LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
- q$ x) X- h3 k- c' e- y* lTHERAPE UTIC PERSPECTIVES
3 M# k- b3 f9 W4 S7 yJ. Mazieres, S. Peters9 F' C5 _) f$ p- Z
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% s0 N6 [/ z+ K' j+ K5 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
7 l1 q% h# k# H" Wtreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2
: t' j" s9 X' n2 [treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
1 l F- s# {! k9 W' D; j0 Eand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;4 Q. |7 n B$ f8 v) C8 H& f
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for+ @4 F/ g8 J% N8 D
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to: X! b! d3 E6 _3 L" ~' Y
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and, V* t, n3 F' s
22.9 months for respectively early stage and stag e IV patients./ {( y( @1 }8 \& e, Z
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,
u) H! q2 A0 F6 p" y" y n4 M+ freinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .6 J2 M* y5 L* c* t9 y3 h6 M
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative7 H0 }8 ]8 p" M! q; E6 S$ G
clinicaltrials.
0 y3 K0 s! X. t2 O5 i |
显身卡
