Personalized Therapy for Lung Cancer

被引:54
作者
Moreira, Andre L. [1 ]
Eng, Juliana [2 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10065 USA
[2] Mem Sloan Kettering Canc Ctr, Dept Med, Thorac Oncol Serv, New York, NY 10065 USA
关键词
TYROSINE KINASE INHIBITORS; ACQUIRED-RESISTANCE; EGFR MUTATIONS; GEFITINIB RESISTANCE; CLINICAL-RESPONSE; ADENOCARCINOMA; HISTOLOGY; REARRANGEMENTS; AMPLIFICATION; PREVALENCE;
D O I
10.1378/chest.14-0713
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The past decade has seen an enormous advancement in the therapy for lung cancer, predominantly seen in adenocarcinoma, ranging from the introduction of histology-based drugs to the discovery of targetable mutations. These events have led to a personalized therapeutic approach with the delivery of drugs that target specifi c oncogenic pathways active in a given tumor with the intent of acquiring the best response rate. The discovery of sensitizing mutation in the epidermal growth factor receptor gene as the basis for clinical response to tyrosine kinase inhibitors led to a systematic search for other molecular targets in lung cancer. Currently, there are several molecular alterations that can be targeted by experimental drugs. These new discoveries would not be possible without a parallel technological evolution in diagnostic molecular pathology. Next-generation sequencing (NGS) is a technology that allows for the evaluation of multiple molecular alterations in the same sample using a small amount of tissue. Selective evaluation of targeted cancer genes, instead of whole-genome evaluation, is the approach that is best suited to enter clinical practice. This technology allows for the detection of most molecular alteration with a single test, thus saving tissue for future discoveries. The use of NGS is expected to increase and gain importance in clinical and experimental approaches, since it can be used as a diagnostic tool as well as for new discoveries. The technique may also help us elucidate the interplay of several genes and their alteration in the mechanism of drug response and resistance.
引用
收藏
页码:1649 / 1657
页数:9
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