LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND: i6 m7 M4 g' g
THERAPE UTIC PERSPECTIVES
5 ]6 a, {8 e6 `% i- k' H1 |/ MJ. Mazieres, S. Peters P9 J, j# q, m
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
" N7 K, S- Y6 Houtcomes 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 targeted1 h% N R1 m2 Q) i1 B5 W/ U
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2& U+ ]- N. \8 ^. t& L3 ]; r
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
$ p C: W0 _' p& o% q1 Yand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;7 P: r4 P) D. J
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for3 j0 J. d6 t- B: ^/ U* i
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
# o1 b0 H, E; N: u; n, M: Ilapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and, {3 S) z& `4 I# y' I& }
22.9 months for respectively early stage and stag e IV patients.
3 _# a! `: X) z# H7 K oConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
& k; k# b" T; j+ l# treinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' z2 V3 l! K3 k2 j( |5 gHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
% N- K0 V, s7 z/ t) l! b, {clinicaltrials." b6 ]% A u% q6 ?
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