摘要
背景:乳腺癌是全球最常见的危及生命的恶性肿瘤。由于其独特的生物学和生理特性,HER2阳性是独特的乳腺癌亚型。 结果:HER2基因扩增和17号染色体多体导致HER2的过度表达,这是HER2阳性乳腺癌的重要原因所在。HER2基因变异,以及其他基因/基因变异,涉及其过度表达,疾病的预后和预测HER2阳性乳腺癌的敏感性。Trastuzumab(Herceptin)是最常用的治疗HER2阳性状态的患者的药物。基因组的改变可导致曲妥珠单抗耐药性的发展,从而影响到曲妥珠单抗治疗的反应。 结论:在目前的综述文章中,我们总结了基因组改变HER2的过度表达的原因,因而增加乳腺癌的风险。此外,也讨论了基因突变影响到曲妥珠单抗治疗的反应。
关键词: 乳腺癌,HER2过度表达,基因变异,基因组改变,耐药性,曲妥珠单抗。
图形摘要
Current Cancer Drug Targets
Title:Role of Genomic Alterations in HER2 Positive Breast Carcinoma: Focus on Susceptibility and Trastuzumab-therapy
Volume: 17 Issue: 4
关键词: 乳腺癌,HER2过度表达,基因变异,基因组改变,耐药性,曲妥珠单抗。
摘要: Background: Breast cancer is the most frequently diagnosed life-threatening malignancy among women, across the globe. HER2 positive is a distinct breast cancer subtype, on account of its unique biology and physiological behavior.
Results: Amplification of HER2 oncogene/polysomy 17 leads to HER2 overexpression that is a significant causal implication in HER2 positive breast cancer. HER2 gene variants, as well as other genes/gene variants, are involved in its overexpression, disease prognosis and in predicting the susceptibility towards HER2 positive breast cancer. Trastuzumab (Herceptin) is the most commonly used therapy for treating patients with HER2 positive status. Genomic alterations are incriminated in the development of trastuzumab-resistance, which influences the response towards trastuzumab-therapy. Conclusion: In the current review article, we have summarized the genomic alterations that are responsible for overexpression of HER2 and therefore, increased risk of breast cancer. In addition, the gene variants affecting response towards trastuzumab-therapy have also been discussed.Export Options
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Cite this article as:
Role of Genomic Alterations in HER2 Positive Breast Carcinoma: Focus on Susceptibility and Trastuzumab-therapy, Current Cancer Drug Targets 2017; 17 (4) . https://dx.doi.org/10.2174/1568009616666161216094026
DOI https://dx.doi.org/10.2174/1568009616666161216094026 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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