LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
+ Q1 \1 o' w. mTHERAPE UTIC PERSPECTIVES6 c2 x. q" o; `* t3 Q- v: M
J. Mazieres, S. Peters
% a& A8 C5 m( A; R$ U7 LIntroduction: 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
% d5 F4 A- @* b& Aoutcomes 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
, w/ f3 f0 W8 G# T5 Ktreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2- J: P+ W0 R) X3 s! o
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations5 N4 ?* ?4 J3 b% @% _8 f- C
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;4 z' N1 B4 V2 X9 J o7 @2 M& }# \
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for+ T6 q; z& S; b+ ]8 Z
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
! p2 m; m: Q5 _$ U# f Blapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and8 f4 ^/ {; [# s; w5 T+ x M
22.9 months for respectively early stage and stag e IV patients.
I7 |( ~* H. r( w& UConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,' M3 T* Y% W& t$ h+ C# M6 E% u* A
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .: J5 i- O* U; T4 f7 K9 t4 u1 |6 u
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative% h- ~$ J$ d& A6 }! E
clinicaltrials.( h: S# S F- @- h
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