LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
$ X" E4 J6 ?# O% }0 vTHERAPE UTIC PERSPECTIVES
" y. w0 Z' h4 G; ~# n5 {! }J. Mazieres, S. Peters
" ]2 m# y G. Y% m- d! AIntroduction: 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
( v( @( _& U1 b) Noutcomes 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% P0 n$ o+ j) J' {- r. ~
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
# I9 ]9 ^; p) O) Ltreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
( ~6 I+ m. t% {& Z$ a3 Y! Cand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
7 g( n& _4 [$ ^6 fdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
/ R) v- t5 F: H7 wtrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
0 ~/ ?- ?# F* [9 A" I8 M. Clapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and+ |3 r; `& m3 `1 u0 R) J
22.9 months for respectively early stage and stag e IV patients.
; o7 Q# J' E$ c& T, {Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
3 b( o! L6 `( U- M) f! p/ S% a, lreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' H) ^4 L6 d0 b) h: uHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
& {, ]6 z& j |: }clinicaltrials.* q8 G Y7 @4 p4 M% f
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