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 Experiment Videos

Tumor-stroma interactions.

Neil A Bhowmick1, Harold L Moses

  • 1Departments of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Current Opinion in Genetics & Development
|January 22, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Extracellular vesicles in fatty liver promote a metastatic tumor microenvironment.

Cell metabolism·2026
Same author

Circulating Inflammatory and Mitochondrial Biomarkers Associated with Cachexia in Advanced Non-Small Cell Lung Cancer.

Cancers·2026
Same author

Radiation reprograms fibroblasts to drive prostate cancer therapy resistance.

Endocrine-related cancer·2025
Same author

A Cyanobacteria-Derived RNA Aptamer Resensitizes Prostate Cancer to Hormone Therapy.

Cancer research·2025
Same author

CD105 blockade restores osimertinib sensitivity in drug-resistant EGFR-mutant non-small cell lung cancer.

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy·2025
Same author

Emerin Dysregulation Drives the Very-Small-Nuclear Phenotype and Lineage Plasticity That Associate with a Clinically Aggressive Subtype of Prostate Cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research·2025
Same journal

Temporal trajectories underlying adult neuronal diversity.

Current opinion in genetics & development·2026
Same journal

Transcription regulation of cell fate plasticity - from embryonic development to tissue regeneration.

Current opinion in genetics & development·2026
Same journal

Shared molecular and cellular programs during regeneration of glandular epithelia.

Current opinion in genetics & development·2026
Same journal

Lineage tracing in human cortical development.

Current opinion in genetics & development·2026
Same journal

Cis-regulatory strategies in developmental patterning.

Current opinion in genetics & development·2026
Same journal

GABAergic neuron fate specification and lineage allocation: from development to disorder.

Current opinion in genetics & development·2026
See all related articles

Stromal cells play a crucial role in cancer development. Recent research indicates that mutations in stromal fibroblasts, not just epithelial cells, can initiate tumors by altering growth factor pathways.

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Stromal cells within epithelial tissues are recognized for their supportive role in carcinogenesis.
  • Traditionally, tumor-initiating mutations were thought to originate solely within epithelial cells.
  • Recent literature emphasizes the significance of stromal cells and their expressed factors in cancer initiation and progression.

Purpose of the Study:

  • To highlight the emerging understanding of stromal cell contributions to cancer.
  • To explore the mechanisms by which stromal fibroblasts can initiate epithelial tumors.
  • To address the unresolved question of tissue-specific responses to growth factors involved in carcinogenesis.

Main Methods:

  • Review of recent scientific literature.

Related Experiment Videos

  • Analysis of findings from mouse models of cancer.
  • Examination of data from xenograft studies.

    • Main Results:

    • Evidence suggests that mutations in stromal fibroblasts can initiate epithelial tumors.
    • Alterations in paracrine growth factor pathways are implicated in many of these stromal-initiated tumors.
    • The tissue-specific nature of epithelial responses to these growth factors remains largely unknown.

    Conclusions:

    • Stromal cells are increasingly recognized as key players in cancer initiation and progression.
    • Stromal fibroblast mutations can drive tumor formation through altered signaling pathways.
    • Further research is needed to elucidate the mechanisms underlying tissue-specific growth factor responses in cancer.