Gene expression analysis studies may shed some light on these
differences. Studies show that the transcriptome of the normal
bronchial epithelium is distinct from that of the lung parenchyma,
that the SCLC transcriptome profi le differs from that of NSCLC,
and that there is in each individual an association between cumulative
tobacco exposure and gene transcription ( 73 , 74 ). Not all genes
are reversible to their pre-smoke exposure transcriptional status
upon cessation of smoke exposure. Those reversible tend to be
genes encoding detoxifi cation/oxidoreductase enzymes, whereas
those not reversible appear to be immune-modifying cancerrelated
genes ( 75 ). The gene expression profi le of the individual’s
lung cells may reveal which disease pathway predominates and
why disease risk persists in ex-smokers ( 32 , 76 ).