Jeffery L. Kutok

NKT Therapeutics (United States) — United States

Medicine · Health Sciences

91h-index31.1kcitations410works0.12yr avg
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Research Topics

Chronic Lymphocytic Leukemia Research(125), Lymphoma Diagnosis and Treatment(96), Protein Degradation and Inhibitors(61), Chronic Myeloid Leukemia Treatments(60), Acute Lymphoblastic Leukemia research(37)

Publications410 total

Supplementary Figure S3 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Figure S1 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Figure S2 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Table S1 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Figure S6 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Figure S5 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Supplementary Figure S4 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model
2025Open Access
Abstract P4-12-18: Discovery and characterization of ETX-636, a potential best-in-class, oral, small molecule, pan-mutant-selective PI3Kα inhibitor
Clinical Cancer Research·2025
Abstract 1659: ETX-636, a novel allosteric pan-mutant-selective PI3Kα dual inhibitor and degrader with best-in-class potential
Cancer Research·2025
T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation
Cancer Cell·2024· 1 citedOpen Access
Corrigendium: Effects of RAS on the genesis of embryonal rhabdomyosarcoma
Genes & Development·2024Open Access
Supplementary Tables S5-8 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Fig. S4 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Fig. S5 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Data from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Table S3 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Fig. S7 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Fig. S6 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Table S4 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
Supplementary Tables S1-2 from EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes
2023Open Access
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Frequent Co-authors

Donna Neuberg(10), Jon C. Aster(7), A. Thomas Look(7), Ifor R. Williams(7), D. Gary Gilliland(7), Margaret A. Shipp(6), Scott J. Rodig(6), Koichi Akashi(6), Klaus Rajewsky(5), Leonard I. Zon(5), John P. Kanki(5), Stefano Monti(4), Vito J. Palombella(4), David M. Langenau(4), Todd R. Golub(3), Stefano Casola(3), Marc Schmidt‐Supprian(3), Przemysław Juszczyński(3), Treeve Currie(3), Kunihiko Takeyama(3)