Predictive molecular markers in non–small cell lung cancer

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Abstract
Recent biotechnologic knowledge has enabled the discovery of a cornucopia of genetic abnormalities commonly involved not only in cancer but also in other diseases ranging from the plague to arteriosclerosis. The wealth of possibilities uncovered by this knowledge inspires the hope that today's dream of a unified concept of common treatment for multiple diseases could become a future reality. This review arbitrarily categorizes recent findings into five major areas. First, cisplatin resistance associated with the nucleotide excision repair pathway can help clinical oncologists to choose between cisplatin and noncisplatin combinations. Second, the relevant role of nuclear factor-kappa B as a predictor of chemosensitivity can lead to the development of new drugs abrogating nuclear factor-kappa B expression. Third, the presence of tubulin mutations, which are directly involved in resistance to microtubule-interactive drugs, can guide chemotherapy based on taxane or nontaxane combinations. In addition, certain chromosomal deletions affect genes involved in deoxyribonucleotide synthesis, like ribonucleotide reductase, that intervene in gemcitabine metabolism; this raises interest in investigating deletion at chromosome 11p15.5 as a potential mechanism of gemcitabine resistance. Finally, an overwhelming number of publications have analyzed genes involved in cell cycle regulation and development as predictive markers of survival; however, where these pieces fit into the puzzle of cancer management is still unclear.