LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
$ Q2 K* T9 L! @7 M+ `, QTHERAPE UTIC PERSPECTIVES
& D% N$ ]" i7 v' ~5 B2 `) WJ. Mazieres, S. Peters
4 [/ M; E) c; lIntroduction: 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
% e, C8 x2 `) e6 m% Eoutcomes 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
V% S; s9 {( wtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her27 m) Z* u! `4 E
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
& i8 Y6 M, R7 b$ k z- iand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
% B5 T6 u% }! e. Xdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
% ~" `: R, g3 |+ w8 Q5 _trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to `8 @! W" A4 @$ D
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and; k* u" [( w, K4 F6 c( D3 J. s* Q" p7 q
22.9 months for respectively early stage and stag e IV patients.
4 V9 c$ O! D/ \' W( [Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
8 M* i1 p4 v7 s( P' sreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .' {- M9 s+ U* m: y$ \$ `# G
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
& h4 q# k/ y8 M$ Fclinicaltrials.) W+ ]# |3 ?" K- a2 h
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