| LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND % n2 ~2 ^' _0 Z2 Y. K6 Z  g2 f& [$ NTHERAPE UTIC PERSPECTIVES- }& `4 C! U# M% ]8 A
 J. Mazieres, S. Peters
 $ V. h7 ?0 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
 . S0 P2 {- B6 P: B4 ^5 J' Voutcomes 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
 % J$ |# @/ Q' \) |* U/ vtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
 0 c3 _; U/ V9 P" streatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
 / F; R' U& V8 w" xand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;3 ~. G9 ]9 {5 c$ [  B1 v" I
 disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for: K! f  @5 q* L; W
 trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to1 Z! X5 R3 Q+ f2 }
 lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
 & m2 q% U( E( a) D: G22.9 months for respectively early stage and stag e IV patients.7 q/ ?( s) I; L
 Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,, L- v! [- G* h/ s
 reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
 - l& M" M6 G9 U1 z3 D% a6 z. dHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
 8 ?- d7 o7 C7 L  L7 V% N4 y3 ^# i/ oclinicaltrials.
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