Jana Von Jan

Koeln, NW, Germany

Last Updated: 09/26/2026

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Found 8 publications

Optimizing drug combinations for T-PLL: restoring DNA damage and P53-mediated apoptotic responses.

Optimizing drug combinations for T-PLL: restoring DNA damage and P53-mediated apoptotic responses.

Journal: Blood

Published: October 12, 2023

Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies.

Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies.

Journal: Blood

Published: October 04, 2021

Development of HDAC Inhibitors Exhibiting Therapeutic Potential in T-Cell Prolymphocytic Leukemia.

Development of HDAC Inhibitors Exhibiting Therapeutic Potential in T-Cell Prolymphocytic Leukemia.

Journal: Journal of medicinal chemistry

Published: June 08, 2021

Corrections: Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.

Corrections: Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.

Journal: Leukemia

Published: October 24, 2020

Advances and Perspectives in the Treatment of T-PLL.

Advances and Perspectives in the Treatment of T-PLL.

Journal: Current hematologic malignancy reports

Published: February 09, 2020

Noncanonical effector functions of the T-memory-like T-PLL cell are shaped by cooperative TCL1A and TCR signaling.

Noncanonical effector functions of the T-memory-like T-PLL cell are shaped by cooperative TCL1A and TCR signaling.

Journal: Blood

Published: September 26, 2019

Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.

Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.

Journal: Leukemia

Published: July 30, 2019

Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL.

Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL.

Journal: Nature communications

Published: December 28, 2016

Showing 1-8 of 8

Last Updated: 09/26/2026