LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND+ B/ }; @' F- I1 z7 ~$ `6 B3 k
THERAPE UTIC PERSPECTIVES
& T* h) T) \4 s6 ^J. Mazieres, S. Peters
$ S' K) F6 \% S# {$ F5 w# |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' l& C" {8 g' U4 l( M
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
1 K+ ]6 J. @% B2 b" rtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2; b! E- p3 r% b& T2 i
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
]- ~2 E; B2 t1 h" R0 h, `and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
9 V% I- L- F0 ~4 a$ {* G- M! z3 Adisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
+ |' {( R: W/ Etrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to+ ~# O# W) [' z" s
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
- @3 U' Q0 A* m9 S! r3 ^22.9 months for respectively early stage and stag e IV patients.
0 E6 u5 Z" M7 P& L/ PConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,$ E$ l7 H" a; I/ A8 M
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
, F a$ w9 n# I) q1 [HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative1 s( s0 z( {# Y: o/ b
clinicaltrials.
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