LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
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4 V# I0 e5 G1 g' O* \# T8 ~J. Mazieres, S. Peters0 m/ n" Y( V& L! g. L4 f
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/ W2 C7 J, Z, q1 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
/ o% o: z- k% R: d# W- e& m) ]treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2! k) {6 `/ R9 c
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
" F9 g- `1 W+ r# Mand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;5 L8 e. W% u) E( v
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for5 ?0 ~9 v- n) M" y& j( [! x) G% l
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to1 I9 c& }( Z" k: v2 G% {) B
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and& Q6 ?* c3 v# l
22.9 months for respectively early stage and stag e IV patients.0 ^# b! Q6 G2 X1 s1 S
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
/ f0 ^3 D; }, C, }' K# d0 a! ] oreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
% ^& v x: w l: v4 F5 }1 W5 [$ w4 mHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative3 `/ s' Q( }# N6 H& G5 @2 {6 B
clinicaltrials.
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