These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Misexpression of disrupted HMGI architectural factors activates alternative pathways of tumorigenesis.
    Author: Tkachenko A, Ashar HR, Meloni AM, Sandberg AA, Chada KK.
    Journal: Cancer Res; 1997 Jun 01; 57(11):2276-80. PubMed ID: 9187132.
    Abstract:
    Cancer arises from aberrations in the genetic mechanisms that control growth and differentiation. HMGI-C and HMGI(Y) are members of the HMGI family of architectural factors expressed in embryonic or undifferentiated cells and highly associated with transformation. Translocations of 12q13-15 in lipomas (fat cell tumors) disrupt HMGI-C and fuse its DNA-binding domains to novel transcriptional regulatory domains. This study shows that in a rare, karyotypically distinct group of human lipomas, rearrangements of 6p21-23 produce internal deletions within HMGI(Y). Activation of the rearranged alleles leads to expression of aberrant HMGI(Y) transcripts in differentiated adipocytes. A molecular analysis of these transcripts demonstrates that fusion of HMGI DNA-binding domains to putative transcriptional regulatory domains was not necessary for lipoma formation. However, such fusions may facilitate tumor development because activation of the wild-type HMGI allele, normally required for tumorigenesis, is bypassed in lipomas which express chimeric HMGI proteins. We hypothesize that HMGI misexpression in a differentiated cell is a pivotal event in benign tumorigenesis, and the molecular pathway of tumor development depends upon the precise nature of HMGI disruption.
    [Abstract] [Full Text] [Related] [New Search]