LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND; M. x$ g4 t) i0 U! y
THERAPE UTIC PERSPECTIVES) y5 N0 d& q8 H; p) \! L& _
J. Mazieres, S. Peters8 z; D$ h5 K$ d/ U( h5 C, {- k3 @
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 {9 ` q) I1 d- h5 Loutcomes 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 F' q( ^. k: z8 g9 Y/ u
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
$ D) t: t: S* w+ B% e6 Ytreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
K" Q6 W6 d; Z$ m* zand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;! |+ o |! J- o" o4 M- w
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
/ K' i5 }) O3 h i( utrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to# Y# \! w1 }( R9 {( q7 i8 T$ \
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
% g7 n" ^7 h8 r9 s# N22.9 months for respectively early stage and stag e IV patients., |* G; F$ n$ z" _# Y c8 _
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,$ V5 t4 Y. U( q5 c7 |7 x, V
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
1 Y, x& H. o" e' K( D( @HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
( |& t: q7 G* [clinicaltrials.
: J- c. C1 j# K |