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Article ; Online: Comprehensive Proteomic Profiling-derived Immunohistochemistry-based Prediction Models for BRCA1 and BRCA2 Germline Mutation-related Breast Carcinomas.

Vos, Shoko / Elias, Sjoerd G / van der Groep, Petra / Smolders, Yvonne H / van Gils, Carla H / van Diest, Paul J

The American journal of surgical pathology

2018 Volume 42, Issue 9, Page(s) 1262–1272

Abstract: Heredity, mostly due to BRCA germline mutations, is involved in 5% to 10% of all breast cancer cases. Potential BRCA germline mutation carriers may be missed following the current eligibility criteria for BRCA genetic testing. The purpose of this study ... ...

Abstract	Heredity, mostly due to BRCA germline mutations, is involved in 5% to 10% of all breast cancer cases. Potential BRCA germline mutation carriers may be missed following the current eligibility criteria for BRCA genetic testing. The purpose of this study was to, therefore, develop an immunohistochemistry-based model to predict likelihood of underlying BRCA1 and BRCA2 germline mutations in unselected female breast cancer patients. The study group consisted of 100 BRCA1-related, 46 BRCA2-related, and 94 sporadic breast carcinomas. Tumor expression of 44 proteins involved in (BRCA-related) breast carcinogenesis was assessed by immunohistochemistry. A prediction model for BRCA-related versus non-BRCA-related breast cancer was developed using Lasso logistic regression analysis with cross-validation. The model was assessed for its discriminative value and clinical usefulness. The optimal prediction model included 14 predictors (age, cyclinD1, ERα, ERβ, FGFR2, FGFR3, FGFR4, GLUT1, IGFR, Ki67, mitotic activity index, MLH1, p120, and TOP2A), showed excellent discriminative performance (area under the receiving operating characteristic curve=0.943; 95% confidence interval=0.909-0.978), and reasonable calibration. To enhance possible implementation, we developed an alternative model only considering more widely available immunostains. This model included 15 predictors (age, BCL2, CK5/6, CK8/18, cyclinD1, E-cadherin, ERα, HER2, Ki67, mitotic activity index , MLH1, p16, PMS2, PR, and vimentin), and still showed very good discriminative performance (area under the receiving operating characteristic curve=0.853; 95% confidence interval=0.795-0.911). We present a well-applicable and accurate tool to predict which breast cancer patients may have an underlying BRCA germline mutation, largely consisting of immunohistochemical markers independent of clinical characteristics. This may improve identification of potential BRCA germline mutation carriers and optimize referral for germline mutation testing.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Biomarkers, Tumor/analysis ; Biomarkers, Tumor/genetics ; Breast Neoplasms/chemistry ; Breast Neoplasms/genetics ; Case-Control Studies ; Cross-Sectional Studies ; Female ; Genetic Carrier Screening/methods ; Genetic Predisposition to Disease ; Germ-Line Mutation ; Heterozygote ; Humans ; Immunohistochemistry ; Middle Aged ; Neoplasm Grading ; Phenotype ; Predictive Value of Tests ; Proteomics/methods ; Reproducibility of Results ; Risk Assessment ; Risk Factors ; Young Adult
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; BRCA2 Protein ; BRCA2 protein, human ; Biomarkers, Tumor
Language	English
Publishing date	2018-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752964-8
ISSN	1532-0979 ; 0147-5185
ISSN (online)	1532-0979
ISSN	0147-5185
DOI	10.1097/PAS.0000000000001115
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Article ; Online: miRNA expression patterns in normal breast tissue and invasive breast cancers of BRCA1 and BRCA2 germ-line mutation carriers.

Vos, Shoko / Vesuna, Farhad / Raman, Venu / van Diest, Paul J / van der Groep, Petra

Oncotarget

2015 Volume 6, Issue 31, Page(s) 32115–32137

Abstract: miRNA deregulation has been found to promote carcinogenesis. Little is known about miRNA deregulation in hereditary breast tumors as no miRNA expression profiling studies have been performed in normal breast tissue of BRCA1 and BRCA2 mutation carriers. ... ...

Abstract	miRNA deregulation has been found to promote carcinogenesis. Little is known about miRNA deregulation in hereditary breast tumors as no miRNA expression profiling studies have been performed in normal breast tissue of BRCA1 and BRCA2 mutation carriers. miRNA profiles of 17 BRCA1- and 9 BRCA2-associated breast carcinomas were analyzed using microarrays. Normal breast tissues from BRCA1 and BRCA2 mutation carriers (both n = 5) and non-mutation carriers (n = 10) were also included. Candidate miRNAs were validated by qRT-PCR. Breast carcinomas showed extensive miRNA alteration compared to normal breast tissues in BRCA1 and BRCA2 mutation carriers. Moreover, normal breast tissue from BRCA1 mutation carriers already showed miRNA alterations compared to non-mutation carriers. Chromosomal distribution analysis showed several hotspots containing down- or up-regulated miRNAs. Pathway analysis yielded many similarities between the BRCA1 and BRCA2 axes with miRNAs involved in cell cycle regulation, proliferation and apoptosis. Lesser known pathways were also affected, including cellular movement and protein trafficking. This study provides a comprehensive insight into the potential role of miRNA deregulation in BRCA1/2-associated breast carcinogenesis. The observed extensive miRNA deregulation is likely the result of genome-wide effects of chromosomal instability caused by impaired BRCA1 or BRCA2 function. This study's results also suggest the existence of common pathways driving breast carcinogenesis in both BRCA1 and BRCA2 germ-line mutation carriers.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Biomarkers, Tumor/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinoma, Ductal, Breast/genetics ; Carcinoma, Ductal, Breast/metabolism ; Carcinoma, Ductal, Breast/pathology ; Carcinoma, Lobular/genetics ; Carcinoma, Lobular/metabolism ; Carcinoma, Lobular/pathology ; Carcinoma, Medullary/genetics ; Carcinoma, Medullary/metabolism ; Carcinoma, Medullary/pathology ; Case-Control Studies ; Chromosomes, Human/genetics ; Female ; Follow-Up Studies ; Genetic Predisposition to Disease ; Germ-Line Mutation/genetics ; Humans ; Immunoenzyme Techniques ; MicroRNAs/genetics ; Microarray Analysis ; Middle Aged ; Neoplasm Grading ; Neoplasm Invasiveness ; Prognosis ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptor, ErbB-2/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Young Adult
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; BRCA2 Protein ; BRCA2 protein, human ; Biomarkers, Tumor ; MicroRNAs ; RNA, Messenger ; Receptors, Estrogen ; Receptors, Progesterone ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2015-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.5617
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Article ; Online: Pathology of hereditary breast cancer.

van der Groep, Petra / van der Wall, Elsken / van Diest, Paul J

Cellular oncology (Dordrecht)

2011 Volume 34, Issue 2, Page(s) 71–88

Abstract: Background: Hereditary breast cancer runs in families where several members in different generations are affected. Most of these breast cancers are caused by mutations in the high penetrance genes BRCA1 and BRCA2 accounting for about 5% of all breast ... ...

Abstract	Background: Hereditary breast cancer runs in families where several members in different generations are affected. Most of these breast cancers are caused by mutations in the high penetrance genes BRCA1 and BRCA2 accounting for about 5% of all breast cancers. Other genes that include CHEK2, PTEN, TP53, ATM, STK11/LKB1, CDH1, NBS1, RAD50, BRIP1 and PALB2 have been described to be high or moderate penetrance breast cancer susceptibility genes, all contributing to the hereditary breast cancer spectrum. However, in still a part of familial hereditary breast cancers no relationship to any of these breast cancer susceptibility genes can be found. Research on new susceptibility genes is therefore ongoing. Design: In this review we will describe the function of the today known high or moderate penetrance breast cancer susceptibility genes and the consequences of their mutated status. Furthermore, we will focus on the histology, the immunophenotype and genotype of breast cancers caused by mutations in BRCA1 and BRCA2 genes and the other high or moderate penetrance breast cancer susceptibility genes. Finally, an overview of the clinical implications of hereditary breast cancer patients will be provided. Conclusion: This information leads to a better understanding of the morphological, immunohistochemical and molecular characteristics of different types of hereditary breast cancers. Further, these characteristics offer clues for diagnosis and new therapeutic approaches.
MeSH term(s)	BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Family Health ; Female ; Gene Frequency ; Genetic Predisposition to Disease/genetics ; Humans ; Mutation
Chemical Substances	BRCA1 Protein ; BRCA2 Protein
Language	English
Publishing date	2011-02-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-011-0010-3
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Article ; Online: Subcellular FIH-1 expression patterns in invasive breast cancer in relation to HIF-1α expression.

Hyseni, Agon / van der Groep, Petra / van der Wall, Elsken / van Diest, Paul J

Cellular oncology (Dordrecht)

2011 Volume 34, Issue 6, Page(s) 565–570

Abstract: Background: Hypoxia Inducible Factor-1α (HIF-1α) expression in breast cancer is associated with a poor clinical outcome. HIF-1α shows two expression patterns: the canonical poor prognosis hypoxia-related perinecrotic pattern and a diffuse expression ... ...

Abstract	Background: Hypoxia Inducible Factor-1α (HIF-1α) expression in breast cancer is associated with a poor clinical outcome. HIF-1α shows two expression patterns: the canonical poor prognosis hypoxia-related perinecrotic pattern and a diffuse expression pattern that seems to have less downstream effects and is clearly associated with poor survival. Factor-inhibiting hypoxia-inducible factor 1 (FIH-1) inhibits HIF-1 activity by hydroxylating the C-terminal trans-activation domain of the HIF-1α subunit, thus preventing HIF-1 from recruiting co-activators CPB/p300, which are important for inducing the transcription of target genes. The aim of this study was to investigate the expression patterns of FIH-1 in breast cancer and evaluate the relationship between FIH-1 and HIF-1α expression in breast cancer as a possible explanation for apparently less downstream effects of diffuse HIF-1α expression. Methods: Tissue sections from 92 consecutive invasive breast carcinomas were stained by immunohistochemistry for FIH-1, HIF-1α, glucose transporter 1 (GLUT-1) and carbonic anhydrase IX (CAIX). Results: 45 cases overexpressed HIF-1α, 5 of which in a perinecrotic fashion while FIH-1 was positive in 73 of the 92 cases studied. Contrary to our expectations, three out of five cases with perinecrotic HIF-1α expression were also positive for FIH1. Cytoplasmic FIH-1 correlated with HIF-1α expression (P = 0.03) and tumor grade (P = 0.01). HIF-1α overexpression predicted poorer prognosis as usual (P = 0.02). FIH expression had no additional prognostic value to HIF-1α. Conclusions: FIH1 is expressed in the majority of invasive breast carcinomas and shows distinct subcellular localization patterns. FIH-1 expression does not seem to explain the proposed functional differences between diffuse and perinecrotic HIF-1α expression in breast cancer.
MeSH term(s)	Breast Neoplasms/metabolism ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Immunohistochemistry ; In Vitro Techniques ; Mixed Function Oxygenases/metabolism ; Repressor Proteins/metabolism
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; Repressor Proteins ; Mixed Function Oxygenases (EC 1.-) ; HIF1AN protein, human (EC 1.14.11.-)
Language	English
Publishing date	2011-07-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-011-0053-5
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Article ; Online: p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice.

Tenhagen, Milou / Klarenbeek, Sjoerd / Braumuller, Tanya M / Hofmann, Ilse / van der Groep, Petra / Ter Hoeve, Natalie / van der Wall, Elsken / Jonkers, Jos / Derksen, Patrick W B

Journal of mammary gland biology and neoplasia

2016 Volume 21, Issue 3-4, Page(s) 81–88

Abstract: Loss of E-cadherin expression is causal to the development of invasive lobular breast carcinoma (ILC). E-cadherin loss leads to dismantling of the adherens junction and subsequent translocation of p120-catenin (p120) to the cytosol and nucleus. Although ... ...

Abstract	Loss of E-cadherin expression is causal to the development of invasive lobular breast carcinoma (ILC). E-cadherin loss leads to dismantling of the adherens junction and subsequent translocation of p120-catenin (p120) to the cytosol and nucleus. Although p120 is critical for the metastatic potential of ILC through the regulation of Rock-dependent anoikis resistance, it remains unknown whether p120 also contributes to ILC development. Using genetically engineered mouse models with mammary gland-specific inactivation of E-cadherin, p120 and p53, we demonstrate that ILC formation induced by E-cadherin and p53 loss is severely impaired upon concomitant inactivation of p120. Tumors that developed in the triple-knockout mice were mostly basal sarcomatoid carcinomas that displayed overt nuclear atypia and multinucleation. In line with the strong reduction in ILC incidence in triple-knockout mice compared to E-cadherin and p53 double-knockout mice, no functional redundancy of p120 family members was observed in mouse ILC development, as expression and localization of ARVCF, p0071 or δ-catenin was unaltered in ILCs from triple-knockout mice. In conclusion, we show that loss of p120 in the context of the p53-deficient mouse models is dominant over E-cadherin inactivation and its inactivation promotes the development of basal, epithelial-to-mesenchymal-transition (EMT)-type invasive mammary tumors.
MeSH term(s)	Animals ; Cadherins/metabolism ; Carcinoma, Lobular/metabolism ; Carcinoma, Lobular/pathology ; Catenins/metabolism ; Cell Nucleus/metabolism ; Cytosol/metabolism ; Female ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mice ; Mice, Knockout ; Neoplasm Invasiveness ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Cadherins ; Catenins ; Tumor Suppressor Protein p53 ; delta catenin
Language	English
Publishing date	2016-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-016-9358-3
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Zs.A 4478: Show issues

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Article ; Online: Differential expression of growth factor receptors and membrane-bound tumor markers for imaging in male and female breast cancer.

Vermeulen, Jeroen F / Kornegoor, Robert / van der Wall, Elsken / van der Groep, Petra / van Diest, Paul J

PloS one

2013 Volume 8, Issue 1, Page(s) e53353

Abstract: Introduction: Male breast cancer accounts for 0.5-1% of all breast cancers and is generally diagnosed at higher stage than female breast cancers and therefore might benefit from earlier detection and targeted therapy. Except for HER2 and EGFR, little is ...

Abstract	Introduction: Male breast cancer accounts for 0.5-1% of all breast cancers and is generally diagnosed at higher stage than female breast cancers and therefore might benefit from earlier detection and targeted therapy. Except for HER2 and EGFR, little is known about expression of growth factor receptors in male breast cancer. We therefore investigated expression profiles of growth factor receptors and membrane-bound tumor markers in male breast cancer and gynecomastia, in comparison with female breast cancer. Methods: Tissue microarrays containing 133 male breast cancer and 32 gynecomastia cases were stained by immunohistochemistry for a panel of membrane-bound targets and compared with data on 266 female breast cancers. Results: Growth factor receptors were variably expressed in 4.5% (MET) up to 38.5% (IGF1-R) of male breast cancers. Compared to female breast cancer, IGF1-R and carbonic anhydrase 12 (CAXII) were more frequently and CD44v6, MET and FGFR2 less frequently expressed in male breast cancer. Expression of EGFR, HER2, CAIX, and GLUT1 was not significantly different between male and female breast cancer. Further, 48.1% of male breast cancers expressed at least one and 18.0% expressed multiple growth factor receptors. Since individual membrane receptors are expressed in only half of male breast cancers, a panel of membrane markers will be required for molecular imaging strategies to reach sensitivity. A potential panel of markers for molecular imaging, consisting of EGFR, IGF1-R, FGFR2, CD44v6, CAXII, GLUT1, and CD44v6 was positive in 77% of male breast cancers, comparable to female breast cancers. Conclusions: Expression patterns of growth factor receptors and hypoxia membrane proteins in male breast cancer are different from female breast cancer. For molecular imaging strategies, a putative panel consisting of markers for EGFR, IGF1-R, FGFR2, GLUT1, CAXII, CD44v6 was positive in 77% of cases and might be considered for development of molecular tracers for male breast cancer.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/genetics ; Breast Neoplasms, Male/diagnosis ; Breast Neoplasms, Male/genetics ; Carbonic Anhydrases/genetics ; Female ; Gene Expression ; Glucose Transporter Type 1/genetics ; Gynecomastia/diagnosis ; Gynecomastia/genetics ; Humans ; Hyaluronan Receptors/genetics ; Immunohistochemistry ; Insulin-Like Growth Factor I/genetics ; Male ; Middle Aged ; Molecular Imaging/standards ; Receptors, Growth Factor/genetics ; Sex Factors ; Tissue Array Analysis
Chemical Substances	Biomarkers, Tumor ; CD44v6 antigen ; Glucose Transporter Type 1 ; Hyaluronan Receptors ; Receptors, Growth Factor ; SLC2A1 protein, human ; Insulin-Like Growth Factor I (67763-96-6) ; Carbonic Anhydrases (EC 4.2.1.1) ; carbonic anhydrase XII (EC 4.2.1.1)
Language	English
Publishing date	2013-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0053353
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Article ; Online: Influence of decalcification procedures on immunohistochemistry and molecular pathology in breast cancer.

Schrijver, Willemijne A M E / van der Groep, Petra / Hoefnagel, Laurien Dc / Ter Hoeve, Natalie D / Peeters, Ton / Moelans, Cathy B / van Diest, Paul J

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

2016 Volume 29, Issue 12, Page(s) 1460–1470

Abstract: Distant breast cancer metastases are nowadays routinely biopsied to reassess receptor status and to isolate DNA for sequencing of druggable targets. Bone metastases are the most frequent subgroup. Decalcification procedures may negatively affect ... ...

Abstract	Distant breast cancer metastases are nowadays routinely biopsied to reassess receptor status and to isolate DNA for sequencing of druggable targets. Bone metastases are the most frequent subgroup. Decalcification procedures may negatively affect antigenicity and DNA quality. We therefore evaluated the effect of several decalcification procedures on receptor status and DNA/RNA quality. In 23 prospectively collected breast tumors, we compared ERα, PR and HER2 status by immunohistochemistry in (non-decalcified) tissue routinely processed for diagnostic purposes and in parallel tissue decalcified in Christensen's buffer with and without microwave, EDTA and Formical-4. Furthermore, HER2 fluorescence in situ hybridization and DNA/RNA quantity and quality were assessed. We found that the percentage of ERα-positive cells were on average lower in EDTA (P=0.049) and Formical-4 (P=0.047) treated cases, compared with controls, and PR expression showed decreased antigenicity after Christensen's buffer treatment (P=0.041). Overall, a good concordance (weighted kappa) was seen for ERα, PR and HER2 immunohistochemistry when comparing the non-decalcified control tissues with the decalcified tissues. For two patients (9%), there was a potential influence on therapeutic decision making with regard to hormonal therapy or HER2-targeted therapy. HER2 fluorescence in situ hybridization interpretation was seriously hampered by Christensen's buffer and Formical-4, and DNA/RNA quantity and quality were decreased after all four decalcification procedures. Validation on paired primary breast tumor specimens and EDTA-treated bone metastases showed that immunohistochemistry and fluorescence in situ hybridization were well assessable and DNA and RNA yield and quality were sufficient. With this, we conclude that common decalcification procedures have only a modest negative influence on hormone and HER2 receptor immunohistochemistry in breast cancer. However, they may seriously affect DNA/RNA-based diagnostic procedures. Overall, EDTA-based decalcification is therefore to be preferred as it best allows fluorescence in situ hybridization and DNA/RNA isolation.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/analysis ; Bone Neoplasms/genetics ; Bone Neoplasms/secondary ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; DNA, Neoplasm/analysis ; Decalcification Technique ; Female ; Humans ; Immunohistochemistry ; Middle Aged ; Pathology, Molecular/methods
Chemical Substances	Biomarkers, Tumor ; DNA, Neoplasm
Language	English
Publishing date	2016-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645073-8
ISSN	1530-0285 ; 0893-3952
ISSN (online)	1530-0285
ISSN	0893-3952
DOI	10.1038/modpathol.2016.116
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Zs.A 2450: Show issues

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Article ; Online: HIF-1α and NOTCH signaling in ductal and lobular carcinomas of the breast.

Ercan, Cigdem / Vermeulen, Jeroen F / Hoefnagel, Laurien / Bult, Peter / van der Groep, Petra / van der Wall, Elsken / van Diest, Paul J

Cellular oncology (Dordrecht)

2012 Volume 35, Issue 6, Page(s) 435–442

Abstract: Background: NOTCH signaling is involved in every step of metazoan development and maintenance of adult tissue homeostasis. It is frequently deregulated by mutations and overexpression in different cancer types including solid tumors such as breast ... ...

Abstract	Background: NOTCH signaling is involved in every step of metazoan development and maintenance of adult tissue homeostasis. It is frequently deregulated by mutations and overexpression in different cancer types including solid tumors such as breast cancer. Another common feature of solid tumors is hypoxia, which occurs due to defective or insufficient vascularization. Hypoxia-inducible factors (HIFs) are key regulators of the homeostatic response to low oxygen levels. HIF-1α is overexpressed in many solid tumors, including breast cancer. Hypoxia-induced stabilization of HIF transcription factors has been shown to lead to NOTCH activation in vitro in different contexts and tissues, causing differentiation arrest and induction of proliferation and migration. Methods: Since the link between HIF-1α and NOTCH signalling has hardly been studied, we set out to closely investigate associations between the expression of HIF-1α and NOTCH pathway members in primary and metastatic human breast cancer specimens and their prognostic value. Results: Co-expression of NOTCH1 intracellular domain (N1ICD) and HIF-1α was associated with a high grade and a high proliferation rate in invasive breast cancer. HIF-1α expression was low in classic, but high in pleomorphic lobular cancers, which also frequently showed stromal HIF-1α expression. NOTCH1 pathway activation was prognostically unfavorable. Conclusion: In breast cancer, NOTCH pathway activation appears to be associated with a poor prognosis, but NOTCH and HIF signaling do not seem to be functionally associated.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Breast Neoplasms/metabolism ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Carcinoma, Ductal, Breast/metabolism ; Carcinoma, Ductal, Breast/mortality ; Carcinoma, Ductal, Breast/pathology ; Carcinoma, Lobular/metabolism ; Carcinoma, Lobular/mortality ; Carcinoma, Lobular/pathology ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Immunohistochemistry ; Kaplan-Meier Estimate ; Middle Aged ; Prognosis ; Receptors, Notch/metabolism ; Signal Transduction/physiology
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Receptors, Notch
Language	English
Publishing date	2012-09-25
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-012-0102-8
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Article ; Online: Genomic evolution from primary breast carcinoma to distant metastasis: Few copy number changes of breast cancer related genes.

Moelans, Cathy B / van der Groep, Petra / Hoefnagel, Laurien D C / van de Vijver, Marc J / Wesseling, Pieter / Wesseling, Jelle / van der Wall, Elsken / van Diest, Paul J

Cancer letters

2014 Volume 344, Issue 1, Page(s) 138–146

Abstract: Cancer initiation and progression is characterized by (epi)genetic aberrations. However, little is known about the changes that occur during breast cancer metastasis. In the present study, multiplex ligation-dependent probe amplification was used to ... ...

Abstract	Cancer initiation and progression is characterized by (epi)genetic aberrations. However, little is known about the changes that occur during breast cancer metastasis. In the present study, multiplex ligation-dependent probe amplification was used to compare copy numbers of 21 established oncogenes and tumor suppressor genes between 55 primary breast cancer samples and corresponding distant metastases. Distant breast cancer metastases generally showed similar gene copy number aberrations compared to their corresponding primary tumors. The few genes that showed differences between primary tumor and metastasis (PRDM14, MED1, CCNE1, TRAF4, MTDH, CDH1) have been implicated in the development of therapy resistance.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Gene Dosage ; Genes, Tumor Suppressor ; Genomics ; Humans ; Middle Aged ; Multiplex Polymerase Chain Reaction ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis/genetics ; Oncogenes/genetics
Language	English
Publishing date	2014-03-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2013.10.025
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Article ; Online: The molecular genetic make-up of male breast cancer.

Moelans, Cathy B / de Ligt, Joep / van der Groep, Petra / Prins, Pjotr / Besselink, Nicolle J M / Hoogstraat, Marlous / Ter Hoeve, Natalie D / Lacle, Miangela M / Kornegoor, Robert / van der Pol, Carmen C / de Leng, Wendy W J / Barbé, Ellis / van der Vegt, Bert / Martens, John / Bult, Peter / Smit, Vincent T H B M / Koudijs, Marco J / Nijman, Isaac J / Voest, Emile E /

Selenica, Pier / Weigelt, Britta / Reis-Filho, Jorge S / van der Wall, Elsken / Cuppen, Edwin / van Diest, Paul J

Endocrine-related cancer

2019 Volume 26, Issue 10, Page(s) 779–794

Abstract: Male breast cancer (MBC) is extremely rare and accounts for less than 1% of all breast malignancies. Therefore, clinical management of MBC is currently guided by research on the disease in females. In this study, DNA obtained from 45 formalin-fixed ... ...

Abstract	Male breast cancer (MBC) is extremely rare and accounts for less than 1% of all breast malignancies. Therefore, clinical management of MBC is currently guided by research on the disease in females. In this study, DNA obtained from 45 formalin-fixed paraffin-embedded (FFPE) MBCs with and 90 MBCs (52 FFPE and 38 fresh-frozen) without matched normal tissues was subjected to massively parallel sequencing targeting all exons of 1943 cancer-related genes. The landscape of mutations and copy number alterations was compared to that of publicly available estrogen receptor (ER)-positive female breast cancers (smFBCs) and correlated to prognosis. From the 135 MBCs, 90% showed ductal histology, 96% were ER-positive, 66% were progesterone receptor (PR)-positive, and 2% HER2-positive, resulting in 50, 46 and 4% luminal A-like, luminal B-like and basal-like cases, respectively. Five patients had Klinefelter syndrome (4%) and 11% of patients harbored pathogenic BRCA2 germline mutations. The genomic landscape of MBC to some extent recapitulated that of smFBC, with recurrent PIK3CA (36%) and GATA3 (15%) somatic mutations, and with 40% of the most frequently amplified genes overlapping between both sexes. TP53 (3%) somatic mutations were significantly less frequent in MBC compared to smFBC, whereas somatic mutations in genes regulating chromatin function and homologous recombination deficiency-related signatures were more prevalent. MDM2 amplifications were frequent (13%), correlated with protein overexpression (P = 0.001) and predicted poor outcome (P = 0.007). In conclusion, despite similarities in the genomic landscape between MBC and smFBC, MBC is a molecularly unique and heterogeneous disease requiring its own clinical trials and treatment guidelines.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms, Male/genetics ; Breast Neoplasms, Male/pathology ; DNA Copy Number Variations ; Female ; Gene Amplification ; Genome, Human/genetics ; Humans ; Male ; Middle Aged ; Mutation ; Oncogenes/genetics ; Prognosis
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2019-07-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1530/ERC-19-0278
Database	MEDical Literature Analysis and Retrieval System OnLINE

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