TMPRSS2-ERG的机理认识和分子诊断:从融合阳性前列腺癌信号图谱的调控到作为诊断标记物的评估历程概述。

IF 3.3 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Ammad Ahmad Farooqi, Assiya Turgambayeva, Aigul Almabayeva, Marina Zhanaliyeva, Lyazat Orakbay, Zhanara Shabanbayeva, Oryngul Narmanova, Marat Kelissovich Syzdykbayev
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引用次数: 0

摘要

染色体重排和复发性基因融合以前被认为是血液恶性肿瘤的主要致癌机制。然而,不同癌症中基因融合的发现为全面研究细胞类型特异性融合癌蛋白如何调节信号级联打开了新的视野。前列腺癌(PCa)是一种多方面的、具有治疗挑战性的疾病,功能基因组学帮助我们更好地了解了前列腺癌、耐阉PCa和转移的发生机制。考虑到在 PCa 中也发现了基因融合,分子肿瘤学领域得到了迅速扩展,研究人员正在揭示融合肿瘤蛋白对信号通路的机理调控的新面貌。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanistic Insights and Molecular Diagnostics of TMPRSS2-ERG: Overview of the Journey from Regulation of Signaling Landscape in Fusion Positive Prostate Cancer to Appraisal as a Diagnostic Marker.

Chromosomal rearrangements and recurrent gene fusions were previously presumed to be the primary oncogenic mechanisms of hematological malignancies. However, the discovery of gene fusions in different cancers has opened new horizons to comprehensively investigate how cell type-specific fusion oncoproteins modulate signaling cascades. Prostate cancer (PCa) is a multifaceted and therapeutically challenging disease, and functional genomics have helped us develop a better understanding of the mechanisms underlying prostate carcinogenesis, castration-resistant PCa, and metastasis. Keeping in mind the fact that gene fusions have also been discovered in PCa, there has been rapid expansion in the field of molecular oncology and researchers are uncovering new facets regarding the mechanistic regulation of signaling pathways by fusion oncoproteins.

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