LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
" n- f) t1 Z- _. k: s* jTHERAPE UTIC PERSPECTIVES
1 T$ C* _ ]8 n c/ ~J. Mazieres, S. Peters0 ~4 b& r ^- Q- 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
9 A! f' f& ^% s- m9 ?! {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 targeted4 j; w. o) T3 A A1 ^5 A# U
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
0 m C4 p$ g8 ~2 f# |4 z) |% @treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
V" }# _$ s1 N \and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
! J7 T7 d4 `$ hdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for5 r7 U8 b; r- G/ G( N
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
# P( s) v2 |* f- _lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
8 P8 C3 z3 n3 v% x/ X22.9 months for respectively early stage and stag e IV patients.
2 X2 z% l0 U8 R, u; i, uConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,# l. f) ] }( V8 c$ c2 l7 f
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' b+ w U* G7 p n$ D6 }. YHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
0 _) m% ?8 @- v+ q& Cclinicaltrials.3 m8 E4 |0 `4 G+ B0 E4 D
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