LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
2 k% u; D; s; ]7 ?2 zTHERAPE UTIC PERSPECTIVES d' x$ {4 |" A* o( U- X
J. Mazieres, S. Peters: x; U# |: o( k/ c4 p
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
/ Z$ S; R& W$ a, I( {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 targeted. s5 r K! _* A+ e# a
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her23 e( f% Y c: X. n9 B# A, i
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
X& b4 F+ }" ?+ C% uand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
3 S2 o, `( Q, Kdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
/ P, B- o5 {* @' x; Wtrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to; e9 E3 C: L \! _0 E: x
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
0 X/ v& {% s6 p% {) S' B& o22.9 months for respectively early stage and stag e IV patients.; S2 {) [. ^, G$ I9 e1 o3 h8 S7 M
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
! {' K3 F/ P8 r: H/ Y& }2 lreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .: L7 Z7 B; j; n3 d! C. @
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
9 B0 D% U* r' V$ {! l; @' sclinicaltrials.
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