Shilpa R. Patil

Goettingen, NI 37075, Germany

Last Updated: 09/26/2026

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Found 12 publications

Acvr1b Loss Increases Formation of Pancreatic Precancerous Lesions From Acinar and Ductal Cells of Origin.

Acvr1b Loss Increases Formation of Pancreatic Precancerous Lesions From Acinar and Ductal Cells of Origin.

Journal: Cellular and molecular gastroenterology and hepatology
Published: June 07, 2023

Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation.

Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation.

Journal: Cell metabolism
Published: September 13, 2022

TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer.

TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer.

Journal: Cancers
Published: June 09, 2022

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

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

Journal: Cellular and molecular gastroenterology and hepatology
Published: May 23, 2022

HSP90 Inhibition Synergizes with Cisplatin to Eliminate Basal-like Pancreatic Ductal Adenocarcinoma Cells.

HSP90 Inhibition Synergizes with Cisplatin to Eliminate Basal-like Pancreatic Ductal Adenocarcinoma Cells.

Journal: Cancers
Published: November 02, 2021

Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer.

Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer.

Journal: Cells
Published: October 31, 2021

Cell Type of Pancreatic Ductal Adenocarcinoma Origin: Implications for Prognosis and Clinical Outcomes.

Cell Type of Pancreatic Ductal Adenocarcinoma Origin: Implications for Prognosis and Clinical Outcomes.

Journal: Visceral medicine
Published: June 29, 2021

EZH2 Regulates Pancreatic Cancer Subtype Identity and Tumor Progression via Transcriptional Repression of GATA6.

EZH2 Regulates Pancreatic Cancer Subtype Identity and Tumor Progression via Transcriptional Repression of GATA6.

Journal: Cancer research
Published: February 28, 2020

Preclinical Evaluation of 1,2-Diamino-4,5-Dibromobenzene in Genetically Engineered Mouse Models of Pancreatic Cancer.

Preclinical Evaluation of 1,2-Diamino-4,5-Dibromobenzene in Genetically Engineered Mouse Models of Pancreatic Cancer.

Journal: Cells
Published: May 09, 2019

Cytosolic 5'-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites.

Cytosolic 5'-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites.

Journal: EBioMedicine
Published: September 03, 2018

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models.

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models.

Journal: Journal of visualized experiments : JoVE
Published: April 24, 2018

Negative differential resistance in boron nitride graphene heterostructures: physical mechanisms and size scaling analysis.

Negative differential resistance in boron nitride graphene heterostructures: physical mechanisms and size scaling analysis.

Journal: Scientific reports
Published: October 22, 2014
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Last Updated: 09/26/2026