What question did this study set out to answer?

To identify and characterize the tumor-stroma signaling mechanisms driving fibrosis, chemoresistance, and disease progression in pancreatic ductal adenocarcinoma.

January 23, 2018Cancer Research

Tumor–Stroma IL1β-IRAK4 Feedforward Circuitry Drives Tumor Fibrosis, Chemoresistance, and Poor Prognosis in Pancreatic Cancer

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To identify and characterize the tumor-stroma signaling mechanisms driving fibrosis, chemoresistance, and disease progression in pancreatic ductal adenocarcinoma.
Examined IRAK4 and NFκB expression and activation in cancer-associated fibroblasts and pancreatic ductal adenocarcinoma cells.
Performed cytokine array analysis of cancer-associated fibroblasts and microarray profiling of tumor cells to identify key activating signals.
Targeted IRAK4 and IL1β in preclinical pancreatic cancer models receiving gemcitabine and analyzed stromal IL1β expression in human clinical specimens.
Cancer-associated fibroblasts demonstrated robust activation of IRAK4 and NFκB, promoting stromal fibrosis, tumor cell survival, proliferation, and chemoresistance.
IL1β was identified as the principal driver of IRAK4 activation in cancer-associated fibroblasts, and targeting either IL1β or IRAK4 reduced fibrosis and restored gemcitabine sensitivity.
High stromal IL1β expression in clinical pancreatic ductal adenocarcinoma tissue specimens significantly associated with poor patient overall survival.

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Implication

Preclinical study reveals an IL1β-IRAK4 tumor-stroma circuit driving fibrosis and chemoresistance in pancreatic cancer, indicating that pathway inhibition enhances chemotherapy efficacy.

Cite This Study

Zhang et al. (2018) studied this question.

synapsesocial.com/papers/6a92d930de5a63b802a2affe https://doi.org/10.1158/0008-5472.can-17-1366

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Implication

Preclinical study reveals an IL1β-IRAK4 tumor-stroma circuit driving fibrosis and chemoresistance in pancreatic cancer, indicating that pathway inhibition enhances chemotherapy efficacy.

Tumor–Stroma IL1β-IRAK4 Feedforward Circuitry Drives Tumor Fibrosis, Chemoresistance, and Poor Prognosis in Pancreatic Cancer

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Discussion

Implication

Cite This Study

Tumor–Stroma IL1β-IRAK4 Feedforward Circuitry Drives Tumor Fibrosis, Chemoresistance, and Poor Prognosis in Pancreatic Cancer

Key Points

Discussion

Implication

Cite This Study

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