Hendrik Ungefroren

Germany

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Articles (10)

Year:

2023

Year:

2023

Pancreatic cancer is currently the fourth most common cause of cancer-related deaths and is predicted to be the second leading cause of cancer-related mortality by the year 2030 [...]

Year:

2023

Year:

2023

Year:

2022

Year:

2022

Year:

2022

Year:

2022

Year:

2021

Year:

2021

Collaborators (5)

Jens-Uwe Marquardt

GERMANY

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Hauke Busch

Professor

University of Lübeck

GERMANY

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Axel Künstner

Head of Bioinformatics Service Unit

University of Lübeck

GERMANY

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PD Dr. med. Kim C. Honselmann

Assistant Professor of Surgery

Universitätsklinikum Schleswig-Holstein Campus Kiel

GERMANY

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Tobias Keck

Full Professor and Chairman

Universitätsklinikum Schleswig-Holstein Campus Kiel

GERMANY

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Hendrik Ungefroren

Research Interests

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Articles (10)

Establishment and Molecular Characterization of Two Patient-Derived Pancreatic Ductal Adenocarcinoma Cell Lines as Preclinical Models for Treatment Response

Elucidation of the Role of SMAD4 in Epithelial–Mesenchymal Plasticity: Does It Help to Better Understand the Consequences of DPC4 Inactivation in the Malignant Progression of Pancreatic Ductal Adenocarcinoma?

Preclinical Patient-Derived Culture Models for Personalized Treatment of Pancreatic Cancer: A Dream of the Future or Useful Practice?

Tap73 Inhibits EMT and Cell Migration in Pancreatic Cancer Cells through Promoting SMAD4 Expression and SMAD4-Dependent Inhibition of ERK Activation

Differential Effects of Somatostatin, Octreotide, and Lanreotide on Neuroendocrine Differentiation and Proliferation in Established and Primary NET Cell Lines: Possible Crosstalk with TGF-β Signaling

The Use of PDX1 DNA Methylation to Distinguish Two Subtypes of Pancreatic Neuroendocrine Neoplasms with Different Prognoses

Suppressive Role of ACVR1/ALK2 in Basal and TGFβ1-Induced Cell Migration in Pancreatic Ductal Adenocarcinoma Cells and Identification of a Self-Perpetuating Autoregulatory Loop Involving the Small GTPase RAC1b

The Quasimesenchymal Pancreatic Ductal Epithelial Cell Line PANC-1—A Useful Model to Study Clonal Heterogeneity and EMT Subtype Shifting

Activation of a Ductal-to-Endocrine Transdifferentiation Transcriptional Program in the Pancreatic Cancer Cell Line PANC-1 Is Controlled by RAC1 and RAC1b through Antagonistic Regulation of Stemness Factors

A Comparative Endocrine Trans-Differentiation Approach to Pancreatic Ductal Adenocarcinoma Cells with Different EMT Phenotypes Identifies Quasi-Mesenchymal Tumor Cells as Those with Highest Plasticity

Collaborators (5)

Jens-Uwe Marquardt

Hauke Busch

Axel Künstner

PD Dr. med. Kim C. Honselmann

Tobias Keck

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Hendrik Ungefroren

Research Interests

Explore related searches

Contact this professor

Articles (10)

Establishment and Molecular Characterization of Two Patient-Derived Pancreatic Ductal Adenocarcinoma Cell Lines as Preclinical Models for Treatment Response

Elucidation of the Role of SMAD4 in Epithelial–Mesenchymal Plasticity: Does It Help to Better Understand the Consequences of DPC4 Inactivation in the Malignant Progression of Pancreatic Ductal Adenocarcinoma?

Preclinical Patient-Derived Culture Models for Personalized Treatment of Pancreatic Cancer: A Dream of the Future or Useful Practice?

Tap73 Inhibits EMT and Cell Migration in Pancreatic Cancer Cells through Promoting SMAD4 Expression and SMAD4-Dependent Inhibition of ERK Activation

Differential Effects of Somatostatin, Octreotide, and Lanreotide on Neuroendocrine Differentiation and Proliferation in Established and Primary NET Cell Lines: Possible Crosstalk with TGF-β Signaling

The Use of PDX1 DNA Methylation to Distinguish Two Subtypes of Pancreatic Neuroendocrine Neoplasms with Different Prognoses

Suppressive Role of ACVR1/ALK2 in Basal and TGFβ1-Induced Cell Migration in Pancreatic Ductal Adenocarcinoma Cells and Identification of a Self-Perpetuating Autoregulatory Loop Involving the Small GTPase RAC1b

The Quasimesenchymal Pancreatic Ductal Epithelial Cell Line PANC-1&mdash;A Useful Model to Study Clonal Heterogeneity and EMT Subtype Shifting

Activation of a Ductal-to-Endocrine Transdifferentiation Transcriptional Program in the Pancreatic Cancer Cell Line PANC-1 Is Controlled by RAC1 and RAC1b through Antagonistic Regulation of Stemness Factors

A Comparative Endocrine Trans-Differentiation Approach to Pancreatic Ductal Adenocarcinoma Cells with Different EMT Phenotypes Identifies Quasi-Mesenchymal Tumor Cells as Those with Highest Plasticity

Collaborators (5)

Jens-Uwe Marquardt

Hauke Busch

Axel Künstner

PD Dr. med. Kim C. Honselmann

Tobias Keck

Make your next move.

The Quasimesenchymal Pancreatic Ductal Epithelial Cell Line PANC-1—A Useful Model to Study Clonal Heterogeneity and EMT Subtype Shifting