FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2018498303> ?p ?o ?g. }

• W2018498303 endingPage "1809" @default.
• W2018498303 startingPage "1795" @default.
• W2018498303 abstract "Established histopathological criteria divide invasive breast carcinomas into defined groups. Ductal of no specific type and lobular are the two major subtypes accounting for around 75 and 15% of all cases, respectively. The remaining 10% include rarer types such as tubular, cribriform, mucinous, papillary, medullary, metaplastic, and apocrine breast carcinomas. Molecular profiling technologies, on the other hand, subdivide breast tumors into five subtypes, basal-like, luminal A, luminal B, normal breast tissue-like, and ERBB2-positive, that have different prognostic characteristics. An additional subclass termed “molecular apocrine” has recently been described, but these lesions did not exhibit all the histopathological features of classical invasive apocrine carcinomas (IACs). IACs make up 0.5–3% of the invasive ductal carcinomas, and despite the fact that they are morphologically distinct from other breast lesions, there are presently no standard molecular criteria available for their diagnosis and as a result no precise information as to their prognosis. Toward this goal our laboratories have embarked in a systematic proteomics endeavor aimed at identifying biomarkers that may characterize and subtype these lesions as well as targets that may lead to the development of novel targeted therapies and chemoprevention strategies. By comparing the protein expression profiles of apocrine macrocysts and non-malignant breast epithelial tissue we have previously reported the identification of a few proteins that are specifically expressed by benign apocrine lesions as well as by the few IACs that were available to us at the time. Here we reiterate our strategy to reveal apocrine cell markers and present novel data, based on the analysis of a considerably larger number of samples, establishing that IACs correspond to a distinct molecular subtype of breast carcinomas characterized by the expression of 15-prostaglandin dehydrogenase alone or in combination with a novel form of acyl-CoA synthetase medium-chain family member 1 (ACSM1). Moreover we show that 15-prostaglandin dehydrogenase is not expressed by other breast cancer types as determined by gel-based proteomics and immunohistochemistry analysis and that antibodies against this protein can identify IACs in an unbiased manner in a large breast cancer tissue microarray making them potentially useful as a diagnostic aid. Established histopathological criteria divide invasive breast carcinomas into defined groups. Ductal of no specific type and lobular are the two major subtypes accounting for around 75 and 15% of all cases, respectively. The remaining 10% include rarer types such as tubular, cribriform, mucinous, papillary, medullary, metaplastic, and apocrine breast carcinomas. Molecular profiling technologies, on the other hand, subdivide breast tumors into five subtypes, basal-like, luminal A, luminal B, normal breast tissue-like, and ERBB2-positive, that have different prognostic characteristics. An additional subclass termed “molecular apocrine” has recently been described, but these lesions did not exhibit all the histopathological features of classical invasive apocrine carcinomas (IACs). IACs make up 0.5–3% of the invasive ductal carcinomas, and despite the fact that they are morphologically distinct from other breast lesions, there are presently no standard molecular criteria available for their diagnosis and as a result no precise information as to their prognosis. Toward this goal our laboratories have embarked in a systematic proteomics endeavor aimed at identifying biomarkers that may characterize and subtype these lesions as well as targets that may lead to the development of novel targeted therapies and chemoprevention strategies. By comparing the protein expression profiles of apocrine macrocysts and non-malignant breast epithelial tissue we have previously reported the identification of a few proteins that are specifically expressed by benign apocrine lesions as well as by the few IACs that were available to us at the time. Here we reiterate our strategy to reveal apocrine cell markers and present novel data, based on the analysis of a considerably larger number of samples, establishing that IACs correspond to a distinct molecular subtype of breast carcinomas characterized by the expression of 15-prostaglandin dehydrogenase alone or in combination with a novel form of acyl-CoA synthetase medium-chain family member 1 (ACSM1). Moreover we show that 15-prostaglandin dehydrogenase is not expressed by other breast cancer types as determined by gel-based proteomics and immunohistochemistry analysis and that antibodies against this protein can identify IACs in an unbiased manner in a large breast cancer tissue microarray making them potentially useful as a diagnostic aid. Breast cancer is the leading cause of cancer deaths in women today and the most common cancer among women in the Western world (1Kamangar F. Dores G.M. Anderson W.F. Patterns of cancer incidence, mortality, and prevalence across five continents: defining priorities to reduce cancer disparities in different geographic regions of the world.J. Clin. Oncol. 2006; 24: 2137-2150Crossref PubMed Scopus (3068) Google Scholar). According to the World Health Organization more than 1.2 million people will be diagnosed with breast cancer this year worldwide, and the global incidence rates are increasing. In Denmark, ∼4,200 women were diagnosed with the disease in 2005; this means that the number of new cases diagnosed every year has tripled in the past 40 years. As a result, the lifetime risk of a woman developing breast cancer has increased from 1 in 28 just 50 years ago to 1 in 8 today. The 5-year survival rate is about 97% when breast cancer is detected at a more curable stage, indicating that early detection is crucial both for treatment intervention and for improving survival (2Gondos A. Bray F. Brewster D.H. Coebergh J.W. Hakulinen T. Janssen-Heijnen M.L. Kurtinaitis J. Brenner H. The EUNICE Survival Working Group Recent trends in cancer survival across Europe between 2000 and 2004: a model-based period analysis from 12 cancer registries.Eur. J. Cancer. 2008; 44: 1463-1475Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar). Breast cancer is a heterogeneous disease that encompasses a wide range of histopathological types. Established histopathological criteria classify invasive breast cancer into defined groups: two major subtypes, ductal of no specific type (NST) 1The abbreviations used are: NST, no specific type; ERα, estrogen receptor α; IAC, invasive apocrine carcinoma; IDC, invasive ductal carcinoma; PgR, progesterone receptor; AR, androgen receptor; IHC, immunohistochemistry; 2D, two-dimensional; GCDFP-15, gross cystic disease fluid protein-15; ACSM1, acyl-CoA synthetase medium-chain family member 1; 15-PGDH, 15-prostaglandin dehydrogenase; TMA, tissue microarray; CK, cytokeratin; AKR1A1, aldo-keto reductase family 1 member A1; apo, apolipoprotein; B-FABP, brain fatty acid-binding protein; SOD, superoxide dismutase; HMG, hydroxymethylglutaryl; SCP2, steroid carrier-binding protein 2; DCTB, Danish Centre for Translational Breast Cancer Research. and lobular accounting for around 75 and 15% of all cases, respectively, in addition to rare special types, e.g. tubular, cribriform, mucinous, medullary, metaplastic, and apocrine breast carcinomas (3Perry N. Broeders M. de Wolf C. Toürnberg S. Holland R. von Karsa L. European Guidelines for Quality Assurance in Breast Cancer Screening and Diagnosis. 4th Ed. European Commission, Brussels, Belgium2006: 221-311Google Scholar). However, molecular profiling technologies subdivide breast cancer tumors into five clinically relevant clusters with different prognostic characteristics. These include two estrogen receptor α (ERα)-positive groups (luminal A and B) and three ERα-negative groups comprising basal-like, normal breast tissue-like, and ERBB2/Her2-positive lesions (4Perou C.M. Sørlie T. Eisen M.B. van de Rijn M. Jeffrey S.S. Rees C.A. Pollack J.R. Ross D.T. Johnsen H. Akslen L.A. Fluge O. Pergamenschikov A. Williams C. Zhu S.X. Lønning P.E. Børresen-Dale A.L. Brown P.O. Botstein D. Molecular portraits of human breast tumours.Nature. 2000; 406: 747-752Crossref PubMed Scopus (11864) Google Scholar, 5Sørlie T. Perou C.M. Tibshirani R. Aas T. Geisler S. Johnsen H. Hastie T. Eisen M.B. van de Rijn M. Jeffrey S.S. Thorsen T. Quist H. Matese J.C. Brown P.O. Botstein D. Eystein Lønning P. Børresen-Dale A.L. Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications.Proc. Natl. Acad. Sci. U. S. A. 2001; 98: 10869-10874Crossref PubMed Scopus (8659) Google Scholar). This classification, however, is by no means exhaustive as work by Farmer et al. (6) recently identified a novel subset of breast tumors with increased androgen signaling and an apocrine expression profile that they termed “molecular apocrine” given that these lesions do not exhibit all the histopathological features of classical apocrine carcinomas. Molecular apocrine carcinomas encompass tumors that share some common expression characteristics with the ERBB2 class (ERα−/PgR−/ERBB2+) in the Stanford classification as well as with some lesions that exhibit morphological features of the triple negative group (high grade lesions; ERα−/PgR−/ERBB2−). Invasive apocrine carcinomas (IACs) as defined by morphological features correspond to 0.5–3% of all invasive ductal carcinomas (IDCs) (7Frable W.J. Kay S. Carcinoma of the breast. Histologic and clinical features of apocrine tumors.Cancer. 1968; 21: 756-763Crossref PubMed Scopus (53) Google Scholar, 8Mossler J.A. Barton T.K. Brinkhous A.D. McCarty K.S. Moylan J.A. McCarty Jr., K.S. Apocrine differentiation in human mammary carcinoma.Cancer. 1980; 46: 2463-2471Crossref PubMed Scopus (76) Google Scholar, 9Eusebi V. Millis R.R. Cattani M.G. Bussolati G. Azzopardi J.G. Apocrine carcinoma of the breast. A morphologic and immunocytochemical study.Am. J. Pathol. 1986; 123: 532-541PubMed Google Scholar, 10O'Malley F.P. Bane A. An update on apocrine lesions of the breast.Histopathology. 2008; 52: 3-10Crossref PubMed Scopus (65) Google Scholar), and despite the fact that they are histologically distinct from other breast lesions there are currently no standard molecular criteria available for their diagnosis and no precise information as to their prognosis (Refs. 10O'Malley F.P. Bane A. An update on apocrine lesions of the breast.Histopathology. 2008; 52: 3-10Crossref PubMed Scopus (65) Google Scholar, 11Japaze H. Emina J. Diaz C. Schwam R.J. Gercovich N. Demonty G. Morgenfeld E. Rivarola E. Gil Deza E. Gercovich F.G. ‘Pure' invasive apocrine carcinoma of the breast: a new clinicopathological entity?.Breast. 2005; 14: 3-10Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar, 12Page D.L. Apocrine carcinomas of the breast.Breast. 2005; 14: 1-2Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar, 13Wells C.A. El-Ayat G.A. Non-operative breast pathology: apocrine lesions.J. Clin. Pathol. 2007; 60: 1313-1320Crossref PubMed Scopus (53) Google Scholar, 14Tanaka K. Imoto S. Wada N. Sakemura N. Hasebe K. Invasive apocrine carcinoma of the breast: clinicopathologic features of 57 patients.Breast J. 2008; 14: 164-168Crossref PubMed Scopus (38) Google Scholar and references therein). IACs are generally considered as a variant of IDC (8Mossler J.A. Barton T.K. Brinkhous A.D. McCarty K.S. Moylan J.A. McCarty Jr., K.S. Apocrine differentiation in human mammary carcinoma.Cancer. 1980; 46: 2463-2471Crossref PubMed Scopus (76) Google Scholar, 10O'Malley F.P. Bane A. An update on apocrine lesions of the breast.Histopathology. 2008; 52: 3-10Crossref PubMed Scopus (65) Google Scholar, 15Abati A.D. Kimmel M. Rosen P.P. Apocrine mammary carcinoma. A clinicopathologic study of 72 cases.Am. J. Clin. Pathol. 1990; 94: 371-377Crossref PubMed Scopus (81) Google Scholar), although Japaze et al. (11Japaze H. Emina J. Diaz C. Schwam R.J. Gercovich N. Demonty G. Morgenfeld E. Rivarola E. Gil Deza E. Gercovich F.G. ‘Pure' invasive apocrine carcinoma of the breast: a new clinicopathological entity?.Breast. 2005; 14: 3-10Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar) recently defined separate histopathological criteria for the diagnosis of pure IACs, which have a less aggressive behavior than IDC-NST. The identification of apocrine carcinomas is further complicated by the fact that some of the less differentiated carcinomas may actually represent apocrine carcinomas that have lost their apocrine morphological characteristics, making it difficult to distinguish them from IDC-NST using purely morphological criteria (16Celis J.E. Gromov P. Moreira J.M. Cabezón T. Friis E. Vejborg I.M. Proess G. Rank F. Gromova I. Apocrine cysts of the breast: biomarkers, origin, enlargement, and relation with cancer phenotype.Mol. Cell. Proteomics. 2006; 5: 462-483Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar, 17Celis J.E. Gromova I. Gromov P. Moreira J.M. Cabezón T. Friis E. Rank F. Molecular pathology of breast apocrine carcinomas: a protein expression signature specific for benign apocrine metaplasia.FEBS Lett. 2006; 580: 2935-2944Crossref PubMed Scopus (44) Google Scholar). As a result, it is likely that IACs are more frequent than previously estimated. IACs have not been characterized at the molecular level but are generally accepted to be ERα−, progesterone receptor (PgR)-negative, and androgen receptor (AR)-positive (18Tavassoli F.A. Purcell C. Man Y.G. Down regulation of bcl2, ER, PR, associatied with AR expression is triggered by apocrine differentiation of mammary epithelium.Mod. Pathol. 1996; 9: 25 AGoogle Scholar, 19Gatalica Z. Immunohistochemical analysis of apocrine breast lesions. Consistent over-expression of androgen receptor accompanied by the loss of estrogen and progesterone receptors in apocrine metaplasia and apocrine carcinoma in situ.Pathol. Res. Pract. 1997; 193: 753-758Crossref PubMed Scopus (103) Google Scholar, 20Selim A.G. Wells C.A. Immunohistochemical localisation of androgen receptor in apocrine metaplasia and apocrine adenosis of the breast: relation to oestrogen and progesterone receptors.J. Clin. Pathol. 1999; 52: 838-841Crossref PubMed Scopus (44) Google Scholar, 21Sapp M. Malik A. Hanna W. Hormone receptor profile of apocrine lesions of the breast.Breast J. 2003; 9: 335-356Crossref PubMed Scopus (26) Google Scholar) and Bcl-2-negative (19Gatalica Z. Immunohistochemical analysis of apocrine breast lesions. Consistent over-expression of androgen receptor accompanied by the loss of estrogen and progesterone receptors in apocrine metaplasia and apocrine carcinoma in situ.Pathol. Res. Pract. 1997; 193: 753-758Crossref PubMed Scopus (103) Google Scholar, 22Selim A.G. El-Ayat G. Wells C.A. Expression of c-erbB2, p53, Bcl-2, Bax, c-myc and Ki-67 in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast.Virchows Arch. 2002; 441: 449-455Crossref PubMed Scopus (42) Google Scholar), and many are Her2/neu-negative (23Moinfar F. Okcu M. Tsybrovskyy O. Regitnig P. Lax S.F. Weybora W. Ratschek M. Tavassoli F.A. Denk H. Androgen receptors frequently are expressed in breast carcinomas: potential relevance to new therapeutic strategies.Cancer. 2003; 98: 703-711Crossref PubMed Scopus (206) Google Scholar). Moreover some are positive for the gross cystic disease fluid protein-15 (GCDFP-15) (9Eusebi V. Millis R.R. Cattani M.G. Bussolati G. Azzopardi J.G. Apocrine carcinoma of the breast. A morphologic and immunocytochemical study.Am. J. Pathol. 1986; 123: 532-541PubMed Google Scholar, 24Mazoujian G. Pinkus G.S. Davis S. Haagensen Jr., D.E. Immunohistochemistry of a gross cystic disease fluid protein (GCDFP-15) of the breast. A marker of apocrine epithelium and breast carcinomas with apocrine features.Am. J. Pathol. 1983; 110: 105-112PubMed Google Scholar, 25Miller W.R. Shivas A.A. Franchimont P. Haagensen D.E. Breast gross cystic disease protein 15 in human breast cancer in culture.Eur. J. Cancer Clin. Oncol. 1988; 24: 223-228Abstract Full Text PDF PubMed Scopus (29) Google Scholar, 26Honma N. Takubo K. Akiyama F. Sawabe M. Arai T. Younes M. Kasumi F. Sakamoto G. Expression of GCDFP-15 and AR decreases in larger or node-positive apocrine carcinomas of the breast.Histopathology. 2005; 47: 195-201Crossref PubMed Scopus (57) Google Scholar), a marker that it is, however, not specific for these lesions (16Celis J.E. Gromov P. Moreira J.M. Cabezón T. Friis E. Vejborg I.M. Proess G. Rank F. Gromova I. Apocrine cysts of the breast: biomarkers, origin, enlargement, and relation with cancer phenotype.Mol. Cell. Proteomics. 2006; 5: 462-483Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar, 17Celis J.E. Gromova I. Gromov P. Moreira J.M. Cabezón T. Friis E. Rank F. Molecular pathology of breast apocrine carcinomas: a protein expression signature specific for benign apocrine metaplasia.FEBS Lett. 2006; 580: 2935-2944Crossref PubMed Scopus (44) Google Scholar, 25Miller W.R. Shivas A.A. Franchimont P. Haagensen D.E. Breast gross cystic disease protein 15 in human breast cancer in culture.Eur. J. Cancer Clin. Oncol. 1988; 24: 223-228Abstract Full Text PDF PubMed Scopus (29) Google Scholar). p53 expression has been observed in about 50% of invasive apocrine carcinomas (19Gatalica Z. Immunohistochemical analysis of apocrine breast lesions. Consistent over-expression of androgen receptor accompanied by the loss of estrogen and progesterone receptors in apocrine metaplasia and apocrine carcinoma in situ.Pathol. Res. Pract. 1997; 193: 753-758Crossref PubMed Scopus (103) Google Scholar, 27Moriya T. Sakamoto K. Sasano H. Kawanaka M. Sonoo H. Manabe T. Ito J. Immunohistochemical analysis of Ki-67, p53, p21, and p27 in benign and malignant apocrine lesions of the breast: its correlation to histologic findings in 43 cases.Mod. Pathol. 2000; 13: 13-18Crossref PubMed Scopus (62) Google Scholar), and there have been some reports addressing the characteristics of apocrine lesions using loss of heterozygosity (22Selim A.G. El-Ayat G. Wells C.A. Expression of c-erbB2, p53, Bcl-2, Bax, c-myc and Ki-67 in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast.Virchows Arch. 2002; 441: 449-455Crossref PubMed Scopus (42) Google Scholar, 28Washington C. Dalbeègue F. Abreo F. Taubenberger J.K. Lichy J.H. Loss of heterozygosity in fibrocystic change of the breast: genetic relationship between benign proliferative lesions and associated carcinomas.Am. J. Pathol. 2000; 157: 323-329Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar, 29Maitra A. Wistuba I.I. Washington C. Virmani A.K. Ashfaq R. Milchgrub S. Gazdar A.F. Minna J.D. High-resolution chromosome 3p allelotyping of breast carcinomas and precursor lesions demonstrates frequent loss of heterozygosity and a discontinuous pattern of allele loss.Am. J. Pathol. 2001; 159: 119-130Abstract Full Text Full Text PDF PubMed Scopus (127) Google Scholar) and comparative genome hybridization (10O'Malley F.P. Bane A. An update on apocrine lesions of the breast.Histopathology. 2008; 52: 3-10Crossref PubMed Scopus (65) Google Scholar, 30Jones C. Damiani S. Wells D. Chaggar R. Lakhani S.R. Eusebi V. Molecular cytogenetic comparison of apocrine hyperplasia and apocrine carcinoma of the breast.Am. J. Pathol. 2001; 158: 207-214Abstract Full Text Full Text PDF PubMed Scopus (69) Google Scholar). Considering the lack of histological and molecular criteria to reproducibly categorize IACs and the lack of knowledge as to which is the most appropriate treatment for patients bearing these lesions, our laboratories have embarked in a systematic proteomics endeavor aimed at identifying biomarkers that may characterize and subtype these lesions to a greater detail than it is possible today and to search for targets that may lead to the development of novel targeted therapies and chemoprevention strategies. By comparing the protein expression profiles of “blue dome” apocrine cysts and non-malignant breast epithelial tissue we have identified a few markers that are expressed by benign and non-obligatory lesions as well as by some IACs (16Celis J.E. Gromov P. Moreira J.M. Cabezón T. Friis E. Vejborg I.M. Proess G. Rank F. Gromova I. Apocrine cysts of the breast: biomarkers, origin, enlargement, and relation with cancer phenotype.Mol. Cell. Proteomics. 2006; 5: 462-483Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar, 17Celis J.E. Gromova I. Gromov P. Moreira J.M. Cabezón T. Friis E. Rank F. Molecular pathology of breast apocrine carcinomas: a protein expression signature specific for benign apocrine metaplasia.FEBS Lett. 2006; 580: 2935-2944Crossref PubMed Scopus (44) Google Scholar, 31Celis J.E. Moreira J.M.A. Irina Gromova I. Teresa Cabezón T. Gromov P. Shen T. Timmermans V. Rank F. Characterization of breast precancerous lesions and myoepithelial hyperplasia in sclerosing adenosis with apocrine metaplasia.Mol. Oncol. 2007; 1: 97-119Crossref PubMed Scopus (27) Google Scholar). In addition, the identification of differentially expressed proteins that characterize a specific step in the progression from early benign lesions to apocrine cancer has opened a window of opportunity for designing and testing new approaches for chemoprevention (16Celis J.E. Gromov P. Moreira J.M. Cabezón T. Friis E. Vejborg I.M. Proess G. Rank F. Gromova I. Apocrine cysts of the breast: biomarkers, origin, enlargement, and relation with cancer phenotype.Mol. Cell. Proteomics. 2006; 5: 462-483Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar, 17Celis J.E. Gromova I. Gromov P. Moreira J.M. Cabezón T. Friis E. Rank F. Molecular pathology of breast apocrine carcinomas: a protein expression signature specific for benign apocrine metaplasia.FEBS Lett. 2006; 580: 2935-2944Crossref PubMed Scopus (44) Google Scholar). Here we reiterate our strategy to reveal apocrine cell markers and present novel data, based on the analysis of a considerably larger number of samples, establishing that IACs correspond to a distinct molecular subtype of breast carcinomas characterized by the expression of 15-prostaglandin dehydrogenase (15-PGDH) alone or in combination with a novel form of acyl-CoA synthetase medium-chain family member 1 (ACSM1). Moreover we show that 15-PGDH is not expressed by other breast cancer types as determined by gel-based proteomics and immunohistochemistry analysis and that antibodies against this protein can identify IACs in an unbiased manner in a large breast cancer tissue microarray making them potentially useful as a diagnostic aid. Tissue biopsies from clinical high risk patients 2The criteria for high risk cancer applied by the Danish Cooperative Breast Cancer Group are age below 35 years old, and/or tumor diameter of more than 20 mm, and/or histological malignancy grade 2 or 3, and/or negative estrogen and progesterone receptor status, and/or positive axillary status. that underwent mastectomy were collected from the Pathology Department at the Copenhagen University Hospital. Samples for gel analysis were placed in liquid nitrogen and were rapidly transported to the Institute of Cancer Biology where they were stored at −80 °C. Samples were routinely collected within a maximum of 30–45 min from the time of surgical excision. The project was approved by the Scientific and Ethical Committee of the Copenhagen and Frederiksberg Municipalities (KF 01-069/03). We also obtained paraffin-embedded tissue blocks from the Department of Pathology, University of Valencia and Instituto Valenciano de Oncologia, Valencia, Spain. For these patients the personal identification number is unknown. Samples used in this study are described in Table III.Table IIIImmunophenotype of IACsa In years.b D, ductal carcinoma.c The tumor size is given in mm.d The histological malignancy grade was determined according to Elston and Ellis (55Elston C.W. Ellis I.O. Pathological prognostic factors in breast cancer. I. The value of histological grade in breast cancer: experience from a large study with long-term follow-up.Histopathology. 1991; 19: 403-410Crossref PubMed Scopus (4841) Google Scholar).e Her2 status was defined as positive or amplified respectively, either as IHC level of 3+ (HERCEPTEST), or as FISH ratio of 2.0 or higher (DAKO kit). IHC level 2+ was defined as equivocal and followed by FISH (56Dowcett M. Bartlett J. Ellis I.O. Salter J. Hills M. Mallon E. Watters A.D. Cooke T. Paish C. Wencyk P.M. Pinder S.E. Correlation between immunohistochemistry (Hercep Test) and fluorescence in situ hybridization (FISH) for HER-2 in 426 breast carcinomas from 37 centres.J. Pathol. 2003; 199: 418-423Crossref PubMed Scopus (221) Google Scholar).f ALN, axillary lymph node. N+, metastasis in lymph nodes; N−, no metastasis detected in lymph nodes (see also “Experimental Procedures”).g ERα, estrogen receptor alpha; PgR, progesterone receptor; AR, androgen receptor. ERα, and PgR status was determined by IHC analysis according to the Danish Breast Cancer Cooperative Group (DBCG) guidelines. Tumors were regarded as negative when receptors were expressed in less than 10% of tumor cell nuclei.h Pos, positive; Neg, Negative.i Department of Pathology, Copenhagen University Hospital.j Department of Pathology, University of Valencia and Instituto Valenciano de Oncologia.k ND, not determined. Open table in a new tab a In years. b D, ductal carcinoma. c The tumor size is given in mm. d The histological malignancy grade was determined according to Elston and Ellis (55Elston C.W. Ellis I.O. Pathological prognostic factors in breast cancer. I. The value of histological grade in breast cancer: experience from a large study with long-term follow-up.Histopathology. 1991; 19: 403-410Crossref PubMed Scopus (4841) Google Scholar). e Her2 status was defined as positive or amplified respectively, either as IHC level of 3+ (HERCEPTEST), or as FISH ratio of 2.0 or higher (DAKO kit). IHC level 2+ was defined as equivocal and followed by FISH (56Dowcett M. Bartlett J. Ellis I.O. Salter J. Hills M. Mallon E. Watters A.D. Cooke T. Paish C. Wencyk P.M. Pinder S.E. Correlation between immunohistochemistry (Hercep Test) and fluorescence in situ hybridization (FISH) for HER-2 in 426 breast carcinomas from 37 centres.J. Pathol. 2003; 199: 418-423Crossref PubMed Scopus (221) Google Scholar). f ALN, axillary lymph node. N+, metastasis in lymph nodes; N−, no metastasis detected in lymph nodes (see also “Experimental Procedures”). g ERα, estrogen receptor alpha; PgR, progesterone receptor; AR, androgen receptor. ERα, and PgR status was determined by IHC analysis according to the Danish Breast Cancer Cooperative Group (DBCG) guidelines. Tumors were regarded as negative when receptors were expressed in less than 10% of tumor cell nuclei. h Pos, positive; Neg, Negative. i Department of Pathology, Copenhagen University Hospital. j Department of Pathology, University of Valencia and Instituto Valenciano de Oncologia. k ND, not determined. Normal human tissue arrays containing tissues from 33 different anatomic sites (MN0661) were purchased from Pantomics, Inc., San Francisco, CA. We also used a tissue microarray (TMA) containing 498 consecutive cases of primary breast cancer diagnosed at the Department of Pathology, Malmö University Hospital between 1988 and 1992. The median age at the time of diagnosis was 65 years old (range, 27–96 years), and the median follow-up time from diagnosis to recurrent disease was 106 months (range, 0–207 months) (see Table II). The patient cohort represented in this TMA is part of the Malmö Diet and Cancer Study and has been described in detail elsewhere (32Borgquist S. Holm C. Stendahl M. Anagnostaki L. Landberg G. Jirstroüm K.J. Oestrogen receptors α and β show different associations to clinicopathological parameters and their co-expression might predict a better response to endocrine treatment in breast cancer.Clin. Pathol. 2008; 61: 197-203Crossref PubMed Scopus (58) Google Scholar). For the present study, new tissue arrays were constructed using 2 × 1.0-mm cores from 498 cases in the cohort from which donor blocks could be retrieved. Ethical permission for the Malmö Diet and Cancer Study was obtained from the Ethical Committee at Lund University (LU 51-90) (see Table IV). In addition, a TMA (BRC1502) containing 68 human breast carcinomas present in duplicate was purchased from Pantomics, Inc.Table IITMAs of 33 normal tissues incubated with 15-PGDH and ACSM1 antibodiesTissue-anatomic siteaTMA containing 33 types of normal human tissues (MNO661; Pantomics, Inc.) in duplicates. The TMAs were used 1 week after shipment.Histology15-PGDHbThe antibody was used at a dilution of 1:3,000.ACSM1cThe antibody was used at a dilution of 1:400.Adrenal glanddThe tissues were from autopsies.NormalNegativeNegativeBladderNormalPositive (umbrella cells)NegativeBone marrowdThe tissues were from autopsies.NormalNegativeNegativeEyedThe tissues were from autopsies.NormalNegativeNegativeBreastNormalNegativeNegativeCerebellumdThe tissues were from autopsies.NormalNegativeNegativeCerebral cortexdThe tissues were from autopsies.NormalNegativeNegativeFallopian tubeNormalNegativeNegativeEsophagusNormalNegativeNegativeStomachNormalPositive weak (gastric glands)NegativeSmall intestineNormalNegativeNegativeColonNormalNegativeNegativeRectumNormalNegativeNegativeHeartdThe tissues were from autopsies.NormalNegativePositive (cardiac muscle)KidneyNormalPositive weak (proximal convoluted tubes)NegativeLiverNormalNegativeNegativeLungNormalNegativeNegativeOvaryNormalNegativeNegativePancreasdThe tissues were from autopsies.NormalNegativeNegativeParathyroidAdenomaNegativeNegativePituitary glanddThe tissues were fro" @default.
• W2018498303 created "2016-06-24" @default.
• W2018498303 creator A5007234546 @default.
• W2018498303 creator A5020658166 @default.
• W2018498303 creator A5020904085 @default.
• W2018498303 creator A5026977458 @default.
• W2018498303 creator A5029764881 @default.
• W2018498303 creator A5055700396 @default.
• W2018498303 creator A5063496403 @default.
• W2018498303 creator A5071208815 @default.
• W2018498303 creator A5074105781 @default.
• W2018498303 creator A5074468888 @default.
• W2018498303 date "2008-10-01" @default.
• W2018498303 modified "2023-10-17" @default.
• W2018498303 title "15-Prostaglandin Dehydrogenase Expression Alone or in Combination with ACSM1 Defines a Subgroup of the Apocrine Molecular Subtype of Breast Carcinoma" @default.
• W2018498303 cites W1210400071 @default.
• W2018498303 cites W1497322432 @default.
• W2018498303 cites W1536290683 @default.
• W2018498303 cites W1606423922 @default.
• W2018498303 cites W1946975580 @default.
• W2018498303 cites W1966856806 @default.
• W2018498303 cites W1969832327 @default.
• W2018498303 cites W1972086678 @default.
• W2018498303 cites W1976739900 @default.
• W2018498303 cites W1987438979 @default.
• W2018498303 cites W1988592538 @default.
• W2018498303 cites W1996808076 @default.
• W2018498303 cites W2007117595 @default.
• W2018498303 cites W2010871781 @default.
• W2018498303 cites W2011321818 @default.
• W2018498303 cites W2012140938 @default.
• W2018498303 cites W2013833276 @default.
• W2018498303 cites W2015756684 @default.
• W2018498303 cites W2018744320 @default.
• W2018498303 cites W2022169113 @default.
• W2018498303 cites W2043905676 @default.
• W2018498303 cites W2046870043 @default.
• W2018498303 cites W2053281862 @default.
• W2018498303 cites W2053644910 @default.
• W2018498303 cites W2056931917 @default.
• W2018498303 cites W2069837734 @default.
• W2018498303 cites W2070650966 @default.
• W2018498303 cites W2077986050 @default.
• W2018498303 cites W2078594804 @default.
• W2018498303 cites W2082660634 @default.
• W2018498303 cites W2088369265 @default.
• W2018498303 cites W2090277204 @default.
• W2018498303 cites W2094402002 @default.
• W2018498303 cites W2097255042 @default.
• W2018498303 cites W2101249156 @default.
• W2018498303 cites W2102803669 @default.
• W2018498303 cites W2105869199 @default.
• W2018498303 cites W2123124042 @default.
• W2018498303 cites W2127653391 @default.
• W2018498303 cites W2131597845 @default.
• W2018498303 cites W2131994307 @default.
• W2018498303 cites W2143001644 @default.
• W2018498303 cites W2147027178 @default.
• W2018498303 cites W2147343434 @default.
• W2018498303 cites W2157840751 @default.
• W2018498303 cites W4252310904 @default.
• W2018498303 cites W4253739671 @default.
• W2018498303 doi "https://doi.org/10.1074/mcp.r800011-mcp200" @default.
• W2018498303 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18632593" @default.
• W2018498303 hasPublicationYear "2008" @default.
• W2018498303 type Work @default.
• W2018498303 sameAs 2018498303 @default.
• W2018498303 citedByCount "39" @default.
• W2018498303 countsByYear W20184983032012 @default.
• W2018498303 countsByYear W20184983032013 @default.
• W2018498303 countsByYear W20184983032014 @default.
• W2018498303 countsByYear W20184983032015 @default.
• W2018498303 countsByYear W20184983032016 @default.
• W2018498303 countsByYear W20184983032017 @default.
• W2018498303 countsByYear W20184983032018 @default.
• W2018498303 countsByYear W20184983032019 @default.
• W2018498303 countsByYear W20184983032020 @default.
• W2018498303 countsByYear W20184983032021 @default.
• W2018498303 countsByYear W20184983032022 @default.
• W2018498303 crossrefType "journal-article" @default.
• W2018498303 hasAuthorship W2018498303A5007234546 @default.
• W2018498303 hasAuthorship W2018498303A5020658166 @default.
• W2018498303 hasAuthorship W2018498303A5020904085 @default.
• W2018498303 hasAuthorship W2018498303A5026977458 @default.
• W2018498303 hasAuthorship W2018498303A5029764881 @default.
• W2018498303 hasAuthorship W2018498303A5055700396 @default.
• W2018498303 hasAuthorship W2018498303A5063496403 @default.
• W2018498303 hasAuthorship W2018498303A5071208815 @default.
• W2018498303 hasAuthorship W2018498303A5074105781 @default.
• W2018498303 hasAuthorship W2018498303A5074468888 @default.
• W2018498303 hasBestOaLocation W20184983031 @default.
• W2018498303 hasConcept C121608353 @default.
• W2018498303 hasConcept C126322002 @default.
• W2018498303 hasConcept C142724271 @default.
• W2018498303 hasConcept C143998085 @default.
• W2018498303 hasConcept C150875184 @default.
• W2018498303 hasConcept C2777546739 @default.
• W2018498303 hasConcept C3018521938 @default.

• next