No abstract

We have identified a gene, fos B, encoding a nuclear protein of 338 amino acids presenting a 70% homology with c‐fos, whose expression is activated during G0/G1 transition. Growth factor stimulation of quiescent cells leads to a rapid and transient accumulation of fos B mRNA, with kinetics similar to those of c‐fos. The induction of fos B mRNA levels is in part due to a dramatic increase in the transcription of the gene. The half‐life of fos B mRNA is in the order of 10‐15 min. Both transcriptional activation and mRNA stability are substantially increased in the presence of protein synthesis inhibitors. Immunoprecipitation studies showed that fos B as c‐fos protein, forms a complex in vitro with c‐jun and jun B proteins in the absence of a target binding sequence. Gel retardation assays demonstrated that fos B protein positively influences the binding of c‐jun and jun B proteins to an AP‐1 binding consensus sequence, suggesting that fos B protein plays a role in control of gene expression.

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p16(INK4a) promoter hypermethylation and p53 mutations can occur in chronic smokers before any clinical evidence of neoplasia and may be indicative of an increased risk of developing lung cancer or of early disease. K-ras mutations occur exclusively in the presence of clinically detectable neoplastic transformation. Molecular analysis of sputum for such markers may provide an effective means of screening chronic smokers to enable earlier detection and therapeutic intervention of lung cancer.

No abstract