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

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.9K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
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...
3.9K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

6.0K
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,...
6.0K
Other Glycolytic Pathways01:24

Other Glycolytic Pathways

304
The pentose phosphate pathway (PPP) operates in parallel with glycolysis, facilitating the metabolism of both pentoses and glucose. This pathway consists of two distinct phases: the oxidative and non-oxidative phases. While it does not directly generate ATP, the intermediates formed during the process can integrate into glycolysis, contributing to cellular energy metabolism when required.Oxidative Phase: NADPH ProductionThe oxidative phase of the pentose phosphate pathway is primarily...
304
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

15.3K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
15.3K
Tumor Progression02:07

Tumor Progression

6.6K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.6K

You might also read

Related Articles

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

Sort by
Same author

Integrated Molecular and Clinical Analysis of Thymic Epithelial Tumors.

JCO precision oncology·2026
Same author

Multidisciplinary care in the management of pleomorphic dermal sarcoma: A single-center case series and review.

JAAD case reports·2026
Same author

Urgent radiotherapy for superior vena cava syndrome in metastatic non-small cell lung cancer: a case report.

Technical innovations & patient support in radiation oncology·2026
Same author

HIV and lung cancer: a single cancer center experience.

Frontiers in oncology·2025
Same author

Extracellular Matrix-MYCAF Signatures Correlate with Resistance to Neoadjuvant aPD-L1 Immune Checkpoint Inhibition with Durvalumab + Metformin in HPV+ HNSCC.

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

Pansarcoma Analysis of Cyclin-Dependent Kinase and Cyclin Outlier Gene Expression Highlights CDK7 as a Potential Therapeutic Target in Chordoma.

JCO precision oncology·2025

Related Experiment Video

Updated: Oct 9, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
08:07

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

7.3K

Metabolic Pathways and Targets in Chondrosarcoma.

Ida Micaily1, Megan Roche1, Mohammad Y Ibrahim2

  • 1Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA, United States.

Frontiers in Oncology
|December 23, 2021
PubMed
Summary

Chondrosarcomas, a rare bone cancer, exhibit poor outcomes due to resistance to standard treatments. This review explores metabolic alterations and signaling pathways driving cancer aggressiveness and resistance, offering new therapeutic targets.

Keywords:
IDHLdhAPI3K - AKT pathwaychondrosarcomalactate dehydrogenasemTORmetabolism

More Related Videos

Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
09:25

Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma

Published on: October 14, 2016

19.3K
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.6K

Related Experiment Videos

Last Updated: Oct 9, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
08:07

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

7.3K
Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
09:25

Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma

Published on: October 14, 2016

19.3K
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.6K

Area of Science:

  • Oncology
  • Cancer Metabolism
  • Epigenetics

Background:

  • Chondrosarcomas are the second most common primary bone cancer.
  • These tumors produce cartilaginous matrix and are typically resistant to radiation and chemotherapy, leading to poor patient outcomes.
  • Understanding the mechanisms behind chondrosarcoma aggressiveness and therapeutic resistance is crucial.

Purpose of the Study:

  • To review metabolic alterations in chondrosarcoma.
  • To explore the relationship between metabolic changes, epigenetic state, and the tumor microenvironment.
  • To discuss potential therapeutic strategies targeting metabolism, including immunotherapy combinations.

Main Methods:

  • Literature review focusing on metabolic pathways in chondrosarcoma.
  • Analysis of signaling pathways including isocitrate dehydrogenase 1 and 2 (IDH1/IDH2), hedgehog, PI3K-mTOR-AKT, and SRC.
  • Examination of the role of histone acetylation and angiogenesis.

Main Results:

  • Metabolic alterations are linked to epigenetic state and tumor microenvironment in chondrosarcoma.
  • Specific signaling pathways (IDH1/IDH2, hedgehog, PI3K-mTOR-AKT, SRC) are implicated in cancer aggressiveness and resistance.
  • Histone acetylation and angiogenesis are associated with chondrosarcoma progression.

Conclusions:

  • Metabolic reprogramming is a key driver of chondrosarcoma aggressiveness and treatment resistance.
  • Targeting metabolic pathways presents a promising therapeutic avenue.
  • Combination therapies, potentially including immunotherapies, may enhance treatment efficacy.