LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND6 U% d; Q- d2 k& Y, }' O" N
THERAPE UTIC PERSPECTIVES
' e/ r2 D, J6 \, R, O1 I6 MJ. Mazieres, S. Peters, j9 [! a3 k+ S
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
. j4 [* [3 n4 c: M e$ foutcomes 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 targeted2 d) R4 P0 O+ q: G5 Q, e
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2. o8 b7 L0 U& F2 N9 U$ t# o" l
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations9 q8 F/ w' n' M1 I v
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
$ N( |4 g+ p- j- [disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
0 b! m6 R5 _! X btrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to5 N6 ^" g# Y1 O- J8 v* V. |+ j
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and0 w7 H w6 t0 j- P* A
22.9 months for respectively early stage and stag e IV patients.- {. z; e% H4 w! @2 a' S
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,6 G7 q: M4 K5 ]/ B8 y6 I, i T
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas ." P" s. k$ L4 m8 S1 f; `: b5 M
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative& x% _1 r' j" k7 _$ c& K* b( z
clinicaltrials. G! z7 ~0 q" o/ u5 d+ I4 m _
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