No evidence of clonal somatic genetic alterations in cancer-associated fibroblasts from human breast and ovarian carcinomas

Wen Qiu, Min Hu, Anita Sridhar, Ken Opeskin, Stephen Fox, Michail Shipitsin, Melanie Trivett, Ella R. Thompson, Manasa Ramakrishna, Kylie L. Gorringe, Kornelia Polyak, Izhak Haviv, Ian G. Campbell

Research output: Contribution to journalArticlepeer-review

238 Scopus citations


There is increasing evidence showing that the stromal cells surrounding cancer epithelial cells, rather than being passive bystanders, might have a role in modifying tumor outgrowth. The molecular basis of this aspect of carcinoma etiology is controversial. Some studies have reported a high frequency of genetic aberrations in carcinoma-associated fibroblasts (CAFs), whereas other studies have reported very low or zero mutation rates. Resolution of this contentious area is of critical importance in terms of understanding both the basic biology of cancer as well as the potential clinical implications of CAF somatic alterations. We undertook genome-wide copy number and loss of heterozygosity (LOH) analysis of CAFs derived from breast and ovarian carcinomas using a 500K SNP array platform. Our data show conclusively that LOH and copy number alterations are extremely rare in CAFs and cannot be the basis of the carcinoma-promoting phenotypes of breast and ovarian CAFs.

Original languageEnglish
Pages (from-to)650-655
Number of pages6
JournalNature Genetics
Issue number5
StatePublished - May 2008
Externally publishedYes

Bibliographical note

Funding Information:
We thank the Peter MacCallum Cancer Centre Tissue Bank, and particularly L. Devereux, for their assistance in accessing tumor samples. We also thank the Peter MacCallum Cancer Centre Microarray and Bioinformatics core facilities for their assistance in the SNP array analysis. This work was supported by a grant (ID 400107) from the National Health and Medical Research Council of Australia (NHMRC). W.Q. is supported by NHMRC Dora Lush Postgraduate Scholarship. E.R.T. is supported by National Breast Cancer Foundation Postgraduate Scholarship. M.R. is supported by Melbourne Research Scholarship from University of Melbourne, Australia. I.H. is supported by US Department of Defense WXH1-1-06-0643 and the Komen for the Cure grants. This work was supported in part by US National Institutes of Health (CA116235) and American Cancer Society (RSG-05-154-01-MGO) grants to K.P.


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