LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
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5 h" f, s( a- m& w" h4 Y5 d dJ. Mazieres, S. Peters
" w+ y) O7 R( N$ o9 T( }4 J xIntroduction: 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 B0 ^$ i* u& E- |
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+ f3 f; I) u9 b4 [/ c+ B
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2* @$ J/ Q7 p, S' l1 z% Y" C
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
# l9 x% P" |2 I3 c' ~' _# p uand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
& y* U# d2 o1 `6 w8 e% ]disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
' Y9 c$ e J- btrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
; d" I9 x- D7 q5 Z9 Llapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
7 B4 y/ _- Z3 Q# H! U22.9 months for respectively early stage and stag e IV patients.
4 R) @. n/ B6 F. ^5 c0 y9 s; C3 W% ?Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,& _, h) K7 v' w% x$ v
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .+ _4 l) x( |- c! L9 H" w
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative8 s% _, D" N) u/ n5 a* o0 w
clinicaltrials.
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