LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
$ u" O3 T- J* @! @' R( I. u% WTHERAPE UTIC PERSPECTIVES3 R$ v! I8 k) k7 m0 Y
J. Mazieres, S. Peters' D F8 f) l# p4 [/ c! ]6 x4 l, @! r
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
+ Z9 K: l& Y$ s; d0 f' Foutcomes 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* z8 J% m- k" K' D7 a" _
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
( b+ Z. J' @! C- H: I. xtreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
1 u; A( d, j6 }* }! `( ~and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
$ W: M" E! n5 x, Bdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
T, r9 N' g% M4 g3 y, ctrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to0 w. t8 x/ ~+ R
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and% }% J! o, G( v
22.9 months for respectively early stage and stag e IV patients.+ d( S+ c/ z; I# O
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
z* x s6 F0 P' A: C( U$ Z) T0 v& mreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
6 h4 g$ e% B) W8 ~. N0 THER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative& k0 [" v% x. I4 w: J
clinicaltrials.- c: g9 @: ?& K, ]
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