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

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 Survival Analysis

Cancer Survival Analysis

Cancer survival analysis focuses on quantifying and interpreting the time from a key starting point, such as diagnosis or the initiation of treatment, to a specific endpoint, such as remission or death. This analysis provides critical insights into treatment effectiveness and factors that influence patient outcomes, helping to shape clinical decisions and guide prognostic evaluations. A cornerstone of oncology research, survival analysis tackles the challenges of skewed, non-normally...

Cancer

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

You might also read

Related Articles

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

Sort by

Same author

Long Term Patient Reported Urinary Function Following External Beam Radiotherapy for Prostate Cancer.

Clinical oncology (Royal College of Radiologists (Great Britain))·2017

Same author

Potential roles of cytokines and chemokines in human intervertebral disc degeneration: interleukin-1 is a master regulator of catabolic processes.

Osteoarthritis and cartilage·2015

Same author

Implications of neuro-developmental deviations in low birthweight and mechanically ventilated infants.

The Australian journal of physiotherapy·2014

Same author

Dynamic ultrasonic contact detection using acoustic emissions.

Ultrasonics·2013

Same author

Cannabinoid WIN-55,212-2 mesylate inhibits interleukin-1β induced matrix metalloproteinase and tissue inhibitor of matrix metalloproteinase expression in human chondrocytes.

Osteoarthritis and cartilage·2013

Same author

Ecological and molecular maintenance strategies of mobile genetic elements.

FEMS microbiology ecology·2009

Search research articles

Related Experiment Video

Updated: Jun 21, 2026

Adaptation of Semiautomated Circulating Tumor Cell (CTC) Assays for Clinical and Preclinical Research Applications

Adaptation of Semiautomated Circulating Tumor Cell (CTC) Assays for Clinical and Preclinical Research Applications

Published on: February 28, 2014

ADAMs and ADAMTSs in cancer.

S L Turner¹, M E Blair-Zajdel, R A D Bunning

¹Biomedical Research Centre, Sheffield Hallam University, Howard Street, Sheffield S1 1WB, UK. sharon.l.turner@student.shu.ac.uk

British Journal of Biomedical Science

|July 30, 2009

Summary

ADAMs and ADAMTSs are proteins involved in cancer. Their dysregulated expression can promote or inhibit cancer progression by affecting the tumor microenvironment and cell signaling.

Area of Science:

Biochemistry
Molecular Biology
Oncology

Background:

ADAMs (a disintegrin and metalloproteinase domain) and ADAMTSs (ADAMs with thrombospondin motifs) are multi-domain protein families.
These proteins possess metalloproteinase and disintegrin-like domains, with ADAMs typically being transmembrane proteins and ADAMTSs being secreted.
Dysregulated expression of ADAMs and ADAMTSs is frequently observed in human cancers, often correlating with cancer progression.

Purpose of the Study:

To review recent developments in the role of ADAM and ADAMTS proteins in human cancer.
To elucidate how these proteins modulate the tumor microenvironment and influence cancer progression.
To explore the dual roles of ADAMs and ADAMTSs as both promoters and inhibitors of cancer.

Main Methods:

More Related Videos

Adapting 3' Rapid Amplification of CDNA Ends to Map Transcripts in Cancer

Adapting 3' Rapid Amplification of CDNA Ends to Map Transcripts in Cancer

Published on: March 28, 2018

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Related Experiment Videos

Last Updated: Jun 21, 2026

Adaptation of Semiautomated Circulating Tumor Cell (CTC) Assays for Clinical and Preclinical Research Applications

Adaptation of Semiautomated Circulating Tumor Cell (CTC) Assays for Clinical and Preclinical Research Applications

Published on: February 28, 2014

Adapting 3' Rapid Amplification of CDNA Ends to Map Transcripts in Cancer

Adapting 3' Rapid Amplification of CDNA Ends to Map Transcripts in Cancer

Published on: March 28, 2018

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Literature review of recent research on ADAM and ADAMTS proteins in cancer.

Analysis of the proteolytic activities of ADAMs (ectodomain shedding) and ADAMTSs (ECM proteoglycan degradation).

Examination of the mechanisms by which these proteins influence cancer cell proliferation, migration, angiogenesis, and dissemination.

Main Results:

ADAMs function as ectodomain sheddases, releasing bioactive molecules that impact cancer.
ADAMTSs degrade extracellular matrix proteoglycans, remodeling the tumor microenvironment.
Both protein families can promote cancer progression (e.g., via proliferation, migration, angiogenesis) or inhibit it (e.g., via integrin interaction, antiangiogenic activity).

Conclusions:

ADAM and ADAMTS proteins play complex and often opposing roles in human cancer.
Their involvement spans modulation of the tumor microenvironment, cell signaling, and metastasis.
Targeting ADAMs and ADAMTSs presents potential therapeutic strategies for cancer treatment.