LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
b% @4 |. z" ~2 yTHERAPE UTIC PERSPECTIVES! L; X! @1 |, n3 N% R, `0 g% F7 M$ O7 H% p
J. Mazieres, S. Peters
t* |% L' x. w" BIntroduction: 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
9 X. ?5 r' [1 H% X# F! Toutcomes 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' @1 X8 e4 R9 g0 n: z* `* |
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2( a1 S" n1 D- X( e
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
1 f% P% r! m9 V5 F: ?! d7 `and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;% m6 ?+ Q" J# U* _- n) B# Q
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for1 Q; Z, M: J9 {
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
/ j, f' f8 i7 Plapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
8 ^: }" Z# z% E' v+ M- C22.9 months for respectively early stage and stag e IV patients.7 ?2 a$ M$ x6 p2 C
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
" e" K6 }" |5 r- n( j4 W- ?reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
- n/ v2 j- a |. E" S4 [, n( HHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative! ?! x! g, P1 {' X4 ]; o/ x; `
clinicaltrials.) U$ ^ T# m h7 ~
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