LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
" x& Z5 B" Q0 nTHERAPE UTIC PERSPECTIVES) m! q* o( i7 H" ?
J. Mazieres, S. Peters
' U! L# W, w- F1 F5 x 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
$ e0 \ K) K- moutcomes 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
( f; L( ]; I0 S3 j3 U4 {% |treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her23 u# C2 {; y3 Y- E) w+ t a k
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations- P9 P9 O8 X$ S6 u8 B
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
( W" g% z! e% e7 zdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for* i N8 Y( ]8 B$ @( H
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
. i6 j: b% j# \lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and# D8 S/ E, B; x! q6 L
22.9 months for respectively early stage and stag e IV patients.
- ^( ~, h! G' }% h' f" D3 c6 a4 mConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC," h* K! M; ?: K" J' o/ a6 \& w
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
1 S# {- E! c, M/ P' KHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
) Y, [! s1 Y, yclinicaltrials.
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