LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
3 z: v; P" `% S ^THERAPE UTIC PERSPECTIVES" h8 W1 S/ N$ {. a: s; X+ r6 F5 g
J. Mazieres, S. Peters. D" e% d7 e5 ~) C
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
Y" s( o/ G, ?( _( 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 targeted
- h, z, a6 ~$ _0 K: x* {treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
% L- G: Z( [6 t& q# j( _treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations3 `; b1 M9 o$ E# f
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
# l; f( l. [. ]9 I3 [% L8 |disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for v8 c0 x6 O0 B( B' }: h4 X
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
' W! r r9 q3 Tlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
. ]0 Y& f: v2 i7 R! A4 D22.9 months for respectively early stage and stag e IV patients.2 w- p. o' y# \3 C- U4 h/ N& L
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
2 C* M; g- W. W6 J) f: Z8 Q, ireinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
/ R r# R" n. n/ y! _HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative7 `! y- l! s" E7 F, j+ o, q
clinicaltrials.- i% @. A* m3 h! |, n1 u2 g
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