LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
6 l/ y, r) {' u+ NTHERAPE UTIC PERSPECTIVES2 |8 u/ M. T4 Q/ v0 O% Q6 j
J. Mazieres, S. Peters( T' r% Z8 {2 ^& }, s1 w
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
! ?1 ]) u$ Z: ]4 |1 \" ~* Youtcomes 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: D2 K7 Q) |4 D
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her22 k4 c- ^% P2 f6 ], K& s
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
5 c& T0 g3 f* j9 M& q2 dand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
! P0 w: R& u4 S, i+ Idisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for1 C! r2 C) D) W/ o$ s. r, z g
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to& P! w' A0 T, {- [. \# B8 Q/ x. F
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
7 U3 U/ g' l. ?& C22.9 months for respectively early stage and stag e IV patients.
8 [- i: Z1 X5 [% n% iConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,6 l4 w* a$ ]9 b' Y0 [- P8 z/ g
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .$ Z9 [( x+ L B" W! a5 }
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
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