LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
4 O- F3 h) s; v& I8 M) }' BTHERAPE UTIC PERSPECTIVES
. @4 h- n! u( \' {& kJ. Mazieres, S. Peters8 ~( N& y4 s2 w# m/ Y
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) I8 Z7 Q4 x6 K) g
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
1 P* O$ k# f3 `4 r3 c* Itreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her25 b1 W- Y/ \ y. ^( D
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
7 I' n4 B; B2 u* B; t# fand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;5 R& I- B* J4 l$ Y5 u
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for1 t* }) Y1 @5 B2 o
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
, Z$ o2 Q2 G9 k p( Elapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
) B, @" S3 B' M ?22.9 months for respectively early stage and stag e IV patients.
" a7 f; R S4 I% t# R* I5 FConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
0 L" r8 }& w( Zreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
( v; y% r4 G v1 `; d+ P0 BHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
9 y1 f- q& F, C) e' N- rclinicaltrials.* b6 x7 C4 [. q6 n; p( {
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