LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
4 ~ o% _$ m6 {5 u# JTHERAPE UTIC PERSPECTIVES0 H& S1 [0 ?4 f1 _+ U
J. Mazieres, S. Peters
7 G0 g" d0 j z9 g- hIntroduction: 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
+ \1 g( h0 v( u# {4 s* F$ Eoutcomes 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
/ v) S2 ^; x0 X( u. otreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
) \* r( T9 }. D+ C, T1 ~! ^treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations1 y' B/ B c0 q I
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
. a& H- G# B- x: P {+ i$ pdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for9 q! J, L- g+ ?* k$ L
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to' r* a M1 J, H1 z8 s- n
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and" Y( i+ J/ I5 _+ h% W
22.9 months for respectively early stage and stag e IV patients.
" B) o$ v) J8 a% w, g- j% `- X _. \Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
& F% L) k" N) b3 z7 }5 f" J8 |* O% a2 hreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
1 l6 V* h% C2 t, ?/ x5 hHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
6 t" c5 K8 J4 Z- j+ [( L% [clinicaltrials.
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