LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND+ r& V% u1 r g/ f" C
THERAPE UTIC PERSPECTIVES
7 \8 X4 z# @5 k4 iJ. Mazieres, S. Peters( m1 `+ F2 C7 a( Q# G d) z( C
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 therapeutic3 D" V8 ?3 {- e' 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& l+ p( K4 g4 w7 O! w3 X
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
6 w$ C2 g" C" C3 }: w3 Atreatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
3 A% ?9 g& n. F0 T( jand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ; P! i( M3 \$ B9 v
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
# \ ?& w* \: ^4 Q& Utrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to# }5 O$ [% {* L7 K. A6 J
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and9 P2 v3 a* v% ` T9 s" h, X! n
22.9 months for respectively early stage and stag e IV patients.2 L& o% R; i4 M$ @* v$ o
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,! a5 M) P% w9 \* q6 W& m! k
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
1 Z: `* W. a O" R! M% ^HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
' k& x" z2 h$ T' o) v9 @ Sclinicaltrials.0 \1 w/ }5 k8 f8 t+ j) |. `
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