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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Further Study Necessary To Better Utilize Nature's Medicine Cabinet

Main Category: Pharma Industry / Biotech Industry
Also Included In: Cancer / Oncology
Article Date: 15 Dec 2011 - 0:00 PST

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There are probably at least 500 medically useful chemicals awaiting discovery in plant species whose chemical constituents have not yet been evaluated for their potential to cure or treat disease, according to a new analysis by a New York Botanical Garden scientist who has more than 15 years of experience in collecting plants for natural-products discovery programs.

Currently, 135 drugs on the market are derived directly from plants; the analysis indicates that at least three times as many disease-fighting substances have yet to be found that could be developed into drugs or used as the basis for further drug research.

"Clearly, plant diversity has not been exhausted, and there is still great potential in the plant world," said James S. Miller, Ph.D., Dean and Vice President for Science at the Botanical Garden.

Dr. Miller's analysis, "The Discovery of Medicines from Plants: A Current Biological Perspective," is published in the December issue of the peer-reviewed journal Economic Botany.

To arrive at his estimate, Dr. Miller used a formula based on the ratio of the number of drugs that have been developed from plants to the number of plants that were screened to find those drugs. He then applied that ratio to the number of plant species that have not yet been screened.

Because of uncertainties in some of those numbers, the formula yields a range of potential drug discoveries. While there is no general agreement among botanists about the number of plant species that are likely to exist, Dr. Miller concluded that there are 300,000 to 350,000 species of plants. Of those, he determined that the chemistry of only 2,000 species has been thoroughly studied, and perhaps only 60,000 species have been evaluated even partially for medicinally useful chemicals.

Working with those numbers, Dr. Miller calculated that there are likely to be a minimum of 540 to 653 new drugs waiting to be discovered from plants; the actual number could be much greater.

"These calculations indicate that there is significant value in continuing to screen plants for the discovery of novel bioactive medicinally useful compounds," concludes Dr. Miller, who has run natural-products discovery programs that have collected specimens in North America, Central and Southeast Asia, and Africa for government agencies, pharmaceutical companies, and academic programs.

As part of his Economic Botany paper, Dr. Miller reviews the disappointing history of past plant-screening efforts and evaluates the potential for future programs.

Technological advances in the 1970s and 1980s gave medical researchers the capacity to evaluate large numbers of plant samples. That prompted the federal government and large pharmaceutical companies to institute aggressive plant collecting and screening programs. Those programs led to the development of several important drugs such as Taxol from Taxus brevifolia (used in cancer treatment) and Camptothecin from Camptotheca acuminata (derivatives of which are used to treat cancer). Other drugs indirectly trace their discovery to natural-products research, including the anti-viral Oseltamivir, which derives from Illicium anisatum and is marketed in the United States as Tamiflu.

The number of drug discoveries, however, was substantially less than anticipated. By the early 2000s, many of the large pharmaceutical companies had abandoned their efforts.

Dr. Miller argues that one possible explanation for the low yield is the relatively crude way in which plant extracts were tested for their pharmaceutical potential. Plants may contain as many as 500 to 800 different chemical compounds, but the screening programs of the late 20th century used extracts made from a whole plant or at best extracts that contained many hundreds of compounds.

Under those circumstances, one compound may interfere with the action of another, or the amount of one compound may be too small to register in a mix of hundreds of chemicals.

To correct this problem, new technologies now allow researchers to separate complex mixtures of natural products into a "library" of relatively pure compounds that can be tested individually. A 2002 study demonstrated that testing such libraries dramatically improves discovery rates.

Bringing these advances together with refinements in collecting strategies could lead to what Dr. Miller calls a "second renaissance" of natural-products discovery.

Miller undertook his analysis to highlight the fact that despite past collecting programs, the plant world represents a poorly explored source of potentially lifesaving drugs. That adds urgency, he said, to efforts to conserve natural habitats so that species are not driven to extinction before they can be studied.

"The natural world has a great and diverse array of interesting chemicals that have been only minimally studied and still hold considerable potential," he writes.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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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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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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A New Way To Target Cancer Through Manipulating A Master Switch Responsible For Cancer Cell Growth

Main Category: Cancer / Oncology
Also Included In: Vascular;  Urology / Nephrology;  Eye Health / Blindness
Article Date: 14 Dec 2011 - 0:00 PST

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Scientists have discovered a new way to target cancer through manipulating a master switch responsible for cancer cell growth.

The findings, published in the journal Cancer Cell, reveal how cancer cells grow faster by producing their own blood vessels.

Cancer cells gain the nutrients they need by producing proteins that make blood vessels grow, helping deliver oxygen and sugars to the tumour. These proteins are vascular growth factors like VEGF - the target for the anti-cancer drug Avastin. Making these proteins requires the slotting together of different parts of genes, a process called splicing.

Scientists at UWE Bristol and the University of Bristol discovered that mutations in one specific cancer gene can control how splicing is balanced, allowing a master switch in the cell to be turned on. This master switch of splicing makes cancer cells grow faster, and blood vessels to grow more quickly, as they alter how VEGFs are put together.

In experimental models, the researchers found that by using new drugs that block this master switch they prevented blood vessel growth and stopped the growth of cancers.

Dr Michael Ladomery spearheading the work from UWE Bristol, said: "The research clearly demonstrates that it may be possible to block tumour growth by targeting and manipulating alternative splicing in patients, adding to the increasingly wide armoury of potential anti-cancer therapies."

Professor David Bates who led the team from the University of Bristol's School of Physiology and Pharmacology, said: "This enables us to develop new classes of drugs that target blood vessel growth, in cancer and other diseases like blindness and kidney disease."

The work, which started on kidney cancer, also involved groups at Southmead Hospital, where patients with kidney disease helped by allowing tissues that had been removed during surgery to be used in the research.

Professor Steve Harper, Consultant Nephrologist and part of the research team, said: "This shows how important it is for patients, doctors and scientists to come together in an excellent environment like Bristol to make these groundbreaking discoveries."

Professor Moin Saleem, Consultant Pediatric Nephrologist, whose lab helped to make the cells used, added: "We are really grateful to the patients who allowed their cells to be used in this research, as we hope it will eventually help the development of new drugs."

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 paper, entitled 'WT1 mutants reveal SRPK1 to be a downstream angiogenesis target by altering VEGF splicing', is published today in Cancer Cell. The research was sponsored by a UWE Bristol Faculty PhD studentship, which funded Elianna Amin, the first author on the paper, and by University of Bristol research grants from the British Heart Foundation, Cancer Research UK, Wellcome Trust, Medical Research Council Fight for Sight and the Skin Cancer Research Fund.
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Researchers Find Potential Target For Treating Metastatic Cancer

Main Category: Cancer / Oncology
Article Date: 14 Dec 2011 - 2:00 PST

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Finding ways to counteract or disrupt the invasive nature of cancer cells, called "metastasis," has been a long-term goal of cancer researchers. Now, researchers at Moffitt Cancer Center in Tampa, Fla., have identified an interactive pathway that regulates metastases in some cancers that may be vulnerable to chemical targeting in order to prevent cancer cell proliferation and tumor growth.

Ongoing collaboration by researchers in Moffitt's Departments of Tumor Biology and Drug Discovery has revealed the potential for combating metastatic disease by disrupting the interaction between the retinoblastoma tumor suppressor protein (Rb) and Raf-1 (a gene with a potential to cause cancer) with RRD-251, a selective, chemical disrupter of Rb-Raf-1 interaction.

Their recent study, aimed at understanding the association between Rb-Raf-1 and genes known to be over-expressed in metastatic non-small lung cancer, was published in the recent issue of Cancer Research, a journal of the American Association for Cancer Research. This work, using a mouse model, was a continuation of the researchers' study of RRD-251's successful disruption of Rb-Raf-1 interaction in metastatic melanoma in test mice, a study published in Molecular Cancer Therapeutics in 2010.

"The Rb gene is mutated in a variety of cancers," said study corresponding author Srikumar P. Chellappan, Ph.D., chair of Moffitt's Department of Tumor Biology and scientific director of the National Functional Genomics Center. "Our earlier studies have shown that Raf-1 interacts with Rb early in the cell cycle and facilitates its inactivation."

The ongoing work of Chellappan and his colleagues in Moffitt's Department of Tumor Biology focuses on understanding the mechanisms by which external signals regulate cell proliferation and how a loss of regulation may cause cancer. They work extensively with the Rb protein, the Raf-1 signaling molecule, and E2Fs, genes that affect cell proliferation, differentiation and cell death (apoptosis).

E2Fs, a family of genes that play a role in the mammalian cell cycle and can transform normal cells to have properties of cancer cells, interact with Rb. In addition, E2Fs are important for the development, differentiation and DNA damage repair programs in cells. Their previous studies have shown that RRD-251-mediated disruption of the Rb-Raf-1 interaction could inhibit the activity of E2F. They now show that E2Fs regulate matrix metalloproteinases (MMPs), which are involved in cancer metastasis, and RRD-251 can prevent the expression of MMPs.

"A considerable amount of research has been dedicated to identifying novel E2F- regulated genes, but a clear role for E2Fs in cancer progression and metastasis had not been established," explained Chellappan. "We find that the Rb-E2F pathway contributes to the expression of many genes involved in different aspects of cancer, and that targeting this pathway might fight metastatic disease."

Their study found that a mouse model of non small cell lung cancer metastasis being treated with RRD-251 had "significantly less metastasis to the lung and surrounding areas." They concluded that disrupting the Rb-Raf-1 interaction using RRD-251 could inhibit the regulatory function of E2Fs as an activator of gene promoters that are related to tumor growth and metastases.

"There is a possibility that E2F might indirectly regulate tumor metastasis as a consequence of its activating these genes," suggested Chellappan. "Taken together, our studies link the Rb-E2F cell cycle regulatory pathway to advanced stages of cancer development and metastasis."

Although further studies are underway, their work suggests that disrupting Rb-Raf-1 interaction can prevent cancer cell proliferation, cell vascular growth (angiogenesis), tumor growth, and the metastatic colonization of organs.

"This approach appears to be a fruitful avenue to combat metastatic disease," concluded Chellappan.

Article adapted by Medical News Today from original press release. Source: Moffitt Cancer Center
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How Lymphoma Evolves - A Study Of Two Sisters

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Academic Journal
Main Category: Lymphoma / Leukemia / Myeloma
Also Included In: Cancer / Oncology
Article Date: 13 Dec 2011 - 9:00 PST

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A 41-year-old woman with chronic-phase chronic myeloid leukemia received a bone marrow transplant and subsequent leukocyte infusion from her sister to control her leukemia, however seven years on, both sisters developed follicular lymphoma. Cases whereby donors pass on a malignancy to their recipients are well documented and usually of minimal risk to those in the transplant community, however this case presented scientists with the opportunity to study genetic abnormalities, which led to follicular lymphoma in both cases. Following standard chemotherapy, both sisters are currently in remission.

David Weinstock, M.D., assistant professor of medicine at the Dana-Farber Cancer Institute said:

"We were able to combine clinical activity with laboratory expertise to gain a real insight into the biology involved."

Funded by a Stand Up To Cancer Innovative Research Grant, Weinstock published the case study in a recent issue of Cancer Discovery, the latest journal of the American Association for Cancer Research, and together with his team, they presented their findings at the 2011 American Society of Hematology Annual Meeting and Exposition in San Diego on Dec. 12, 2011.

Weinstock and his team sequenced the DNA of samples derived from both sisters. They also sequenced a frozen sample of the leukocyte infusion to establish the genetic lesions that led to the lymphoma.

Their findings revealed that both sisters had identical BCL2/IGH and V (D) J rearrangements, and also found 15 mutations present in both women's lymphomas.

Using ultra-deep sequencing, they managed to recover 14 of these mutations from the donor lymphocyte infusions. This suggests that a lymphoma ancestor who already contained these mutations, was passed from donor to recipient seven years before becoming clinically active.

According to Weinstock, this kind of knowledge could pave the way to finding an early treatment of follicular lymphoma.

Weinstock declared:

"Currently the only curative approach is stem cell transplantation, but the more we understand about the genetic aberrations that lead to follicular lymphoma, the better we'll be able to manage the disease."

Written by Petra Rattue
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Visit our lymphoma / leukemia / myeloma section for the latest news on this subject. Cancer Discovery

Source: American Association for Cancer Research

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Cancer Vaccine Significantly Reduces Tumor Size

Editor's Choice
Academic Journal
Main Category: Cancer / Oncology
Also Included In: Immune System / Vaccines
Article Date: 13 Dec 2011 - 8:00 PST

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An experimental cancer vaccine has been found to reduce tumor size by an average of 80%, researchers from the Mayo Clinic and the University of Georgia reported in Proceedings of the National Academy of Sciences. In their animal experiment, mouse models that mimic most human pancreatic and breast cancer cases had dramatic reductions in tumor size - even among those that had not responded to standard treatments.

Tumors that share the same distinct carbohydrate signature may be especially treatable with this new vaccine, say the authors. This includes various cancers such as colorectal, ovarian, breast, pancreatic and some others.

Co-senior author Geert-Jan Boons, wrote:

"This vaccine elicits a very strong immune response. It activates all three components of the immune system to reduce tumor size by an average of 80 percent."

Sugars on the surface proteins of cancerous cells are different from those in healthy cells, the authors explain. For several years, researchers have sought ways of getting the immune system to identify the differences and target the cancer cells only, leaving the healthy ones alone. However, this is not easy, because cancer cells start off in the patient's own body, and his/her immune system does not see them as foreign or pathogenic, and does not attack them.

Study co-author, Sandra Gendler, developed some unique mice for this experiment. Tumors in mice overexpress MUC1, a type of protein, on the surface of their cells. The surface of MUC1 found in tumors has a unique, shorter set of carbohydrates (this is not the case with carbohydrates on the surface of healthy cells).

Gendler said:

"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. 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."

MUC1 was found to exist in over 70% of all lethal cancer, Gendler explained. In ovarian, pancreatic and breast cancers, as well as multiple myeloma, in 90% of cases MUC1 is expressed with the shorter carbohydrate.

When a cell becomes cancerous, its structure alters and MUC1 is overproduced - this promotes tumor formation. Hence, the potential for a vaccine that targets MUC1, either as a preventative (prophylactic) measure for high risk patients, or to reduce the risk of cancer recurrence. The vaccine could also be extremely helpful in cancer cases where surgery is not possible, such as pancreatic cancer, to be used together with chemotherapy.

Some cancer patients do not respond to hormonal therapy, such as aromatase inhibitors, Tamoxifen, or Herceptin. In 90% of these patients, MUC1 is overexpressed. Tripe-negative tumors are very aggressive and hard to treat.

Boons wrote:

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

Boons' vaccine is much simpler than other therapeutic ones, such as Provenge (for prostate cancer), because it is fully synthetic and can be manufactured in a laboratory with assembly-line precision.

The vaccine has three components: An adjuvant (an immune system booster)A component that encourages the production of T-helper cells (part of the immune system)A peptide linked to carbohydrate that makes the immune system target those cells that bear the MUC1 proteinsGendler, Boons and team are carrying out tests to see how effective the vaccine is against human cancer cells in culture. They are also planning to see how toxic (safe) it is. If all goes according to plan, Phase I trials to determine safety could be underway before the end of 2013.

Boons said:

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

Written by Christian Nordqvist

Copyright: Medical News Today
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posted by Mark Reddish on 13 Dec 2011 at 8:54 am

Great to see this article that identifies the potential for MUC1 vaccines. To bad it is 15 years after the first articles describing exactly the same thing. This is not a first, it is not even a second, it is after a long line of vaccine candidates long ago published and moved into clinical trials. Sandy knows better, she worked on some of those a long time ago. Shame on the author for not doing proper diligence. Theratope was a vaccine targeting the sugars on MUC1 and Stimuvax is phase III and is peptide core, exactly the same.

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posted by Carlos Rodriguez on 13 Dec 2011 at 10:12 am

I'm wondering if it would be possible for my dog who has a tumor on her lung could be an candidate for this experiment.

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posted by Jim West on 13 Dec 2011 at 10:15 am

If a cancer patient was willing to take all risks and asked for no guarantees, could he/she try the Boons vaccine?

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posted by Esther on 13 Dec 2011 at 10:34 am

There have been many successful treatments for cancer over the past 100 years..but the PHARMA industry will not allow these to be distributed widely because of the billion dollar industry cancer is. What would happen to oncologist, radiologists, etc. if a vaccine was found? The Susan Komen organization and the American Cancer Society would be out of business.
I pray this vaccine will be distributed soon..so many people have died in this holocaust!!

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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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Dana-Farber Cancer Institute. "Dana-Farber Offers Healthy Holiday Recipes And Food Tips To Fight Cancer With Your Fork This Holiday Season." Medical News Today. MediLexicon, Intl., 13 Dec. 2011. Web.
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