LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND" ?* s; @6 H4 H8 k* u2 R/ _9 P
THERAPE UTIC PERSPECTIVES
* t, L) n% C; q% s! ^9 S1 w* ?' HJ. Mazieres, S. Peters
! E2 ^$ A; y# c% F }4 ]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- T! q$ q: [1 q# U& C
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; K% H7 @" a4 Z% t
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
0 q8 ~1 ~ x/ K% n9 Ftreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations( v0 b. w! z: A0 M
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
9 w1 |8 W6 U- wdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
; A$ {% ^6 i8 o8 C5 G- `6 ~trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
9 A& U5 T( ^0 f8 ?lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
% R2 v* p2 _" Z- C% F22.9 months for respectively early stage and stag e IV patients.& Z, Q) F9 ] y9 y6 N4 @; [0 X
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
6 m+ W& c6 Y3 dreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .: Y5 |( b8 t# S! ?) G) ?
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
& n0 \- I* [" y8 e9 Q5 n gclinicaltrials.$ d1 Z2 \2 ^( \7 C8 [" w
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