LUNG CANCER HARB ORING HER2 MUTATION :EPIDE MIOLOGI CAL CHARACTE RISTICS AND. t0 ~+ e+ F6 V
THERAPE UTIC PERSPECTIVES- K& w& {1 |& l
J. Mazieres, S. Peters
' i! d( b8 E; E: o: y- qIntroduction: 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( U+ }) b: }7 A; [6 ^* k
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- D% a5 _' R/ Z# X
treatment was delivered after convention al chemothe rapy. A total of 20 anti-Her25 j0 h a* v. }4 B& F& b
treatments were eval uable. We observed 4 progressive dise ases, 7 disease stabilizations
/ }/ r8 d" @0 n# l) z( dand 9 partial resp onses according to RECIST 1.1 (overall response rate ORR = 45% ;+ N0 o; h i) u7 O5 V- I
disease control rate DCR = 80%). Specifica lly, we obse rved a DCR of 92% for
) T0 x4 z$ J4 T* Q- \ r4 I- ltrastuzum ab-based therapie s (n = 14), 100 % for afatinib (n = 3) but no response to
, C6 {# |5 _4 D) p( {lapatinib (n = 2) and to a multiTKI (n = 1). Median survival was of 68.2 months and" \9 W# Y0 l1 _7 r7 H4 a
22.9 months for respectively early stage and stag e IV patients.
* \- ]1 ]! m- u$ cConclusion: This study, the largest to date dedic ated to HER2 mutated NSCLC,2 s' L, ?; K2 N- q r# v: ?, Z' c, X
reinforces the importance of an HER2 screening strategy in lung adenoc arcinomas .* k( s+ X( \1 W! s' r+ H$ }
HER2-target ed drugs shou ld be tested further, ide ally withi n large collaborative0 V y- v, s: F1 M) z5 D4 g5 V2 y
clinicaltrials.; v7 ]$ Y d0 j9 g5 b% V
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