LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND: [$ a+ P( X, e; Y
THERAPE UTIC PERSPECTIVES/ `6 [3 D8 u e3 |+ c
J. Mazieres, S. Peters( G$ [7 S) ?. q/ R7 V2 Q7 i, n* T. j! E
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# B1 {3 C8 O% W& J
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
: q) I/ c) X3 ftreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2; @9 h3 E V+ w. E% ^
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations' O; n; C* G0 C" S: ?6 a4 S
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
* o0 Z6 t+ `7 s: Hdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for. e s4 ^/ D! ~, G
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to7 q3 D9 L4 z- ]
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and& y, D1 [5 i& o( i/ {
22.9 months for respectively early stage and stag e IV patients." a7 ~ y' ]% `# @2 q
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
% |" @: u" U) @1 `% P+ dreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
, ? T3 W! @* _2 ~) qHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
3 n; ?% v! ~: l& m0 iclinicaltrials.- l1 \8 c# k V0 B' \* s
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