Related Experiment Video
Updated: Nov 27, 2025

04:40
Author Spotlight: Advancing Cancer Associated Thrombosis Research in Rodent Models
Published on: January 5, 2024
2.9K
Cancer and thrombosis: new insights to an old problem
O Leiva1, R Newcomb2, J M Connors3
1Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Journal De Medecine Vasculaire
|December 5, 2020
Summary
Cancer patients frequently develop venous thromboembolism (VTE), a serious condition. Understanding cancer-related hypercoagulability is key to identifying patients who need preventative treatment.
Area of Science:
- Oncology
- Hematology
- Thrombosis Research
Background:
- Venous thromboembolism (VTE) is a frequent and serious complication in cancer patients.
- Malignancy triggers a pro-thrombotic state through venous stasis, endothelial injury, and imbalanced coagulation factors.
- Historical understanding of cancer-related hypercoagulability, including Virchow's triad, provides a foundation for current research.
Purpose of the Study:
- To elucidate the complex pathophysiology of VTE in cancer patients.
- To identify patient-specific, treatment-related, and tumor-specific factors contributing to thrombosis.
- To underscore the importance of understanding these factors for effective thromboprophylaxis.
Main Methods:
- Review of existing literature on cancer and VTE pathophysiology.
- Analysis of factors contributing to hypercoagulability in malignancy.
- Synthesis of knowledge regarding venous stasis, endothelial injury, and coagulation factor imbalance.
Main Results:
- Cancer inherently induces a hypercoagulable state.
- Multiple factors (patient, treatment, tumor) exacerbate thrombosis risk.
- A comprehensive understanding of these factors is crucial for clinical decision-making.
Conclusions:
- Cancer-associated thrombosis is multifactorial, involving intrinsic malignancy effects and external factors.
- Identifying patients at high risk for VTE is essential for implementing appropriate preventative strategies.
- Further research into thromboprophylaxis in cancer patients is warranted.
Keywords:
AnticoagulationCancerCancer-associated thrombosisDriver mutationThrombosisVenous thromboembolismMore Related Videos
Related Concept Videos
Adaptive Mechanisms in Cancer Cells
6.3K
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,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
6.3K
Intracellular Signaling Affects Focal Adhesions
3.2K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
3.2K
mTOR Signaling and Cancer Progression
4.2K
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...
The mTOR pathway or the...
4.2K
Metastasis
6.1K
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...
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...
6.1K
Cancer
52.4K
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.
52.4K
Cancer Survival Analysis
535
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...
535

