LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND9 L2 T- I6 i: a* _( A! S
THERAPE UTIC PERSPECTIVES
5 r( u n8 y; f; W1 B7 FJ. Mazieres, S. Peters$ B1 f3 l v% ^8 u+ t- m
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 therapeutic7 a( \5 w* Y7 t* U1 F
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
/ e# g) P' F. d0 i3 Htreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
8 T# g( z1 \: Otreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
+ y A8 T! n% I+ band 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;3 E) \& U# d$ F
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for, G9 D0 y, x5 m h# |4 c
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
1 a: |, F0 |" e9 ~8 e |$ a/ ~6 xlapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
: H9 x- n% _- U7 J. P* U' M" \8 Y' b22.9 months for respectively early stage and stag e IV patients.
9 }# i% L$ Q( w/ n S# S/ _Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
* a8 u8 ]" a; \1 j! mreinforces the importance of an HER2 screening strategy in lung adenoc arcinomas ., K. w. ^! m7 B* x O$ `& X
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative3 M- b- ~3 u' i6 F. I2 ^
clinicaltrials.* t% s. v- r: B) x1 o' Y, Y$ o7 ?9 }
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