Authors: | Perk, J.; Iavarone, A.; Benezra, R. |
Article Title: | Id family of helix-loop-helix proteins in cancer |
Abstract: | Over the past few decades, biologists have identified key molecular signatures associated with a wide range of human cancers. Recently, animal models have been particularly useful in establishing whether such signatures have functional relevance; the overexpression of pro-oncogenic or loss of anti-oncogenic factors have been evaluated for their effects on various tumour models. The aim of this review is to analyze the potential role of the inhibitor of DNA binding (Id) proteins in cancer and examine whether deregulated Id activity is tumorigenic and contributes to hallmarks of malignancy, such as loss of differentiation (anaplasia), unrestricted proliferation and neoangiogenesis. |
Keywords: | protein expression; unclassified drug; oncoprotein; review; nonhuman; protein function; neoplasms; cell proliferation; phenotype; cell cycle; gene overexpression; inhibitor of differentiation 1; protein depletion; tumor markers, biological; genotype; cell renewal; cell differentiation; neovascularization, pathologic; carcinogenesis; transcription factors; cancer invasion; endothelium cell; models, animal; cancer inhibition; oncogene; transcription regulation; carcinogenicity; inhibitor of differentiation protein 1; inhibitor of differentiation 2; tumor growth; tumor vascularization; retinoblastoma protein; repressor proteins; anaplasia; anaplastic carcinoma; knockout mouse; transcription factor ets; inhibitor of differentiation 3; helix loop helix protein; helix-loop-helix motifs; inhibitor of differentiation 4 |
Journal Title: | Nature Reviews Cancer |
Volume: | 5 |
Issue: | 8 |
ISSN: | 1474-175X |
Publisher: | Nature Publishing Group |
Date Published: | 2005-08-01 |
Start Page: | 603 |
End Page: | 614 |
Language: | English |
DOI: | 10.1038/nrc1673 |
PUBMED: | 16034366 |
PROVIDER: | scopus |
DOI/URL: | |
Notes: | --- - "Cited By (since 1996): 205" - "Export Date: 24 October 2012" - "CODEN: NRCAC" - "Source: Scopus" |