LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
% q& j, d( N# K. ~/ d* p3 nTHERAPE UTIC PERSPECTIVES8 ?" d5 \8 @+ q: \* B
J. Mazieres, S. Peters1 A( z9 i5 {: w, Z+ t
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
3 Z( c. M" J% F( s; ?1 boutcomes 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 targeted0 V( t6 o/ \" ?- S
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
. d; j$ J2 ^9 Y+ I+ Y u8 `; Qtreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations' s; L+ D6 f3 o1 v+ X9 S
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
; M$ b( ?6 ^ o" R8 \disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
" T$ B/ J, s- N+ F+ {trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
0 T& a0 I' |5 B* Q. e- Blapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and6 M1 N* \. v0 ?! \; Q/ H2 [
22.9 months for respectively early stage and stag e IV patients.* i/ M$ d0 k: I
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
4 L0 ~) C6 O+ V5 o9 { Z0 B4 v6 ]3 m! Freinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
( u, D1 L4 H ~8 s$ \/ ?& YHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative5 n5 P9 F# ?; j- O/ ?, K' L
clinicaltrials.
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