LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
. C+ Q5 }3 G6 k3 kTHERAPE UTIC PERSPECTIVES \) {) ^2 f& n3 E" X/ V- V
J. Mazieres, S. Peters) Q9 y, _+ L# B% p+ B
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& E$ o, m3 I+ Z W
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
3 s8 S' h. U. L" v4 Y' _treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
5 [; q# y% D# F9 ztreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations8 z7 l7 n) h2 u4 J
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;2 s: [& f5 ]& m- J9 z1 F
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for9 h, A! p( J: U# K
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
5 h4 Y" O& D) Plapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and& [+ k5 ]0 K' ]: k# Z
22.9 months for respectively early stage and stag e IV patients.) S1 P" \1 d4 x6 z& I9 R. [
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
) S5 ]- e% F6 z! d5 N6 Q \% E3 lreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
0 x0 h, |- v! `# x* N7 yHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative3 @( G3 b: F, [4 A, s0 {
clinicaltrials.1 R0 S8 [6 W9 {4 S
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