Cancer results from an accumulation of a wide range of genomic alterations in normal cells. Advances in DNA sequencing technology have accelerated the large-scale complete sequencing of cancer genomes to reveal the evolutionary processes that underlie tumor origin, progression and metastasis. This comprehensive cancer genome data provides new insights for the treatment of cancers. Thousands of somatically acquired mutations are often associated with solid tumors. However, only some of the mutations, termed as driver mutations, play an important role in driving cancer biology. Targeting oncogenic driver mutations has been proven to produce effective therapeutic interventions to control the tumor growth and progression. Although a cancer is traditionally classified according to the tissue from which the cancerous cells are generated, it could be more completely characterized by its key genomic abnormalities. For example, lung cancer is a general term for a number of genetically distinct diseases, each with its own unique potential genetic targets for drug therapy. The oncogenic driver EML4-ALK is presented in ~5% of non-small cell lung cancer (NSCLC) and CD74-ROS in ~1% of NSCLC. Crizotinib, a multi-targeted kinase inhibitor for MET/ALK/ROS, has demonstrated marked efficacy in patients with abnormal ALK or ROS genes. The success of crizotinib has shifted the traditional one-pill-for-all chemotherapy to a new paradigm of molecularly targeted therapy, and represents the true transition of cancer to orphan diseases.

Precision cancer therapy: The transition of cancer to orphan diseases

247th National Meeting (2014)

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