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Oct. 1, 2002 |
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Browse Archives n Lung n Breast n General n Prostate n Leukemia n Lymphoma n Colon n News/Issues |
New discovery of gene's role in tumor formation COLD SPRING HARBOR, NY -- Oct. 1, 2002 -- In a discovery that could lead to new anti-cancer drugs, scientists have found that a gene, long known for its role in cancer development, is essential for growing the added blood vessels tumors need to continue growing. The c-Myc gene is commonly activated in a variety of human tumors. Now, a research team led by Dr. John Cleveland at St. Jude Children's Research Hospital, have discovered that c-Myc regulates factors necessary for the growth of blood vessels into tumors, a process called angiogenesis. The new report appears in tomorrow's issue of Genes & Development. The Myc family of genes (c-Myc, N-Myc, and L-Myc) function in the control of cell proliferation, differentiation, and tumorigenesis. They have long been implicated in cancer as many tumor types contain cells that overproduce these genes. Despite identifying c-Myc's pivotal role in cell proliferation and how abnormal copies of it can contribute to cancer development, scientists have also suspected that c-Myc has additional roles in the progression of malignancy. Cleveland's team discovered that c-Myc is essential for tumor angiogenesis. "The goal of this study was to determine the role of c-Myc in development," Cleveland said in a prepared statement. "These studies established that c-Myc is essential for the formation of the vasculature that distributes blood throughout the organism, and that it did so by functioning as a master regulator of factors that are necessary for the growth of blood vessels and capillaries. The surprising result was that these studies also revealed why the Myc family of genes are activated in 70 percent of all human cancers," he said. Growing tumors need oxygen and nutrients to survive. Once a tumor's demand for oxygen and nutrients exceeds what the existing blood vessels can provide, a new vascular network is established (vasculogenesis) and new capillaries are formed (angiogenesis) to meet the tumor's increasing needs. Since the late nineties, when the first anti-angiogenic drugs entered clinical trials, much interest has centered upon the therapeutic approach to thwart a tumor's growth by cutting off its blood supply. By showing that c-Myc is essential for promoting vasculo- and angiogenesis, Cleveland and colleagues have revealed another possible route in this anti-angiogenic strategy. To evaluate the physiological role of c-Myc, Cleveland's team re-derived a strain of transgenic mice that are deficient in the gene. The c-Myc-deficient mice die as embryos due to cardiac and neural defects, but also display marked defects in vasculogenesis, angiogenesis, and the formation of red blood cells. The researchers found that the vascular defects in the c-Myc-deficient mice arise from the mis-expression of intercellular signals that coordinate blood vessel formation during development. Cleveland's team went on to show that c-Myc plays a similar role in orchestrating vasculogenesis during tumor formation. The researchers demonstrated that c-Myc-deficient embryonic stem cells have a diminished ability to form tumors in mice with compromised immune systems, and that the small tumors that sometimes form have dramatically less vasculature. Further study of the role of c-Myc in promoting human tumorigenesis is needed, but as it stands, this study presents strong evidence to suggest that the disruption of c-Myc may prove successful as an anti-angiogenic tool in cancer therapy. |
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