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

Leukemic transformation.

Ying-Wei Lin1, Peter D Aplan

  • 1Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20889-5105, USA. aplanp@mail.nih.gov

Cancer Biology & Therapy
|January 17, 2004
PubMed
Summary
This summary is machine-generated.

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

Azanucleoside treatment leads to B-cell precursor acute lymphoblastic leukemia.

Blood neoplasia·2025
Same author

5-Azacytidine and decitabine induce C > G transversions in both murine and human cells.

Leukemia·2025
Same author

Disruption of normal stem cell function and transmission of myelodysplastic syndrome by self-renewal of committed myeloid lineage cells.

Stem cell reports·2025
Same author

Mechanism of cytarabine-induced neurotoxicity.

Nature·2025
Same author

HoxBlinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98-rearranged leukemia.

The Journal of clinical investigation·2025
Same author

Advancing drug development in myelodysplastic syndromes.

Blood advances·2025
Same journal

Effective treatment of human breast tumors by chimeric CCL2 and CCL8 diphtheria toxin cytotoxic peptides.

Cancer biology & therapy·2026
Same journal

<i>NSUN2</i> mediates <i>SALL2</i> m5C methylation to inhibit ferroptosis and promote breast cancer progression.

Cancer biology & therapy·2026
Same journal

Targeting the PI3K/AKT pathway in prostate cancer: the role of PTEN deficiency and biomarker-guided therapy.

Cancer biology & therapy·2026
Same journal

ABHD17C regulates the efficacy of lenvatinib in suppressing hepatocellular carcinoma.

Cancer biology & therapy·2026
Same journal

Advances in SEC61G research: from ER translocon subunit to emerging pan-cancer oncogenic roles.

Cancer biology & therapy·2026
Same journal

Efficacy and safety profiles of CDK4/6 inhibitor in patients with hormone receptor-positive and human epidermal growth factor receptor 2-negative (HR+/HER2-) advanced breast cancer (ABC) from the high-altitude <i>versus</i> low-altitude regions: a multi-center retrospective study.

Cancer biology & therapy·2026
See all related articles

Leukemia arises from accumulated mutations in blood stem cells that disrupt cell growth and differentiation. Understanding these genetic changes is key to developing targeted therapies for this cancer.

Area of Science:

  • Hematology
  • Cancer Biology
  • Molecular Genetics

Background:

  • Leukemia is characterized by the uncontrolled proliferation of immature blood cells.
  • This uncontrolled growth stems from the accumulation of genetic and epigenetic alterations in hematopoietic precursor cells.
  • Key mutations impact pathways regulating cell accumulation and hematopoietic differentiation.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying leukemic transformation.
  • To identify critical genetic and epigenetic changes driving leukemia development.
  • To provide a foundation for developing novel, targeted therapeutic strategies.

Main Methods:

  • Analysis of point mutations (insertions, deletions, substitutions).
  • Characterization of chromosomal rearrangements (deletions, insertions, amplifications, translocations).

Related Experiment Videos

  • Assessment of epigenetic modifications in hematopoietic precursor cells.

    • Main Results:

    • Identified diverse mutation types contributing to leukemia, including point mutations and chromosomal abnormalities.
    • Highlighted the necessity of mutations in at least two distinct pathways for leukemic development.
    • These pathways control cell proliferation and the differentiation of blood cells.

    Conclusions:

    • Leukemic transformation is a multi-step process driven by accumulating mutations.
    • Targeting specific leukemogenic proteins offers a promising therapeutic avenue.
    • Further understanding of leukemia mechanisms will facilitate the development of effective treatments.