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H. Lee Moffitt Researchers Discover Potential Targets to Reduce Risk of Stem Cell Transplants
By Dross at 2007-02-21 00:58

Inhibiting one gene -- even temporarily -- can improve cure rates for blood cancer patients who receive stem cell transplants. This strategy may also help patients with genetic and autoimmune diseases who are also treated with stem cell transplants. Researchers at H. Lee Moffitt Comprehensive Cancer Center in Tampa, led by William Kerr Ph.D., and funded by The Leukemiaterm & Lymphomaterm Society, have discovered that the SHIP gene plays a critical role in graft vs. host disease (GvHD), in which a donor's immune cells (the "graft") attack a stem cell transplant patient's healthy tissue (the "host") as well as cancer cells. By using genetically engineered mice, the researchers have shown that inactivating the SHIP gene for just one week protects transplant recipients from acute GvHD. This protection is seen even when the graft contains extra immune cells to help the graft "take" or when the graft cells are completely mismatched to the recipient. The findings will be published in the March 1st issue of the "Journal of Immunology."

read more | 1938 reads

Cancer drug can extend survival in patients with deadly brain tumors
By Dross at 2007-02-20 23:56

DURHAM, N.C. -- Avastinterm, a relatively new type of drug that shrinks cancerous tumors by cutting off their blood supply, can slow the growth of the most common and deadly form of brain cancer, a pilot study conducted at Duke University Medical Center has found. The study marks the first time that Avastin has been tested against brain tumors, the researchers said. The drug, whose chemical name is bevacizumabtermterm, currently is used to treat lung and colorectal cancers. The researchers tested the effectiveness of Avastin in conjunction with a standard chemotherapyterm agent in patients with recurrent cancerous brain tumors called gliomas. They found that the two drugs together halted tumor growth up to twice as long as comparative therapies.

read more | 3343 reads

Researchers identify cell pathway in colon cancer
By Dross at 2007-02-20 23:38

CLEVELAND, OH - For the one in 18 men and women who will be diagnosed with cancer of the colon and rectum during their lifetime and over 150,000 people diagnosed on a yearly basis, today's genetic research news offers some optimism. In a study to be published in the Proceedings of the National Academy of Sciences, {PNAS Online Edition Feb. 20-23, 2007} led by Zhenghe John Wang, Ph.D., Assistant Professor, Department of Genetics at Case Western Reserve University School of Medicine and Case Comprehensive Cancer Center, researchers have identified a cell pathway which plays a critical role in the development of colon cancer. This pathway may also play a role in the development of lung and stomach cancers. Investigators say they have identified STAT3 {signal transducer and activator of transcription 3}, as a target regulated by PTPRT {Receptor Protein tyrosine phosphatase T}, which was previously identified to be mutated in colon, lung and stomach cancer patients.

read more | 1183 reads

Gene profiling predicts resistance to breast cancer drug Herceptin
By Dross at 2007-02-20 23:36

PHILADELPHIA -- Using gene chips to profile tumors before treatment, researchers at Harvard and Yale Universities found markers that identified breast cancer subtypes resistant to Herceptin, the primary treatment for HER2-positive breast cancer. They say this advance could help further refine therapy for the 25 to 30 percent of breast cancer patients with this class of tumor. In the February 15 issue of Clinical Cancer Research, the researchers found that HER2-positive tumors that did not respond to Herceptin expressed certain basal markers, growth factors and growth factor receptors. One of these, insulin-growth factor receptor 1(IGF-1R), was associated with a Herceptin response rate that was half that of tumors that did not express IGF-1R. They also discovered that resistant tumors continue to over-express the HER2 growth factor protein -- an important finding given that many scientists had thought that loss of HER2 was likely responsible for Herceptin resistance. "Herceptin has revolutionized the care of HER2-positive breast cancer for many patients, but unfortunately, not for some.

read more | 1 comment | 1435 reads

Antibody signal may redirect inflammation to fuel cancer
By Dross at 2007-02-19 21:19

As evidence mounts that the body's normally protective inflammation response can drive some precancerous tissues to become fully malignant, UCSF scientists report discovering an apparent trigger to this potentially deadly process. Typically, the "innate" immune system's Pac-Man-like white blood cells, or leukocytes, engulf and destroy invading microbes when receptors on their surface receive a signal from serum in the blood -- often an antibodyterm produced by a B cell in the separately evolved "acquired" immune system.

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Scientists uncover new target in cancer mutation puzzle
By Dross at 2007-02-19 09:28

University of Rochester scientists, while investigating the two most frequent types of mutations in cancer, discovered a possible new route to treatment that would take advantage of the mutations instead of trying to repair them. The research is reported online this week in the journal Nature Structural & Molecular Biology. In experiments with rodent and human cells, co-authors Mingxuan Xia, Ph.D., and Hartmut Land, Ph.D., explored how the Rho family of proteins, which are involved in cell movement, and thus in the progression from benign to malignant cancer, are controlled by two well-known cancer genes, p53 and Ras. By closing in on this deadly collaboration, researchers showed for the first time why some molecules such as Rho are targeted by cancer genes and how they might lead to a promising way to intervene against cancer.

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Cancer that colonizes our bodies
By Dross at 2007-02-19 09:25

To Robert C. von Borstel, cancer is a metaphorical example of the perfect invasion by a founder species. Like the first pregnant finch that landed on a deserted island in the Galapagos Archipelago, the first cancer cell in the human body has to undergo many mutations through many generations to establish itself as an invader of different organs in the body. But once it is there, like any newly stabilized species in different ecological niches, cancer is tough to get rid of. The former University of Alberta biologist has been working with DNA - the molecule that carries our cells genetic information - ever since 1947, six years before its structure was described by Watson and Crick. His fundamental Natural Sciences and Engineering Research Council (NSERC) work on how radiation can kill cells, how the DNA molecule itself can control mutation, and other research has earned him a fellowship in the American Association for the Advancement for Science (AAAS). Now, von Borstel, at the AAAS conference in San Francisco, to be held between Feb. 15 and 19, will deliver a talk about how cancer cell mutation and selection are metaphorically similar to how a new species begins its evolution.

read more | 774 reads

Cancer cells more likely to genetically mutate
By Dross at 2007-02-19 09:23

When cells become cancerous, they also become 100 times more likely to genetically mutate than regular cells, researchers have found. The findings may explain why cells in a tumor have so many genetic mutations, but could also be bad news for cancer treatments that target a particular gene controlling cancer malignancy. The research was led by Dr. Lawrence Loeb, professor of pathology and biochemistry at the University of Washington School of Medicine in Seattle. Loeb will present his research Feb. 18 at the meeting of the American Association for the Advancement of Science in San Francisco. Most types of cancer are believed to begin with a random genetic mutation that makes a normal cell go horribly awry. This is followed by mutations, which endow the cancer cells with properties allowing them to grow without normal controls to become a tumor. These mutated genes would be targets for chemotherapyterm. But Loeb had another idea that he originally hatched many years ago, what if the cancer cells changed somehow, and became much more likely to mutate? These "mutator" cells would develop dangerous genetic mutations at a much faster rate than normal cells, which might account for the high number of mutations seen in tumor cells. Since the technology of cancer genetics has dramatically improved, Loeb and his colleagues have only recently been able to test this hypothesis. They found that tumor tissue had random mutation rates up to 100 times higher than normal tissue from the same patient. The "mutator" hypothesis seems to be correct.

read more | 3 comments | 741 reads

Geron’s GRN163L Headed to Phase I Clinical Trials in Lung Cancer Patients
By HCat at 2007-02-17 08:26

    Geron Corporation has published preclinical data on GRN163L indicating anti-tumor and anti-metastaticterm activity. Released in this month’s Cancer Research, the new study ascribes the anti-metastatic effects of GRN163L to its unique structure, and not it known human telomerase RNA (hTR) inhibition. By successive shortening of this oligonucleotide (specifically N3’ to P5’ Thio-Phosphoramidate), the authors show that cell adhesion in a lung cell line is reduced due the structural aspects of GRN163L and not is inhibitory effect on hTR. Also, in mice models of metastatic lung cancer, the researchers show a reduced tumor burden in mice treated with GRN163L upon inoculation with the cancer cells.

read more | 3972 reads

HIV protein enlisted to help kill cancer cells
By Dross at 2007-02-17 03:50

        Cancer cells are sick, but they keep growing because they don't react to internal signals urging them to die. Now researchers at Washington University School of Medicine in St. Louis have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around - HIV. "HIV knows how to insert itself into many different types of cells," says senior author William G. Hawkins, M.D., assistant professor of surgery and a member of the Siteman Cancer Center at the School of Medicine and Barnes-Jewish Hospital. "A portion of the HIV protein called TAT can transport biologically active compounds into cells. TAT is small, but it can move massive molecules. You could almost hook TAT up to a train, and TAT would drag it inside a cell. So we've taken advantage of this ability."

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Adult Stem Cells Decide the Fate of Their Daughters
By Dross at 2007-02-16 22:45

The amount of the signaling protein Delta, shown in red, in an intestinal stem cell (ISC) determines the fate of its daughter cells. In panel A, an ISC that has just produced an enterocyte (EC) shows a high level of Delta (arrow). In panel B, an ISC that has just produced an enteroendocrine cell (ee) lacks detectable Delta. Adult stem cells call the shots when it comes to their daughters' destinies. That's the take-home lesson for adult stem cells in the intestines of fruit flies, according to new studies by researchers at the Howard Hughes Medical Institute (HHMI). The researchers found that intestinal stem cells make important decisions about their fate by communicating directly with their daughter cells, instructing them to become one of two possible cell types.

read more | 1473 reads

Seattle Genetics Granted Orphan Drug Designation for AML and Hodgkin’s Disease Drugs
By HCat at 2007-02-16 06:15

    The FDA has approved orphan drug status for Seattle Genetic’s two drugs SGN-33 and SGN-35. Orphan drug status allows Seattle Genetics to obtain marketing exclusivity of the drug upon approval. More importantly, it also allows Seattle Genetics an opportunity to obtain grant funding from the U.S. government to support clinical trials and defray costs. The Orphan Drug Act encourages companies to develop treatment for diseases that affect fewer than 200,000 people a year.

    SGN-33 has shown anti-tumor effects in phase I studies. SGN-33 (lintuzumab) is a humanized monoclonal antibodyterm that targets the CD33 antigen. SGN-33 is expected to enter clinical phase II by the end of 2007 testing mainly older patients with AML and MDS.

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Genta Cites Publication of Study Showing Improved Outcomes in CLL Patients Treated With Genasense(R) Plus Chemotherapy
By Dross at 2007-02-16 03:11

BERKELEY HEIGHTS, N.J., Feb. 14 -- Genta Incorporated (NASDAQ:GNTA) today announced the publication of findings from a Phase 3 trial of the Company's lead anticancer drug, Genasense(R) (oblimersen sodium) Injection, when used in combination with chemotherapyterm for treatment of patients with relapsed or refractory chronic lymphocytic leukemiaterm (CLL). The findings were published on-line this week in the Journal of Clinical Oncology, ahead of its tentatively scheduled print publication date of March 20, 2007. Conducted at 100 centers in the U.S., Europe, Canada, Australia and South America, patients with relapsed or refractory CLL received fludarabine plus cyclophosphamide (Flu/Cy) chemotherapy with or without Genasense. This trial -- the first randomized study ever conducted in this population -- achieved its primary endpoint, which was a statistically significant increase in the proportion of patients who achieved a complete or nodular partial response (CR/nPR) (17% vs. 7%; P=0.025). Patients who achieved CR/nPR experienced the disappearance of all predefined CLL symptoms, including fever, night sweats, fatigue, abdominal discomfort due to an enlarged spleen, and impaired mobility due to swollen lymph nodes. The key secondary endpoint -- duration of CR/nPR -- was also significantly longer for patients treated with Genasense (median = not reached but will exceed 36 months in the Genasense group vs. 22 months for patients treated with chemotherapy alone). Among patients who achieved a CR/nPR with Genasense, 70 percent were alive at three years versus 38 percent for the control arm. Among patients who achieved a partial response, 45 percent who received Genasense were alive at three years compared to 33 percent for the control arm. The lead and senior authors of the article are, respectively, Dr. Susan O'Brien, Professor of Medicine, Department of Leukemia, M.D. Anderson Cancer Center, and Dr. Kanti R. Rai, Chief, Hematology and Oncology, North Shore/Long Island Jewish Medical Center, and Professor of Medicine, Albert Einstein College of Medicine. An abstract of this article that addresses safety and efficacy in the trial can be accessed at:

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Active lifestyle reduces risk of invasive breast cancer
By Dross at 2007-02-15 23:55

PHILADELPHIA -- Six or more hours per week of strenuous recreational activity may reduce the risks of invasive breast cancer by 23 percent, according to researchers from the University of Wisconsin Paul P. Carbone Comprehensive Cancer Center (UWCCC). Their report in the February issue of Cancer Epidemiology Biomarkers & Prevention, based on a survey of over 15,000 women, shows that exercise has a protective effect against invasive breast cancer throughout a woman's lifetime.


The results provide further evidence that for most women physical activity may reduce the risk of invasive breast cancer, the researchers concluded. To gain further insights into the mechanisms of risk reduction for breast cancer, the researchers investigated the relationship between physical activity and breast cancer risk in a population-based case control study in Massachusetts, New Hampshire, and Wisconsin. During structured telephone interviews, the researchers questioned 7,630 women without breast cancer, 1,689 survivors of in situ, or non-invasive, breast cancer and 6,391 survivors of invasive breast cancer, all between the ages of 20 and 69. They asked detailed questions about physical activity, occupation, family history of breast cancer, menopausal status, and body mass index. According to the researchers, women who exercised had a reduced risk of developing invasive breast cancer provided they didn't have a family history of breast cancer. This reduction in risk was apparent whether the physical activity took place early in life, in the postmenopausal years, or in the recent past. "A woman's hormone levels naturally fluctuate throughout her life, and we have found that exercise likely offers protection against breast cancer regardless of a woman's stage in life," said Brian Sprague, a UWCCC research assistant and lead author of the study.

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Shortening chromosomes cause for earlier cancer onset in families with rare syndrome
By Dross at 2007-02-15 23:53

PHILADELPHIA -- In families with a high incidence of Li-Fraumeni syndrome, the ends of individuals chromosomes act somewhat like a lit fuse, according to researchers at The Hospital for Sick Children in Toronto. Their findings detail how telomeres, the ends of the chromosomes, shorten with every successive generation, leading to more severe cancers at an earlier age. Their results, published in the February 15 issue of the journal Cancer Research, could represent the first biological marker for clinical monitoring in families with Li-Fraumeni syndrome, and could shed light on the important area of aging in cancer research "We have known since 1990 that Li-Fraumeni was associated with inheritance of a mutated form of the p53 tumor suppressor gene, but we also noticed each generation developed cancer earlier than the preceding generation," said David Malkin, M.D., the study's principal investigator, and co-director of the Cancer Genetics Program at The Hospital for Sick Children at the University of Toronto. "By studying blood samples taken from families in which members have Li-Fraumeni, we have discovered that telomeres become shorter in each generation of disease carriers, leading to a genetic instability that primes them for progressively earlier cancers."

read more | 941 reads


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