LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND- V9 L7 ?, O) p, v" o( c" j4 V
THERAPE UTIC PERSPECTIVES, ?6 N7 y Y$ M3 ?' [* A
J. Mazieres, S. Peters
& z8 k! ]7 \3 u/ SIntroduction: 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; t- S" T5 X) W/ L+ K' j
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. i+ b- m1 o! j% h# l
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2+ U7 c4 b, n" ~
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations2 {4 S" y. P# `& r, o1 A1 u( O
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;6 w# }$ [5 d/ }) J, z
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
! j/ z& x; H) H. N4 @2 @% T$ }trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to% y5 ^- U( U3 t% d7 z% ^
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
$ Q" O/ K! J2 m+ w22.9 months for respectively early stage and stag e IV patients.
; m- I( U( [: F( _Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,7 i- @6 T. `2 A: s
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
8 E7 ~0 j, Q; M$ Y! ?, |/ `( b/ _3 LHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
0 J+ o) U0 {# B/ ]/ mclinicaltrials.$ I C: K7 U/ D! u" `, Z' ~1 b
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