LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND- L! K5 _3 `, d0 M- b* Z& A
THERAPE UTIC PERSPECTIVES) `& D, z2 k/ \; {6 V) ]) L2 E
J. Mazieres, S. Peters
- c, b1 {) ?, x8 X1 U- g) 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 therapeutic
8 a3 k$ l/ F: poutcomes 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 targeted8 N: S/ S4 B/ e/ U
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
. ?( j% G1 M" q! `0 a0 Dtreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations% @' D! H# a& B" s q& X; h
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;4 D% w& l. z% @6 q6 N7 N
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for, F0 V# Z0 [5 {+ v! [3 Z; B
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to) z7 e! `+ H0 p* x
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
1 W$ c0 ?7 H r' D( K" F22.9 months for respectively early stage and stag e IV patients.$ B0 }! v& c/ O$ }
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
% y/ N' e$ D0 Hreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
3 y4 v1 ^0 `4 o( D; P: [" mHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
5 w* [* c/ x4 _clinicaltrials./ v0 z1 `, B/ K, L$ l: v, x( s ?+ y
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