LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND8 L. M1 y: G0 F: n0 S! a3 F! M
THERAPE UTIC PERSPECTIVES% N) ?5 |9 L. X% p) s% H. A6 [
J. Mazieres, S. Peters
# \4 s% N' R5 ~# 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
* |+ \& `3 s# _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' w7 N, x# }. ?7 X
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2: O. X2 d* p" H7 ~
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations& x* T& E% v# u8 X: \! P
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;( M8 _" y A8 h$ b3 y2 x! B
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
9 {2 K, r/ k% {8 \1 Ctrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
7 H* a3 e+ r) [; x. d% I( Zlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and7 c! h: n0 P* g1 C
22.9 months for respectively early stage and stag e IV patients.
8 w$ |. H; N/ |( k6 Q2 pConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
6 C+ t$ t( D, O. j# t- ?4 areinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .% F" v$ o* q: c" |& l1 w
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
( X+ j3 g; A. w1 zclinicaltrials.( T3 P. [* b% L* e2 X" C! n' {& D
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