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Oncogenes☆

Cancer Letters, 1988
Particular eukaryotic genes which play integral roles in the control of normal growth and differentiation programs are targets for mutagenic events which lead to the generation of malignancies. These genes, called proto-oncogenes can be activated to the oncogenic state by amplification, point mutation, deletion or chromosomal translocation. The protein
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Enabling oncogenes

Science, 2021
Melanoma can arise only from cells with a permissive chromatin ...
David W, Vredevoogd, Daniel S, Peeper
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Oncogenic Osteomalacia

Seminars in Musculoskeletal Radiology, 2002
Oncogenic osteomalacia is a rare paraneoplastic syndrome caused by bone and soft tissue tumors. The characteristic clinical, metabolic, and imaging findings are reviewed, as is the radiologist's role in evaluation and diagnosis. New insight into the pathophysiology of oncogenic osteomalacia is also presented.
Kelli Andresen, Edmister   +1 more
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Human oncogenes

Human Genetics, 1984
The information published on human oncogenes up to the fall of 1983 is reviewed. Retroviral oncogenes, proto-oncogenes, and cellular transforming genes are compared. Transforming genes derived from the ras gene family are described in detail. The different mechanisms of activation of proto-oncogenes are summarized.
K, Willecke, R, Schäfer
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Recessive oncogenes

Cancer, 1993
Tumor-suppressor genes (antioncogenes or recessive oncogenes) are cancer genes that achieve their oncogenic effect by mutational inactivation of both normal alleles. By contrast, oncogenes are created from protooncogenes by mutations that lead to aberrant functional activation. Mutation of multiple suppressor genes and/or oncogenes probably is required
R, Bookstein, D C, Allred
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RET oncogene

Current Opinion in Genetics & Development, 1996
RET mutations have been identified as the underlying cause of two congenital diseases that predominately affect tissues of neural crest origin: the MEN 2 cancer syndromes and a proportion of cases of dominantly inherited Hirschsprung disease, a disorder of gut development.
Y F, Mak, B A, Ponder
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Oncogenic signaling

Current Opinion in ONCOLOGY, 1996
Cancer develops when one or more cells begin to grow uncontrollably, presumably as a result of alterations in the highly regulated processes of normal cell division. These changes may result from germline or somatic mutations in genes that control normal cell proliferation, resulting in oncogenes.
C L, Jones, M A, Kane
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Oncogenes and anti-oncogenes

Current Opinion in Cell Biology, 1990
The study of oncogenes offers insights into many steps in signal transduction. Rapid progress is possible because of the combination of biochemistry and genetics--unique in vertebrate cell biology--the availability of specific clones and antibodies, sequence information, dominant mutants, and biochemical assays of function.
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Nuclear oncogenes

Current Opinion in Cell Biology, 1991
Ample evidence has accumulated in recent years to establish that most, if not all, nuclear proto-oncogenes are in fact sequence-specific DNA-binding proteins that modulate gene expression. Their synthesis or activity is modulated by extracellular signals or by cross talk between different classes of transcription factors.
J, Ghysdael, M, Yaniv
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Transient oncogenes

Medical Hypotheses, 2010
A given cancer is produced by a unique combination of genetic alterations that target specific genes, most often leading to activation of oncogenes and inactivation of tumor suppressor genes. Traditional oncogenes, such as RasV12, are involved in maintaining pro-survival and proliferation signals activated in the cell.
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