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

p16ink4a gene and hematological malignancies

B Quesnel1, C Preudhomme, P Fenaux

  • 1Service des maladies du sang CHU Lille, France.

Leukemia & Lymphoma
|June 1, 1996
PubMed
Summary

The p16ink4a and p15ink4b genes, critical for cell cycle regulation, are frequently deleted in hematological malignancies like acute lymphoblastic leukemia. Their inactivation, primarily through deletion, impacts cancer progression and offers therapeutic targets.

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

[GATA2 gene mutations: 3 cases].

La Revue de medecine interne·2022
Same author

Effects of azacitidine in 93 patients with <i>IDH1/2</i> mutated acute myeloid leukemia/myelodysplastic syndromes: a French retrospective multicenter study.

Leukemia & lymphoma·2020
Same author

[Thoracic air bubbles of unusual cause].

La Revue de medecine interne·2020
Same author

Immature platelet fraction (IPF): A reliable tool to predict peripheral thrombocytopenia.

Current research in translational medicine·2019
Same author

Outcomes and mutational analysis of patients with lower-risk non-del5q myelodysplastic syndrome treated with antithymocyte globulin with or without ciclosporine A.

Leukemia research·2018
Same author

Targeting MYC in multiple myeloma.

Leukemia·2018

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Cell cycle progression relies on cyclin-dependent kinases (CDKs) and their regulators.
  • CDK inhibitors (CDKis), including p16ink4a and p15ink4b, are crucial for controlling cell division.
  • These genes are located on chromosome 9p21 and are frequently altered in various cancers.

Purpose of the Study:

  • To review the functions of p16ink4a and p15ink4b.
  • To analyze the implications of p16ink4a and p15ink4b alterations in hematological malignancies.
  • To highlight the role of these genes in cell cycle regulation and cancer development.

Main Methods:

  • Literature review of recent studies on p16ink4a and p15ink4b.
  • Analysis of genetic alterations (deletions, mutations) in cancer cell lines and tumors.
  • Examination of functional data regarding CDK inhibition and cell cycle control.

Main Results:

  • p16ink4a and p15ink4b inhibit cyclin D-CDK4/6 complexes, regulating the G1/S phase transition.
  • Biallelic deletion is the predominant mechanism for p16ink4a/p15ink4b inactivation in cancers.
  • Homozygous deletions are frequent in acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML) blast crisis, and adult T-cell leukemia (ATL), with p16ink4a deletions being more common.

Conclusions:

  • p16ink4a and p15ink4b play a significant role in cell cycle control and are frequently inactivated in hematological malignancies.
  • The high frequency of deletions in ALL suggests their importance in leukemogenesis.
  • Understanding these genetic alterations is vital for comprehending cancer progression and developing targeted therapies.

Related Experiment Videos