Targeted drug development in melanoma and nonsmall cell lung cancer: BRAF, MEK, and ALK inhibitors

被引：1
作者：
Chi M. [1 ]
Puzanov I. [2 ]
机构：
[1] Department of Internal Medicine, St Joseph Hospital, University of Illinois at Chicago
[2] Division of Hematology-Oncology, Vanderbilt University Medical Center, 777 Preston Research Building, 37232-6307 Nashville TN
来源：
memo - Magazine of European Medical Oncology | 2012年 / 5卷 / 4期
关键词：
ALK inhibitor; BRAF inhibitor; MEK inhibitor; Melanoma; Nonsmall cell lung cancer;
D O I：
10.1007/s12254-012-0058-4
中图分类号：
学科分类号：
摘要：
In the past few decades, many advances have been witnessed in the development of personalized molecular therapies, especially in the areas of melanoma and nonsmall cell lung cancer (NSCLC) among all other medical oncology fields. These therapies can be roughly divided into three categories at present: (1) targeting membrane-bound receptor tyrosine kinase (RTK), using either monoclonal antibodies or tyrosine kinase inhibitor (TKI), (2) targeting intracellular mitogen-activated protein kinase (MAPK) pathway, and (3) targeting intracellular phosphoinositide 3-kinase (PI3K) pathway. Currently, melanoma research focuses on MAPK pathway, spending efforts to clarify the intricate interactions in RAS-MEK-ERK-signaling cascades, whereas in the field of NSCLC, most achievements have been made targeting RTKs. This review will discuss the recent movements of drug development in these two areas, specifically BRAF and MEK inhibitors in melanoma, and ELM4-ALK inhibitors in lung cancer, along with the mechanisms of drug resistance and potential future strategies. © 2012 Springer-Verlag Wien.
引用
收藏
页码：302 / 308
页数：6
相关论文
共 62 条
  • [1] Fipil J., Garrido-Laguna I., Lubos B.P., Novel therapeutic targets in non-small cell lung cancer, J Thorac Oncol, 6, pp. 1601-1612, (2011)
  • [2] Downward J., Targeting RAS signalling pathways in cancer therapy, Nat Rev Cancer, 3, 1, pp. 11-22, (2003)
  • [3] Platz A., Egyhazi S., Ringborg U., Hansson J., Human cutaneous melanoma
  • [4] A review of NRAS and BRAF mutation frequencies in relation to histogenetic subclass and body site, Mol Oncol., 1, 4, pp. 395-405, (2008)
  • [5] Kelleher C.F., Solomon B., McArthur A.G., Molecular therapeutic advances in personalized therapy of melanoma and non-small cell lung cancer, J Pers Med., 2, 2, pp. 35-49, (2012)
  • [6] Zuidervaart W., Van Nieuwpoort F., Stark M., Dijkman R., Packer L., Borgstein A.M., Activation of the MAPK pathway is a common event in uveal melanomas although it rarely occurs through mutation of BRAF or RAS, Br J Cancer., 92, 11, pp. 2032-2038, (2005)
  • [7] Davies H., Bignell G.R., Cox C., Stephens P., Edkins S., Clegg S., Mutations of the BRAF gene in human cancer, Nature, 417, 6892, pp. 949-954, (2002)
  • [8] Puzanov I., Flaherty K.T., Sosman J.A., Vemurafenib, Drugs Fut, 36, 3, (2011)
  • [9] Lemech C., Infante J., Arkenau H.T., The potential for BRAF V600 inhibitors in advanced cutaneous melanoma: Rationale and latest evidence, Ther Adv Med Oncol., 4, 2, pp. 61-73, (2012)
  • [10] Ott P.A., Hamilton A., Min C., Safarzadeh-Amiri S., Goldberg L., Yoon J., A phase II trial of sorafenib in metastatic melanoma with tissue correlates, PLoS One., 5, 12, (2010)
1234567