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 Experiment Videos

Primary polycythemias

J T Prchal1

  • 1University of Alabama, Birmingham, USA.

Current Opinion in Hematology
|March 1, 1995
PubMed
Summary
This summary is machine-generated.

Primary polycythemias stem from mutations in blood cells. Understanding these genetic causes, including polycythemia vera, aids in treating blood disorders and normal blood cell development.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Adaptive genetic changes related to haemoglobin concentration in native high-altitude Tibetans.

Experimental physiology·2015
Same author

Presence of polyclonal hematopoiesis in females with Ph-negative myeloproliferative neoplasms.

Leukemia·2015
Same author

End-tidal carbon monoxide as an indicator of the hemolytic rate.

Blood cells, molecules & diseases·2015
Same author

The relationship of JAK2(V617F) and acquired UPD at chromosome 9p in polycythemia vera.

Leukemia·2014
Same author

Whole-exome sequencing of polycythemia vera revealed novel driver genes and somatic mutation shared by T cells and granulocytes.

Leukemia·2014
Same author

Establishing optimal quantitative-polymerase chain reaction assays for routine diagnosis and tracking of minimal residual disease in JAK2-V617F-associated myeloproliferative neoplasms: a joint European LeukemiaNet/MPN&MPNr-EuroNet (COST action BM0902) study.

Leukemia·2013
Same journal

Dynamic myeloid suppressor states in cancer and inflammation and their therapeutic potential.

Current opinion in hematology·2026
Same journal

Factor XIa inhibition for the prevention of thrombosis: mechanism, clinical trial signals, and indication-specific positioning.

Current opinion in hematology·2026
Same journal

Nutrition as a regulator of hematopoietic stem cell biology and transplantation.

Current opinion in hematology·2026
Same journal

From biomimicry to clinical actionability: rethinking high-shear thrombosis as a mechanobiological system.

Current opinion in hematology·2026
Same journal

Bidirectional relationship between metabolic and thrombotic disease mechanisms.

Current opinion in hematology·2026
Same journal

The dual role of the brain-derived neurotrophic factor as a regulator of hemostasis and thrombotic risk.

Current opinion in hematology·2026
See all related articles

Area of Science:

  • Hematology
  • Genetics
  • Molecular Biology

Background:

  • Primary polycythemias involve mutations affecting hematopoietic and erythroid cells.
  • Polycythemia vera, a common type, arises from acquired somatic mutations in hematopoietic stem cells, with unclear molecular origins.
  • Primary familial and congenital polycythemias result from inherited mutations, with some molecular mechanisms already identified.

Purpose of the Study:

  • To review primary polycythemic states alongside other polycythemic disorders.
  • To highlight the genetic basis of primary polycythemias.
  • To explore the implications of understanding molecular defects for broader hematologic and leukemic disorders.

Main Methods:

  • Literature review of primary polycythemic states.

Related Experiment Videos

  • Discussion of genetic mutations (acquired and inborn) in hematopoietic and erythroid cells.
  • Analysis of molecular mechanisms and signal transduction pathways.

    • Main Results:

    • Primary polycythemias are categorized based on acquired or inborn mutations.
    • Polycythemia vera's molecular pathogenesis remains largely undefined.
    • Defined molecular mechanisms exist for some primary familial and congenital polycythemias.

    Conclusions:

    • Advances in defining molecular defects offer insights into primary polycythemias.
    • Understanding these defects can illuminate pathogenesis of leukemic disorders and normal hematopoiesis.
    • This knowledge is crucial for developing effective therapies for myeloproliferative and leukemic disorders.