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Steven Johnsen

Scientific Director

Robert Bosch Center for Tumor Diseases

Germany

Research Interests

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Professors in Germany Professors in Cell Biology Cell Biology professors in Germany

Articles (19)

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2026

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2026

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2026

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2025

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2024

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2023

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2023

Collaborators (10)

Ulrich Sax

Univ-Prof. Dr., Head of Translational Research Informatics Research Group

Universitätsmedizin Göttingen

GERMANY

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Andrew Clark

Group Leader

University of Stuttgart

GERMANY

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SAJJAD HUSSAIN

Assistant Professor

Mayo Clinic

UNITED STATES

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Silke Kaulfuß

Head of NGS

University Medical Center Göttingen

GERMANY

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Markus Glatzel

University Medical Center Hamburg-Eppendorf

GERMANY

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Mark Truty

Chair

Mayo Clinic

UNITED STATES

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Patrick Metzger

GERMANY

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Ronald Simon

University Medical Center Hamburg-Eppendorf

GERMANY

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Stephan Hahn

Head

Ruhr-Universität Bochum

GERMANY

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Lena Levien

University Medical Center

GERMANY

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Steven Johnsen

Research Interests

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Articles (19)

KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival

Epigenetic context defines the transcriptional activity of canonical and noncanonical NF-κB signaling in pancreatic cancer.

BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer.

GSK3β<sup>high</sup>/NFATc1<sup>high</sup> subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair.

Patient‐derived tumor organoids highlight the potential of precision medicine in managing pancreatic ductal adenocarcinoma

Transcriptional pause release at enhancers mediates cell identity

Therapeutic targeting of FOSL1 and RELA-dependent transcriptional mechanisms to suppress pancreatic cancer metastasis.

CRISPR GENome and epigenome engineering improves loss-of-function genetic-screening approaches.

SWI/SNF complexes govern ontology-specific transcription factor function in MYC-subtype atypical teratoid rhabdoid tumor.

Glucocorticoid receptor suppresses GATA6-mediated RNA polymerase II pause release to modulate classical subtype identity in pancreatic cancer.

An NFATc1/SMAD3/cJUN Complex Restricted to SMAD4-Deficient Pancreatic Cancer Guides Rational Therapies

USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming

USP22 supports the aggressive behavior of basal-like breast cancer by stimulating cellular respiration.

Pancreatic cancer acquires resistance to MAPK pathway inhibition by clonal expansion and adaptive DNA hypermethylation.

The FOXP3+ Pro-Inflammatory T Cell: A Potential Therapeutic Target in Crohn's Disease.

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

NFATc1 Is a Central Mediator of EGFR-Induced ARID1A Chromatin Dissociation During Acinar Cell Reprogramming

Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma.

Interactive enhancer hubs (iHUBs) mediate transcriptional reprogramming and adaptive resistance in pancreatic cancer.

Collaborators (10)

Ulrich Sax

Andrew Clark

SAJJAD HUSSAIN

Silke Kaulfuß

Markus Glatzel

Mark Truty

Patrick Metzger

Ronald Simon

Stephan Hahn

Lena Levien

Make your next move.

Steven Johnsen

Research Interests

Explore related searches

Articles (19)

KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival

Epigenetic context defines the transcriptional activity of canonical and noncanonical NF-κB signaling in pancreatic cancer.

BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer.

GSK3β&lt;sup&gt;high&lt;/sup&gt;/NFATc1&lt;sup&gt;high&lt;/sup&gt; subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair.

Patient‐derived tumor organoids highlight the potential of precision medicine in managing pancreatic ductal adenocarcinoma

Transcriptional pause release at enhancers mediates cell identity

Therapeutic targeting of FOSL1 and RELA-dependent transcriptional mechanisms to suppress pancreatic cancer metastasis.

CRISPR GENome and epigenome engineering improves loss-of-function genetic-screening approaches.

SWI/SNF complexes govern ontology-specific transcription factor function in MYC-subtype atypical teratoid rhabdoid tumor.

Glucocorticoid receptor suppresses GATA6-mediated RNA polymerase II pause release to modulate classical subtype identity in pancreatic cancer.

An NFATc1/SMAD3/cJUN Complex Restricted to SMAD4-Deficient Pancreatic Cancer Guides Rational Therapies

USP44 Overexpression Drives a MYC-Like Gene Expression Program in Neuroblastoma through Epigenetic Reprogramming

USP22 supports the aggressive behavior of basal-like breast cancer by stimulating cellular respiration.

Pancreatic cancer acquires resistance to MAPK pathway inhibition by clonal expansion and adaptive DNA hypermethylation.

The FOXP3+ Pro-Inflammatory T Cell: A Potential Therapeutic Target in Crohn's Disease.

RNF40 epigenetically modulates glycolysis to support the aggressiveness of basal-like breast cancer

NFATc1 Is a Central Mediator of EGFR-Induced ARID1A Chromatin Dissociation During Acinar Cell Reprogramming

Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma.

Interactive enhancer hubs (iHUBs) mediate transcriptional reprogramming and adaptive resistance in pancreatic cancer.

Collaborators (10)

Ulrich Sax

Andrew Clark

SAJJAD HUSSAIN

Silke Kaulfuß

Markus Glatzel

Mark Truty

Patrick Metzger

Ronald Simon

Stephan Hahn

Lena Levien

Make your next move.

GSK3β<sup>high</sup>/NFATc1<sup>high</sup> subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair.