LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND. X9 r" z0 Z9 w( C) Y
THERAPE UTIC PERSPECTIVES: U" O. ~# ~% P4 U+ c0 @
J. Mazieres, S. Peters
7 h& {0 Z0 a7 o6 CIntroduction: 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 therapeutic7 X' w: K0 h4 `2 V! n! \
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# m( ^: N( L1 Y, m. n3 ]
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2* A! }; ^6 V4 [& [. r
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations, ?4 U [& [' N
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
& J7 k7 _0 k7 Y: ~disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
! s' y7 z" f: g3 W0 |; Ktrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
$ K8 K4 Z; S. o: A) b' V+ x- plapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
5 q8 c. Y) D9 r3 V" A- o22.9 months for respectively early stage and stag e IV patients." `( c+ n- G% L3 z
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
0 ?: F8 C& F+ Q+ @4 u) ireinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
( @! v8 i0 t% ^# J3 h; U3 gHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
+ w; ?4 _ w8 J- r( l% b3 Wclinicaltrials.
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