LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND0 E5 }5 A8 X. c7 ~ o
THERAPE UTIC PERSPECTIVES" V, V* f! N5 o, K8 w
J. Mazieres, S. Peters; h) G; V9 p! L& z$ N
Introduction: HER2 oncogene is a memb er of the EGFR family, encoding atransmembrane receptor that drives and regulates cell proliferation. HER2 mutations are identified in about 2% of non small cell lung cancer (NSCLC) , mainly located in exon 20, and appear to be critical for lung cancer carcinogenesis . Very scarce data are available to define a clinical profile of the patients harboring HER2 mutated NSCLC. We aimed to study clinic opatholog ical characteristics an d therapeutic- T" i- O4 g5 {- Q/ Z T. [: `
outcomes of patients harboring HER2 mutation in a large European series. Result s:We retrospec tively ide ntified 46 NSCLC patients diagn osed with HER2 exon 20 mut ation. HER2 mutation was mainly exclusive as only one concomitan t KRas mutation was des cribed. Our population was characterized by a median age of 60 yr (31 to 86 yr), a high proportion of women (30 vs. 16 men, 65% ), and of never smokers (24, 52%). All tumors were adenoc arcinomas (two with lepidic features). Half of the patients had stage IV dise ase at the time of diagnosis. HER2 targeted ^- O, y7 h+ v5 l+ i* S3 F, v& q
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2& _* F( ?2 u8 D* `4 k
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
! t6 g& V: B9 Rand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
5 Q) i' ~2 b Q/ A* v+ Mdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for8 c( g% x$ Z$ W9 @: q
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to" P& f$ {6 R) d* T% m; O
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
- {+ S! Z! P, [* x22.9 months for respectively early stage and stag e IV patients.
6 y' N- Z0 L# a: P; D CConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
# @% d/ K5 M1 D$ X7 freinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
2 X j1 U! N& | \% Z" `0 VHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative. G9 K, h h5 k8 B
clinicaltrials.
1 _9 Z' ~8 Y: J$ Q3 D( x" W& a |