{"title":"Breast cancer during pregnancy of Luminal A type overexpressed CXCL13.","authors":"Fumi Nozaki, Yoko Nakanishi, Tomoyuki Tanino, Tomohiro Ochi, Reika In, Yuka Kajiura, Kumiko Kida, Junko Takei, Atsushi Yoshida, Naoki Kanomata, Atsuko Kitano, Hideko Yamauchi, Shinobu Masuda","doi":"10.1111/pin.13474","DOIUrl":null,"url":null,"abstract":"<p><p>Pregnancy-associated breast cancer has been increasing. In this study, we analyzed patients with breast cancer that occurred during pregnancy (PrBC) and compared their genetic profiles with those of patients with breast cancer that did not occur during pregnancy, within 1 year after childbirth nor during lactation (non-PrBC). We performed gene expression analyses of patients with PrBC and non-PrBC using microarrays and qRT-PCR. Microarray analysis showed that 355 genes were upregulated in the luminal-type PrBC group compared to those in the non-PrBC group. The C-X-C motif chemokine ligand 13 (CXCL13) gene was the most upregulated in the PrBC group compared to that in the non-PrBC group, especially in the luminal A-type (p = 0.016). This result was corroborated by the qRT-PCR analysis of microdissected cancer cells (p < 0.001). A negative correlation was observed between CXCL13 and estrogen receptor 1 (ESR1) mRNA expression levels in luminal A-type breast carcinoma (p < 0.001). Our results provide clues for a better understanding of breast cancer pathogenesis during pregnancy.</p>","PeriodicalId":19806,"journal":{"name":"Pathology International","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pathology International","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/pin.13474","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/28 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PATHOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Pregnancy-associated breast cancer has been increasing. In this study, we analyzed patients with breast cancer that occurred during pregnancy (PrBC) and compared their genetic profiles with those of patients with breast cancer that did not occur during pregnancy, within 1 year after childbirth nor during lactation (non-PrBC). We performed gene expression analyses of patients with PrBC and non-PrBC using microarrays and qRT-PCR. Microarray analysis showed that 355 genes were upregulated in the luminal-type PrBC group compared to those in the non-PrBC group. The C-X-C motif chemokine ligand 13 (CXCL13) gene was the most upregulated in the PrBC group compared to that in the non-PrBC group, especially in the luminal A-type (p = 0.016). This result was corroborated by the qRT-PCR analysis of microdissected cancer cells (p < 0.001). A negative correlation was observed between CXCL13 and estrogen receptor 1 (ESR1) mRNA expression levels in luminal A-type breast carcinoma (p < 0.001). Our results provide clues for a better understanding of breast cancer pathogenesis during pregnancy.
期刊介绍:
Pathology International is the official English journal of the Japanese Society of Pathology, publishing articles of excellence in human and experimental pathology. The Journal focuses on the morphological study of the disease process and/or mechanisms. For human pathology, morphological investigation receives priority but manuscripts describing the result of any ancillary methods (cellular, chemical, immunological and molecular biological) that complement the morphology are accepted. Manuscript on experimental pathology that approach pathologenesis or mechanisms of disease processes are expected to report on the data obtained from models using cellular, biochemical, molecular biological, animal, immunological or other methods in conjunction with morphology. Manuscripts that report data on laboratory medicine (clinical pathology) without significant morphological contribution are not accepted.