Evidence for transformation of fibroadenoma of the breast to malignant phyllodes tumor.

Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Applied immunohistochemistry & molecular morphology: AIMM / official publication of the Society for Applied Immunohistochemistry (Impact Factor: 1.63). 04/2009; 17(4):345-50. DOI: 10.1097/PAI.0b013e318194d992
Source: PubMed

ABSTRACT Fibroadenoma (FA) and phyllodes tumor (PT) of the breast are biphasic tumors composed of variable proportions of epithelial and stromal cells. We identified a case of synchronous FA and PT in the same breast mass. Using laser capture microdissection, loss of heterozygosity analysis was performed on these components to gain potential insight into the histogenetic relationship between FA and PT. Genomic DNA was analyzed at 10 microsatellite loci by polymerase chain reaction. Both tumors showed allelic loss at D7S522. In addition, phylloid tumor showed allelic loss at TP53 and D22S264, not observed in FA. Our data suggest that FA and PT are clonally related and allelic loss at TP53 and D22S264 may be implicated in the progression of FA to phyllode tumor.

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    ABSTRACT: Breast phyllodes tumors are fibroepithelial neoplasms with variable risk of aggressive local recurrence and distant metastasis, and the molecular pathogenesis is unclear. Here, we systematically study p16 and Rb expression in 34 phyllodes tumors in relation to proliferation. Tissue microarrays were constructed from 10 benign, 10 borderline, and 14 malignant phyllodes (5 cores/tumor) and from 10 fibroadenomas (2 cores/tumor). Tissue microarrays were labeled by immunohistochemistry for p16, Rb, and Ki-67 and by in situ hybridization for high-risk human papillomavirus. Cytoplasmic and nuclear p16 were scored by percentage labeling (0%-100%, diffuse >95%) and intensity. Nuclear Rb was scored by percentage labeling (0%-100%, diffuse >75%) and intensity. p16 and Rb labeling were repeated on whole sections of cases with Rb loss on the tissue microarray. Twenty-nine percent (4/14) malignant phyllodes showed diffuse strong p16 labeling with Rb loss in malignant cells (diffuse p16+/Rb-), whereas 21% (3/14) malignant phyllodes showed the reverse pattern of p16 loss with diffuse strong Rb (p16-/diffuse Rb+). Results were consistent between tissue microarrays and whole sections. No borderline phyllodes, benign phyllodes, or fibroadenoma showed diffuse p16+/Rb- or p16-/diffuse Rb+ phenotypes. No cases contained high-risk human papillomavirus. Average Ki-67 proliferation indices were 15% in malignant phyllodes, 1.7% in borderline phyllodes, 0.5% in benign phyllodes, and 0% in fibroadenoma. Ki-67 was highest in malignant phyllodes with diffuse p16+/Rb- labeling. In summary, 50% malignant phyllodes display evidence of Rb/p16 pathway alterations, likely reflecting p16 or Rb inactivation. These and other mechanisms may contribute to the increased proliferation in malignant phyllodes relative to other fibroepithelial neoplasms.
    Human pathology 07/2013; DOI:10.1016/j.humpath.2013.06.009 · 2.81 Impact Factor


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Feb 11, 2015