In a new study described in the journal Oncogene, researchers reveal how a key player in cell growth, immunity and the inflammatory response can be transformed into a primary contributor to tumor growth.
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A University of Colorado Cancer Center study recently published in the journal Cell Death & Disease shows that turning up a few microRNAs a little may offer as much anti-breast-cancer activity as turning up one microRNA a lot - and without the unwanted side effects.
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Cancer is a complex disease, in which cells undergo a series of alterations, including changes in their architecture; an increase in their ability to divide, to survive and to invade new tissues or metastasis.
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Researchers at Moffitt Cancer Center have found that a deficiency in an important anti-tumor protein, p53, can slow or delay DNA repair after radiation treatment. They suggest that this is because p53 regulates the expression of two enzymes (JMJD2b and SUV39H1) that control the folding of DNA.
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Presence of the genetic mutation BRAF V600E was significantly associated with increased cancer-related death among patients with papillary thyroid cancer (PTC); however, because overall mortality in PTC is low and the association was not independent of tumor characteristics, how to use this information to manage mortality risk in patients with PTC is unclear, according to a study in the April 10 issue of JAMA, a Genomics theme issue.
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Researchers have discovered a new mechanism by which the human papilloma virus (HPV) causes head and neck cancer, and they have designed a drug to block that mechanism. Though further research is needed, the new agent might offer a safer treatment for these tumors when combined with a tapered dose of standard chemotherapy.
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The American Cancer Society, the largest non-government, not-for-profit funding source of cancer research in the United States, has awarded 175 national research and training grants totaling $79,073,250 for fiscal year 2013.
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Researchers from The Wistar Institute explain a new molecular mechanism behind the phenomenon of oncogene-induced senescence. By depriving the cell of the ability to make new nucleotides-the building blocks of DNA molecules-cells can suppress cancer development by forcing a damaged cell into a senescent state, where the cell remains alive yet cannot reproduce.
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Researchers at Moffitt Cancer Center have determined that the overexpression of microRNA-155 (miR-155), a short, single strand of ribonucleic acid encoded by the miR-155 host gene, promotes the growth of blood vessels in tumors, tumor inflammation, and metastasis.
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Trovagene, Inc., today announced the commercial availability of its urine-based HPV-HR (high-risk) assay, a molecular human papillomavirus test.
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Researchers at the University of North Carolina at Chapel Hill have discovered that a protein found in the cells surrounding pancreatic cancers play a role in the spread of the disease to other parts of the body.
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Molecular driven therapeutic targets have resulted in a paradigm shift in the treatment of advanced lung adenocarcinoma. However, in early non-small cell lung cancer, surgical resection remains the treatment of choice with adjuvant chemotherapy.
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A team of Canadian and international cancer researchers led by Dr. Brenda Gallie at the Princess Margaret Cancer Centre, University Health Network, has discovered a new type of retinoblastoma, a rapidly developing eye cancer that affects very young babies- a finding that can immediately change clinical practice and optimize care for these children.
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Two University of Colorado Cancer Center studies show that the protein receptor Mer is overexpressed in many leukemias, and that inhibition of this Mer receptor results in the death of leukemia cells - without affecting surrounding, healthy cells.
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Some cellular proteins have multiple, and occasionally opposing, functions. Professor Adrian Krainer and colleagues at Cold Spring Harbor Laboratory demonstrate in a paper published online today in Molecular Cell that the oncogenic protein SRSF1 can also trigger a stop in cell growth and prevent cancerous proliferation by stabilizing p53, the powerful tumor-suppressor protein.
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Dr. Lewis Cantley, a leading cancer researcher credited with discovering a family of enzymes fundamental to understanding cancer, was named a winner of the inaugural Breakthrough Prize in Life Sciences, the world’s richest academic prize for medicine and biology. The prize, which carries a $3 million cash award, recognizes excellence in research aimed at curing intractable diseases and human life.
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Napoleone Ferrara, MD, PhD, the molecular biologist credited with helping decipher how tumors grow and now senior deputy director for basic sciences at the University of California, San Diego Moores Cancer Center, was today named one of 11 recipients of the inaugural Breakthrough Prize in Life Sciences, which comes with a $3 million cash award.
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Researchers at Moffitt Cancer Center have found a potential targeted therapy for patients with tobacco-associated non-small cell lung cancer. It is based on the newly identified oncogene IKBKE, which helps regulate immune response.
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Though a small group of proteins, the family called Ras controls a large number of cellular functions, including cell growth, differentiation, and survival. And because the protein has a hand in cellular division, mutated Ras, which can be detected in one-third of all tumors, contributes to many human cancers by allowing for the rapid growth of diseased cells.
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Biologists at Tufts University School of Arts and Sciences have discovered a bioelectric signal that can identify cells that are likely to develop into tumors. The researchers also found that they could lower the incidence of cancerous cells by manipulating the electrical charge across cells' membranes.
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