Targeting FOLR1 in high-risk CBF2AT3-GLIS2 pediatric AML with STRO-002 FOLR1–antibody-drug conjugate

,

[1]  B. Hadland,et al.  CBFA2T3-GLIS2 oncogenic fusion is sufficient for leukemic transformation , 2021 .

[2]  C. Klein,et al.  Protease-activation using anti-idiotypic masks enables tumor specificity of a folate receptor 1-T cell bispecific antibody , 2020, Nature Communications.

[3]  U. Banerji,et al.  Exploiting the folate receptor α in oncology , 2020, Nature Reviews Clinical Oncology.

[4]  H. Bolouri,et al.  Comprehensive Transcriptome Profiling of Cryptic CBFA2T3-GLIS2 Fusion-Positive AML Defines Novel Therapeutic Options — a COG and Target Pediatric AML Study , 2018, Blood.

[5]  Heather L. Mulder,et al.  Pediatric non–Down syndrome acute megakaryoblastic leukemia is characterized by distinct genomic subsets with varying outcomes , 2017, Nature Genetics.

[6]  M. Fornerod,et al.  Recurrent abnormalities can be used for risk group stratification in pediatric AMKL: a retrospective intergroup study. , 2016, Blood.

[7]  Kristina M. Ilieva,et al.  Targeting folate receptor alpha for cancer treatment , 2016, Oncotarget.

[8]  R. Casadio,et al.  CBFA2T3-GLIS2 fusion transcript is a novel common feature in pediatric, cytogenetically normal AML, not restricted to FAB M7 subtype. , 2013, Blood.

[9]  Heather L. Mulder,et al.  An Inv(16)(p13.3q24.3)-encoded CBFA2T3-GLIS2 fusion protein defines an aggressive subtype of pediatric acute megakaryoblastic leukemia. , 2012, Cancer cell.

[10]  D. Gautheret,et al.  Characterization of novel genomic alterations and therapeutic approaches using acute megakaryoblastic leukemia xenograft models , 2012, The Journal of experimental medicine.

[11]  Xuan Zheng,et al.  Enhancement of folate receptor alpha expression in tumor cells through the glucocorticoid receptor: a promising means to improved tumor detection and targeting. , 2005, Cancer research.