| LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND: {  A! V( n( {; v: q THERAPE UTIC PERSPECTIVES
 , [# q6 \+ E9 X- j+ G/ cJ. Mazieres, S. Peters8 A9 L* l; h* o
 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 therapeutic4 f0 C- `3 l# D5 \
 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 targeted2 z- h5 z2 @/ B6 A! e- Y
 treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
 - X' W) R# T& Z4 P: M& }% V- ytreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations! O9 @5 {7 ~7 r" B# T
 and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;) x, e7 o( H: s& w- l" E( h
 disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
 / u2 }: x! C. e% U3 c) i5 |( ptrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
 0 e8 W% h, p2 M! Rlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
 , H4 r- P& b/ p' w22.9 months for respectively early stage and stag e IV patients.% L6 W+ S) x  W8 m
 Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,: k% C6 ~( e/ a1 P$ N
 reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas ." [: P: c6 }' _) y. y9 d
 HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative$ d, L! i. q; d8 b" v4 B- W
 clinicaltrials.' b& U( Q) o4 {- m9 z
 
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