LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND' K1 Z& t0 p3 _" O' e
THERAPE UTIC PERSPECTIVES d0 K- c% F( _& \2 |
J. Mazieres, S. Peters2 s5 k5 k/ M6 _4 Y+ u0 d
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
) \' _4 N: K6 q, Y6 r1 zoutcomes 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- V" p1 s" \0 o& R9 e' k
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2& @9 V5 [0 f# |. _ H8 _2 N
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
; u5 i+ M$ n F9 _and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
/ l y* Y$ {7 udisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for: r6 r c# M0 g K( P
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to* [9 q8 L1 \2 b
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
1 ~$ ~0 o+ i' L$ I/ k. k8 F22.9 months for respectively early stage and stag e IV patients.
) \2 n0 f9 v. j9 WConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,- G9 i' p2 V1 a' j% h
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
7 v4 L7 N9 g5 a" D9 S$ x7 [: G' KHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
$ X( K. V! ~ R, pclinicaltrials.9 l( `$ Y& p* _' H' `
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