LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
# v4 b' n. P1 |1 NTHERAPE UTIC PERSPECTIVES! v0 D. v% Q7 b
J. Mazieres, S. Peters* l7 ^* s2 D% `3 j. ?; 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
9 \ r' f* X1 boutcomes 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 targeted9 x: a3 o9 n/ m, [
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her27 U8 g" F. [* i
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
' ?; j/ Q$ x8 P/ g' Zand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
* }" g" W/ t- T5 G" bdisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for) ~# U7 T1 |, O- A3 z/ D' L$ o
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to! P1 G; f& D8 |+ J
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
5 q. \* V& W1 x! ]& o2 f$ y22.9 months for respectively early stage and stag e IV patients.
1 T; t; s# P6 ^ w$ \' r* S% S+ |Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC," m7 b+ G1 C& s# ~8 e6 Z
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas ." L; j. m7 Q/ J, ]3 p' k1 F0 F
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
8 x& Q5 |5 I, Q' s/ d3 d- ~( cclinicaltrials. N. L3 P9 S) S* P; h+ v
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