Metaplastic Breast Carcinoma with Squamous Differentiation: Molecular and Clinical Analysis of Six Cases

Kochhar, Ruby; Howard, Eugene M.; Umbreit, Jay N.; Lau, Stephen K.

doi:10.1111/j.1075-122x.2005.00031.x

Cited by 21 publications

(12 citation statements)

References 18 publications

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“…p53 protein overexpression analysed by immunohistochemistry has been demonstrated in MBC with squamous differentiation (66% of six cases)51 and in up to 61% of MBC, compared with 20%–40% of IDC NST 49. Lien et al 43 found p53 overexpression in 71% of 14 cases of MBC, but p53 mutations identified by direct sequencing were only found in four of the 10 cases, possibly due to decreased sensitivity of Sanger sequencing on formalin fixed, paraffin embedded material.…”

Section: Molecular Features Of Mbcmentioning

confidence: 99%

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Molecular alterations in metaplastic breast carcinoma

et al. 2013

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Metaplastic carcinoma of the breast is a rare and heterogeneous subtype of breast carcinoma with a generally poor outcome, and few therapeutic options once disease recurs or progresses. Metaplastic carcinomas of the breast are usually of a larger size at diagnosis, with less frequent nodal metastasis compared with invasive ductal carcinoma no special type, and lack hormone and HER2 receptor expression. Recent research has revealed some potentially actionable genetic changes in a subset of these rare tumours. However, ongoing efforts to further characterise the genetic basis and the molecular alterations underlying the distinctive morphological and clinical characteristics of these tumours are needed in order to identify new targets for treatment. This review will describe the theories of pathogenesis of metaplastic breast carcinoma, and highlight genetic changes and potential therapeutic targets in this generally poor prognosis malignancy.

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Section: Molecular Features Of Mbcmentioning

confidence: 99%

“…High levels of the angiogenesis markers VEGF and hypoxia inducible factor (HIF)-1α have been observed in metaplastic carcinomas, particularly in MBC with squamous differentiation 51 53 54…”

Section: Molecular Features Of Mbcmentioning

confidence: 99%

Molecular alterations in metaplastic breast carcinoma

et al. 2013

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“…Although p53 status is not available for this dataset, we note that medullary breast cancers, which are poorly differentiated and aggressive if left untreated, are known to harbor frequent p53 mutations (26). Metaplastic breast cancer, which is characterized by the coexistence of carcinoma with nonepithelial cellular elements suggestive of defects in differentiation commitment, also frequently contains mutant p53 (27). We also investigated claudin-low breast cancer, which is defined by low expression of a set of 23 genes (claudin signature), including several claudin tight junction proteins and their genes, which have been reported as a stem cell-like class (28).…”

Section: Additional Measures Supporting Relevance Between the P53mentioning

confidence: 99%

Inactivation of p53 in breast cancers correlates with stem cell transcriptional signatures

Mizuno

Spike

Wahl

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

148

132

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Breast cancer comprises a heterogeneous set of diseases distinguishable from one another by pathologic presentation and molecular signatures. However, each breast cancer subtype is also heterogeneous. Some of the heterogeneity may be attributable to genetic instability, but recent data emphasize that developmental plasticity may also contribute. The p53 tumor suppressor could constitute a nodal control point underlying both sources of heterogeneity because it is frequently inactivated during malignant progression and has recently been shown to function as a potent barrier preventing fully differentiated cells from reverting to pluripotent stem cells after expression of appropriate oncogenes. Using archival microarray datasets, we tested the hypothesis that a p53 mutation could allow cells within a tumor to acquire a stem cell-like state by looking for coordinate expression of stem cell identity genes. We show that breast and lung cancers with p53 mutations do exhibit stem cell-like transcriptional patterns. Such tumors were also depleted for differentiation genes regulated by the polycomb repressor complex 2. These data are consistent with a model in which loss of p53 function enables acquisition of stem cell properties, which are positively selected during tumor progression.

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“…loss was associated with poorly differentiated thyroid cancers (Fagin et al, 1993), breast cancer (de Cremoux et al, 1999;Kochhar et al, 2005;Miller et al, 2005;Mizuno et al, 2010) lung cancer (Junttila et al, 2010), hematopoetic system malignacies (Chylicki et al, 2000;Feinstein et al, 1992), collateral mutations of p53 and PTEN are the most common tumor suppressor aberrations in glioblastomas, which are poorly differentiated, developmentally plastic brain tumors derived from the neuronal stem/progenitor cells (Zheng et al, 2008). Deletion of the three RB family proteins triggers the reprogramming of MEFs to generate CSC-like cells ).…”

Section: Tumor Suppressor Loss Differentiation and Oncogenic Tranformentioning

confidence: 99%

Reprogramming and Carcinogenesis—Parallels and Distinctions

Wasik

Grabarek

Pantovic

et al. 2014

International Review of Cell and Molecular Biology

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Abbreviations: CDK -Cyclin-Dependent Kinase; CSC -cancer stem cells; DSB -double strand breaks ; ECM -extracellular matrix; ES cell -embryonic stem cell; GFP -green fluorescent protein; GSK3 -glycogen synthase kinase-3; HN -Hemagglutininneuraminidase; iPS -induced pluripotent stem cells; MSFs -myocardial scar fibroblasts; RB -Retinoblastoma protein; RGD -arginine-glycine-aspartic acid; RISC -RNA-induced silencing complex; Shc -Src homology 2 domain-containing.

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Metaplastic Breast Carcinoma with Squamous Differentiation: Molecular and Clinical Analysis of Six Cases

Cited by 21 publications

References 18 publications

Molecular alterations in metaplastic breast carcinoma

Molecular alterations in metaplastic breast carcinoma

Inactivation of p53 in breast cancers correlates with stem cell transcriptional signatures

Reprogramming and Carcinogenesis—Parallels and Distinctions

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