LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND1 |- z* [4 o' U# G8 S" b
THERAPE UTIC PERSPECTIVES
4 m$ w: r7 Q- J' {& ZJ. Mazieres, S. Peters$ M4 N \ A) P4 x3 S# N- 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
7 z) S! ]7 |% C/ Woutcomes 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 targeted4 |0 k$ s- W3 }* F2 _% U
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2$ G# }* x0 i# U5 p, U
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
) b% W$ k$ L. Xand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
+ ]0 _0 }( r# k5 A% Y& N# Ydisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
1 ~4 N g, O" atrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
) J) A( j0 F6 A2 dlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
4 a5 m/ \( s# ^3 ? I* {22.9 months for respectively early stage and stag e IV patients.$ g! `* q' j8 D1 e6 Z
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
. j. O2 ?' `* Q6 N* R8 A6 z8 k7 mreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' ~& w) T5 E4 H. q3 THER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
; z' w f/ _) m8 a# xclinicaltrials.
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