EGFR, ESR1, BCL2和TP53通路的协同靶向:多管齐下的晚期乳腺癌治疗方法

IF 2.3 4区 医学 Q3 ONCOLOGY
Harneet Marwah, Hitesh Kumar Dewangan
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引用次数: 0

摘要

乳腺癌是一种由复杂的分子信号通路驱动的异质性疾病,影响肿瘤的进展、转移和治疗耐药性。本文对乳腺癌的分子机制进行了全面的分析,重点关注了EGFR、ESR1、BCL2和TP53等关键通路。我们研究了这些通路在调节关键细胞过程中的作用,包括增殖、存活、凋亡和迁移。讨论了EGFR参与细胞增殖和迁移,以及其在乳腺癌中的过表达和突变,以及ESR1信号在激素受体阳性乳腺癌中的影响和对内分泌治疗的抵抗。此外,本综述强调了BCL2在细胞凋亡调控中的作用及其在耐药中的过表达,同时探讨了TP53在细胞周期控制和细胞凋亡中的作用,特别是其突变导致预后不良。此外,这些分子途径之间的相互作用,如EGFR和ESR1之间的串扰,BCL2-TP53的相互作用,以及EGFR- tp53的突变关系,说明了耐药机制的复杂性和对多靶向治疗策略的需求。本文探讨了协同靶向的概念,包括PI3K/AKT/mTOR通路的整合,并有证据支持克服耐药和改善治疗结果的潜力。我们还讨论了个性化医疗的新兴作用,强调生物标志物驱动的患者选择和量身定制的治疗方法。最后,综述了纳米颗粒为基础的药物传递系统的进展,指出了它们在提高治疗效果和解决当前癌症治疗挑战方面的潜力。这篇综述强调了了解乳腺癌分子基础的重要性,以及需要综合的、多靶向的方法来克服治疗耐药,为改善乳腺癌治疗的临床结果提供了未来的方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Synergistic Targeting of EGFR, ESR1, BCL2, and TP53 Pathways: A Multi-Pronged Approach for Advanced Breast Cancer Therapy.

Breast cancer is a heterogeneous disease driven by complex molecular signaling pathways that influence tumor progression, metastasis, and treatment resistance. This review provides a comprehensive analysis of the molecular mechanisms underlying breast cancer, with a focus on key pathways such as EGFR, ESR1, BCL2, and TP53. We examine the roles of these pathways in regulating critical cellular processes, including proliferation, survival, apoptosis, and migration. EGFR's involvement in cell proliferation and migration, as well as its overexpression and mutations in breast cancer, are discussed, alongside the impact of ESR1 signaling in hormone-receptor-positive breast cancer and resistance to endocrine ther-apies. Additionally, the review highlights the function of BCL2 in apoptosis regulation and its overexpression in conferring resistance while also exploring the role of TP53 in cell cycle control and apoptosis, particularly its mutations that contribute to poor prognosis. Further-more, the interplay between these molecular pathways-such as the crosstalk between EGFR and ESR1, BCL2-TP53 interactions, and the EGFR-TP53 mutational relationships-illustrates the complexity of resistance mechanisms and the need for multi-targeted thera-peutic strategies. The concept of synergistic targeting, including the integration of the PI3K/AKT/mTOR pathway, is explored, with evidence supporting the potential for over-coming resistance and improving therapeutic outcomes. We also discuss the emerging role of personalized medicine, emphasizing biomarker-driven approaches for patient selection and tailored treatments. Finally, advancements in nanoparticle-based drug delivery systems are reviewed, addressing their potential to enhance therapeutic efficacy and address current challenges in cancer therapy. This review highlights the critical importance of understanding the molecular underpinnings of breast cancer and the need for integrated, multi-targeted ap-proaches to overcome therapeutic resistance, offering insights into future directions for im-proving clinical outcomes in breast cancer treatment.

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来源期刊
Current cancer drug targets
Current cancer drug targets 医学-肿瘤学
CiteScore
5.40
自引率
0.00%
发文量
105
审稿时长
1 months
期刊介绍: Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes and genes. Current Cancer Drug Targets publishes original research articles, letters, reviews / mini-reviews, drug clinical trial studies and guest edited thematic issues written by leaders in the field covering a range of current topics on drug targets involved in cancer. As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.
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