LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND4 ]+ K: S5 J/ c/ J! Q: N0 l
THERAPE UTIC PERSPECTIVES. B" V3 w4 c" Q$ s A p( I
J. Mazieres, S. Peters: ?1 G7 g: k+ p o9 V+ G
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
$ e, r& @; m. q8 Z4 xoutcomes 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
: a( R$ n) x3 ?! mtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her21 H& {8 m) [* u
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
$ k! C* J* k: u: E" B, tand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;1 \$ M0 {/ V' }& C' f
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for- m% P+ W; r3 q) X! D% u" H
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
+ K: h1 W* C) I) c3 o: K# s, @lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
5 q# @( j9 }, x3 r% \3 w- \22.9 months for respectively early stage and stag e IV patients.
, ~, Q& _. ?; Y& n5 `Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,* b, ]( G2 W3 _% o% K, A5 p
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .8 W* V& N6 |1 L. d
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative4 J9 D0 t3 i& q5 T4 n: J8 R" D
clinicaltrials.
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