LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
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0 }4 {$ I$ P, ?, w1 rJ. Mazieres, S. Peters
4 J! M& f! A* a3 }0 |/ k* mIntroduction: 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+ B$ u/ Z. [/ g
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
6 }* h/ v: q) p: E$ jtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
: j0 c& f# X: j) C \% |treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations4 P$ s7 y& J; I' |0 P' [
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
5 ~, G: i* o( kdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for' N0 o% a) X( p% o2 d
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to+ Y H- R& ^7 d; M7 G' h
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and* M1 b5 [! d" u# K4 V0 P, _3 ]. n
22.9 months for respectively early stage and stag e IV patients.% P& W1 D1 K* S
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC, f* s7 D4 u+ x# y y% K4 ]/ o1 _
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' A3 s4 @- C, }6 A4 c, GHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative: C2 V( N5 z! P* c( [( t
clinicaltrials.
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