LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND( k- Q) [4 g/ I: a0 a9 z( H( q
THERAPE UTIC PERSPECTIVES9 _/ W6 {" J) ?, g* ]
J. Mazieres, S. Peters- P$ j4 f6 O# e0 v* a3 W2 V
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 v. T/ k Z& S/ m) Noutcomes 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, N, a8 M m# z' D/ [
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her24 f. F+ h6 [ k3 X
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
6 g5 f; `1 }5 [: kand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
/ p' Q* f" [" k4 F# r4 b% k: Vdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for0 ~! @' U; ~9 }8 [8 h; v- l# G3 C
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to8 f7 |- U% r) w
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and A9 u" N; h q5 K+ M' S
22.9 months for respectively early stage and stag e IV patients.
) A; L- j, p& y* \Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,! Z! [; H( R, N) J. K8 W6 k( K
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
) V' c6 ?- ?4 m; }. ZHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
1 ~6 O+ k" O% J! C3 ]/ t7 T" }clinicaltrials.6 j6 q/ o, _' L, i0 `/ ?2 v6 ^
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