LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
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( ^7 s: I3 L4 z1 m( {) LJ. Mazieres, S. Peters8 D, X0 r% ~+ X4 e$ @$ K' k2 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) Y, @) j+ w- j& h
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
5 r/ w' e6 |6 Vtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2) C# X9 o; p' x- h0 b: r; }
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations2 M5 g- t+ S( Q' O
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;# [, ]+ I u2 e' g+ p" s( \- R/ _# _$ h
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
: F' K( _2 `% ~, m8 X% l* `7 \trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to7 T7 a$ m: }; o. }' V
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and% ^; f8 E( D6 l4 T
22.9 months for respectively early stage and stag e IV patients.
4 B8 ^! F3 G* n: H6 e* V4 yConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
0 _& l6 f) v$ S! breinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
3 Q( D+ O$ X; u6 {9 W( ?3 BHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
7 s2 [. x, Y) x; Z1 B7 n! kclinicaltrials.
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