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      Genetic characterization of breast cancer and implications for clinical management

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          Abstract

          Breast cancer is a genetic disease caused by the accumulation of mutations in neoplastic cells. In the last few years, high-throughput microarray-based molecular analysis has provided increasingly more coherent information about the genetic aberrations in breast cancer. New biomarkers and molecular techniques are slowly becoming part of the diagnostic and prognostic armamentarium available for pathologists and oncologists to tailor the therapy for breast cancer patients. In this review, we will focus on the contribution of breast cancer somatic genetics to our understanding of breast cancer biology and its impact on breast cancer patient management.

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          Gene expression and benefit of chemotherapy in women with node-negative, estrogen receptor-positive breast cancer.

          Soonmyung Paik, Gong Tang, Steven Shak … (2006)
          The 21-gene recurrence score (RS) assay quantifies the likelihood of distant recurrence in women with estrogen receptor-positive, lymph node-negative breast cancer treated with adjuvant tamoxifen. The relationship between the RS and chemotherapy benefit is not known. The RS was measured in tumors from the tamoxifen-treated and tamoxifen plus chemotherapy-treated patients in the National Surgical Adjuvant Breast and Bowel Project (NSABP) B20 trial. Cox proportional hazards models were utilized to test for interaction between chemotherapy treatment and the RS. A total of 651 patients were assessable (227 randomly assigned to tamoxifen and 424 randomly assigned to tamoxifen plus chemotherapy). The test for interaction between chemotherapy treatment and RS was statistically significant (P = .038). Patients with high-RS (> or = 31) tumors (ie, high risk of recurrence) had a large benefit from chemotherapy (relative risk, 0.26; 95% CI, 0.13 to 0.53; absolute decrease in 10-year distant recurrence rate: mean, 27.6%; SE, 8.0%). Patients with low-RS (< 18) tumors derived minimal, if any, benefit from chemotherapy treatment (relative risk, 1.31; 95% CI, 0.46 to 3.78; absolute decrease in distant recurrence rate at 10 years: mean, -1.1%; SE, 2.2%). Patients with intermediate-RS tumors did not appear to have a large benefit, but the uncertainty in the estimate can not exclude a clinically important benefit. The RS assay not only quantifies the likelihood of breast cancer recurrence in women with node-negative, estrogen receptor-positive breast cancer, but also predicts the magnitude of chemotherapy benefit.
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            Stromal gene expression predicts clinical outcome in breast cancer.

            Greg Finak, Nicholas Bertos, François Pépin … (2008)
            Although it is increasingly evident that cancer is influenced by signals emanating from tumor stroma, little is known regarding how changes in stromal gene expression affect epithelial tumor progression. We used laser capture microdissection to compare gene expression profiles of tumor stroma from 53 primary breast tumors and derived signatures strongly associated with clinical outcome. We present a new stroma-derived prognostic predictor (SDPP) that stratifies disease outcome independently of standard clinical prognostic factors and published expression-based predictors. The SDPP predicts outcome in several published whole tumor-derived expression data sets, identifies poor-outcome individuals from multiple clinical subtypes, including lymph node-negative tumors, and shows increased accuracy with respect to previously published predictors, especially for HER2-positive tumors. Prognostic power increases substantially when the predictor is combined with existing outcome predictors. Genes represented in the SDPP reveal the strong prognostic capacity of differential immune responses as well as angiogenic and hypoxic responses, highlighting the importance of stromal biology in tumor progression.
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              Breast cancer molecular subtypes respond differently to preoperative chemotherapy.

              Roman Rouzier, Charles Perou, W Symmans … (2005)
              Molecular classification of breast cancer has been proposed based on gene expression profiles of human tumors. Luminal, basal-like, normal-like, and erbB2+ subgroups were identified and were shown to have different prognoses. The goal of this research was to determine if these different molecular subtypes of breast cancer also respond differently to preoperative chemotherapy. Fine needle aspirations of 82 breast cancers were obtained before starting preoperative paclitaxel followed by 5-fluorouracil, doxorubicin, and cyclophosphamide chemotherapy. Gene expression profiling was done with Affymetrix U133A microarrays and the previously reported "breast intrinsic" gene set was used for hierarchical clustering and multidimensional scaling to assign molecular class. The basal-like and erbB2+ subgroups were associated with the highest rates of pathologic complete response (CR), 45% [95% confidence interval (95% CI), 24-68] and 45% (95% CI, 23-68), respectively, whereas the luminal tumors had a pathologic CR rate of 6% (95% CI, 1-21). No pathologic CR was observed among the normal-like cancers (95% CI, 0-31). Molecular class was not independent of conventional cliniocopathologic predictors of response such as estrogen receptor status and nuclear grade. None of the 61 genes associated with pathologic CR in the basal-like group were associated with pathologic CR in the erbB2+ group, suggesting that the molecular mechanisms of chemotherapy sensitivity may vary between these two estrogen receptor-negative subtypes. The basal-like and erbB2+ subtypes of breast cancer are more sensitive to paclitaxel- and doxorubicin-containing preoperative chemotherapy than the luminal and normal-like cancers.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (publisher-id): jcmm
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley & Sons, Ltd (Chichester, UK )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Print): October 2009
                Publication date (Electronic): 14 September 2009
                Volume: 13
                Issue: 10
                Pages: 4090-4103
                Affiliations
                Molecular Pathology Laboratory, The Breakthrough Breast Cancer Research Centre, Institute of Cancer Research London, UK
                Author notes
                *Correspondence to: Jorge S. REIS-FILHO, M.D., Ph.D., F.R.C.Path, The Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, 237 Fulham Road, London, SW3 6JB, UK. Tel.: +44 2071535167 Fax: +44 2071535533 E-mail: Jorge.Reis-Filho@ 123456icr.ac.uk

                Guest Editor: G. Bussolati

                Article
                DOI: 10.1111/j.1582-4934.2009.00906.x
                PMC ID: 4496116
                PubMed ID: 19754664
                SO-VID: cae64887-a5b9-4c35-b112-3feccf808a03
                Copyright © © 2009 The Authors Journal compilation © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
                History
                Date received : 14 August 2009
                Date accepted : 08 September 2009
                Categories
                Subject: Reviews

                ScienceOpen disciplines: Molecular medicine
                Keywords: microarray,comparative genomic hybridization,gene expression,biomarker,therapeutic target
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: microarray, comparative genomic hybridization, gene expression, biomarker, therapeutic target

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