Department of Pathology Division of Internal Medicine and Dermatology, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands.
Endocr Relat Cancer. 2012 Jun 18;19(4):R115-29. doi: 10.1530/ERC-12-0060. Print 2012 Aug.
Cancer treatments are increasingly focusing on the molecular mechanisms underlying the oncogenic processes present in tumors of individual patients. Fibroblast growth factor receptors (FGFRs) are among the many molecules that are involved in oncogenesis and are currently under investigation for their potential as drug targets in breast cancer patients. These receptor tyrosine kinases play a role in several processes including proliferation, angiogenesis, and migration. Alterations in these basal processes can contribute to the development and progression of tumors. Among breast cancer patients, several subgroups have been shown to harbor genetic aberrations in FGFRs, including amplifications of FGFR1, FGFR2, and FGFR4 and mutations in FGFR2 and FGFR4. Here, we review in vitro and in vivo models that have partly elucidated the molecular implications of these different genetic aberrations, the resulting tumor characteristics, and the potential of FGFRs as therapeutic targets for breast cancer treatment.
癌症治疗越来越关注个体患者肿瘤中致癌过程的分子机制。成纤维细胞生长因子受体 (FGFRs) 是参与致癌作用的众多分子之一，目前正在研究其作为乳腺癌患者药物靶点的潜力。这些受体酪氨酸激酶在包括增殖、血管生成和迁移在内的几个过程中发挥作用。这些基础过程的改变可能导致肿瘤的发生和发展。在乳腺癌患者中，已经证实几个亚组存在 FGFR 中的遗传异常，包括 FGFR1、FGFR2 和 FGFR4 的扩增以及 FGFR2 和 FGFR4 的突变。在这里，我们回顾了部分阐明这些不同遗传异常的分子意义、由此产生的肿瘤特征以及 FGFR 作为乳腺癌治疗的治疗靶点的潜力的体外和体内模型。
