LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
( e8 U R: G6 b* I: yTHERAPE UTIC PERSPECTIVES
9 m. X' y+ F6 e9 v8 TJ. Mazieres, S. Peters( }, y6 K9 w: b* j
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' g! E/ \5 Loutcomes 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, Y/ A* ^- W9 F+ q1 n$ M1 K
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
$ {, C/ I) @5 B+ H8 ?; T5 N e1 C* jtreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations* y1 L; { t5 T/ o
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;9 a" |% `- @) q3 h
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
P; b+ }) ^5 Dtrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to/ e: Y$ v/ Z q
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
& b; E1 Z" y V* l2 j4 U22.9 months for respectively early stage and stag e IV patients., X4 d+ t) A1 g& _7 l/ v/ I
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,; X7 Q( k) N$ N
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .* D+ a3 ^# P" i- }1 C& Y
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
# M* B* S* P+ ~clinicaltrials.
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