首页> 美国卫生研究院文献>Breast Cancer Research : BCR >p53 deficiency linked to B cell translocation gene 2 (BTG2) loss enhances metastatic potential by promoting tumor growth in primary and metastatic sites in patient-derived xenograft (PDX) models of triple-negative breast cancer
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p53 deficiency linked to B cell translocation gene 2 (BTG2) loss enhances metastatic potential by promoting tumor growth in primary and metastatic sites in patient-derived xenograft (PDX) models of triple-negative breast cancer

机译:与B细胞易位基因2(BTG2)丢失有关的p53缺乏症通过促进三阴性乳腺癌患者源性异种移植(PDX)模型中原发和转移部位的肿瘤生长来增强转移潜力

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摘要

BackgroundDespite advances in early diagnosis and treatment of cancer patients, metastasis remains the major cause of mortality. TP53 is one of the most frequently mutated genes in human cancer, and these alterations can occur during the early stages of oncogenesis or as later events as tumors progress to more aggressive forms. Previous studies have suggested that p53 plays a role in cellular pathways that govern metastasis. To investigate how p53 deficiency contributes to late-stage tumor growth and metastasis, we developed paired isogenic patient-derived xenograft (PDX) models of triple-negative breast cancer (TNBC) differing only in p53 status for longitudinal analysis.
机译:背景技术尽管在癌症患者的早期诊断和治疗方面取得了进步,但转移仍然是导致死亡的主要原因。 TP53是人类癌症中最常见的突变基因之一,这些改变可以发生在肿瘤发生的早期阶段,也可以随着肿瘤发展为更具侵略性的形式而发生。先前的研究表明,p53在控制转移的细胞途径中起作用。为了研究p53缺乏如何导致晚期肿瘤生长和转移,我们开发了三阴性乳腺癌(TNBC)的配对同基因患者异种移植(PDX)模型,仅在p53状态上有所不同,以进行纵向分析。

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