LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND7 {$ W8 Y6 A2 |! \ X/ X+ t5 H8 f
THERAPE UTIC PERSPECTIVES. s7 G6 [4 d7 \ i3 E8 K
J. Mazieres, S. Peters4 L. O8 W+ p0 n/ b# X$ D
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
- ]! G7 d- | D S$ e( Q% Toutcomes 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' r# ]6 h( [- p' G9 _4 o
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her2$ D' P- M$ D+ K0 C5 M
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations+ W8 b; O, h, J( f/ u' N
and 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;
/ R% R4 r- K/ w+ U5 Adisease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
# i6 R" c% L0 _$ J otrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
* [ P$ G& e8 B5 t9 `( A- k6 Flapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and% H# C# V: K p
22.9 months for respectively early stage and stag e IV patients.3 h" G# y# X6 \7 Z
Conclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,, ?! H6 I" A5 g( g+ ]- s7 t; I$ Z) y' A
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .
' w6 ^2 |" L4 p1 w9 M: ^% zHER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative- c4 ]$ |* k" ~
clinicaltrials.7 ?. h3 m* L* a J. n
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