Related Experiment Video
Updated: Jun 2, 2026

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
Published on: November 28, 2019
Endogenous Myc maintains the tumor microenvironment
Nicole M Sodir1, Lamorna Brown Swigart, Anthony N Karnezis
1Department of Pathology, University of California at San Francisco, San Francisco, California 94143, USA.
Abstract:
The ubiquitous deregulation of Myc in human cancers makes it an intriguing therapeutic target, a notion supported by recent studies in Ras-driven lung tumors showing that inhibiting endogenous Myc triggers ubiquitous tumor regression. However, neither the therapeutic mechanism nor the applicability of Myc inhibition to other tumor types driven by other oncogenic mechanisms is established. Here, we show that inhibition of endogenous Myc also triggers ubiquitous regression of tumors in a simian virus 40 (SV40)-driven pancreatic islet tumor model. Such regression is presaged by collapse of the tumor microenvironment and involution of tumor vasculature. Hence, in addition to its diverse intracellular roles, endogenous Myc serves an essential and nonredundant role in coupling diverse intracellular oncogenic pathways to the tumor microenvironment, further bolstering its credentials as a pharmacological target.
Insights
Inhibiting Myc, a key cancer gene, triggers tumor regression in pancreatic cancer models. This highlights Myc
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Myc deregulation is common in human cancers, presenting it as a potential therapeutic target.
- Previous studies demonstrated Myc inhibition's efficacy in Ras-driven lung tumors, leading to tumor regression.
- The precise therapeutic mechanisms and broader applicability of Myc inhibition across different cancer types remain unclear.
Purpose of the Study:
- To investigate the therapeutic effects of inhibiting endogenous Myc in a simian virus 40 (SV40)-driven pancreatic islet tumor model.
- To elucidate the underlying mechanisms of Myc inhibition-induced tumor regression.
- To assess the role of Myc in connecting oncogenic pathways to the tumor microenvironment.
Main Methods:
- Utilized a simian virus 40 (SV40)-driven pancreatic islet tumor model in preclinical studies.
- Administered targeted inhibition of endogenous Myc.
- Monitored tumor regression, tumor microenvironment changes, and tumor vasculature involution.
Main Results:
- Inhibition of endogenous Myc led to widespread regression of pancreatic islet tumors.
- Tumor regression was preceded by the collapse of the tumor microenvironment.
- Involution of tumor vasculature was observed concurrently with tumor regression.
Conclusions:
- Endogenous Myc plays a critical and non-redundant role in linking various intracellular oncogenic pathways to the tumor microenvironment.
- Myc inhibition demonstrates therapeutic potential beyond Ras-driven lung cancers, including in pancreatic cancer.
- These findings strengthen the rationale for targeting Myc pharmacologically across diverse cancer types.
Related Concept Videos
The Tumor Microenvironment
The Tumor Microenvironment
Abnormal Proliferation
Induced Pluripotent Stem Cells
Somatic cells are...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Cancer Stem Cells and Tumor Maintenance
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
