LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND4 r/ b! ?( t O9 Q2 X1 |6 Z
THERAPE UTIC PERSPECTIVES
2 F/ r* \: z0 J$ l6 M0 r4 rJ. Mazieres, S. Peters
, q" f) C* I" b& Q! O1 SIntroduction: 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
/ g$ _) V8 w5 \* Houtcomes 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
5 }6 Q& k& j" {8 e, w; Ttreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2+ d+ ^8 C/ i( [; j* {& v" `! J
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
) [/ }( s7 q/ Uand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;! T( O) `3 `' `0 _3 y
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for* [7 Q- F( p- F( y# S; X
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to- Q" W/ l5 V% n
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
5 {) F2 i2 w! P; ~+ l22.9 months for respectively early stage and stag e IV patients.3 e$ X4 j6 P" B
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,5 ?, I) \& l% r, O
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .2 F f8 a; L1 Y6 L! k3 {+ n; a
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
$ x; m6 S4 s, H/ q. @# Pclinicaltrials.0 @- i. {# b. Y/ I+ R
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