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c-myc and cutaneous vascular neoplasms.

Identifieur interne : 001E17 ( PubMed/Curation ); précédent : 001E16; suivant : 001E18

c-myc and cutaneous vascular neoplasms.

Auteurs : John K. Feller [États-Unis] ; Meera Mahalingam

Source :

RBID : pubmed:23221487

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English descriptors

Abstract

The c-myc proto-oncogene is involved in various cellular processes including cell growth, proliferation, and apoptosis. Overexpression and deregulated expression of the gene have been previously linked to several lineage-unrelated, aggressive, and poorly differentiated tumors. The expression of c-myc has also been implicated in hematopoiesis and has been shown to play a crucial role in angiogenesis via a vascular endothelial growth factor-dependent mechanism. This gives c-myc a dual oncogenic function in that tumor growth requires both cell proliferation and angiogenesis to ensure survival and confer an effective malignancy. Amplification of c-myc has been recently reported to be a recurrent genetic alteration in angiosarcomas secondary to irradiation and/or chronic lymphedema. Of note, however, no c-myc gene abnormalities have been demonstrated in cases of primary angiosarcomas or postradiation atypical vascular lesions. More recently, our own experience indicates that c-myc amplification is not normally found in the Kaposi sarcoma and cannot be correlated with expression of the c-Myc protein. This comprehensive review outlines the structure, normal functions, and effects of the deregulated expression of c-myc with particular emphasis on its role in angiogenesis and select cutaneous vascular neoplasms.

DOI: 10.1097/DAD.0b013e31827aad83
PubMed: 23221487

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Le document en format XML

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<div type="abstract" xml:lang="en">The c-myc proto-oncogene is involved in various cellular processes including cell growth, proliferation, and apoptosis. Overexpression and deregulated expression of the gene have been previously linked to several lineage-unrelated, aggressive, and poorly differentiated tumors. The expression of c-myc has also been implicated in hematopoiesis and has been shown to play a crucial role in angiogenesis via a vascular endothelial growth factor-dependent mechanism. This gives c-myc a dual oncogenic function in that tumor growth requires both cell proliferation and angiogenesis to ensure survival and confer an effective malignancy. Amplification of c-myc has been recently reported to be a recurrent genetic alteration in angiosarcomas secondary to irradiation and/or chronic lymphedema. Of note, however, no c-myc gene abnormalities have been demonstrated in cases of primary angiosarcomas or postradiation atypical vascular lesions. More recently, our own experience indicates that c-myc amplification is not normally found in the Kaposi sarcoma and cannot be correlated with expression of the c-Myc protein. This comprehensive review outlines the structure, normal functions, and effects of the deregulated expression of c-myc with particular emphasis on its role in angiogenesis and select cutaneous vascular neoplasms.</div>
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