LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND" @$ k# g6 n3 H
THERAPE UTIC PERSPECTIVES
; c& H$ ~ H. P4 |% yJ. Mazieres, S. Peters
: g; b" I6 p4 q" X' | v7 OIntroduction: 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* M2 \8 k0 z8 o. {: { W
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 targeted3 ^$ C! X/ o) F
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her21 f7 s% m: A2 t. e2 i
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
2 @) [, B: L9 |$ g& U4 fand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
, b+ l% `, [: J+ e0 |disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for1 q- U) k# p1 d2 K) _% _" d* O
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
5 p* g( V9 x( f2 y( H F1 m. c; W! plapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
" q, z5 z1 F$ W3 r22.9 months for respectively early stage and stag e IV patients.7 h6 ^ e. p1 n9 v% t
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,0 U; P6 c( [) y
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas ." P, P/ y, W' n f% k/ A4 r
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
- s( R' _# G/ B, t. k( wclinicaltrials.
' l- k+ T. Z: [9 {* [ |
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