Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Metastasis

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

Metastasis

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Cancer Cell Migration through Invadopodia

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...

Cancer Stem Cells and Tumor Maintenance

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...

You might also read

Related Articles

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

Sort by

Same author

Retraction Note to: Roles of MicroRNAs and Other Non-coding RNAs in Breast Cancer Metastasis.

Journal of mammary gland biology and neoplasia·2016

Same author

Roles of microRNAs and other non-coding RNAs in breast cancer metastasis.

Journal of mammary gland biology and neoplasia·2012

Same author

Tumor metastasis: molecular insights and evolving paradigms.

Cell·2011

Same author

Activation of miR-31 function in already-established metastases elicits metastatic regression.

Genes & development·2011

Same author

Roles for microRNAs in the regulation of cell adhesion molecules.

Journal of cell science·2011

Same author

Metastasis suppression: a role of the Dice(r).

Genome biology·2010

Search research articles

Related Experiment Video

Updated: May 26, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

Endogenous anticancer mechanisms: metastasis.

Scott Valastyan¹

¹Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. scott_valastyan@hms.harvard.edu

Frontiers in Bioscience (Elite Edition)

|December 29, 2011

Summary

Metastases cause most cancer deaths. This study highlights four natural protective mechanisms against breast cancer metastasis and discusses targeting them for treatment.

Area of Science:

Oncology
Cell Biology
Cancer Metastasis Research

Background:

Metastasis, the spread of cancer cells, is responsible for over 90% of cancer mortality.
The invasion-metastasis cascade describes the multi-step process of cancer cell dissemination and adaptation.
Endogenous mechanisms normally prevent metastatic progression, but these must be overcome for metastasis to occur.

Purpose of the Study:

To identify and discuss four endogenous anti-metastasis mechanisms in breast carcinomas.
To explore how these protective gene expressions are reduced during cancer progression.
To examine clinical opportunities for targeting these endogenous anti-metastasis pathways.

Main Methods:

Review and analysis of endogenous anti-metastasis mechanisms in breast cancer.

More Related Videos

Injection of Syngeneic Murine Melanoma Cells to Determine Their Metastatic Potential in the Lungs

Injection of Syngeneic Murine Melanoma Cells to Determine Their Metastatic Potential in the Lungs

Published on: May 24, 2016

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Published on: July 7, 2023

Related Experiment Videos

Last Updated: May 26, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

Injection of Syngeneic Murine Melanoma Cells to Determine Their Metastatic Potential in the Lungs

Injection of Syngeneic Murine Melanoma Cells to Determine Their Metastatic Potential in the Lungs

Published on: May 24, 2016

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Published on: July 7, 2023

Discussion of gene expression changes during malignant progression.

Exploration of therapeutic strategies targeting these mechanisms.

Main Results:

Four key endogenous mechanisms that protect against metastatic disease in breast carcinomas were identified.
Expression of protective genes is often downregulated during malignant progression.
Therapeutic reactivation of these endogenous mechanisms presents a potential treatment strategy.

Conclusions:

Understanding endogenous anti-metastasis mechanisms is crucial for comprehending metastasis etiology.
Targeting and reactivating these natural safeguards may offer effective treatment for metastatic breast cancer.
This knowledge can guide the development of novel therapeutic interventions for human tumors.