MTDH expression in invasive micropapillary carcinoma of the breast

Hao, Jinyan; Yang, Yiling; Liu, Fangfang; Li, Shuai; Li, Weidong; Qian, Xiaolong; Paulos, Estifanos; Fu, Li

doi:10.1007/s11805-011-0568-6

Cited by 5 publications

(7 citation statements)

References 36 publications

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“…33,58 Many genes related to maintaining polarity, cilia formation, and cell morphology are located in these regions. Hao et al 59 compared the expression of prostate stem cell antigen (PSCA) gene located at 8q24 in 66 cases of IMPCs and 67 cases of ICD-NOSs and found that its expression was significantly greater at both the protein and messenger RNA levels in IMPC than it was in IDC-NOS. They concluded that PSCA might have an important role in the LNM of IMPC.…”

Section: Mechanism Of Metastasismentioning

confidence: 99%

Invasive Micropapillary Carcinoma of the Breast: An Update

Yang¹,

Liu²,

Zhang³

et al. 2016

Archives of Pathology &Amp; Laboratory Medicine

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107

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Context.-Invasive micropapillary carcinoma (IMPC) is a distinct variant of mammary carcinoma in which tumor cells are arranged in morulelike clusters devoid of fibrovascular cores and situated within empty stromal spaces. Identification of IMPC can be achieved by the assessment of morphologic features in conjunction with the characteristic ''inside-out'' staining pattern of epithelial membrane antigen and sialyl Lewis X highlighted by immunohistochemical analysis. Although recognizing micropapillary architecture is often not challenging, the criteria for distinguishing between mixed and pure IMPC remain imprecise. Some mucin-producing carcinomas can also have micropapillary histology, but there is no consensus on whether these tumors are variants of IMPC or mucinous carcinomas. The molecular genetic studies demonstrate that IMPCs have distinct molecular genetic profiles, supporting the theory that they constitute distinct pathologic entities. However, genomic analyses have not identified any specific genomic aberration that may explain the distinctive morphology and clinical behavior of IMPC.Objective.-To provide an overview on the current concepts in the diagnosis and pathogenesis of IMPC of the breast, incorporating recent molecular genetic advances and prognosis-based reclassification.Data Sources.-PubMed search and the cited references were reviewed.Conclusions.-The recent evolution of prognosis-based reclassification and molecular genetic advances has enhanced our knowledge of the pathogenesis of IMPC of the breast. Additional studies might reveal consistent molecular alterations that underlie the formation of the inside-out growth pattern, and they might elucidate the molecular mechanisms responsible for the unfavorable clinical behavior of IMPC.

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Section: Mechanism Of Metastasismentioning

confidence: 99%

Invasive Micropapillary Carcinoma of the Breast: An Update

Yang¹,

Liu²,

Zhang³

et al. 2016

Archives of Pathology &Amp; Laboratory Medicine

Self Cite

107

View full text Add to dashboard Cite

show abstract

“…rs2294008 or rs2978974) are associated with increased risk of developing breast cancer [ 24 ]. Moreover, there is some evidence by two preliminary studies suggesting that PSCA-protein might be expressed in at least a subpopulation of breast cancer patients [ 25 , 26 ]. However one of these studies only focusses on a limited set of patients with micropapillary carcinoma of the breast.…”

Section: Introductionmentioning

confidence: 99%

Exploratory investigation of PSCA-protein expression in primary breast cancer patients reveals a link to HER2/neu overexpression

et al. 2017

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BackgroundProstate stem cell antigen (PSCA) has been suggested as biomarker and therapeutic target for prostate cancer. Recent advances showed that PSCA is up-regulated in other cancer entities, such as bladder or pancreatic cancer. However, the clinical relevance of PSCA-expression in breast cancer patients has not yet been established and is therefore addressed by the current study.MethodsPSCA-protein expression was assessed in 405 breast cancer patients, using immunohistochemistry (PSCA antibody MB1) and tissue microarrays.ResultsPSCA-expression was detected in 94/405 patients (23%) and correlated with unfavorable histopathological grade (p=0.011) and increased Ki67 proliferation index (p=0.006). We observed a strong positive correlation between PSCA-protein expression and HER2/neu receptor status (p<0.001). PSCA did not provide prognostic information in the analyzed cohort. Interestingly, the distribution of PSCA-expression among triple negative patients was comparable to the total population.ConclusionWe identified a subgroup of PSCA-positive breast cancer patients, which could be amenable for a PSCA-targeted therapy. Moreover, given that we found a strong positive correlation between PSCA- and HER/neu expression, targeting PSCA may provide an alternative therapeutic option in case of trastuzumab resistance.

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“…Additionally, recent GWAS studies have shown that two single-nucleotide polymorphisms (SNPs) in PSCA gene are associated with gastric cancer [44]. Hao et al (2011) have reported the PSCA expression in invasive micropapillary carcinoma of breast [45]. CYP11B2 residing in the same region has been associated with adrenocortical tumor development [46].…”

Section: Discussionmentioning

confidence: 99%

A systematic comparison of copy number alterations in four types of female cancer

et al. 2016

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BackgroundDetection and localization of genomic alterations and breakpoints are crucial in cancer research. The purpose of this study was to investigate, in a methodological and biological perspective, different female, hormone-dependent cancers to identify common and diverse DNA aberrations, genes, and pathways.MethodsIn this work, we analyzed tissue samples from patients with breast (n = 112), ovarian (n = 74), endometrial (n = 84), or cervical (n = 76) cancer. To identify genomic aberrations, the Circular Binary Segmentation (CBS) and Piecewise Constant Fitting (PCF) algorithms were used and segmentation thresholds optimized. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was applied to the segmented data to identify significantly altered regions and the associated genes were analyzed by Ingenuity Pathway Analysis (IPA) to detect over-represented pathways and functions within the identified gene sets.Results and DiscussionAnalyses of high-resolution copy number alterations in four different female cancer types are presented. For appropriately adjusted segmentation parameters the two segmentation algorithms CBS and PCF performed similarly. We identified one region at 8q24.3 with focal aberrations that was altered at significant frequency across all four cancer types. Considering both, broad regions and focal peaks, three additional regions with gains at significant frequency were revealed at 1p21.1, 8p22, and 13q21.33, respectively. Several of these events involve known cancer-related genes, like PPP2R2A, PSCA, PTP4A3, and PTK2. In the female reproductive system (ovarian, endometrial, and cervix [OEC]), we discovered three common events: copy number gains at 5p15.33 and 15q11.2, further a copy number loss at 8p21.2. Interestingly, as many as 75% of the aberrations (75% amplifications and 86% deletions) identified by GISTIC were specific for just one cancer type and represented distinct molecular pathways.ConclusionsOur results disclose that some prominent copy number changes are shared in the four examined female, hormone-dependent cancer whereas others are definitive to specific cancer types.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2899-4) contains supplementary material, which is available to authorized users.

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MTDH expression in invasive micropapillary carcinoma of the breast

Cited by 5 publications

References 36 publications

Invasive Micropapillary Carcinoma of the Breast: An Update

Invasive Micropapillary Carcinoma of the Breast: An Update

Exploratory investigation of PSCA-protein expression in primary breast cancer patients reveals a link to HER2/neu overexpression

A systematic comparison of copy number alterations in four types of female cancer

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