Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

5.3K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K
The Ras Gene02:38

The Ras Gene

7.4K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
7.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.9K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.9K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

8.7K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
8.7K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

5.7K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
5.7K
T Cell Types and Functions01:24

T Cell Types and Functions

2.7K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Ex situ heart perfusion: a novel model for drug validation and translation.

Frontiers in cardiovascular medicine·2026
Same author

Corrigendum: Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice.

Genes & development·2026
Same author

Covalent pan-TEAD inhibitors block YAP activity and demonstrate brain penetrance in a Hippo-dependent cancer model.

Nature communications·2026
Same author

Integrated stress response couples mitochondrial fitness with lineage reprogramming to drive cancer evolution.

Nature cell biology·2026
Same author

Peripheral blood transcriptional profiling predicts tumor subtype and neoadjuvant chemoimmunotherapy outcomes in human breast cancer.

Science translational medicine·2026
Same author

Harnessing glucocorticoid receptor antagonism to enhance the efficacy of cardiac regenerative growth factors and cytokines.

Nature cardiovascular research·2026

Related Experiment Video

Updated: Feb 17, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

8.6K

Myc Cooperates with Ras by Programming Inflammation and Immune Suppression.

Roderik M Kortlever1, Nicole M Sodir1, Catherine H Wilson2

  • 1Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK; Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA.

Cell
|December 2, 2017
PubMed
Summary

The oncogenes KRas and Myc drive cancer by reprogramming the tumor microenvironment. Blocking signals CCL9 and IL-23 inhibits tumor growth, revealing therapeutic targets.

Keywords:
CCL9IL-23MycNK cellsRasimmune suppressioninflammationlung canceroncogene cooperationtumor microenvironment

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

829
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.8K

Related Experiment Videos

Last Updated: Feb 17, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

8.6K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

829
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.8K

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • KRas and Myc oncogenes collaborate in tumorigenesis.
  • The precise mechanisms of KRas-Myc cooperation in driving tumor progression are not fully understood.
  • Understanding the tumor microenvironment's role is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To elucidate the mechanism by which KRas and Myc cooperate to drive tumorigenesis.
  • To identify the key signaling pathways involved in stromal reprogramming during tumor progression.
  • To evaluate the therapeutic potential of targeting these pathways in a KRas-driven lung cancer model.

Main Methods:

  • Utilized a mouse lung cancer model with KRasG12D-driven adenomas.
  • Investigated the effects of Myc co-activation on tumor growth, proliferation, and invasion.
  • Analyzed the composition and immune landscape of the tumor stroma.
  • Identified and characterized epithelial-derived signaling molecules (CCL9 and IL-23) responsible for stromal reprogramming.
  • Assessed the impact of co-blockading CCL9 and IL-23 on tumor progression.
  • Examined the effects of Myc deactivation on established tumors and stromal changes.
  • Evaluated the role of T cells and NK cells in tumor regression.

Main Results:

  • Myc co-activation in KRas-driven adenomas rapidly promotes the development of invasive adenocarcinomas.
  • Tumor progression is characterized by an inflammatory, angiogenic, and immune-suppressed stroma.
  • Epithelial-derived CCL9 and IL-23 are identified as key signals driving stromal reprogramming.
  • CCL9 mediates macrophage recruitment, angiogenesis, and PD-L1-dependent T and B cell exclusion.
  • IL-23 orchestrates the exclusion of adaptive T and B cells, as well as NK cells.
  • Co-blockade of CCL9 and IL-23 effectively inhibits Myc-induced tumor progression.
  • Deactivation of Myc in established tumors leads to rapid reversal of stromal changes and tumor regression.
  • Tumor regression upon Myc deactivation is independent of CD4+CD8+ T cells but relies on NK cells.

Conclusions:

  • Myc extensively reprograms the tumor stroma to create an immune-suppressive environment that is essential for tumor progression.
  • Targeting CCL9 and IL-23 represents a promising therapeutic strategy for KRas-driven lung cancers.
  • The interplay between oncogenes and the tumor microenvironment is critical in cancer development and progression.
  • NK cells play a significant role in tumor regression following the withdrawal of oncogenic signaling.