have thyroid cancer, malignant melanomas, and cancers of the kidney. The cancer incident rates for adolescent's ages 15 to 19 were 210 per one million, while the rate of incidence in children under 14 were approximately 151 per one million. The race of children most likely to have cancer was shown to be white, with an incidence rate of 173 per one million. The rate for children that were black was 18 per one million, Hispanics were 164 per one million, and Asian/ Pacific Islanders were 131 per one million. The American Indians and Alaskan natives held the lowest rates at 97 per one million. In the study, geography appeared to also make as difference. The children in the Northeastern part of the country are most likely to develop cancers, with the incidence rate of 179 per one million. In the Midwest region, the incidence rate was 166 per one million. In the Southern region, the incidence rate was 159 per one million, and in the Western region the incidence rates were 165 per one million. The study also interestingly showed that children in the Northeast, despite having the highest rate of cancers, also had the lowest rate of deaths from pediatric cancers. Li said that the researchers were not able to find the reasons for the differences in the study, but he does believe that the data will lay groundwork for research in the future. He also added that knowing these differences could help other scientists target their research. Dr. Adam Levy, a pediatric hematologist, oncologist, and a director of pediatric neuro-oncology at the Children's Hospital at Montefiore in New York city, said, " This is an interesting study, but as a practicing oncologist, I won't be advising families any differently. And, as a father of three sons, I wouldn't have any added concern as a parent living in the Northeast." He fears that people may over-interpret this new study, and the parents really don't need the added anxiety. This study is talking about very rare pediatric cancers and very mild differences. This study gives mostly clues to epidemiological researchers clues. He concluded by stating that parents do not need to become overly worried by the information from this study. |
Male breast cancer treatment often delayed
Yes, men can and do get breast cancer -- and the disease is often treated at a late stage, according to research presented Sunday in Lugano, Switzerland. Dr. Marina Garassino of the University of Study of Milan, Italy and colleagues reviewed the medical records of 146 men, about 62 years old on average, who were diagnosed with breast cancer. The researcher reported the findings at a conference organized by the European Society for Medical Oncology.
Doctors and patients may both play a part in delayed diagnosis of male breast cancer, Garassino surmises. "Physicians may not recognize the tumor in men; they see a lump but don't think that it may be breast cancer. Also men might not suspect that they have a tumor and they arrive to the physician later than females." "Male breast cancer is a very hormonal-dependent disease," Garrasino said, and there is some evidence that, if treated early, "prognosis may be better" than in women. All of the men underwent surgery to remove their cancer, 48 men then received radiation treatment, and 100 received add-on chemotherapy or hormonal therapy. "Of note," the investigators say, is the finding that 42 men (30 percent) received no further treatment after surgery. Overall 10-year survival rates were 47 percent for men with earlier-stage disease, and 44 percent for men with more advanced disease. "The message for men," Garassino said, "is this: if you have a lump in your breast, go immediately to the physician. Don't wait, because you may have a tumor." |
Vitamin D levels tied to colorectal cancer survival
Patients diagnosed with colorectal cancer who had abundant vitamin D in their blood prior to diagnosis were less likely to die during a follow-up period than those who were deficient in the vitamin, researchers report. |
The Fact of Colon Cancer and Genetic Testing
There has been much excitement during the past decade because of the identification of defective genes (mutations) associated with colon cancer in families where colon cancer is common. When a defective gene can be identified, it is possible to examine other members of the family to see if they also carry the defective gene. Those individuals who carry the defective gene are at a very high risk (75%-100%) for developing colon cancer. The reason for the excitement is that if an individual is found to have the defective gene, his or her colon can be removed before the cancer occurs. |
Understanding Kidney Cancer
It is important to realize that with timely diagnosis and treatment, kidney cancer can be cured. If found early, the survival rate for patients with kidney cancer ranges from 79 to 100 percent. More than 100,000 survivors of kidney cancer are alive in the United States today. The following information addresses the most common questions about kidney tumors and serves as a supplement to the discussion that you have with your physician. What is a kidney tumor? A kidney tumor is an abnormal growth within the kidney. The terms "mass," "lesion" and "tumor" are often used interchangeably. Tumors may be benign (non-cancerous) or malignant (cancerous). The most common kidney lesion is a fluid-filled area called a cyst. Simple cysts are benign and have a typical appearance on imaging studies. They do not progress to cancer and usually require no followup or treatment. Solid kidney tumors can be benign, but are cancerous more than 90 percent of the time. What are some facts about kidney cancer?
What risk factors are associated with kidney cancer? The following associations may increase the risk of developing kidney cancer. * smoking What are the symptoms for kidney cancer? Many kidney tumors do not produce symptoms, but may be detected incidentally during the evaluation of an unrelated problem or during routine screening for people who are in high-risk categories (e.g. Von Hippel Lindau disease, tuberous sclerosis). Compression, stretching and invasion of structures near the kidney may cause pain (in the flank, abdomen or back), palpable mass, and blood in the urine (microscopic or grossly visible). If cancer spreads (metastasizes) beyond the kidney, symptoms depend upon the involved organ. Shortness of breath or coughing up blood may occur when cancer is in the lung, bone pain or fracture may occur when cancer is in the bone and neurologic symptoms may occur when cancer is in the brain. In some cases, the cancer causes associated clinical or laboratory abnormalities called paraneoplastic syndromes. These syndromes are observed in approximately 20 percent of patients with kidney cancer and can occur in any stage (including cancers confined to the kidney). Symptoms from paraneoplastic syndromes include weight loss, loss of appetite, fever, sweats and high blood pressure. Laboratory findings include elevated red blood cell sedimentation rate, low blood count (anemia), high calcium level in the blood, abnormal liver function tests, elevated alkaline phosphatase in the blood, and high blood count. In many cases, the paraneoplastic syndrome resolves after the cancer is removed. How is kidney cancer diagnosed? Unfortunately, there are no blood or urine tests that directly detect the presence of kidney tumors. When a kidney tumor is suspected, a kidney imaging study is obtained. The initial imaging study is usually an ultrasound or CT scan. In some cases, a combination of imaging studies may be required to completely evaluate the tumor. If cancer is suspected, the patient should be evaluated to see if the cancer has spread beyond the kidney (metastasis). An evaluation for metastasis includes an abdominal CT scan or MRI, chest X-ray and blood tests. A bone scan is also recommended if the patient has bone pain, recent bone fractures, or certain abnormalities on their blood tests. Additional tests may be obtained when indicated. Kidney cancer has the tendency to grow into the renal vein and vena cava. The portion of the cancer that extends into these veins is called "tumor thrombus." Imaging studies, particularly MRI, can help determine if tumor thrombus is present. What are the different stages of kidney cancer? The most commonly used staging system for kidney cancer was developed by the American Joint Committee on Cancer (AJCC). The most current version is the 2002 AJCC Staging System. This staging system includes the extent of the primary kidney tumor (T stage), the status of lymph nodes near the kidney (N stage) and the presence or absence of metastases (M stage). In kidney cancer, the lymph nodes near the kidney are referred to as regional lymph nodes. Clinical stage is based on radiographic imaging before surgery, whereas pathologic stage is based on the analysis of surgically removed tissue. Staging the cancer helps predict prognosis and survival. In general, cancers with higher T stage, lymph node metastasis, or distant metastasis have a worse prognosis and shorter survival rates, and these patients need to consider more aggressive treatments. Grade: Tumor grade is a subjective measure of how aggressive the tumor looks under the microscope; therefore, it is determined from a surgical specimen. Grade cannot be determined from radiographic imaging, blood tests or urine tests. Grade usually ranges from one to three or one to four, with higher numbers indicating a more aggressive tumor. Thus, higher grade implies a worse prognosis. Stage I: The tumor is confined to the kidney. There is no spread to lymph nodes or distant organs. Stage II: The tumor is locally invasive into the fat around the kidney or the adrenal gland above the kidney. There is no spread to lymph nodes or distant organs. Stage III: There are several combinations of T and N categories that are included in this stage. These include tumors of any size, with spread into the lymph nodes adjacent to the kidney or into the large veins leading from the kidney to the heart (venous tumor thrombus). This stage does not include tumores that invade into other adjacent organs or those with distant metastasis. Stage IV: There are several combinations of T, N, and M categories that included in this stage. This stage includes any cancers that have invaded into adjacent organs such as the colon (large bowel) or the abdominal wall, and those with distant metastases. Primary tumor (T): N - Regional lymph nodes M - Distant metastasis What are the treatment options for tumors that appear confined to the kidney? When the tumor appears confined to the kidney (a "localized" tumor), there are three main treatment options: tumor removal, tumor ablation and surveillance. Chemotherapy, hormone therapy and radiation therapy are not effective treatments for kidney cancer. Tumor removal: Tumor removal is considered the standard mode of therapy for most patients and is accomplished by performing a surgery called nephrectomy. Radical nephrectomy is surgical removal of everything within Gerota's fascia, including the whole kidney. Partial nephrectomy is surgical removal of part of the kidney (in this case, the part that contains the tumor). The goal of partial nephrectomy is to remove the entire tumor while preserving as much normal kidney tissue as possible. The kidney tissue that is conserved may prevent the need for dialysis if subsequent kidney damage occurs. Nephrectomy can be performed through a traditional incision (open surgery) or through several small incisions (laparoscopic or retroperitoneoscopic surgery). Open nephrectomy (radical and partial): Traditional open nephrectomy (partial or radical) is performed through a flank or abdominal incision. This incision is typically 10 to 20 inches in length and may include removal of a rib. In the past, open radical nephrectomy was considered the treatment of choice for tumors that appeared to be confined to the kidney. However, five- to 10-year follow up reveals that partial and radical open nephrectomies provide equally effective cancer treatment for many patients with a single, small, localized tumor. Therefore, partial and radical nephrectomies are now considered standard treatments. If you are interested in partial nephrectomy, it is important that you seek a urologist who has experience with this technique. As stated before, partial nephrectomy is performed to preserve as much normal kidney tissue as possible; however, its complication rate may be slightly higher than radical nephrectomy. Open partial nephrectomy should be considered in any patient with a small (ideally less than four centimeters) localized kidney tumor and a normal kidney on the opposite side. Open partial nephrectomy is usually the treatment of choice when radical nephrectomy results in either immediate dialysis or a high risk for subsequent dialysis, such as when the patient has a single functioning kidney, poor overall kidney function, medical or genetic diseases that threaten kidney function or bilateral kidney tumors. Partial nephrectomy is usually not recommended in patients with tumors that have any of the following characteristics: extension into the renal vein, close proximity to the main kidney vessels or factors that would make complete tumor resection unlikely. When the tumor cannot be safely removed by partial nephrectomy, radical nephrectomy is performed. If you elect to undergo a partial nephrectomy, there is always a risk that the entire kidney may need to be removed. Laparoscopic radical nephrectomy: Laparoscopic nephrectomy is performed using telescopes that are inserted into the abdominal cavity through small "key hole" incisions; however, a somewhat larger incision is often made to permit removal of an intact kidney. Nephrectomy performed by inserting the telescopes into the cavity that surrounds the kidney (rather than into the abdominal cavity) is called retroperitoneoscopic nephrectomy. Current data indicate that open and laparoscopic radical nephrectomies have similar complication rates and provide equally effective cancer treatment for patients with tumors that appear confined to the kidney. Compared to open radical nephrectomy, laparoscopic radical nephrectomy has less postoperative pain, shorter hospital stay and shorter recovery time. If you elect to undergo a laparoscopic radical nephrectomy, there is a low risk (usually less than five percent) that the surgeon will need to convert to an open nephrectomy (i.e., convert the "key hole" incisions to a larger incision). Not all patients are candidates for laparoscopic nephrectomy. Laparoscopic radical nephrectomy is best suited for small, localized tumors that have not invaded the lymph nodes or renal vein. Open nephrectomy is preferred in patients with severe scarring around the kidney or a history of extensive abdominal surgery. Surgeons who are experienced with retroperitoneoscopy may consider this approach in patients with a history of extensive abdominal surgery. Laparoscopic and retroperitoneoscopic partial nephrectomy: Information is accumulating on laparoscopic and retroperitoneoscopic partial nephrectomy, but the data on complications and cancer control is still premature. In general, this approach is best suited for relatively small, peripherally located tumors that are relatively easy to remove and for which reconstruction of the kidney is straightforward. Tumor ablation: Tumor ablation destroys the tumor without surgically removing it. Examples of ablative technologies include cryotherapy, interstitial radiofrequency ablation, high- intensity focused ultrasound, microwave thermotherapy and laser coagulation. Ablation can be accomplished during open surgery, laparoscopy, retroperitoneoscopy or percutaneously (through the skin). Since renal tumor ablation is a relatively new procedure, long-term results are unknown. However, ablation may be less invasive than nephrectomy and may be useful in patients who cannot tolerate a more extensive surgery. Tumor ablation may also permit a better chance of preserving kidney function in situations when multiple tumors are present. In general, tumor ablation is best reserved for older or somewhat frail patients. The risk to tumor recurrence with these approaches is somewhat higher than with surgical excision. Embolization: This is not a standard treatment option, but may be considered in patients who cannot tolerate tumor removal or ablation. It may also be considered as an adjunct to standard forms of treatment, especially when the tumor is actively bleeding. Embolization can stop the bleeding and permits physicians to stabilize the patient before surgery. Embolization is usually performed under sedation and is accomplished by advancing a long narrow catheter from a peripheral artery (such as in the groin) into the artery of the kidney. The catheter is used to deposit small embolic material particles in the vessels of the kidney. These particles block the flow of blood to the tumor and, therefore, stop active bleeding. Furthermore, without a blood supply, the tumor eventually dies. Since it is unclear whether or not embolization completely eliminates the tumor, it is not considered a primary form of therapy for kidney cancer. What are the treatment options for tumors that invade the renal vein or vena cava? When tumor invades into the renal vein or vena cava, open surgery is recommended to remove the affected kidney and to extract the tumor from the veins. It is important that you seek a urologist who has experience with this type of surgery. This is a major operation that requires isolation and clamping of the inferior vena cava, the largest vein in the body. After the blood flow is blocked the vein is opened and the tumor thrombus is extracted. The vein is then sutured closed. Sometimes embolization is performed before tumor removal. Embolization may also be considered in patients who cannot tolerate surgery. What are the treatment options for tumors that have spread to other organs? When the tumor has spread to other organs, there have traditionally been four primary treatment options: nephrectomy followed by immunotherapy, initial treatment with immunotherapy, clinical research trials and surveillance. More recently, a new category of treatment has been added, namely treatment with drugs that block the blood flow into the cancer (anti-angiogenic agents, see below). Immunotherapy: Immunotherapy stimulates your immune system to attack cancer. Hopefully, the immune system will eliminate cancer in much the same way it eliminates the flu. The most commonly used immunotherapy agents are interleukin-2 (IL-2) and interferon. Until recently, IL-2 was the only effective therapy approved by the Food and Drug Administration (FDA) for the treatment of metastatic kidney cancer. Approximately 20 percent of patients respond to immunotherapy with some degree of tumor regression. Approximately 5-7 percent of patients have complete cancer regression—most of those patients have been treated with the high dose IL-2 protocol. Many different immunotherapy regimens have been studied. One of the most effective regimens is high dose bolus IL-2, which requires inpatient hospitalization. During the initial hospitalization, intravenous IL-2 is administered over five days. The patient is usually allowed to go home for a rest period of five to10 days. Then, the patient is readmitted to the hospital for another five-day course of intravenous IL-2. The most common side effects of immunotherapy are similar to flu symptoms and include fever, chills, nausea, vomiting, diarrhea and fatigue. Other side effects include low blood pressure, fluid accumulation in the lungs (pulmonary edema), impaired liver function, impaired kidney function, mental status changes (such as confusion, agitation, disrupted sleep pattern), rapid heartbeat and irregular heartbeat. Most side effects are temporary and subside when the immunotherapy is stopped. To be a candidate for immunotherapy, the patient must be in good general condition, have adequate function of vital organs (such as the heart, lungs and kidneys) and have no brain metastasis. Immunotherapy is not effective against cancer in the brain. Before immunotherapy, patients must have tests to assess vital organ function and a scan to determine if brain metastases are present. Nephrectomy followed by immunotherapy or anti-angiogenic therapies: In patients with metastases, the best chance of survival is achieved by removing the affected kidney before administering immunotherapy. The kidney may be removed by open or laparoscopic surgery. This treatment option is only offered when the patient is a candidate for both nephrectomy and immunotherapy. Therefore, patients should not undergo any treatment until they have been evaluated by both an oncologist who specializes in immunotherapy and a urologic surgeon. Treatment should only be initiated after the surgeon and oncologist agree that the patient is a candidate for both nephrectomy and immunotherapy. Patients must be relatively healthy and the burden of disease must be limited. Initial treatment with immunotherapy: In some patients, surgery may be too risky. These patients may be treated initially with immunotherapy. If they respond adequately and if their medical condition improves, they may undergo surgical removal of the remaining tumor. Anti-angiogenic therapies: Tumors must stimulate the ingrowth of blood vessels to provide them with nutrients and oxygen. This process, also known as angiogenesis, is essential for a tumor to continue to grow and to metastasize to other areas of the body. Kidney cancers are very angiogenic and are known to be some of the most vascular tumors in the body. They do this by secreting a protein called vascular endothelial growth factor, or VEGF. VEGF acts on nearby blood vessels stimulating them to sprout new vessels to supply the tumor. Recently new drugs have been developed that block the action of VEGF, and thereby cause the vessels supplying the tumor to regress. This starves the tumor and slows it down. These are known as anti-angiogenic treatments. The 2 anti-angiogenic drugs that are now approved by the FDA for the treatment of patients with advanced kidney cancer are sorafenib (Nexavar) and sunitinib (Sutent). Recent studies show that these drugs can slow the progress of kidney cancer and allow patients to live longer. While a complete cure is still an uncommon event, this is still a step forward. These drugs are taken orally, but they can be associated with side effects including fatigue, hypertension, and skin rashes. But most patients are able to tolerate these drugs fairly well and appear to benefit from them. Clinical research trials: Research protocols are not available to all patients. If you are interested in finding out more about these protocols, ask your doctor, check with your local academic institution or search the Internet. There are many non-standard therapies that are being studied in research trials. Some of these therapies include cellular immunotherapy, tumor vaccines, gene therapy, stem cell transplants, anti-angiogenesis therapy, inhibitors of growth factors, etc. Although these therapies appear promising, they are still experimental and it is unclear whether or not they are effective treatments for kidney cancer. Radiation: Radiation therapy is not used to cure kidney cancer, but rather for alleviation of symptomatic metastasis. For example, the pain from bone metastases can be relieved by radiation to bone lesions. It may be used alone or in combination with other therapies. Surveillance: May be appropriate when any of the following are present: the kidney tumor has a low probability of being cancer; the patient cannot tolerate treatment; the patient has a short life expectancy (i.e., they are likely to pass away from other causes); or the patient does not want treatment. With lesions that have a low probability of being cancer, regular follow up with a physician is mandatory. Angiomyolipoma, a benign tumor, is the only kidney tumor that can be diagnosed by CT scan. Patients with angiomyolipoma may undergo surveillance with periodic imaging studies. However, embolization or surgical removal (preferably by partial nephrectomy) may be necessary when the angiomyolipoma is symptomatic, bleeding or greater than four centimeters in size. |
Overweight women more prone to breast cancer
Overweight women and those who show early signs of type 2 diabetes are more prone to advanced breast cancer, a study has revealed. The study, involving around 60,000 female subjects, found that women who are overweight, insulin-resistant or have high blood sugar levels are 50 per cent more likely to be diagnosed with the advanced forms of the disease. The research was conducted by a group of doctors from the University of Melbourne, Umea University in Sweden and the German Cancer Research Centre. Swedish women tracked by researchers between 1985 and 2005 were found to be cancer-free at the time of re cruitment and had their blood tested for glucose and insulin levels and other hormones associated with obesity and diabetes risk.
However, around 600 of them were later diagnosed with breast cancer, with those who showed early signs of diabetes more likely to develop the disease than those who showed no risk factors, it was found. Women, who were insulin resistant or overweight were less likely to be diagnosed with stage one breast cancers but were at greater risk of being diagnosed with stage two to four tumours, which are larger, said Ms Cust, a researcher. “In a way, it's a good thing that these risk factors are converging for all these diseases our society is afflicted with... because the answer is the same: do whatever you can to avoid being overweight or obese by having a healthy diet and being more phy sically active,” said Mr Graham Giles, Director of epidemiology at the Cancer Council Victoria. |
Combat Ovarian Cancer
An Edinburgh University study found an anti-oestrogen drug could help prolong patients' lives by up to three years. A hormone therapy treatment used to tackle breast tumours has also proved successful in combating ovarian cancer, according to research. It also delayed the need for some patients to undergo chemotherapy. The professor who led the research programme described its findings as an "important landmark" in the research and treatment of ovarian cancer. Professor John F Smyth said: "Despite intense scientific research over the past 20 years, there have been few new leads in our understanding of how this disease operates. "But this study suggests that the addition of hormone therapy to our treatment strategy could extend and improve the lives of women with cancer."
Hormone therapy Ovarian cancer affects one in 48 women, with almost 7,000 new cases being diagnosed in the UK every year. The current treatment involves surgery and chemotherapy, but most ovarian cancers return within two years. The results of the Edinburgh research, funded by Cancer Research UK, were published in Clinical Cancer Research. The treatment, known as Letrozole hormone therapy, has already been successful in tackling breast tumours. Track progress It turns off the supply of the hormone oestrogen, a substance which is essential for the growth of some cancers. The study involved 44 women who were sensitive to oestrogen and whose cancer had relapsed after surgery and chemotherapy. Scientists were able to track the progress of the tumours during treatment by looking at levels of a molecule in the blood which is secreted by ovarian cancer. A quarter of the women showed no tumour growth after six months of anti-oestrogen therapy, while 33% of the group most sensitive to oestrogen showed a positive response which allowed chemotherapy to be delayed. |
Understanding Lymphoma
Lymphoma is a type of cancer involving cells of the immune system, called lymphocytes. Just as cancer represents many different diseases, lymphoma represents many different cancers of lymphocytes—about 35 different subtypes, in fact. Lymphoma is a group of cancers that affect the cells that play a role in the immune system, and primarily represents cells involved in the lymphatic system of the body.
* The lymphatic system is part of the immune system. It consists of a network of vessels that carry a fluid called lymph, similar to the way that the network of blood vessels carry blood throughout the body. Lymph contains white blood cells called lymphocytes. Lymphocytes attack a variety of infectious agents as well as many cells in the precancerous stages of development. * Lymph nodes are small collections of lymph tissue that occur throughout the body. The lymphatic system involves lymphatic channels that connect thousands of lymph nodes scattered throughout the body. Lymph flows through the lymph nodes, as well as through other lymphatic tissues including the spleen, the tonsils, the bone marrow, and the thymus gland. * These lymph nodes filter the lymph, which may carry bacteria, viruses, or other microbes. The lymph nodes, or glands as they may be called, filter the lymph, which may on various occasions carry different microbial organisms. At infection sites, large numbers of these microbial organisms collect in the regional nodes and produce the swelling and tenderness typical of a localized infection. These enlarged and occasionally confluent collections of lymph nodes (so-called lymphadenopathy) are often referred to as "swollen glands." Lymphocytes recognize pathogens (infections and abnormal cells) and destroy them. There are 2 major subtypes of lymphocytes: B lymphocytes and T lymphocytes, also referred to as B cells and T cells. * B lymphocytes produce antibodies (proteins that circulate through the blood and lymph and attach to infectious organisms and abnormal cells). The combination attachment cell or antibody microbial organism essentially alerts other cells of the immune system recognize and destroy these intruders, also known as pathogens. * T cells, when activated, can kill pathogens directly. T cells also play a part in the mechanisms of immune system control, to prevent the system from inappropriate overactivity or underactivity. * After fighting off an invader, some of the B and T lymphocytes "remember" the invader and are prepared to fight it off if it returns. Cancer occurs when normal cells undergo a transformation whereby they grow and multiply uncontrollably. Lymphoma is a malignant transformation of either lymphocytes B or T cells or their subtypes. * As the abnormal cells multiply, they may collect in 1 or more lymph nodes or in other lymph tissues such as the spleen. * As the cells continue to multiply, they form a mass often referred to as a tumor. * Tumors often overwhelm surrounding tissues by invading their space, thereby depriving them of the necessary oxygen and nutrients needed to survive and function normally. * Because of their uncontrolled growth, lymphomas can encroach on and/or invade neighboring tissues or distant organs. * In lymphoma, abnormal lymphocytes travel from one lymph node to the next, and sometimes to remote organs, via the lymphatic system. * While lymphomas are often confined to lymph nodes and other lymphatic tissue, they can spread to other types of tissue almost anywhere in the body. Lymphoma development outside of lymphatic tissue is called extranodal disease. Lymphomas fall into 1 of 2 major categories. Hodgkin lymphoma (HL, previously called Hodgkin's disease) and all other lymphomas (non-Hodgkin lymphomas or NHLs). * These 2 types occur in the same places, may be associated with the same symptoms, and often have similar gross physical characteristics. However, they are readily distinguishable via microscopic examination. * Hodgkin disease develops from a specific abnormal B lymphocyte lineage. NHL may derive from either abnormal B or T cells and are distinguished by unique genetic markers. * There are 5 subtypes of Hodgkin disease and about 30 subtypes of non-Hodgkin lymphoma. * Because there are so many different subtypes of lymphoma, the classification of lymphomas is complicated and includes both the microscopic appearance and well-defined genetic and molecular rearrangements. * Many of the NHL subtypes look similar, but they are functionally quite different and respond to different therapies with different probabilities of cure. HL subtypes are microscopically distinct, and typing is based upon the microscopic differences as well as extent of disease. Lymphoma is the most common type of blood cancer in the United States. It is the sixth most common cancer in adults and the third most common in children. Non-Hodgkin lymphoma is far more common than Hodgkin disease. * In the United States, about 54,000 new cases of NHL and 7000 new cases of HL were diagnosed in 2004, and the overall incidence is increasing. * About 24,000 people die of NHL and 1400 of HL each year, with the survival rate of all but the most advanced cases of HL greater than that of other lymphomas. * Lymphoma can occur at any age, including childhood. Hodgkin disease is most common in 2 age groups: young adults aged 16-34 years and in older people aged 55 years and older. Non-Hodgkin lymphoma is more likely to occur in older people. |
Infectious Mononucleosis is Associated with Hodgkins Lymphoma in Young Adults
Researchers from Denmark and Sweden have clarified the relationship between documented Epstein Barr Virus (EBV) infectious mononucleosis and EBV associated Hodgkin’s lymphoma. They concluded that young adults with serologically documented EBV infection had an increased risk of EBV associated Hodgkin’s lymphoma but not EBV negative Hodgkin’s lymphoma. These results appeared in the October 2, 2003 issue of the New England Journal of Medicine.
It has been known for some time that young adults with infectious monocucleosis were at increased risk for the development of Hodgkin’s lymphoma. This risk has been estimated to be approximately one case of Hodgkin’s lymphoma per 1000 individuals with infectious mononucleosis. However, it is unknown if there is truly a causal relationship between EBV virus infection and Hodgkin’s lymphoma. These authors compared the incidence rates of Hodgkin’s lymphoma in a cohort of over 17,000 patients with serologic evidence of infectious mononucleosis to a cohort of over 24,000 individuals without evidence of infectious mononucleosis. They used molecular techniques to determine the presence of EBV virus in biopsy specimens of those with Hodgkin’s lymphoma. The researchers reported that “Only serologically confirmed infectious mononucleosis was associated with a persistently increased risk of Hodgkin’s lymphoma.” This increased incidence (relative risk = 4.0) was related only to EBV positive and not EBV negative Hodgkin’s lymphoma. “The estimated median incubation time from mononucleosis to EBV-positive Hodgkin’s lymphoma was 4.1 years.” |
Who gets ovarian cancer?
A woman can inherit an increased risk for this disease, particularly if a "first degree" relative (a mother, sister or daughter) has or had ovarian, breast or colon cancer. In fact, if she has a strong family history of ovarian cancer, she is more likely to develop the disease at an early age (younger than 50). Other risk factors include: Ashkenazi (Eastern European) Jewish ethnicity, if the condition has already affected one or more family members Unfortunately, there is no reliable screening tool available for ovarian cancer. If you have any unusual symptoms, consult with your health care professional. Diagnosis starts with a pelvic exam and Pap smear, a relatively painless test that involves taking a scraping of cells from your cervix and examining them under a microscope. Although the Pap doesn't detect ovarian cancer, it may detect cancer cells that have migrated to the uterine cervix from the ovaries or abnormal cells in the uterine cervix. After the Pap smear, other tests your health care professional may perform include: CA-125 blood test, which can signal the presence of advanced ovarian cancer; however, experts do not consider this a stand-alone, reliable test. This test is used to determine the level of a tumor marker called CA-125, but is not a screening option because it is unreliable. For example, CA-125 levels are normal when ovarian cancer is confined to the ovaries in half of postmenopausal women. Some ovarian cancers do not produce enough CA-125 to cause a positive result. Other benign conditions may increase CA-125 levels. This test is most effective in women who have been treated for ovarian cancer to determine if cancer has recurred. abdominal or transvaginal ultrasound, sound waves are used to distinguish fluid-filled cysts from solid ones. If cancer is suspected, the surgeon usually removes the entire affected ovary to ensure that all potentially abnormal areas are removed. A pathologist evaluates the tissue and if cancer is confirmed, typically the second ovary, the uterus and the fallopian tubes are removed. |
Circulating Tumor Cells Can Reveal Genetic Signature Of Dangerous Lung Cancers
Massachusetts General Hospital (MGH) investigators have shown that an MGH-developed, microchip-based device that detects and analyzes tumor cells in the bloodstream can be used to determine the genetic signature of lung tumors, allowing identification of those appropriate for targeted treatment and monitoring genetic changes that occur during therapy. A pilot study of the device called the CTC-chip will appear in the July 24 New England Journal of Medicine and is receiving early online release. "The CTC-chip opens up a whole new field of studying tumors in real time," says Daniel Haber, MD, director of the MGH Cancer Center and the study's senior author. "When the device is ready for larger clinical trials, it should give us new options for measuring treatment response, defining prognostic and predictive measures, and studying the biology of blood-borne metastasis, which is the primary method by which cancer spreads and becomes lethal."
The researchers tested blood samples from patients with non-small-cell lung cancer (NSCLC), the leading cause of cancer death in the U.S. In 2004, MGH researchers and a team from Dana-Farber Cancer Institute both discovered that mutations in a protein called EGFR determine whether NSCLC tumors respond to a group of drugs called TKIs, which includes Iressa and Tarceva. Although the response of sensitive tumors to those drugs can be swift and dramatic, eventually many tumors become resistant to the drugs and resume growing. The CTC-chip was used to analyze blood samples from 27 patients -- 23 who had EGFR mutations and 4 who did not -- and CTCs were identified in samples from all patients. Genetic analysis of CTCs from mutation-positive tumors detected those mutations 92 percent of the time. In addition to the primary mutation that leads to initial tumor development and TKI sensitivity, the CTC-chip also detected a secondary mutation associated with treatment resistance in some participants, including those whose tumors originally responded to treatment but later resumed growing. "Patients found to have resistance mutations before treatment probably won't benefit as much or as long from single-agent TKI therapy as those without such baseline mutations," says Lecia Sequist, MD, MPH, of the MGH Cancer Center, a co-lead author of the NEJM paper. "For those patients we may need to consider other modes of therapy, including combinations+ of targeting agents or second-generation TKIs that can overcome the most common resistance mutation." Blood samples were taken at regular intervals during the course of treatment from four patients with mutation-positive tumors. In all of those patients, levels of CTCs dropped sharply after TKI treatment began and began rising when tumors resumed growing. In one patient, adding additional chemotherapy caused CTC levels to drop again as the tumor continued shrinking. Throughout the course of therapy, the tumors' genetic makeup continued to evolve. Not only did the most common resistance mutation emerge in tumors where it was not initially present, but new activating mutations -- the type that causes a tumor to develop in the first place -- appeared in seven patients' tumors, indicating that these cancers are more genetically complex than expected and that continuing to monitor tumor genotype throughout the course of treatment may be crucial. "If tumor genotypes don't remain static during therapy, it's essential to know exactly what you're treating at the time you are treating it," says Haber. "Biopsy samples taken at the time of diagnosis can never tell us about changes emerging during therapy or genotypic differences that may occur in different sites of the original tumor, but the CTC-chip offers the promise of noninvasive continuous monitoring." Haber is the Kurt J. Isselbacher/Peter D. Schwartz Professor of Medicine at Harvard Medical School. |
Breast Cancer in Teens
Breast cancer is very rare in teenagers. One in every 231 women under the age of 40 gets breast cancer, but almost all of those women are at least thirty years old. Even though teens hardly ever get breast cancer, it's a good idea to learn about your breasts and how to check for any signs of problems. If you ever do get breast cancer, finding it early can make all the difference.
You should also examine your own breasts once a month for any changes or signs of breast cancer or other problems. This is called breast self exam or BSE for short. Try to do it shortly after you have your period, since it's common for breasts to get a bit swollen and sore just before or during your period. Breast self-exam is really easy and only takes a few minutes. Here's how to do it: Look in the mirror. First stand with your arms at your sides, then raise your arms above your head. If you're in your teens, your breasts are probably growing and changing. Look for any big changes, not just in size but also in color and shape. Look for changes in your nipples, too. Gently squeeze each nipple and check for any kind of discharge. Feel each breast for any lumps or other changes. Some women do this part when they're in the shower, but you can also do it while you're standing in front of the mirror or when you're sitting down. Use your right hand to feel your left breast and your left hand to feel your right breast. Press firmly. Start at the nipple and work your way toward the edge of your breast, moving in bigger and bigger circles until you've covered your whole breast. Feel for lumps or anything that just feels different than it felt the last time you checked. Now lie down and do the same thing you just did in step three. Now, pay attention to this part. If you find a lump or have some nipple discharge or something about your breasts seems different, it does NOT mean you have breast cancer. Don't panic. You'll want to get it checked out by a doctor just to make sure, but there are lots of other things that could be causing those symptoms. Especially when you're a teenager, your changing hormones can cause lumps and other changes in your breasts. It's also normal for your breasts to feel tender or sore sometimes. |
How Broccoli Protect You from Cancer
| Broccoli, though an unpopular vegetable(especially with children), is now known to reduce the risk of cancer. A recently published scientific study sheds light on why men who eat a lot of broccoli are less likely to develop prostate cancer. Scientists have already observed that diets rich in cruciferous vegetables -- including broccoli, cauliflower, cabbage, Brussels sprouts, bok choy and kale -- may reduce the risk of prostate cancer and other chronic disease. But the new research by scientists at Britain's Institute of Food Research, is the first attempt to show how that works in a clinical study involving people, as opposed to animals or cell models.
The researchers took samples of prostate gland tissue from the men at the start of the study, at six months and at 12 months, to monitor changes in genes linked to cancer. "There were more changes in gene expression in men who were on the broccoli-rich diet than on the pea diet, and these changes may be associated with the reduction in the risk of developing cancer," said a statement by the Public Library of Science, which published the work Wednesday in its online journal PLoS ONE. "The results of the study suggested that relatively low amounts of cruciferous vegetables in the diet -- a few portions per week -- can have large effects on gene expression by changing cell signalling pathways," the statement said. The signalling pathways are the routes by which information is transmitted to the nucleus of the cell where gene expression occurs. "Other fruits and vegetables have been shown to also reduce the risk of prostate cancer and are likely to act through other mechanisms," said lead researcher Richard Mithen. "Once we understand these, we can provide much better dietary advice in which specific combinations of fruit and vegetable are likely to be particularly beneficial. "Until then, eating two or three portions of cruciferous vegetable per week ... should be encouraged." Prostate cancer is the most common form of non-skin cancer affecting men in western countries. |
Herpes Cause Brain Cancer
The deadliest and most common type of brain cancer has a strange bedfellow: cytomegalovirus, a kind of herpes present in about 80 percent of the U.S. population. Now scientists are exploiting this coincidence to treat the cancer with a vaccine that targets the virus and slows tumor regrowth. In 2002 scientists showed that cytomegalovirus, or CMV, was active in the brain tumors but not the surrounding healthy tissue of all 27 patients they tested who had glioblastoma multiforme. CMV is dormant and undetectable in most people. Neuroscientist Duane Mitchell of Duke University Medical Center and his colleagues confirmed in 2007 that CMV is active in at least 90 percent of glioblastoma tumors. Now Mitchell’s team has developed an experimental vaccine that triggers the immune system to attack CMV, thereby attacking its tumor tissue home. As reported at the American Society of Clinical Oncology meeting in June, the vaccine, together with radiation and chemotherapy, prevented the brain tumor from reemerging after surgery for 12 months as compared with the typical six to seven months with no vaccine. Patients’ average life span increased from 14 months to more than 20.
“Most evidence to date does not support CMV being a cancer-causing virus,” Mitchell says. Don Diamond, a virologist at the City of Hope Cancer Center near Los Angeles, agrees: his extensive research on CMV and cancer has convinced him the virus does not cause tumors. But for patients it does not matter whether the connection between herpes and brain cancer is causal or not—the vaccine appears to work. Mitchell hopes to have the vaccine ready for market in a few years. |
Tumor Cells Break Free
When tumor cells acquire the capacity to move around and invade other tissues, there is a risk of metastases and cancer treatment becomes more difficult. At the Institut Curie, CNRS Director of Research Philippe Chavrier and his group have just discovered how breast cancer cells break the bonds that tether them to the tumor. The basement membrane around the mammary gland is a barrier to the spread of cancer cells. Three proteins in the tumor cells transport enzymes needed to perforate this barrier, and another protein puts these enzymes in the right place. These discoveries, published in the 16 June 2008 issue of The Journal of Cell Biology and in Current Biology on 8 July 2008, shed light on the early mechanisms of the formation of metastases in certain breast cancers. These findings constitute an essential step in the quest for the early identification of highly invasive tumors, or even the blocking of formation of metastases.
When tumor cells break loose Tumor cells accumulate errors, become totally anarchic, and flout all the rules. Some even become detached from the tumor through complex and poorly understood mechanisms. The Membrane and Cytoskeleton Dynamics Group headed by Philippe Chavrier(1) (UMR 144 CNRS/Institut Curie) has now shed new light on the way cells, in this case breast cancer cells, escape their shackles. The mammary gland is separated from the neighboring tissue by the basement membrane, which the tumor cells will have to cross before continuing on their way. The cell first forms protrusions called invadopodia and anchors them in the basement membrane. These “feet” provide everything needed to breach the membrane. The tumor cells produce a whole range of proteases that degrade the proteins of the extracellular matrix that hems them in, part of which is the basement membrane. These proteases cut a hole in the basement membrane through which the cells can escape. In a first publication, the researchers used a model of metastatic breast cancer cells to show that the proteins sec3, sec8 and IQGAP1 transport vesicles containing proteases to the invadopodia. Without sec3, sec8 and IQGAP1 the vesicles cannot be fastened to the ends of the invadopodia and so the cells fail to escape into the neighboring tissue. Before the proteases can degrade the membrane, they must first be released from the vesicles. In a second publication, Philippe Chavrier and colleagues show that the protein Vamp7 fuses protease-containing vesicles with the membrane of tumor cells. Only then can the proteases at the ends of the invadopodia progressively erode the basement membrane of the mammary gland. Inactivation of Vamp7 greatly reduces the ability of the breast cancer cells to degrade the extracellular matrix. So tumor cells can only escape from the mammary gland by accomplishing a whole series of modifications. Philippe Chavrier and his group have shown how they hijack cellular mechanisms to leave their original tissue, after which they can spread throughout the body and form metastases. These discoveries may help to explain why certain breast cancers are more aggressive than others, or even to identify highly invasive tumors at an early stage. It is also conceivable that tumor invasion could be blocked by acting on the underlying mechanisms identified by Philippe Chavrier and colleagues. |
Smokeless Tobacco Products Do Raise Cancer Risk
Smokeless tobacco products (STPs), which include products such as snuff and chew tobacco, do increase the user's risk of cancer — just not as much as smoking does. So say researchers who examined worldwide patterns of STP use and the associated risk of cancer. Reporting in the July issue of The Lancet Oncology, a team led by Dr. Paolo Boffeta, of the International Agency for Research on Cancer, in France, noted that STPs contain more than 30 carcinogens, including nitrosamines and metals.
Cancer rates associated with STPs vary between countries. For example, more than 50 percent of oral cancers in India and Sudan are attributable to STPs, compared with 4 percent in the U.S. The findings are published in a special edition of the journal devoted to lung cancer. Overall, studies do support a strong association between STPs and cancer, said the authors, who did not recommend smokeless tobacco as a substitute for smoking. "We do not intend to address explicitly the use of smokeless tobacco to reduce the risk from tobacco smoking — e.g., by promoting smokers to switch to smokeless products or by introducing these products in a population where the habit is not prevalent," the researchers concluded. "Nevertheless, several conclusions can be reached based on the available data ... the risk of cancer, especially that of oral and lung cancer, is probably lower in smokeless tobacco users in the USA and northern Europe than in smokers, and the risk of cancer is higher in smokeless tobacco users than in non-users of any form of tobacco," the team wrote. "Available data for a possible benefit of switching from smoking to smokeless tobacco come from few studies and models from the USA and Sweden." Another article in the July issue of The Lancet Oncology suggests that DNA screening for certain biomarkers could help assess lung cancer risk in people exposed to secondhand smoke. Many carcinogens in cigarette smoke are known to cause DNA lesions called DNA adducts and many carcinogens are known to leave unique signatures on cancer-related genes in the form of specific mutations at specific locations, noted Dr. Ahmad Besaratinia and Dr. Gerd Pfeifer, of the Beckman Research Institute of the City of Hope National Medical Center in Duarte, Calif. They noted that a technique called DNA-lesion footprinting, in conjunction with mutagenicity analysis, is currently used to find carcinogen signatures. They proposed this technique be used in cancer-relevant genes, which are commonly mutated in smoke-related lung cancer. In fact, this method has already been used successfully to find adducts connected with various smoke-derived carcinogens, the researchers said. |
Gastric bands may reduce cancer risk
Obese women who have weight loss surgery dramatically reduce their chances of getting cancer, a major new study shows. The procedures include gastric band surgery, which the television presenter Fern Britton admitted earlier this month is behind her recent weight loss. Researchers found that having the surgery can reduce the likelihood of being diagnosed with some cancers by up to 80 per cent. Obesity is known to raise the risk of developing many types of cancer, including breast, colon, and kidney cancer, as well as other diseases like diabetes. The study looked at 1,035 morbidly obese patients who underwent weight loss surgery between 1986 and 2002, and compared their health with almost 6,000 who did not. Patients who had the operation lost up to 70 per cent of their excess weight and were also much less likely to be subsequently diagnosed with cancer, the research shows. Those who had the surgery were 85 per cent less likely to develop breast cancer, the most common form of the disease in women, and 70 per cent less likely to be diagnosed with colon or pancreatic cancer.
"The relationship between obesity and many forms of cancer is well established," said Dr. Christou. "This is one of the first studies to suggest that (weight loss) surgery might prevent the risk of cancer for a significant percentage of morbidly obese people." Dr Christou said that because obesity affects the body in many ways there was no single reason why the surgery cut the risk of cancer. However, he pointed to research which suggests that excess body fat increases hormone production, a major risk factor for breast and colon cancer. Obesity is measured using the body mass index (BMI), which calculates a person's weight in comparison to their height. A BMI of between 20 and 25 is considered as normal weight, while people classed as morbidly obese have a BMI of more than 40. |
New Drug Slows The Growth Rate of Thyroid Cancer
| An experimental drug that inhibits tumor blood vessel formation slows the progression of metastatic thyroid cancer in some patients, an international study finds. Of the 93 patients with rapidly progressing cancer, 49 had a positive response to treatment with motesanib diphosphate. Of those 49 patients, 14 percent had their tumors shrink and 35 had their tumors stabilize for more than 24 weeks. Median progression-free survival was about 40 weeks. Genetic analysis of 25 patients revealed that drug response was better in those with a mutation known as BRAF V600E in their tumors than in those without the mutation. Further research into this genetic connection is needed, the researchers said.
"This is the first of the various thyroid cancer trials to identify specific mutations that might allow us to individualize or personalize therapy," he said. The study, published in the July 3 issue of the New England Journal of Medicine, was funded by drug maker Amgen Inc. Motesanib diphosphate — a VEGF inhibitor — targets a protein called vascular endothelial growth factor (VEGF), which plays a critical role in the formation of new blood vessels that allow tumors to grow and spread. Currently, there are few treatment options for metastatic thyroid cancer. "There is no standard accepted chemotherapy for advanced metastatic differentiated thyroid cancer, and response rates have typically been 25 percent or less," Sherman said. "Most patients are not treated with systemic chemotherapy, because the limited benefit rarely justifies the side effects. Treatment of thyroid cancer has been a completely unmet need." |
Robot’s are better cancer surgeon!!!
There is a revolution going on in prostate cancer surgery over the past several years since the introduction of robot assisted surgery in 2000. But the question that has not been answered to date in a meaningful way is whether or not all the hype about the robot is in fact born out by the evidence. A recent article in the Journal of Clinical Oncology (JCO), along with an accompanying editorial, suggests that the advantages of the robot may be real in some respects, but may not be so great when it comes to the most important outcome, which is whether or not a man’s prostate cancer is effectively treated. Where to get prostate cancer surgery is one of the more common questions I am asked by people who ask my advice.
That’s part of the hype that can come along with any new procedure. You learn as a doctor that sometimes what seems so new and special may not be so new and special after all. Just more “space age,” more “gee whiz”, more “fancy.” But not necessarily better. I have asked some of my expert urology colleagues—the type that deal with urology related issues of national interest—who they think the best prostate cancer surgeons are. They give me a list, and frequently these surgeons do the traditional “open” prostate operation. They are not all using the robot. When I ask my surgical friends why this is, they tell me very straightforwardly that having a robot doesn’t make up for the experience of a surgeon who does a lot of open prostate cancer operations. Nonetheless, the medical arms race continues. So what does the evidence say? The JCO article looked at Medicare data from 2003 to 2005, and examined the claims records of about 2700 men who had either a robot-assisted surgery or a traditional open operation during that time. They found that the men who underwent the robot procedure had shorter hospital stays after surgery (1.4 compared to 4.4 days) and fewer complications (29.8% vs. 36.4%). However, the researchers also found that the odds of requiring further treatment within the 6 months after the surgery (meaning that the prostate specific antigen levels, a marker of complete resection of the prostate and possibly cancer containing tissue, didn’t fall low enough) was 27.8% for the men who had robotic surgery compared to 9.1% of the men who had the standard operation. In plainer words, over 1 out of 4 men failed to get an adequate resection of their cancer with the robot compared to about 1 out of 11 men who underwent the open procedure. The men who underwent robot surgery also had a higher incidence of strictures (scarring) of the urethra after the surgery compared to the men with the open procedure. This meant more difficulty urinating and more chances they would have to undergo additional procedures over time which could result in further discomfort and a higher chance of incontinence. One important cautionary note about these numbers is that the men who underwent robotic surgery tended to be older and had a higher number of other serious medical conditions, so one would expect they would be at greater risk of problems. The study found just the opposite. The study also found that there was a significant shift in urology practice over the two years of the study, with the percentage of men treated with the open procedure dropping from 82% to 66.1%, and the number of men treated with the robot increasing from 12.1% to 31.4%. Clearly, the robot is catching the fancy of both doctors and patients. This study wasn’t ideal, as the authors pointed out, since the information was gleaned from Medicare claims data. There is a lot about these men that the researchers couldn’t determine, and this was not a randomized trial which hopefully would eliminate differences between the two groups. That said, however, this is at least a study that gives us some idea of the differences in the benefits and risks of the two procedures. The authors also point out that “open radical prostatectomy is preformed through a relatively small incision that is infrequently associated with significant pain”, and that length of sty in the hospital for the open procedure are relatively short, averaging 1 to 3 days at high volume referral centers. “Nevertheless, many patients intuitively perceive minimally invasive approaches to reduce complications compared with conventional open operations and prefer them due to smaller incisions requiring less analgesics and shorter hospital stays even at greater costs.” But you can’t ignore the recurrence data, which is significantly higher in the robot patients as well as the risks of becoming incontinent because of the strictures in the urethra postoperatively. The authors also point out that doctors who do a lot of robotic surgery do have lower complication rates, fewer strictures and less risk of salvage therapy at 6 months. The same, however, is also true for doctors who do a lot of open procedures. What is the “right” number of surgeries your doctor should do in order to demonstrate they are good at either of these operations? For robotic surgery, the paper says your doctor should have done at least 40 to 150 robotic surgeries before they do one on you. They also say that in a recent survey, 37% of urologists “reported doing fewer than 11 radical prostatectomies per year, while 84% reported doing fewer than 31 per year. Consequently, the learning curve may be extended for years. Paradoxically, there is no formal certification process…Surgeons may perform the procedure after completing brief courses lasting 2 days or less.” My friends, I urge you to ask your doctor about their qualifications and the number of procedures—both open and robotic—they perform a year and how many in their career. If the answers don’t add up to a lot, then find someone who does have the experience you want and you need. In an editorial published in the same issue of the Journal, a urologist from the Mayo Clinic points out that the numbers of complications in the “open” group is much higher than that seen in centers that do a high volume of the traditional radical prostatectomy, or open procedure. The length of stay in these centers is also much less than that reported in this paper, on the order of two days as opposed to the four days reported in this study. This doctor also points out that the long term recurrence and survival results from open surgery are well documented and well known, while similar statistics for the robotic surgery don’t exist since the procedure is so new. He concludes, “Currently, open technique is the state-of-the-art procedure in experienced hands, as the long term results for (robotic surgery) do not exist. The published literature fails to answer whether (robotic surgery) meets ‘quality standards.’” So what do you do? What this paper and my discussions with my experienced colleagues tell me is that robotic surgery remains an option for prostate cancer surgery, but it is only an option. If you are going to drive down the street and pass by the world expert because they don’t do robotic surgery, I would think twice. Experience clearly matters when you are having your cancerous prostate removed, and I suspect that a highly experienced surgeon who does open surgery is every bit as good as a highly experienced robot surgeon. Just remember: the operative word here is “experienced.” Which leads me to another observation, which I have also discussed with several colleagues recently. Experience counts, as noted above. The way you find out about experience is to ask the doctor how many procedures they have performed in a week, or a year, or in their career. Increasingly, we hear back from people that when they ask their doctor how many of these robotic operations they do, the answer is frequently in the hundreds if not over one thousand. I guess that’s possible, but some of us are beginning to question some of those numbers, especially from young doctors. There simply aren’t enough prostates to go around. Yes, the world experts have those kinds of numbers, but not a whole lot of doctors are world experts. So when you hear a number, just keep in the back of your mind that there just may some “number inflation” going on here. Unfortunately, there is no way for you to confirm the accuracy of a doctor’s reported experience. Perhaps it is time for the hospitals—when they certify doctors to perform certain procedures—to determine accurately how many procedures of a certain type they have performed over the past year or so as part of the credentialing process. One thing is clear, however, and that is if your doctor doesn’t do a lot of either type of operation, experts would advise you to find one that does. This is simply a procedure where research has shown that “practice makes perfect.” |
How to Avoid Melanoma
This time of year women are anxious to get to the beach to get that perfect tan. Of course, tanning is not limited to summer since a lot of women go to tanning beds all year round to keep that perfect tan. Most people know tanning beds and too much sun is dangerous, yet they still do it. Of course everyone knows to use the right sunscreen but do they use enough? According to Glamour magazine, the answer is no and that is skin cancer waiting to happen. A young woman wrote in to Glamour to warn other women how deadly skin cancer is if not found and treated early enough. This young woman was only 28 years old when she found a lesion on the top of her head. She went to the doctor and found out it was the deadliest type of skin cancer, Melanoma. I read her story in Glamour and instantly thought of my sister because she goes to a tanning bed all year round and, when she has the time, goes to the beach to lay out in the sun. Sure she uses sunscreen but I don't think she uses enough. It's a scary thing to think that lying out in the sun or using a tanning bed can kill you, but it's true.
After more than 20 surgeries, several rounds of immunotherapy, and seven weeks of radiation, this young woman died at the young age of 28 just because she did not know she had melanoma and did not get it found and treated early enough. Don't let this happen to you! Even those tiny moles and freckles you might have could turn into skin cancer if out in the sun or in a tanning bed too long without protecting yourself with sunscreen. You need to check those moles and freckles and see a doctor immediately if you think you might have skin cancer or even if there is a chance for it in the future. Better to be safe than sorry. What You Need to Know about Sunscreen You also need to know the rules of sunscreen before going to the beach or to that tanning bed. Make sure you have a sunscreen with SPF 30 or higher, to fight UVB rays. Also make sure your sunscreen contains ingredients like zinc, oxide, titanium dioxide, oxybenzone or abobenzone, or Mexoryl to block UVA rays. Make sure you use it everywhere such as your face, neck, the V of your chest, your legs, the backs of your hands, and any other area that is not covered. This should be as routine as brushing your teeth in the morning. This is serious stuff and if you do not listen you could pay with your life. When it comes to using sunscreen there are lots of different options you can choose from. You can try the stick, wipes, or lotion and you should use a squirt about the same length as your thumb to cover your face, neck, chest and hands. For your entire body you need at least two tablespoons which is one ounce per application. Like I said it is better to be safe than sorry so please make sure to use enough sunscreen to avoid getting skin cancer. You can go to this website and read this young woman's story she shared with Glamour before she died of this horrible disease. You can also take the two minute skin cancer test to avoid this deadly disease. Be careful in the sun and at the tanning beds. Just because the tanning bed isn't real sunlight, it can still cause cancer. Please send this article to a friend or relative who might be at risk, it could save their life! |
