Alluri N, Jimeno A
Division of Hematology and Oncology, University of Colorado Cancer Center, Aurora, Colorado, USA.
Drugs Today (Barc). 2013 Aug;49(8):491-8. doi: 10.1358/dot.2013.49.8.1990151.
Advanced melanoma traditionally has had poor prognosis with limited, modestly effective and relatively toxic systemic treatment options like cytotoxic chemotherapy (dacarbazine) and immunomodulating agents (high-dose interleukin-2 and ipilimumab) which have response rates of 6-20%. With the identification of BRAF mutations found to be present in 50% of melanomas and the clinical success of serine/threonine-protein kinase B-raf inhibitors the prognostic landscape of melanoma has changed considerably. Vemurafenib and dabrafenib have been at the forefront of antimelanoma-targeted agents with a tolerable side effect profile and efficacy that compared well with the standard chemotherapy. These characteristics have led to the regulatory approval of both agents for the treatment of melanoma. However, these agents are not curative and have a short life span primarily due to rapidly occurring drug resistance. More recently, mitogen-activated protein kinase kinase (MEK) inhibitors have been found to have strong anticancer activity independently as well as when combined with other agents like B-raf inhibitors due to their activity downstream of RAF. Preclinical data and limited clinical data suggest that MEK inhibitors may be a component of effective therapy for a broad spectrum of cancers with other oncogenic drivers.
传统上,晚期黑色素瘤预后较差,可用的全身治疗选择有限、疗效一般且毒性相对较大,如细胞毒性化疗(达卡巴嗪)和免疫调节药物(高剂量白细胞介素-2和伊匹单抗),其缓解率为6%-20%。随着发现50%的黑色素瘤存在BRAF突变,以及丝氨酸/苏氨酸蛋白激酶B-raf抑制剂在临床上取得成功,黑色素瘤的预后情况已发生了很大变化。维莫非尼和达拉非尼一直处于抗黑色素瘤靶向药物的前沿,具有可耐受的副作用和与标准化疗相当的疗效。这些特性使得这两种药物均获得了治疗黑色素瘤的监管批准。然而,这些药物并非治愈性药物,且主要由于迅速出现的耐药性而使用寿命较短。最近,有研究发现,丝裂原活化蛋白激酶激酶(MEK)抑制剂单独使用时以及与其他药物(如B-raf抑制剂)联合使用时均具有很强的抗癌活性,这是因为其在RAF下游发挥作用。临床前数据和有限的临床数据表明,MEK抑制剂可能是针对具有其他致癌驱动因素的广泛癌症进行有效治疗的一个组成部分。