LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND
! I$ M! I- ], m- u! {THERAPE UTIC PERSPECTIVES/ d) g$ f, A* H( k5 h
J. Mazieres, S. Peters2 l7 h* q" B, F0 ^
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
7 u' A' j* m- J/ ^' Q0 noutcomes 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
1 S& f% Y* `/ `0 \( Q, ctreatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2) \; G) O4 d7 _
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations$ |1 Q4 k$ n5 l
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;) ^9 g- k# x+ i& D9 s \8 m5 o2 ^! h
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for" D( W; |5 o( s/ ^6 h7 j0 _( \- C
trastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to* s) L$ ?, {' L0 e
lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and
" X4 o3 ]1 S/ s: m. W) e! O5 z; R22.9 months for respectively early stage and stag e IV patients.
1 p2 k# h G9 qConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,# U# ~9 d$ s' f1 |* q& P5 u6 l3 `0 ]
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
4 v: `; I7 ~3 L$ K5 {9 PHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative
0 M2 l( O" n2 U1 _3 O2 n% K* Aclinicaltrials.
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