Dasatinib Is an Effective Treatment for Angioimmunoblastic T-cell Lymphoma.
Tran B NguyenMamiko Sakata-YanagimotoManabu FujisawaSharna Tanzima NuhatHiroaki MiyoshiYasuhito NannyaKoichi HashimotoKota FukumotoOlivier A BernardYusuke KiyokiKantaro IshitsukaHaruka MomoseShinichiro SukegawaAtsushi ShinagawaTakuya SuyamaYuji SatoHidekazu NishikiiNaoshi ObaraManabu KusakabeShintaro YanagimotoSeishi OgawaKoichi OhshimaShigeru ChibaPublished in: Cancer research (2020)
Recurrent hotspot (p.Gly17Val) mutations in RHOA encoding a small GTPase, together with loss-of-function mutations in TET2 encoding an epigenetic regulator, are genetic hallmarks of angioimmunoblastic T-cell lymphoma (AITL). Mice expressing the p.Gly17Val RHOA mutant on a Tet2-null background succumbed to AITL-like T-cell lymphomas due to deregulated T-cell receptor (TCR) signaling. Using these mice to investigate therapeutics for AITL, we found that dasatinib, a multikinase inhibitor prolonged their survival through inhibition of hyperactivated TCR signaling. A phase I clinical trial study of dasatinib monotherapy in 5 patients with relapsed/refractory AITL was performed. Dasatinib was started at a dose of 100 mg/body once a day and continued until days 10-78 (median day 58). All the evaluable patients achieved partial responses. Our findings suggest that AITL is highly dependent on TCR signaling and that dasatinib could be a promising candidate drug for AITL treatment. SIGNIFICANCE: Deregulated T-cell receptor signaling is a critical molecular event in angioimmunoblastic T-cell lymphoma and can be targeted with dasatinib.
Keyphrases
- chronic myeloid leukemia
- clinical trial
- regulatory t cells
- combination therapy
- ejection fraction
- end stage renal disease
- acute lymphoblastic leukemia
- randomized controlled trial
- acute myeloid leukemia
- newly diagnosed
- high fat diet induced
- small molecule
- wild type
- dna methylation
- transcription factor
- diffuse large b cell lymphoma
- prognostic factors
- metabolic syndrome
- drug delivery
- copy number
- adverse drug
- single molecule
- binding protein
- smoking cessation