LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND: j+ [' E! @8 o: W
THERAPE UTIC PERSPECTIVES$ p# b i8 `+ }9 I W% ?9 z/ d
J. Mazieres, S. Peters
$ l9 a, O. A0 _# J5 G# [6 Y5 FIntroduction: 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! ^" j9 y: X& b1 Q$ J0 [0 U
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
7 Y: v) y/ K4 Ptreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
$ w* K* p" `* f& i/ L; Ltreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations; W: {6 H! ^, @& `8 u* w
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
7 H4 X/ `0 c3 f1 X8 udisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
, z9 Q K8 R0 N g! [" ^5 z# o# ~trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
7 @/ A3 P) U y& mlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
- S4 @" v* {" N22.9 months for respectively early stage and stag e IV patients.
+ M5 L. l8 h( A9 X. p% JConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
8 e/ _& P$ P6 h" B6 ^! treinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .: m8 Q2 x1 |+ _/ u2 ~0 U& I$ ]1 I
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative/ U; T0 ~+ W# y3 h/ ~
clinicaltrials.
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