LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND x6 _* B* J1 B6 l& k- P
THERAPE UTIC PERSPECTIVES
4 ~" b6 x* h2 d+ P) A) |' GJ. Mazieres, S. Peters5 {9 Q% C2 U* Q7 S% {- J
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
+ ?/ p( N6 d6 S$ soutcomes 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
. |0 A& |( `$ a- L3 Otreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2% c! u, Q4 n1 j2 M+ ]8 B
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
: v' P+ @9 x& m2 r! p; uand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
( D2 j9 B/ s0 ?! x- e7 `disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for: d0 Q# \/ i# {$ X% ]9 P
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
+ H) k6 O6 a+ qlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
. q& F2 o" j. ]9 j22.9 months for respectively early stage and stag e IV patients.
6 T. u3 m: X: ~ v! GConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
! ^7 ^1 K7 q. j4 S' Sreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .4 w) U! k3 A ] ^ l- k
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
* Q( d& P3 f1 [clinicaltrials.& W; _0 A3 i: x# l( j' x. m. M
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