Translational Advances in Oncogene and Tumor-Suppressor Gene Research.

IF 4.5 2区 医学 Q1 ONCOLOGY
Cancers Pub Date : 2025-03-17 DOI:10.3390/cancers17061008
Radoslav Stojchevski, Edward Agus Sutanto, Rinni Sutanto, Nikola Hadzi-Petrushev, Mitko Mladenov, Sajal Raj Singh, Jitendra Kumar Sinha, Shampa Ghosh, Bhuvaneshwar Yarlagadda, Krishna Kumar Singh, Prashant Verma, Sonali Sengupta, Rakesh Bhaskar, Dimiter Avtanski
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引用次数: 0

Abstract

Cancer, characterized by the uncontrolled proliferation of cells, is one of the leading causes of death globally, with approximately one in five people developing the disease in their lifetime. While many driver genes were identified decades ago, and most cancers can be classified based on morphology and progression, there is still a significant gap in knowledge about genetic aberrations and nuclear DNA damage. The study of two critical groups of genes-tumor suppressors, which inhibit proliferation and promote apoptosis, and oncogenes, which regulate proliferation and survival-can help to understand the genomic causes behind tumorigenesis, leading to more personalized approaches to diagnosis and treatment. Aberration of tumor suppressors, which undergo two-hit and loss-of-function mutations, and oncogenes, activated forms of proto-oncogenes that experience one-hit and gain-of-function mutations, are responsible for the dysregulation of key signaling pathways that regulate cell division, such as p53, Rb, Ras/Raf/ERK/MAPK, PI3K/AKT, and Wnt/β-catenin. Modern breakthroughs in genomics research, like next-generation sequencing, have provided efficient strategies for mapping unique genomic changes that contribute to tumor heterogeneity. Novel therapeutic approaches have enabled personalized medicine, helping address genetic variability in tumor suppressors and oncogenes. This comprehensive review examines the molecular mechanisms behind tumor-suppressor genes and oncogenes, the key signaling pathways they regulate, epigenetic modifications, tumor heterogeneity, and the drug resistance mechanisms that drive carcinogenesis. Moreover, the review explores the clinical application of sequencing techniques, multiomics, diagnostic procedures, pharmacogenomics, and personalized treatment and prevention options, discussing future directions for emerging technologies.

癌基因和肿瘤抑制基因的翻译研究进展。
癌症的特点是细胞不受控制地增殖,是全球主要死亡原因之一,大约五分之一的人在其一生中患上这种疾病。虽然许多驱动基因在几十年前就被发现了,而且大多数癌症可以根据形态和进展进行分类,但在遗传畸变和核DNA损伤方面的知识仍然存在重大差距。对两组关键基因的研究——抑制肿瘤细胞增殖和促进细胞凋亡的肿瘤抑制基因和调节肿瘤细胞增殖和生存的癌基因——可以帮助我们了解肿瘤发生背后的基因组原因,从而为诊断和治疗提供更个性化的方法。肿瘤抑制基因(经历两次撞击和功能丧失突变)和癌基因(经历一次撞击和功能获得突变的激活形式的原癌基因)的畸变导致了调节细胞分裂的关键信号通路的失调,如p53、Rb、Ras/Raf/ERK/MAPK、PI3K/AKT和Wnt/β-catenin。基因组学研究的现代突破,如下一代测序,为绘制导致肿瘤异质性的独特基因组变化提供了有效的策略。新的治疗方法使个性化医疗成为可能,有助于解决肿瘤抑制因子和癌基因的遗传变异。本文综述了肿瘤抑制基因和癌基因背后的分子机制、它们调节的关键信号通路、表观遗传修饰、肿瘤异质性以及驱动癌变的耐药机制。此外,本文还探讨了测序技术、多组学、诊断方法、药物基因组学以及个性化治疗和预防方案的临床应用,并讨论了新兴技术的未来发展方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cancers
Cancers Medicine-Oncology
CiteScore
8.00
自引率
9.60%
发文量
5371
审稿时长
18.07 days
期刊介绍: Cancers (ISSN 2072-6694) is an international, peer-reviewed open access journal on oncology. It publishes reviews, regular research papers and short communications. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced.
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