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The literature dedicated to the functional properties of the p53 gene can make one wish that there were more genes i nt he human genome an df ar fewer functions for each protein product. p53, arguably the most heavily studied gene product, can interact with aw ide array of nuclear and cytoplasmic binding partners. These interactions, as well as subtle posttranslational changes i np hosphorylation, acetylation, sumoylation, and other modifications, can modulate the central activity of p53—the transcriptional activation (and occasional repression) o fd ownstream target genes. Although there is increasing evidence for unexpected nontranscriptional roles for p53 (1), the regulation of target gene expression in concert wit hi ndividual components of parallel an di nterconnecting cell signaling cascade pathways mediates the primary function of p53, which has been reviewed extensively (2). This function can be summarized as th ea bility to sense and respond to cellular stresses that can range from dramati co r su btle DNA damage to hypoxi ao r a berrant growth signals from oncogene activation. The ability of wild-type p5 3t o restrai nc e ll growth or to kill affected cell st hat are at ris kf or aberrant clonal expansion helps explain, therefore, why loss of wild-type p53 function is among the most common mutational events detecte di n human cancers. In this issue of the Journal ,A hrend te t a l. (3) report their findings on a dataset of 245 patients with operable non-smallcell lung cancer (NSCLC), i nw hich 188 patients with confirmed stage I, II, or IIIa lung cancer were prospectively analyze df or the presence of p53 mutations. p53 mutation status was then examine di nr e lation to matched clinical outcome an dd emographic information for each patient. The authors detected p53 mutations in approximately 50% of the primary lung cancer samples, and they determined that the presence of a p53 mutation was a statisticall ys ignificant predictor of poor surviva li n th es u bset of patients with stage I disease (n 106) but not in patients with more advanced stages o fd i sease. The conclusion of the authors, reflecting the hope o fi nvestigators throughout the broa df i eld of molecular prognostic factors, i st hat thi st ype of specific prognostic information may ultimately lead to better treatment strategies an di mproved outcomes for patients suffering from NSCLC.

New Leads Suggest a Clinically Relevant Genotype-Phenotype Relationship for the p53 Gene