Table 5 Some genetic alterations in small cell lung cancer (SCLC) [23, 24]
Gene (locus)AlterationPossible drug/therapeutic targeting abnormalities
FHIT (3p14.2)Loss (80% of SCLC)
RASSF1 (3p21.3)Loss (>90% of SCLC)
RARB (3p24)Loss (72% of SCLC)
TP53 (17p13.1)Mutation and deletion (>75% of SCLC)p53 adenoviral vector (Advexin)
c-KitOverexpressedTyrosine kinase inhibitor (imatinib)
SrcConstitutively activatedSrc inhibitor (dasatinib)
c-MetAmplified, overexpressed or mutatedsiRNA, c-Met inhibitor SU11274
RB1Altered (>90% of SCLC)
PI3K/Akt/mTORConstitutively activatedPI3K inhibitor (LY294002) mTOR inhibitor (rapamycin) and its derivatives (CCI-779, RAD001, AP23576)
Bcl-2OverexpressedAntisense oligonucleotide (oblimersen sodium) Inhibitor of Bcl-2 (ABT-737)
VEGFOverexpressedHumanised monoclonal antibody (bevacizumab) VEGFR-2 and EGFR inhibitor (ZD6474)
  • FHIT: fragile histidine triad; RASSF: Ras-association domain family; RARB: retinoic acid receptor-β; TP53: tumour protein p53; RB: retinoblastoma; PI3K: phosphoinositide 3-kinase; mTOR: mammalian target of rapamycin; Bcl: B-cell lymphoma; VEGF: vascular endothelial growth factor; siRNA: small interfering RNA; EGFR: epidermal growth factor.