LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND9 N1 K8 Z$ X0 o/ q$ T
THERAPE UTIC PERSPECTIVES
( S, h' K: Y1 d9 ?J. Mazieres, S. Peters
/ ^6 n9 U: a- U5 l7 K, rIntroduction: 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
) {4 n/ [- b& routcomes 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* _8 [% ?5 N4 W& V
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her21 {+ [# y( l: f8 U6 O- K" g$ w
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
+ d/ l3 w+ n0 dand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
# b$ W _: c$ r% {( h x- }disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
5 X2 `: D, e( N% X5 h; T% \trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to5 {3 R+ ~% W' V
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
3 B% t' K4 }1 W22.9 months for respectively early stage and stag e IV patients.3 |& ^0 k) v3 U: q" P. r# j- e
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,5 ~ h; a0 f' S. t# _, g' \
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .+ x1 t: d! C x8 a9 l6 U
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
$ Z$ }; n) l2 M5 e$ s# V9 E; b' Kclinicaltrials.; Z( f8 g1 T; o( D
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