The role of epigenetic modifi cations in the common pathogenesis
of COPD and lung cancer also deserves attention. Although
there is growing evidence implicating DNA methylation, histone
deacetylation, and protein phosphorylation in lung cancer pathogenesis
( 33 – 35 ), this knowledge is only now being applied to
COPD, alone or when associated with lung cancer ( 36 , 37 ). It is
plausible that several candidate risk genes and pathways identifi ed
by lung cancer studies may be shared by these two diseases and
could constitute potential targets for the newly developed drugs
(eg, demethylating agents and histone deacetylase – inhibiting
agents) that modify epigenetic alterations.