Deconstructing the molecular portrait of basal-like breast cancer

Yehiely, Fruma; Moyano, José V.; Evans, Joseph R.; Nielsen, Torsten O.; Cryns, Vincent L.

doi:10.1016/j.molmed.2006.09.004

Cited by 134 publications

(141 citation statements)

References 76 publications

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“…Furthermore, we would postulate that gene-expression profiling, clinical presentation and response to therapy also differ in the five FBC IHC subtypes, as already reported in SBC subtypes (Perou et al, 2000;Sorlie et al, 2001Sorlie et al, , 2003Carey et al, 2006;Hu et al, 2006). Taking into account these differences, the BC subtypes should be studied as distinct entities to better describe their features, as has been done for basal-like tumors Yehiely et al, 2006;VincentSalomon et al, 2007). …”

Section: Resultsmentioning

confidence: 99%

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

et al. 2007

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Five breast cancer subtypes have been described in sporadic breast cancer (SBC) using expression arrays: basal-like, ERBB2, normal breast-like, luminal A and B. These molecular subtypes show different genomic aberration patterns (GAPs). Recently, our group described these breast cancer subtypes in 50 non-BRCA1/2 familial tumors using immunohistochemistry assays. We extended this study to the other classes of familial breast cancer (FBC), including 62 tumors (18 BRCA1, 16 BRCA2 and 28 non-BRCA1/2), with the same panel of 25 immunohistochemical (IHC) markers and histological grade obtaining a similar classification. We combined these data with results generated by a 1 Mb BAC array-based CGH study to evaluate the genomic aberrations of each group. We found that BRCA1-related tumors are preferentially basal-like, whereas non-BRCA1/2 familial tumors are mainly luminal A subtype. We described distinct GAPs related to each IHC subtype. Basal tumors had a greater number of gains/losses, while luminal B tumors had more high-level DNA amplifications. Our data are similar to those obtained in SBC studies, highlighting the existence of distinct genetic pathways of tumor evolution, common to both SBC and FBC.

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Section: Resultsmentioning

confidence: 99%

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

et al. 2007

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“…The striking heterogeneity of BC in terms of tumor histology, clinical presentation, and response to treatment has been analyzed at the molecular level by gene-expression profiling, which has revealed that each breast tumor has its own unique molecular portrait, providing the basis for an improved molecular taxonomy of this disease [5,6]. BC is classified into major BC subtype signatures: ER-positive and ER-negative groups, which can be further subdivided into additional subgroups with distinct biological and clinical significance [7] (Figure 2).…”

Section: Classification Of Bcmentioning

confidence: 99%

“…Several basal-like gene products are important structural elements of basal epithelial cell such as the extracellular matrix (ECM) receptor α6β4 integrin, subunits of laminin-5 (an ECM ligand of α6β4 integrin), and bullous pemphigoid antigen (BPAG1). These proteins are components of hemidesmosomes specialized adhesive structures that anchor basal epithelial cells to the ECM via basal CK intermediate filament network (Table 2) [2,6]. These alterations can be related to the biologically aggressive phenotype of these TN tumors although this remains to be established in order to better guides current efforts to develop meaningful targeted approaches.…”

Section: Molecular Profile Of Blbcmentioning

confidence: 99%

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Molecular insights on basal-like breast cancer

Dominguez‐Valentin

Silva

Privat

et al. 2012

Breast Cancer Res Treat

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Molecular classification of breast cancer (BC) identified diverse subgroups that encompass distinct biological behaviour and clinical implications, in particular in relation to prognosis, spread, and incidence of recurrence. Basal like breast cancers (BLBC) compose up to 15% of BC and are characterized by lack of estrogen receptor (ER), progesterone receptor (PR), and HER-2 amplification with expression of basal cytokeratins 5/6, 14, 17, epidermal growth factor receptor (EGFR), and/or c-KIT. There is an overlap in definition between triple-negative BC and BLBC due to the triple-negative profile of BLBC. Also, most BRCA1-associated BCs are BLBC, triple negative, and express basal cytokeratins (5/6, 14, 17) and EGFR.There is a link between sporadic BLBC (occurring in women without germline BRCA1 mutations) with dysfunction of the BRCA1 pathway. Despite the molecular and clinical similarities, these subtypes respond differently to neoadjuvant therapy. BLBCs are associated with an aggressive phenotype, high histological grade, poor clinical behavior, and high rates of recurrences and/or metastasis. Their molecular features render these tumors especially refractory to anti-hormonal-based therapies and the overall prognosis of this subset remains poor. In this article the molecular profile, genomic and epigenetic characteristics as well as BRCA1 pathway dysfunction, clinicopathological behavior, and therapeutic options in BLBC are presented, with emphasis on the discordant findings in current literature.

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“…One of the most aggressive is the basal-like breast carcinoma (BLBC) often referred to as 'triple-negative' breast cancers because they do not express estrogen or progesterone receptors and they do not overexpress HER-2 (Yehiely et al, 2006). BLBC accounts for 15-25% of all breast cancers, and women diagnosed with it have short survival time and increased rates of relapse (Sorlie et al, 2001).…”

Section: Introductionmentioning

confidence: 99%