LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND: Q0 `0 l: y- F+ N' B# b0 @
THERAPE UTIC PERSPECTIVES7 X* H& m' q0 W3 H# i$ G
J. Mazieres, S. Peters$ G4 A: S+ n- n" C4 H
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; e7 h' J, s O4 n
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 targeted9 g) r7 W$ R6 x
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2, T: ]/ D$ ?6 G: ^ c, Q% `/ O
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
# T- A# L: x9 i6 {and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;: W' u8 G7 \/ ]1 u$ v( g
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for- n2 g6 U* s8 r
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
5 _) f- U6 O( G6 W( |9 Ilapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and( N; r8 W7 {6 @. D) e
22.9 months for respectively early stage and stag e IV patients.
2 G3 O# O# }; s* }" yConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,/ J1 ? F# q5 I" S( [
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
; q( v X* {( d! \4 cHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative! }* p! M! n- i0 E# Q
clinicaltrials.9 ~1 T J/ l9 k* q; {0 R! g
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