LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND, w8 S H! q1 C* U- d9 C2 Q
THERAPE UTIC PERSPECTIVES! m# Q, b! m1 s( r4 d6 j5 y
J. Mazieres, S. Peters4 B( D9 n2 G/ Q; m6 O0 |
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% ?/ ]7 n4 ~* Z
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 targeted6 b& }! d9 R. j$ |+ h. v0 U
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
% g1 a; I" k0 [1 ^treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
# G) n' y2 h& _) Z1 Gand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;& r |5 p( `; H8 p
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
1 R# R5 m* n. V% l& Ctrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
. ?. T) A) ^! Clapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
/ e( j& H9 L2 j* l6 c* B5 e5 g22.9 months for respectively early stage and stag e IV patients." H4 E2 S5 M6 \
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
$ H7 {8 m" A( O1 r. G& @1 x: kreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
6 m( g$ {: Y2 |* N$ a; F/ y4 GHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative# T+ Y y' I' I
clinicaltrials.# G# B: c0 y- w% N& h! z
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