LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
, l: v$ t! B4 M# f; {( G4 S4 JTHERAPE UTIC PERSPECTIVES
5 y7 q: v3 Q3 {J. Mazieres, S. Peters, n4 y0 Z! h# ], Z$ P; q
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
: ~* ?) o% C/ F% moutcomes 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
4 n1 {4 D9 c' g% wtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2" ~: c0 P1 Z, y& P
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
1 P$ u9 L* Z' p0 a+ Yand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;- C1 P# x1 ]- C: D
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
1 {. W% H- o- F# p4 y, h0 c/ ltrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
8 c7 M$ l; a# D" P2 w. d8 q! {lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
! d, c- c' q, R22.9 months for respectively early stage and stag e IV patients.
7 R6 O( D$ V: Z+ \2 ]% lConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
3 A/ k8 y5 n1 @$ o+ U/ u( u4 W: areinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .) W+ \; D- A: t$ d+ `+ f
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
2 L( [5 f, _+ h" m l; Iclinicaltrials.
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