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duminică, 5 august 2012

Critical Tumor Suppressor Identified For Cancer

Scientists from the Florida campus of The Scripps Research Institute have identified a protein that impairs the development and maintenance of lymphoma (cancer of the lymph nodes), but is repressed during the initial stages of the disease, allowing for rapid tumor growth.

While the study, published in the journal Cell, largely focuses on the role of this new tumor suppressor in lymphoma induced by Myc oncoproteins (the cancer-promoting products of Myc oncogenes), the authors show this circuit is apparently operational in all human tumors with MYC involvement, which is more than half of all human tumor types.

"This opens a new therapeutic avenue to exploit for cancers with Myc involvement - including relapsed metastatic tumors and refractory tumors, those that have not responded to treatment," said John Cleveland, a Scripps Research professor and chair of the Department of Cancer Biology, who led the study.

The Myc family of oncoproteins (c-Myc, N-Myc, and L-Myc) regulate critical pathways that contribute to tumors; c-Myc expression, which is activated in human Burkitt lymphoma, is sufficient to induce the growth of several tumor types in animal models.

In the new study, the scientists focused on precancerous and malignant Myc-expressing B cells, part of the immune system affected in human lymphoma. Using transgenic animal models, Cleveland and his team, led by the efforts of senior postdoctoral fellow Robert Rounbehler, showed that Myc-directed repression of a protein called tristetraprolin (TTP/ZFP36) was important for both the development and maintenance of cancer. The suppression of TTP is a hallmark of human cancers with MYC involvement, Cleveland noted.

The scientists' results showed that overriding this pathway by forced expression of TTP more than doubled the lifespan of Myc transgenic mice. Strikingly, Rounbehler discovered that re-introduction of TTP into Myc-driven lymphoma totally disabled these tumors, indicating an important therapeutic target.

The authors showed that Myc regulates hundreds of genes that contain adenylate-uridylate-rich elements (AU-rich elements), which play an important role in RNA stability and are found in many messenger RNAs (mRNAs) that code for oncogenes, nuclear transcription factors, and cytokines. AU-rich elements direct the mRNA for degradation; they are thought to be vital for controlling expression during cell growth.

"Myc regulates the expression of select AU-binding proteins to control the destruction of certain mRNAs," Cleveland said. "Also, our study strongly suggests that other AU-binding proteins may also, in fact, function as tumor suppressors in other cancers."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our lymphoma / leukemia / myeloma section for the latest news on this subject. The first author of the study, "Tristetraprolin is a Tumor Suppressor That Impairs Myc-Induced Lymphoma and Abolishes the Malignant State," is Robert J. Rounbehler of Scripps Research. Other authors include Mohammad Fallahi, Chunying Yang, Meredith A. Steeves, Weimin Li, Joanne R. Doherty, and Franz X. Schaub of Scripps Research; Sandhya Sanduja and Dan A. Dixon of the University of South Carolina; and Perry J. Blackshear of the National Institute of Environmental Health Sciences.
The study was supported by the National Institutes of Health (grant numbers DK44158, CA167093, F32-CA115075, and CA134609), ThinkPink Kids Foundation, the State of Florida, the National City Charitable Contributions Committee, the Glenn W. Bailey Postdoctoral Fellowship, and the PGA National Women’s Cancer Awareness Days.
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First Genome-Wide Analysis Of Peripheral T-cell Lymphomas Identifies 13 Novel Alterations In This Aggressive Blood Cancer

Breast Cancer Slowed By Plant-Based Compound In Mouse Model

The natural plant compound phenethyl isothiocyanate (PEITC) hinders the development of mammary tumors in a mouse model with similarities to human breast cancer progression, according to a study published in the Journal of the National Cancer Institute.

Edible plants are gaining ground as chemopreventative agents. PEITC has shown to be effective as a chemopreventative agent in mice for colon, intestinal, and prostate cancer, by inducing apoptosis.

In order to determine the efficacy of PEITC in mammary tumors in mice, Shivendra V. Singh, Ph.D., of the University of Pittsburgh Cancer Institute and colleagues, placed mice on two diets: a control diet, and a diet supplemented with PEITC for 29 weeks. The researchers performed histopathological assessments, and measured the incidence and size of the mammary tumors, along with cell proliferation, apoptosis, and neoangiogenesis, which were determined in tumor sections.

The researchers found that administering PEITC for 29 weeks was linked with a 56.3% reduction in mammary carcinoma lesions greater than 2mm. "Although PEITC administration does not confer complete protection against mammary carcinogenesis, mice placed on the PEITC-supplemented diet, compared with mice placed on the control diet, clearly exhibited suppression of carcinoma progression," the authors write. PEITC was also well-tolerated. Since chemoprevention trials are both expensive and time-consuming and necessitate years of follow-up, the authors feel that, "The discovery of biomarker(s) associated with exposure and activity is critical for clinical development of promising cancer chemopreventative agents." This study was able to identify certain biomarkers that may be useful in future clinical investigations.

The authors also point out certain limitations of their study, namely that the results may be different in humans than in mice; also both the relevance of other altered proteins from PEITC and the mechanism by which PEITC causes apoptosis are unclear.

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Self-Help For Men Supporting Their Spouses Through Breast Cancer

Male partners of breast cancer patients are likely to take a pass on spousal support groups in favour of exercise or an evening out with friends to cope with stresses associated with the disease, according to new research from the University of Alberta.

Faculty of Nursing professor Wendy Duggleby said spouses of women with breast cancer have unique needs when it comes to retaining a sense of hope at a time when they provide important physical and emotional support for their partners.

"There are many programs out there for women, but for men a lot of support mechanisms are support groups, and it was very clear from the participants in our study that's not what they wanted," said Duggleby, Endowed Nursing Research Chair in Aging and Quality of Life.

"What these spouses needed was help finding ways to do things for themselves to help reduce their stress."

The study, published in this month's Oncology Nursing Forum, is the first to look at the hope experience of male spouses of breast cancer patients, said Duggleby. Ensuring men have a sense of hope not only helps decrease their risk for depression, it helps their partners, too.

"If their husbands lose hope, the wives are really, really worried about them and they often lose hope themselves. For women with breast cancer, it actually helps with their own quality of life if we can do something to help the men. It's very interconnected."

In the study, men in Edmonton and Saskatoon were surveyed about hope and their ability to cope with their spouses' disease. Many reported that their partner's diagnosis was their darkest day, and that they struggled to find hope and balance after juggling career, added household duties and care.

Fighting back

Warren Tasker called upon a fighter's will when his partner Gwen Borowski was diagnosed with breast cancer on March 1, 2007. He made Borowski's needs a priority and together they put everything toward the fight, learning all they could about the disease and pressing physicians to explain treatment in detail.

"It was all I thought about, night and day," said Tasker, an Edmonton-based writer and editor, who wrote about the experience for the Canadian Breast Cancer Foundation - Prairies/NWT chapter.

After years of writing about boxing for the Edmonton Journal, he took up the sport to cope with stress, in addition to his regular running and cycling routine.

"I was getting hit and I was getting to hit back. It felt good - it felt really good," he said. "You need an outlet, you need to find something to release all the pent-up frustration, the fear, the apprehension, the anxiety."

In study interviews, filmed and posted online, spouses reported similar experiences, turning to exercise, music, hobbies and time away with friends to find balance. Many expressed a strong desire to be able to talk to or hear from other spouses who went through similar struggles - without taking time from work or family to attend support groups, Duggleby said.

Work schedules also presented challenges with attending medical appointments with their spouses to hear information first-hand, which was another strong need spouses expressed.

"If you're a working man, it becomes difficult to go to some appointments, although some of that is just perception. They're not being excluded but they feel like they're being excluded. It's part of breaking down some of those barriers in cancer care," said Duggleby.

Duggleby said the findings should help health-care providers and agencies provide the specific support and resources these men need. For many spouses, an easy solution would be a guide showing where to find online information about breast cancer without information overload.

"They really do want something that's specific for them, tailored for their needs. It doesn't have to be done through a research study. There is a lot that can be done just based on what these spouses said and the ideas they provided. It would make a huge, huge difference."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our men's health section for the latest news on this subject. The study was funded by the Canadian Breast Cancer Foundation - Prairies/NWT.
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Potential Weapon In The Fight Against Cancer

By identifying a key protein that tells certain breast cancer cells when and how to move, researchers at Michigan State University hope to better understand the process by which breast cancer spreads, or metastasizes.

When breast cancer metastasizes, cancer cells break away from a primary tumor and move to other organs in the body, including the lungs, liver and brain. In work published recently in the journal Cancer Research, MSU researchers Kathy Gallo and Jian Chen show a protein called MLK3 (mixed lineage kinase 3) is a critical driver of breast cancer cell migration and invasion.

More importantly, Chen and Gallo showed that in triple-negative breast tumor cells, which are more aggressive and for which targeted therapies are needed, it is possible to thwart that cell migration and invasion.

"While the classical approach to cancer drugs has been to find drugs that kill tumor cells, there recently also is an interest in finding drugs that interrupt metastasis," said Gallo, a professor in MSU's Department of Physiology. "The hope is that such drugs in combination with conventional therapies may lead to better outcomes in patients."

As part of their study, Gallo and Chen, a biochemistry graduate student, also found that eliminating MLK3 prevented tumors in animals from metastasizing to the lungs, providing the foundation for future research on targeting MLK3 pathways as an approach to preventing the spread of cancer.

The researchers identified how key cellular proteins were instructed by the MLK3 protein - through the addition of molecular tags called phosphates - to interact with one another, leading cancer cells to move. Specifically, MLK3 promotes the addition of phosphates to another protein called paxillin, which is known to control how cells move.

Gallo and Chen then stopped cell movement in breast cancer models by eliminating MLK3 altogether or using a drug called CEP-1347 to block MLK3's ability to add phosphates to other proteins. The experimental results indicate that when certain cancer cells lose MLK3, the ability to add phosphates is impaired, eventually crippling the cell migration machinery and diminishing cell movement.

"Our research suggests that the intracellular pathways involving MLK3 that control cell movement could provide new targets for the treatment of patients with metastatic cancer," Chen said. "Drugs developed for combating the MLK3 activity may be useful in reducing the spread of breast cancer."

Gallo added that MLK3 is a protein kinase, and these types of proteins have proven to be good drug targets in cancers and other diseases.

"While drugs such as chemotherapy kill all cells, research has shown drugs that inhibit kinases often can be effective with fewer side effects," she said.

The next step for the researchers is to test whether an MLK3 inhibitor can prevent cancer from metastasizing in animal models.

"Cancer is a very complex collection of diseases, but we believe that certain types of cancers may be sensitive to MLK inhibitors," Gallo said, "and targeting MLK3 may provide a very useful weapon in the fight against cancer."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. The team’s research was supported by grants from the Department of Defense’s Breast Cancer Research Program and the Elsa U. Pardee Foundation. The MLK inhibitor, CEP-1347, was provided by Cephalon Inc., a wholly owned, indirect subsidiary of Teva Pharmaceuticals Industries Ltd.
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joi, 15 decembrie 2011

Cancer Spread Can Be Predicted Through Molecular Markers

Main Category: Cancer / Oncology
Also Included In: Radiology / Nuclear Medicine; Lung Cancer
Article Date: 15 Dec 2011 - 0:00 PST

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Molecular markers found in cancer cells that have spread from a primary tumor to a limited number of distant sites can help physicians predict which patients with metastatic cancer will benefit from aggressive, targeted radiation therapy.

In a study published online in the journal PloS One, researchers from the University of Chicago show that if cells from metastatic tumors have high levels of a particular type of microRNA - a tool cells use to silence certain genes - not even aggressive treatment of those tumors would help. But if the cells have lower levels of that biological marker, then focused local treatment could be effective, even curative.

"We previously demonstrated that we could provide lasting disease-free survival to a percentage of patients with metastatic disease," said study author Ralph Weichselbaum, MD, professor and chair of radiation and cellular oncology and Director of the Ludwig Center for Metastasis Research at the University of Chicago. "This finding means we can have a pretty good sense in advance of which patients we can help. Patients unlikely to benefit from focused, local therapy can move on to systemic treatment."

When patients die from cancer, it is usually caused by distant metastases, numerous cancer sites established by malignant cells that split off from the primary cancer and began growing in new settings. In 1994, Weichselbaum and colleague Samuel Hellman proposed that there was a potentially curable intermediate state between cancer that had not spread at all and cancer that had spread extensively. They named this phenomenon "oligometastasis," meaning cancer that had spread to a few distant sites.

In 2004, they began a small clinical trial to test that theory. Patients with stage IV cancer with one to five distant metastases and no tumors bigger than 10 centimeters in diameter were enrolled. The results, published in 2008, showed that precisely targeted radiation therapy could eradicate all evidence of disease in about 20 percent of those patients.

"We were pleased to get such encouraging results in patients with stage IV cancers that had spread to distant sites," Weichselbaum said. "This was proof of principle in patients who had already failed standard therapies."

A follow-up study, published in October 2011, found that 18 percent of the patients in that initial trial had seen no progression of their cancers for the duration of the study and 27 percent developed no new tumor sites.

The next step was to determine in advance which patients were most likely to benefit from such targeted therapy and which ones should move on to whole-body treatments, such as chemotherapy. So they compared cells from secondary tumors from patients who did well in the original studies with those whose cancers went on to establish multiple metastatic sites.

They found that tumors that were highly proliferative, producing many metastases, had patterns of microRNA expression that differed from those that produced only a few. The tumors most likely to spread had high levels of a small nucleic acid known as microRNA-200c.

This came as a surprise. MicroRNA-200c was thought to suppress metastasis. But when the researchers boosted microRNA-200c levels in a mouse model of cancer, it significantly increased metastasis. The researchers subsequently showed that microRNA-200c reduced the activity of other genes that acted to prevent the spread of cancer.

Further tests in mouse models showed that boosting microRNA-200c levels significantly increased the metastatic potential of tumors that were not as prone to spread.

"Our findings are an initial step in discriminating between patients with a few treatable sites where the tumor has spread and those who will develop widespread metastasis, which is not curable with focused radiation therapy," Weichselbaum said. "It is encouraging to find a common molecular basis for this treatable state across a broad variety of metastases from solid tumors."

Oligometastases are "more common than generally recognized," the authors note. "Potentially, 50 percent of patients with metastatic non-small cell lung cancer, the leading cause of cancer death in men and women, may be oligometastatic."

When combined with other factors - the number and size of metastasis, the interval from treatment of a primary tumor to the appearance of metastasis, the microscopic structure and appearance of tumor tissue - the presence of microRNA-220c could become a key element of patient selection for targeted radiation therapy, Weichselbaum said, distinguishing between patients who have treatable tumors and those who have widespread metastasis, including many tumors too small to detect.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. The National Institutes of Health, the Ludwig Center for Metastasis Research, the University of Chicago Center for Radiation Therapy, the Chicago Tumor Institute, Dr. Lloyd Old, Mr. And Mrs. Vincent Foglia and the Foglia Family Foundation, the Lung Cancer Research Foundation, the University of Chicago Cancer Research Foundation, the University of Chicago Comprehensive Cancer Center and the Center for the Multiscale Analysis of Genomic and Cellular Networks supported this study. Additional authors include Yves Lussier of the University of Illinois at Chicago; Rosie Xing, Nikolai Khodarevi, Yong Huang, Qingbei Zhang, Sajid Khan, Xinan Yang, Michael Hasselle, Thomas Darga, Renuka Malik, Hanli Fan, Samantha Perakis, Matthew Filippo, Kimberly Corbin, Younghee Lee, Mitchell C. Posner, Steven J. Chmura, and Samuel Hellman of the University of Chicago Medical Center, and Joseph Salama of Duke University Medical Center.
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Prognostic Model Developed For MDS Related To Prior Cancer Therapy

Main Category: Cancer / Oncology
Article Date: 15 Dec 2011 - 2:00 PST

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A large-scale analysis of patients whose myelodysplastic syndrome is related to earlier cancer treatment overturns the notion that all of them have a poor prognosis, researchers from The University of Texas MD Anderson Cancer Center report at the 53rd Annual Meeting of the American Society of Hematology.

"MDS patients whose disease springs from earlier radiation, chemotherapy or both treatments are usually told that they have a poor prognosis. But by analyzing survival risk factors in a large patient population, we've found these patients fall into good, intermediate and poor prognostic groups," said study leader Guillermo Garcia-Manero, M.D., Ph.D., professor in MD Anderson's Department of Leukemia.

Understanding their differing characteristics will better inform treatment decisions for these patients, Garcia-Manero said.

Myelodysplastic syndrome consists of a group of diseases in which the bone marrow progenitor cells that normally morph into red and white blood cells and platelets fail to respond to normal growth controls. That results in too many progenitor cells (also known as blasts) and too few mature blood cells, and in about 30 percent of patients, the disease progresses to acute myeloid leukemia (AML).

Treatment-related MDS is often more resistant to therapy

Therapy-related MDS generally differs from other MDS cases by having more chromosomal abnormalities, a higher rate of conversions to acute myeloid leukemia and high resistance to standard MDS therapy. Even so, Garcia-Manero notes, a one-size-fits-all poor prognosis is not accurate.

The research team analyzed 1,950 MD Anderson patients treated between 1998 and 2007. It found 438 had a history of one or more previous cancers that were treated before their MDS diagnosis. Of these, 279 cases who had received chemotherapy, radiotherapy or both were analyzed.

A first round of analysis identified at least 15 factors associated with overall survival when considered as isolated, single variables.

Next, the researchers conducted a multi-variable analysis that narrowed factors reducing overall survival to seven:

Age 65 or older.

ECOG performance status scores of 2-4. (Eastern Cooperative Oncology Group criteria range from 0, which means fully active, to 4, signifying complete disability).

Cytogenetics. Having at least seven chromosomal alterations and/or complex cytogenetics.

Two MDS subgroups as determined by World Health Organization Criteria. RARS and RAEB-1/2.

Serum hemoglobin levels of less than 11g/dL.

Platelet levels of less than 50.

Dependency on blood transfusions.

Prognostic model sorts patients into three risk groups

Garcia-Manero and colleagues created a novel prognostic model that incorporated these multivariate factors and divided patients into three categories:

Good prognosis - 57 patients fell into this group by having 0-2 of the multivariate risk characteristics. Their median survival was 34 months.

Intermediate prognosis - 154 patients in this category had 3-4 risk factors and a median survival of 12 months.

Poor prognosis - 61 patients had 5-7 risk factors and a median survival of only five months.

The model also predicted one-year leukemia-free survival of 96 percent in the good category, 84 percent for intermediate, and 72 percent for the poor.

Model validated in a test group of patients

The researchers validated the model by applying it to an additional 189 treatment-related cases diagnosed between 2008 and 2010. Median survival rates in the test group were:

Good - 26 months

Intermediate - 13 months

Poor - 7 months.

"We believe this model will facilitate development of risk-adapted treatment strategies for patients with treatment-related myelodysplastic syndromes," Garcia-Manero said.

Article adapted by Medical News Today from original press release. Source: University of Texas M. D. Anderson Cancer Center
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Gene Mechanism That Stops Colorectal Cancer Modelled In Mice

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Academic Journal
Main Category: Colorectal Cancer
Also Included In: Cancer / Oncology; Genetics
Article Date: 15 Dec 2011 - 6:00 PST

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A research team in France has bred a lab mouse with a gene mutation that allows colorectal cancer tumors to grow because the protein coded by the gene is no longer able to trigger cell suicide ("apoptosis"). They hope their discovery will pave the way for developing a treatment that targets the gene so it reactivates apoptosis in cancer cells. They write about their findings in a letter published online on 11 December in the journal Nature.

The team has been working for some time in trying to understand more about cell death, and apoptosis in particular. Once activatived, the mechanism sets the cell onto a self-destruct path. The team's leader is Patrick Mehlen, Director of the DEVweCAN 'Laboratory of Excellence' at the Lyon Cancer Research Centre at the Université de Lyon, Centre Léon Bérard.

For the past 15 years, researchers in this field have been debating about the tumor-suppressing ability of a gene called DCC which in humans codes for a receptor protein known as Deleted in Colorectal Carcinoma. Receptor proteins sit on the surfaces of cells and are receptive to "ligands", special molecules that engage with them and change their behavior, such as activating or silencing signals that do things like control processes inside the cell.

We already know from previous research that DCC expression is either lost or significantly reduced in the majority of advanced colorectal cancers. We also know, that the DCC receptor triggers apoptosis, unless engaged to its ligand, netrin-1.

Mehlen and colleagues proposed that the receptors act like sentinels on the surface of the cells: these sentinels are constantly looking at what is happening in their environment, which is why they are also called "dependence receptors".

While the ligand is engaged, the DCC receptor protein sends out a signal that "all is well", and so does not activate cell death, and the cell survives. But when the ligand is not there, the receptor effectively interprets this as "all is not well", and releases the cell-death trigger.

When you apply this sentinel idea to cancer cells, then it would suggest that the absence of ligands causes the DCC receptors to signal "all is not well", and so set the cells on a path of self-destruction, thus causing the death of rogue cells that would otherwise grow into a tumor.

But, as Mehlen and colleagues point out in their Nature paper, until now, no animal tests have been able to support the idea that this side of DCC is a cause of aggressive cancer development.

So, to investigate the role that DCC-triggered apoptosis might play in the control of tumor development, they used mice already genetically predisposed to develop colon cancer (they have a particular variant of the APC gene), and further modified them so they carried a mutation of DCC whose apoptosis trigger is silent.

They found that the mice spontaneously developed colon cancer.

Mehlen and colleagues describe their findings in the Nature letter:

"Although the loss of DCC-induced apoptosis in this mouse model is not associated with a major disorganization of the intestines, it leads to spontaneous intestinal neoplasia at a relatively low frequency. Loss of DCC-induced apoptosis is also associated with an increase in the number and aggressiveness of intestinal tumours in a predisposing APC mutant context, resulting in the development of highly invasive adenocarcinomas."

They conclude that these results show that DCC behaves as a tumor suppressor in that it has the ability to trigger apoptosis in cancer cells.

Mehlen told the press:

"The organism is naturally protected from the development of cancers thanks to the presence of this tumour-suppressing gene."

But, unfortunately, there are some cancer cells that manage to escape this control by blocking the dependence receptor mechanism of DCC.

"That is how we know that the DCC gene is extinguished in most human cancers,' he explained.

The researchers hope it won't be long before this work leads to new target treatments that reactivate cell death in cancer cells. This could apply to other cancers too, such as breast and lung cancer.

"Our group has developed several candidate drugs that reactivate the cell death induced by the DCC receptor in animal models, and we hope to be able to carry out human clinical testing of these candidate drugs in three years' time," said Mehlen.

Mehlen has just been awarded Liliane Bettencourt Schueller Life Sciences Prize, which will help to fund his work.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our colorectal cancer section for the latest news on this subject. "DCC constrains tumour progression via its dependence receptor activity"; Marie Castets, Laura Broutier, Yann Molin, Marie Brevet, Guillaume Chazot, and others; Nature published online 11 December 2011; DOI:10.1038/nature10708; Link to Abstract.
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marți, 13 decembrie 2011

Vaccine Developed That Attacks Breast Cancer In Mice; Implications For Ovarian, Colorectal And Pancreatic Cancers

Main Category: Breast Cancer
Also Included In: Pancreatic Cancer; Ovarian Cancer; Immune System / Vaccines
Article Date: 13 Dec 2011 - 3:00 PST

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Researchers from the University of Georgia and the Mayo Clinic in Arizona have developed a vaccine that dramatically reduces tumors in a mouse model that mimics 90 percent of human breast and pancreatic cancer cases - including those that are resistant to common treatments.

The vaccine, described this week in the early edition of the journal Proceedings of the National Academy of Sciences, reveals a promising new strategy for treating cancers that share the same distinct carbohydrate signature, including ovarian and colorectal cancers.

"This vaccine elicits a very strong immune response," said study co-senior author Geert-Jan Boons, Franklin Professor of Chemistry and a researcher in the UGA Cancer Center and its Complex Carbohydrate Research Center. "It activates all three components of the immune system to reduce tumor size by an average of 80 percent."

When cells become cancerous, the sugars on their surface proteins undergo distinct changes that set them apart from healthy cells. For decades, scientists have tried to enable the immune system to recognize those differences to destroy cancer cells rather than normal cells. But since cancer cells originate within the body, the immune system generally doesn't recognize them as foreign and therefore doesn't mount an attack.

The researchers used unique mice developed by Sandra Gendler, Grohne Professor of Therapeutics for Cancer Research at the Mayo Clinic in Arizona and co-senior author on the study. Like humans, the mice develop tumors that overexpress a protein known as MUC1 on the surface of their cells. The tumor-associated MUC1 protein is adorned with a distinctive, shorter, set of carbohydrates that set it apart from healthy cells.

"This is the first time that a vaccine has been developed that trains the immune system to distinguish and kill cancer cells based on their different sugar structures on proteins such as MUC1," Gendler said. "We are especially excited about the fact that MUC1 was recently recognized by the National Cancer Institute as one of the three most important tumor proteins for vaccine development."

Gendler pointed out that MUC1 is found on more than 70 percent of all cancers that kill. Many cancers, such as breast, pancreatic, ovarian and multiple myeloma, express MUC1 with the shorter carbohydrate in more than 90 percent of cases.

She explained that when cancer occurs, the architecture of the cell changes and MUC1 is produced at high levels, promoting tumor formation. A vaccine directed against MUC1 has tremendous potential, Gendler said, as a preventative for recurrence or as a prophylactic in patients at high risk for particular cancers. A vaccine also can be used together with standard therapy such as chemotherapy in cancers that cannot be cured by surgery, such as pancreatic cancer.

Boons noted that MUC1 is also overexpressed in 90 percent of the subset of patients who are not responsive to hormonal therapy, such as Tamoxifen or aromatase inhibitors, or the drug Herceptin. These so-called "triple-negative" tumors are extremely aggressive and difficult to treat, Boons said, and a new treatment option is urgently needed.

"In the U.S. alone, there are 35,000 patients diagnosed every year whose tumors are triple-negative," Boons said. "So we might have a therapy for a large group of patients for which there is currently no drug therapy aside from chemotherapy."

Therapeutic vaccines received renewed attention last year when the Food and Drug Administration approved the first cancer treatment vaccine, a drug known as Provenge that is used to treat metastatic prostate cancer. Treatment with the drug, which is manufactured in Georgia, requires clinicians to isolate immune cells from the patient and then to send the cells to a lab, where they are linked to a protein that stimulates the immune system. The cells are returned to the patient's treating physician, who then infuses the drug over three treatments, usually two weeks apart.

Boons' vaccine, on the other hand, is much simpler. It is fully synthetic, meaning that its components can be manufactured in a lab with assembly-line precision. The vaccine consists of three components - an immune system booster known as an adjuvant, a component that triggers the production of the immune system's T-helper cells, and a carbohydrate-linked peptide molecule that directs the immune response to cells bearing MUC1 proteins with truncated carbohydrates.

Biotechnology is a key industry in Georgia, and this year Boons founded an Athens-based company, known as Viamune, to help develop and commercialize the vaccine and the technologies used to create it. The company is one of nearly 30 that are affiliated with the University's BioBusiness Center, which is an incubator for life sciences start-up companies associated with UGA.

"Companies like these have the potential to create stable, high-paying jobs that have a significant social and economic impact," said Stefan Schulze, associate director of the Georgia BioBusiness Center. He noted that Viamune was a one four finalists selected from 40 companies at an investor's forum hosted this year by the non-profit organization Southeast BIO.

Boons, Gendler and their colleagues are currently testing the vaccine's effectiveness against human cancer cells in culture and are planning to assess its toxicity. If all goes well, they anticipate that phase I clinical trials to test the safety of the vaccine could begin by late 2013.

The vaccine represents nearly a decade of work on the part of Boons and his team. A 2007 study demonstrated the vaccine's effectiveness in another mouse model, and Boons is cautiously optimistic about his most recent results. Although promising results in mice often don't translate to humans, Boons said he is confident that vaccines that target the specific carbohydrate signatures of cancer cells will ultimately play an important role in the treatment of the disease.

"We are beginning to have therapies that can teach our immune system to fight what is uniquely found in cancer cells," Boons said. "When combined with early diagnosis, the hope is that one day cancer will become a manageable disease."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. In addition to co-senior authors Boons, Ph.D., and Gendler, Ph.D., the co-first authors on the paper are Vani Lakshminarayanan, Ph.D., at the Mayo Clinic in Arizona and Pamela Thompson at the University of Georgia. Additional authors include, at UGA, Margreet Wolfert, Ph.D., and Therese Buskas, Ph.D., and, at the Mayo Clinic, Judy Bradley, Latha Pathangey, Cathy Madsen and Peter Cohen, M.D.
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Cancer Screening In Older Patients Very Common

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Main Category: Cancer / Oncology
Also Included In: Seniors / Aging
Article Date: 13 Dec 2011 - 0:00 PST

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U.S. Preventive Services Task Force guidelines recommend against routine cancer screening, especially for breast, cervical, colorectal and prostate cancer, but adults 75 and older are still receiving regular cancer screenings. The report published in the December 12/26 issue of Archives of Internal Medicine, one of the JAMA/Archives journals, is a part of the journal's Less is More series, the aim is to educate healthcare professionals and patients alike in cuttings costs, but having a better service at the same time.

The authors write as background information in the article :

"In the United States, the number of adults 65 years or older, currently estimated at 36.8 million, is expected to double by the year 2030. Providing high-quality care to this growing population while attempting to contain costs will pose a significant challenge ...

While a great deal is known about cancer screening behaviors and trends in young and middle-aged adults, less is known about screening behaviors in older adults from different racial backgrounds."

Keith M. Bellizzi, Ph.D., M.P.H., of the University of Connecticut, Storrs, and colleagues analyzed data from the National Health Interview Survey, an annual in-person nationwide survey used to track health trends in U.S. citizens, to estimate the prevalence of cancer screening among older, racially diverse adults. The study population included 49,575 individuals, 1,697 of whom were 75 to 79 years of age and 2,376 were 80 years of age and older.

Percentages of those reporting cancer screenings are as follows : 62 percent Women age 75 to 79 - A mammogram within the past two years.50 percent of women age 80 and older - A mammogram within the past two years. 53 percent of women ages 75 to 79 - A Papanicolaou screen (also known as a pap smear or pap test) for cervical cancer within the past three years. 38 percent of women ages 80 and older - A pap smear within the past three years.57 percent highest of men and women 75 to 79 - Screenings for colorectal cancer. 57 percent of Men 75-79 - Prostate cancer screening.42 percent of Men 80 and older - Prostate cancer screening.40 percent of Men 50-74 and older - Prostate cancer screeningAnalysis showed large differences in breast, colorectal and prostate cancer screening among older adults, but the authors found that these differences were accounted for by low education.

Individuals without a high school diploma were significantly less likely to be screened for breast, cervical and prostate cancer, compared with adults older than 75 years with a college degree. Adults older than 75 years were also significantly more likely to be screened for breast, colorectal, and prostate cancer if a physician recommended the test.

The authors concluded :

"A high percentage of older adults continue to be screened in the face of ambiguity of recommendations for this group ... Prevalence results from this study can serve as a benchmark for progress as we move the science of cancer screening in older, diverse adults forward."

In additional commentary, Louise C. Walter, M.D., of the University of California, San Francisco and San Francisco Veterans Affairs Medical Center, writes that :

"There are no quality measures that address appropriate target rates for cancer screening in persons older than 75 years ...
While at extremes in older age the likelihood of surviving long enough to benefit from potential detection and treatment of asymptomatic cancer becomes quite small and the likelihood of harm becomes quite large irrespective of other factors, Bellizzi et al were not able to calculate screening rates in subgroups older than 85 years owing to the small number participating in the survey ...
Still, the data by Bellizzi et al raise the issue of whether quality measures should address the overuse of cancer screening."

Dr. Walter concludes :

"While it is useful to determine screening rates among persons in whom screening will likely result in net benefit or net harm, between these two groups is a large number of older persons in whom screening offers small or uncertain net benefit ...
For these persons, the decision about whether the potential benefits of screening outweigh the risks is a value judgment that requires informed decision-making ...
While arguments persists about what is the 'right' rate of cancer screening in older persons, it seems clear that the rate of informed decision-making should approach 100 percent."

Written by Rupert Shepherd
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our cancer / oncology section for the latest news on this subject. Arch Intern Med. 2011;171[22]:2031-2037.

Arch Intern Med. 2011;171[22]:2037-2038.

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Childhood Cancer Survivors' Exposure To Chemotherapy, Radiation Does Not Increase Risk Of Birth Defects In Their Children

Main Category: Pediatrics / Children's Health
Also Included In: Cancer / Oncology
Article Date: 13 Dec 2011 - 1:00 PST

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A large, retrospective study shows that children of childhood cancer survivors who received prior treatment involving radiation to testes or ovaries and/or chemotherapy with alkylating agents do not have an increased risk for birth defects compared to children of survivors who did not have such cancer treatment. The findings provide reassurance that increased risks of birth defects are unlikely for cancer survivors who are concerned about the potential effects of their treatment on their children, and can help guide family planning choices.

"We hope this study will become part of the arsenal of information used by the physicians of childhood cancer survivors if reproductive worries arise," said lead author Lisa Signorello, Sc.D., associate professor of medicine at Vanderbilt University in Nashville, TN, and senior epidemiologist at the International Epidemiology Institute in Rockville, MD.

"Childhood cancer survivors face real reproductive concerns, including unknowns related to the effects of therapy. But, hopefully this study will provide some reassurance that their children are unlikely to be at increased risk for genetic defects stemming from their earlier treatment."

According to Signorello, childhood cancer patients frequently receive aggressive, though life-saving, radiation and chemotherapy treatments that can affect their ability to have children. For girls, radiation to the pelvis and the resulting damage to the uterus has been associated with a risk for pregnancy outcomes such as miscarriage and preterm birth, and effects on the ovaries can lead to infertility. Radiotherapy and chemotherapy with alkylating agents (e.g., busulphan, cyclophosphamide and dacarbazine) are DNA-damaging treatments, affecting both cancer and healthy cells. Studies to date have not adequately addressed the question of whether genetic damage from a parent's treatment could be passed down to their offspring. Genetic-based birth defects are rare in the general population (about 3 percent), and while previous research results indicated little or no increased risk for birth defects among the offspring of cancer survivors, such studies were relatively small in size and lacked detailed information about radiation and chemotherapy treatments, such as specific radiation doses to the testes and ovaries.

In the current study, investigators used information from the Childhood Cancer Survivor Study, a large retrospective study of treatment and outcomes in more than 20,000 childhood cancer survivors diagnosed between 1970 and 1986. Signorello and her colleagues examined data from 4,699 children of 1,128 men and 1,627 women who were 5-year childhood cancer survivors. The survivors reported their children's health problems through questionnaires, and investigators also examined medical records from survivors and their children, focusing on survivors' history of radiation to the testes or ovaries and chemotherapy with alkylating agents.

Of the survivors, 63 percent (1,736) had received radiation for their cancer as children, and 44 percent of men (496) and 50 percent of women (810) had received chemotherapy with alkylating agents. Overall, 2.7 percent (129) of the survivors' children had at least one birth defect, such as Down syndrome, achondroplasia or cleft lip. Researchers found that 3 percent of children of mothers exposed to radiation or treated with alkylating chemotherapy agents had a genetic birth defect, compared to 3.5 percent of children of mothers who were cancer survivors but did not have such exposures. Only 1.9 percent of children of male cancer survivors who received these DNA-damaging treatments had such birth defects, compared to 1.7 percent of children of male survivors who did not have this type of chemotherapy or radiation. The researchers concluded that children of cancer survivors were not at higher risk for birth defects stemming from parents' exposure to chemotherapy and/or radiation.

The researchers also noted that a strength of their study is the comparison they made to the children of other cancer survivors and not to the children of people randomly sampled from the general population. Signorello said that comparing cancer survivors to individuals in the general population can be difficult because the latter may not be as thorough in reporting health problems of their children, and the children of cancer survivors may be under heightened clinical surveillance and may appear to have higher rates of birth defects as a result. The investigators did, however, find that the overall prevalence of birth defects among the cancer survivors' children was very similar to what has been reported in the general population.

The study is among the largest to examine birth defects in children of childhood cancer survivors, and among the first to evaluate birth defects using medical records to validate both the children's health problems and the parents' radiation and chemotherapy exposures.

"The possibility of birth defects in offspring has been a lingering concern among cancer survivors because it's hard to address," Signorello said. "We know these are rare outcomes, and a large study group was needed to address these questions. It took years to validate the parents' self-reported outcomes, and to assemble and use the medical records of radiation and chemotherapy treatment exposures to allow us to quantify their exposure doses. These are the strongest results to date, adding greater certainty to other studies examining this common concern among survivors of childhood cancer."

The researchers would like to continue to sequence the DNA of families of childhood cancer survivors (survivors and their children) to see if there is any evidence of radiation- or chemical-induced genetic damage, even if the children did not have birth defects. They would also like to combine data from all U.S. and international studies on this topic in order to provide even larger, more definitive results.

"As the proportion of childhood cancer survivors within our population grows, it is clear that a very large number of former patients will be impacted by the results of this study. Cancer survivors and newly diagnosed patients worry about the effect that chemotherapy and radiation therapy may have on their future children. While we as oncologists have felt the risk of congenital abnormalities to be low, we now have concrete data from a very large number of children to support us in our conversations with survivors and newly diagnosed patients. These results will reassure survivors that their previous cancer therapy does not appear to result in an increased risk of birth defects in their future offspring."

Article adapted by Medical News Today from original press release. Source: American Society of Clinical Oncology
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Dana-Farber Offers Healthy Holiday Recipes And Food Tips To Fight Cancer With Your Fork This Holiday Season

Main Category: Cancer / Oncology
Article Date: 13 Dec 2011 - 1:00 PST

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The holidays are in full swing and festive food is everywhere. Some are naughty, some are nice, and some may even help fight cancer.

"While these so-called holiday foods are delicious to eat, they can also have the added bonus of containing cancer-preventing nutrients," says Stephanie Meyers, MS, RD/LDN, a nutritionist at Dana-Farber Cancer Institute in Boston. Meyers and her colleagues have put together a list of foods and recipes that definitely belong on the "good" list this holiday season.

Go nuts

Dust off that family nutcracker. Recent research finds that walnuts may help to prevent kidney and colon cancers. In addition, the study suggests that walnuts are a rich source of antioxidants that may help protect cells from oxidative damage. Walnuts contain essential fatty acids, or the so-called "good fats," which are known to help reduce blood pressure and boost the immune system. So go nuts with this simple pesto recipe.

It's not just for pie

Pumpkin is a holiday staple for many families. It is also one of the tastiest ways to enhance the body's own natural cancer-fighting ability, notes Meyers. Pumpkins are packed with nutrients called carotenoids, which have been linked to the prevention of colon, prostate, breast, and lung cancer.

Although many people only eat pumpkin when it is made into a pie, it can also be enjoyed in a variety of other ways, including roasted pumpkin, pumpkin soup and these high-fiber pumpkin muffins.

It's the bright color that gives pumpkins their rich nutrients, so look for other orange vegetables, like sweet potatoes, carrots and butternut and acorn squash. All are also high in carotenoids.

"It is more beneficial to consume carotenoids from whole foods rather than from supplements, because carotenoids in pill form do not appear to have the same protective properties," explains Meyers. In fact, that is true of many of the nutrients in foods. Eating whole foods typically provides greater health benefits than taking a dietary supplement.

An apple a day

Apples are another food packed with cancer-preventing properties, thanks to the nutrient quercitin, which protects DNA in the body's cells from damage that could lead to the development of cancer. Recent research suggests the carbohydrates in apples may help prevent colorectal cancer development as well. To get the most protection against cancer from apples,eat them with the skin on and not combined with sugar and fats, like in a pie.

Not just for the holidays

Meyers reminds her patients at Dana-Farber that cranberries aren't just for the holidays and encourages them to eat the berries year-round. Cranberries contain benzoic acid, which has been shown to inhibit the growth of lung cancer, colon cancer, and some forms of leukemia.

She recommends buying bags of fresh cranberries now, while they are in season and at their nutritional peak, and popping them in the freezer for later use. This will help ensure that the berries will provide the highest level of cancer protection whenever they're used.

Positively pomegranate

Pomegranates are everywhere, from drinks to desserts, and there is good reason why. Recent research suggests that drinking pomegranate juice may be a delicious way to help prevent prostate cancer, as well as prevent the metastasis and spread of prostate cancer cells.

Try combining pomegranates and apples for a delicious, good-for-you dessert that is layered with flavonoids, vitamin C, and other antioxidants that can help lower the risk of cancer.

Color your world

The overall key to finding cancer-fighting foods is to look for a lot of color. In the winter, root vegetables like carrots, parsnips and beets can add a burst of color and taste. The brighter and richer the pigment, the higher the level of nutrients. "You want to load up your plate with as much colorful plant-based foods as you can," explains Meyers. "Eating a plant-based diet is the best way to help lower your risk of cancer all year long."

Article adapted by Medical News Today from original press release. Source: Dana-Farber Cancer Institute
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