TY - JOUR
T1 - X chromosomal abnormalities in basal-like human breast cancer
AU - Richardson, Andrea L.
AU - Wang, Zhigang C.
AU - De Nicolo, Arcangela
AU - Lu, Xin
AU - Brown, Myles
AU - Miron, Alexander
AU - Liao, Xiaodong
AU - Iglehart, J. Dirk
AU - Livingston, David M.
AU - Ganesan, Shridar
N1 - Funding Information:
We would like to thank Dr. Charles Lee of the DF/HCC Cytogenetics Core Facility for the performance of X centromere FISH analysis. We are also grateful for the extraordinarily helpful input of multiple members of the Iglehart and Livingston laboratories. This work was supported by a generous gift in support of cancer research from Deborah and Robert First. It was also supported by the Dana-Farber/Harvard SPORE in Breast Cancer, by other grants from the National Cancer Institute, and by the Breast Cancer Research Foundation. S.G. was a recipient of a Deborah and Robert First Fellowship, and A.d.N. was a fellow of the International Agency for Research on Cancer. D.M.L. serves as a consultant to and is a research grantee of Novartis Oncology.
PY - 2006/2
Y1 - 2006/2
N2 - Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic.
AB - Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic.
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U2 - 10.1016/j.ccr.2006.01.013
DO - 10.1016/j.ccr.2006.01.013
M3 - Article
C2 - 16473279
AN - SCOPUS:32044453343
VL - 9
SP - 121
EP - 132
JO - Cancer Cell
JF - Cancer Cell
SN - 1535-6108
IS - 2
ER -