LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
5 {# K% ?* z) @THERAPE UTIC PERSPECTIVES" c- f2 d3 l0 w/ |; s0 v
J. Mazieres, S. Peters- z7 b; z% `5 ? w1 B
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
5 ]* K: k2 G) G6 h3 Boutcomes 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 F8 F. ?6 v' Ctreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2) b+ A9 b; N+ Z& K1 [2 p- I. d
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations. m* v/ Y0 J& G* m# f" u# L
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
4 H/ X+ a) \% Ydisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for M. f, Q- J# b% ^+ P" R% Z
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
5 P/ s/ |* ~; I! p7 k* [lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and' q4 i; y8 _2 R5 B2 D
22.9 months for respectively early stage and stag e IV patients.
+ ^/ s5 i {- w, ]Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,; u, x: h+ F" f& u- R& v
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
, Q) N8 r& O! n2 K' _0 n$ BHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
9 ?: f) z$ ^/ D' ?% z8 d2 b; Pclinicaltrials.
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