LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND% y# O! s) N0 P' h, C) A3 S
THERAPE UTIC PERSPECTIVES3 P' W9 l+ I7 v# h6 O
J. Mazieres, S. Peters& n b, I8 C/ k/ j* S
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
/ R/ h: {: O, K' d7 R, Y+ doutcomes 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 targeted6 C! m* d- w& v4 N9 e( T7 D+ o+ }
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
# J2 G. T! O' mtreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations3 Q* e- l' W& g* E# z5 \8 X) M
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
% J! H2 L4 p2 b5 a$ qdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
/ Z% f. H/ R2 Vtrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to+ e: Z$ V# ~! F; c/ m7 e
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and/ q4 F9 u/ B' w
22.9 months for respectively early stage and stag e IV patients.$ Y! W7 w6 A* `& Z5 p% k
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,! ?6 x9 r& X3 w# I: z
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .7 j4 B6 a- m ?; Y2 K0 u2 p" M
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative) s. F" s( l4 `
clinicaltrials.8 M) A9 n {& J+ R- Y9 X$ M
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