解密分子图谱:从妇科肿瘤到侵袭性男性乳腺癌的进化过程。

IF 6.6 2区 医学 Q1 Medicine Cellular Oncology Pub Date : 2024-10-01 Epub Date: 2024-06-18 DOI:10.1007/s13402-024-00964-4
Chuang Yang, Zhonglin Wang, Lijun Qian, Jingyue Fu, Handong Sun
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引用次数: 0

摘要

背景:妇科乳腺增生是指腺体乳腺组织的良性增生,是公认的男性乳腺癌的危险因素。然而,人们对从妇科乳腺增生发展为癌症的潜在致癌机制仍然知之甚少:本研究采用单细胞 RNA 测序(scRNA-seq)技术,以单细胞分辨率细致剖析妇科乳腺增生的细胞结构,并揭示其与男性乳腺癌的潜在关联。通过伪时间和进化分析,研究人员划定了妇科肿瘤和男性乳腺癌的不同特征。我们利用 TCGA 数据库以及细胞间通讯分析和免疫组化染色来验证不同基因的表达,特别是 CD13.Result:结果:从拷贝数变异图谱和进化树中,我们推断出这两种疾病的共同突变特征(18p+和18q+)。发育轨迹揭示了妇科炎症与恶性上皮细胞之间令人费解的重叠。此外,与正常乳腺组织相比,差异基因 CD13 成为妇科乳腺病和男性乳腺癌的共同特征。肿瘤微环境中的细胞-细胞相互作用分析和交流动态突出显示了CD13+和CD13-亚群之间的区别,前者表现出FGFR1-FGF7的高表达:我们的研究为从妇科肿瘤到男性乳腺癌的演变过程提供了新的见解,揭示了 CD13 在推动这一转变过程中的关键作用。将 CD13 鉴定为潜在的治疗靶点表明,专门针对男性乳腺癌治疗的 CD13 靶向干预是可行的。
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Deciphering the molecular landscape: evolutionary progression from gynecomastia to aggressive male breast cancer.

Background: Gynecomastia denotes the benign proliferation of glandular breast tissue and stands as a recognized risk factor for male breast cancer. Nonetheless, the underlying carcinogenic mechanisms orchestrating the progression from gynecomastia to cancer remain poorly understood.

Methods: This study employed single-cell RNA sequencing (scRNA-seq) to meticulously dissect the cellular landscape of gynecomastia and unravel potential associations with male breast cancer at a single-cell resolution. Pseudotime and evolutionary analyses were executed to delineate the distinct features characterizing gynecomastia and male breast cancer. The TCGA database, along with cell-cell communication analysis and immunohistochemistry staining, was harnessed to validate differential gene expression, specifically focusing on CD13.

Result: From the copy number variation profiles and evolutionary tree, we inferred shared mutation characteristics (18p+ and 18q+) underpinning both conditions. The developmental trajectory unveiled an intriguing overlap between gynecomastia and malignant epithelial cells. Moreover, the differential gene CD13 emerged as a common denominator in both gynecomastia and male breast cancer when compared with normal mammary tissue. Cell-cell interaction analysis and communication dynamics within the tumor microenvironment spotlighted distinctions between CD13+ and CD13- subsets, with the former exhibiting elevated expression of FGFR1-FGF7.

Conclusions: Our investigation provides novel insights into the evolutionary progression from gynecomastia to male breast cancer, shedding light on the pivotal role of CD13 in driving this transition. The identification of CD13 as a potential therapeutic target suggests the feasibility of CD13-targeted interventions, specifically tailored for male breast cancer treatment.

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来源期刊
Cellular Oncology
Cellular Oncology Biochemistry, Genetics and Molecular Biology-Cancer Research
CiteScore
10.40
自引率
1.50%
发文量
0
审稿时长
16 weeks
期刊介绍: The Official Journal of the International Society for Cellular Oncology Focuses on translational research Addresses the conversion of cell biology to clinical applications Cellular Oncology publishes scientific contributions from various biomedical and clinical disciplines involved in basic and translational cancer research on the cell and tissue level, technical and bioinformatics developments in this area, and clinical applications. This includes a variety of fields like genome technology, micro-arrays and other high-throughput techniques, genomic instability, SNP, DNA methylation, signaling pathways, DNA organization, (sub)microscopic imaging, proteomics, bioinformatics, functional effects of genomics, drug design and development, molecular diagnostics and targeted cancer therapies, genotype-phenotype interactions. A major goal is to translate the latest developments in these fields from the research laboratory into routine patient management. To this end Cellular Oncology forms a platform of scientific information exchange between molecular biologists and geneticists, technical developers, pathologists, (medical) oncologists and other clinicians involved in the management of cancer patients. In vitro studies are preferentially supported by validations in tumor tissue with clinicopathological associations.
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