LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
6 N$ s/ T2 \/ [THERAPE UTIC PERSPECTIVES
5 j3 b8 I- s: |( N3 m" _& CJ. Mazieres, S. Peters Q4 |5 t, |: o
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 therapeutic2 T4 J5 J+ m# G1 ]7 K1 d+ S
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
. V4 z, b2 t) L: L: E' ]. Ctreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2% w" N8 M. z" ~+ c; h
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
: V9 b4 h% Z/ Dand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
' K7 ]+ ~8 `1 ^, B; z8 n+ Q7 h& ^/ adisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
2 B; i; r) U9 l% c+ vtrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
- K6 t9 z$ M, `( @+ B) ulapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
( V5 P* F9 ~4 M; z! Y22.9 months for respectively early stage and stag e IV patients.5 ]9 U m4 v# I7 M: S: q5 @
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
' Q4 B; m# K( \6 N( o6 R3 Ireinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
7 ?, Y4 \5 Z- h' sHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
2 Z; H( l2 F2 Cclinicaltrials.
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