LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
& q1 B$ B j. o% vTHERAPE UTIC PERSPECTIVES
1 S) T6 z. }! G' [/ a1 c% ~" ^J. Mazieres, S. Peters
) c* o2 `6 T( S1 i7 gIntroduction: 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 therapeutic0 M% J" O# a' z, ?4 H6 \
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
( z1 t6 n% o8 q3 `& r& r$ Ctreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
2 N8 m/ n* O% \treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations' ~& E- s$ [ Q/ ^5 H
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
_' x8 O$ ]+ ?0 C8 {disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for4 e3 p O% }, H8 z; r" |* s
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to | D3 r" Y; C6 \2 Y& p7 y% k8 B6 ~
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
6 n2 S$ v0 y w22.9 months for respectively early stage and stag e IV patients.
9 s8 ]4 K- R' Z2 z" EConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,5 L5 c" S. }* D# a
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
8 T$ Y! x" ^- O( HHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
4 k7 E9 X K4 H: [/ X6 Z# Z+ c! K0 M% eclinicaltrials.% E' s7 i6 B5 @* I( m5 _
|
显身卡
