妊娠期 A 型乳腺癌过表达 CXCL13。

IF 2.5 4区 医学 Q2 PATHOLOGY Pathology International Pub Date : 2024-08-28 DOI:10.1111/pin.13474
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
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引用次数: 0

摘要

与妊娠相关的乳腺癌越来越多。在这项研究中,我们对妊娠期乳腺癌(PrBC)患者进行了分析,并将其基因图谱与非妊娠期、产后 1 年内或哺乳期乳腺癌(非 PrBC)患者的基因图谱进行了比较。我们使用芯片和 qRT-PCR 对 PrBC 和非 PrBC 患者进行了基因表达分析。微阵列分析表明,与非PrBC组相比,管腔型PrBC组有355个基因上调。与非管腔型 PrBC 组相比,C-X-C 矩阵趋化因子配体 13(CXCL13)基因在管腔型 PrBC 组中上调最多,尤其是在管腔型 A 组中(p = 0.016)。对微观切片癌细胞的 qRT-PCR 分析也证实了这一结果(p = 0.016)。
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Breast cancer during pregnancy of Luminal A type overexpressed CXCL13.

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.

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来源期刊
Pathology International
Pathology International 医学-病理学
CiteScore
4.50
自引率
4.50%
发文量
102
审稿时长
12 months
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.
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