Molecular Determinants Of The Inflammatory Breast Cancer Phenotype

Main Category: Breast Cancer
Also Included In: Cancer / Oncology
Article Date: 06 Jan 2009 - 0:00 PST

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Despite advances in multimodality treatment, inflammatory breast cancer (IBC) remains the most aggressive and lethal form of breast cancer. The use of primary human IBC cell lines and functional in vivo xenograft cancer models have revealed characteristics innate to IBC thought to confer a strong metastatic potential and aggressive phenotype.

Classic descriptive markers in IBC (eg, estrogen and progesterone receptor status) often guide optimal therapy and aid in development of new diagnostic and prognostic technologies. Recent IBC research has examined two genes, RhoC GTPase and WISP3, which are concordantly altered in the majority of IBC tumors but not in non-IBC specimens. RhoC serves as a transforming oncogene by regulation of genes involved in the cell cycle, secretion of angiogenic factors, and activity of insulin-like growth factor (IGF).

WISP3 functions as a tumor-suppressor gene by modulation of IGF activity and resultant inhibition of cell proliferation, growth, and angiogenesis. Continued research with molecular analysis technology is imperative in order to harness differential gene expression and fully discover a signature profile of IBC. The ultimate goal is to reveal the specific molecular determinants that underlie its aggressive phenotype so that we may accurately identify markers of disease, improve diagnostic tools and predictors of response to treatment, and even suggest targeted IBC-specific therapies that afford improved survival.

Since its early descriptions by Lee and Tannenbaum in 1924, inflammatory breast cancer (IBC) has been recognized as the most aggressive and lethal form of primary breast cancer. With distinct clinical, pathologic, biologic, and molecular features, IBC presents unique challenges and opportunities to breast oncologists and breast cancer researchers.

Nathan W. Houchens, MD, Sofia D. Merajver, MD, PhD
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Source
www.cancernetwork.com