Roman Kischel

Munich, BY, Germany

Last Updated: 09/26/2026

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Found 18 publications

TP53 deficiency in AML induces resistance to T-cell engagers through an immunosuppressive secretome.

TP53 deficiency in AML induces resistance to T-cell engagers through an immunosuppressive secretome.

Journal: Leukemia
Published: December 10, 2025

STING activation improves T-cell-engaging immunotherapy for acute myeloid leukemia.

STING activation improves T-cell-engaging immunotherapy for acute myeloid leukemia.

Journal: Blood
Published: September 13, 2024

An Innovative Approach to Optimize First-In-Human Minimal Anticipated Biological Effect Level Based Starting Dose in Oncology Trials for Bispecific T-Cell Engagers: Experience from A Solid Tumor Bispecific T-Cell Engager.

An Innovative Approach to Optimize First-In-Human Minimal Anticipated Biological Effect Level Based Starting Dose in Oncology Trials for Bispecific T-Cell Engagers: Experience from A Solid Tumor Bispecific T-Cell Engager.

Journal: Clinical pharmacology and therapeutics
Published: March 19, 2024

Evolution of T-cell fitness through AML progression: enhanced bispecific T-cell engager-mediated function of bone marrow T cells at remission compared to initial diagnosis and relapse.

Evolution of T-cell fitness through AML progression: enhanced bispecific T-cell engager-mediated function of bone marrow T cells at remission compared to initial diagnosis and relapse.

Journal: Leukemia
Published: March 13, 2024

Correction to: CD33 BiTE® molecule-mediated immune synapse formation and subsequent T-cell activation is determined by the expression profile of activating and inhibitory checkpoint molecules on AML cells.

Correction to: CD33 BiTE® molecule-mediated immune synapse formation and subsequent T-cell activation is determined by the expression profile of activating and inhibitory checkpoint molecules on AML cells.

Journal: Cancer immunology, immunotherapy : CII
Published: May 08, 2023

CD33 BiTE® molecule-mediated immune synapse formation and subsequent T-cell activation is determined by the expression profile of activating and inhibitory checkpoint molecules on AML cells.

CD33 BiTE® molecule-mediated immune synapse formation and subsequent T-cell activation is determined by the expression profile of activating and inhibitory checkpoint molecules on AML cells.

Journal: Cancer immunology, immunotherapy : CII
Published: December 18, 2022

T-cell exhaustion induced by continuous bispecific molecule exposure is ameliorated by treatment-free intervals.

T-cell exhaustion induced by continuous bispecific molecule exposure is ameliorated by treatment-free intervals.

Journal: Blood
Published: March 21, 2022

Targeting the TIGIT-PVR immune checkpoint axis as novel therapeutic option in breast cancer.

Targeting the TIGIT-PVR immune checkpoint axis as novel therapeutic option in breast cancer.

Journal: Oncoimmunology
Published: July 17, 2019

CD33/CD3-bispecific T-cell engaging (BiTE®) antibody construct targets monocytic AML myeloid-derived suppressor cells.

CD33/CD3-bispecific T-cell engaging (BiTE®) antibody construct targets monocytic AML myeloid-derived suppressor cells.

Journal: Journal for immunotherapy of cancer
Published: August 03, 2018

Immune checkpoints PVR and PVRL2 are prognostic markers in AML and their blockade represents a new therapeutic option.

Immune checkpoints PVR and PVRL2 are prognostic markers in AML and their blockade represents a new therapeutic option.

Journal: Oncogene
Published: October 19, 2017

Harnessing T cells to fight cancer with BiTE® antibody constructs--past developments and future directions.

Harnessing T cells to fight cancer with BiTE® antibody constructs--past developments and future directions.

Journal: Immunological reviews
Published: February 12, 2016

Blockade of the PD-1/PD-L1 axis augments lysis of AML cells by the CD33/CD3 BiTE antibody construct AMG 330: reversing a T-cell-induced immune escape mechanism.

Blockade of the PD-1/PD-L1 axis augments lysis of AML cells by the CD33/CD3 BiTE antibody construct AMG 330: reversing a T-cell-induced immune escape mechanism.

Journal: Leukemia
Published: May 29, 2015
Showing 1-12 of 18

Last Updated: 09/26/2026