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Overexpression of Id-1 protein is a marker in colorectal cancer progression
Department of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Department of Oncology, Institute of Biomedicine and Surgery, Linköping University, Linköping, Sweden / Department of Pathology, Tangshan Gongren Hospital, Tangshan, P.R. China.
Department of Dermatology, Institute of Biomedicine and Surgery, Linköping University, Linköping, Sweden.
Department of Pathology, Tangshan Gongren Hospital, Tangshan, P.R. China.
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2008 (English)In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 19, no 2, p. 419-424Article in journal (Refereed) Published
Abstract [en]

Abstract: The inhibitor of differentiation/DNA binding 1 (Id-1), a negative regulator of basic helix-loop-helix transcription factors, plays an important role in the regulation of cell proliferation and differentiation. We examined the Id-1 expression by immunohistochemistry in 9 adenomas, 79 primary colorectal adenocarcinomas matched with 40 adjacent normal mucosa specimens and its relationship with clinicopathological factors. The Id-1 expression was increased in the carcinoma compared to the adjacent normal mucosa either in the unmatched and matched samples or to the adenoma. There was no significant difference in the Id-1 expression between normal mucosa and adenoma. The Id-1 expression of carcinoma was increased from Dukes' stages A to B, to C and to D. The cases with lymph node metastasis had a higher rate of a stronger Id-1 expression than those without lymph node metastasis. In conclusion, Id-1 overexpression plays an important role in colorectal cancer progression.

Place, publisher, year, edition, pages
Spandidos , 2008. Vol. 19, no 2, p. 419-424
National Category
Biochemistry Molecular Biology
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URN: urn:nbn:se:his:diva-2751DOI: 10.3892/or.19.2.419ISI: 000252648600016PubMedID: 18202790Scopus ID: 2-s2.0-38749123410OAI: oai:DiVA.org:his-2751DiVA, id: diva2:173933
Available from: 2009-02-18 Created: 2009-02-18 Last updated: 2025-02-20Bibliographically approved

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