LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND$ s J7 z6 T# W) q
THERAPE UTIC PERSPECTIVES6 s* q! l F, t9 p0 F
J. Mazieres, S. Peters) P& |0 Z3 _- Q7 h) C6 z% U4 A [, [$ F
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: R+ _6 k7 ] p X! B; q" Q
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 targeted/ y9 g* ^+ g8 D
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
1 v K ^4 E* W6 U7 W1 A$ ytreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations: s' |* b* K7 w1 P9 W6 `; z. B2 O
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
: H, B9 b, t t! T5 H5 Cdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
; ?3 o( Q9 l" }7 q3 ?trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
) s3 g+ D3 l/ }lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
# a# A' e% i* h( c22.9 months for respectively early stage and stag e IV patients.
$ S9 L. O4 C) u4 WConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,2 Q1 i, m7 ] U0 Z. s# E+ {
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
8 n- y5 w& x$ T1 [! o F8 HHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative& W2 W/ |2 d1 F) T
clinicaltrials.6 L6 \, ?" p8 i2 G
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