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Related Concept Videos

Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Role of Hematopoietic Growth Factors01:28

Role of Hematopoietic Growth Factors

Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
Thrombopoietin (TPO), mainly released by the liver,...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...

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Related Experiment Video

Updated: Jul 3, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

Hypercoagulability and tissue factor gene upregulation in hematologic malignancies.

Anna Falanga1, Tiziano Barbui, Frederick R Rickles

  • 1Department Hematology/Oncology, Ospedali Riuniti di Bergamo, Bergamo, Italy. annafalanga@yahoo.com

Seminars in Thrombosis and Hemostasis
|July 23, 2008
PubMed
Summary

Hematologic malignancies like acute leukemia, essential thrombocythemia, and polycythemia vera cause hypercoagulability, increasing thrombosis risk. Understanding these mechanisms is key to preventing blood clots.

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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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Extracellular Vesicle Tissue Factor Activity Assay
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Extracellular Vesicle Tissue Factor Activity Assay

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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Thrombotic complications are frequent in hematologic malignancies, impacting patient morbidity and mortality.
  • A hypercoagulable state is common in Philadelphia chromosome-negative chronic myeloproliferative disorders such as essential thrombocythemia (ET) and polycythemia vera (PV).
  • Thrombosis and bleeding can coexist in acute leukemia as a thrombo-hemorrhagic syndrome.

Purpose of the Study:

  • To review the pathogenic mechanisms underlying the hypercoagulable state in ET and PV.
  • To highlight the role of molecular changes in leukemic cells and hematopoietic progenitor cells.
  • To discuss how neoplastic transformation and specific mutations contribute to hypercoagulability.

Main Methods:

  • Review of molecular studies in experimental models and patient-derived cells.
  • Analysis of gene expression and cellular interactions.
  • Focus on specific genetic alterations like T15-17 translocation and JAK2V617F mutation.

Main Results:

  • Clonal rearrangement in hematopoietic progenitor cells leads to overexpression of procoagulant factors and adhesion molecules.
  • Neoplastic transformation induces activation of blood coagulation.
  • In acute promyelocytic leukemia, T15-17 translocation causes tissue factor (TF) hyperexpression.
  • In PV and ET, the JAK2V617F mutation activates hemostasis, increasing TF microparticles and platelet/neutrophil aggregates.

Conclusions:

  • Understanding the pathophysiology of hypercoagulability in hematologic malignancies is crucial.
  • Molecular alterations drive a prothrombotic state in these conditions.
  • Targeting these mechanisms may help prevent thromboembolic complications.