LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
% ~% k0 d' b& o; ~7 o2 DTHERAPE UTIC PERSPECTIVES
+ {6 j& Y8 e( ]8 l; M& \! UJ. Mazieres, S. Peters
; C+ o1 v. b- @9 i0 w4 I; OIntroduction: 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 Q# C, ^) q8 N. c5 @
outcomes 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 targeted9 s) e# l8 K, b+ K9 V- l
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
# g1 m2 ?1 B7 T5 Ptreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations4 Q3 W6 Y3 v/ |% N
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;$ G. i2 Y1 U0 R) I
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
, u7 ?" M: E1 u ^! ?trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
4 f L5 t: g' ~* {, zlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
2 d' n5 H! z# |' k3 ~" k2 h22.9 months for respectively early stage and stag e IV patients.* m4 _+ F4 x6 Z- l* U) {7 _
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
! t% d. C& z. m( p& m) greinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' C# \* g; W6 ?$ v% VHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
/ v, [# F G3 E1 D7 nclinicaltrials.; q7 W% H* _3 H. A3 _% A( P$ f
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