Related Experiment Video

Updated: Aug 10, 2026

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation
09:09

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

Published on: November 10, 2017

Mutational analysis of the cell cycle inhibitor Kip1/p27 in childhood leukemia

E-A Markaki1, E Stiakaki, A Zafiropoulos

  • 1Department of Pediatric Hematology-Oncology, University of Crete, Medical School, Heraklion Crete, Greece.

Pediatric Blood & Cancer
|March 10, 2006
PubMed
Abstract

Insights

Mutations in the Kip1/p27 gene were found in childhood leukemia, particularly in T-cell acute lymphoblastic leukemia and acute myeloid leukemia. These Kip1/p27 mutations correlate with leukemia type and risk group, suggesting their use in risk stratification.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Cyclin-dependent kinases (CDKs) regulate cell-cycle progression.
  • Kip1/p27 is a key inhibitor of cell division, crucial in preventing G1-S transition.
  • Reduced Kip1/p27 expression is linked to poor prognosis in adult solid tumors.

Purpose of the Study:

  • To investigate mutations in the Kip1/p27 gene in pediatric leukemia.
  • To determine the correlation of Kip1/p27 mutations with leukemia subtypes and clinical parameters.

Main Methods:

  • Bone marrow samples from 49 children with leukemia (37 ALL, 12 AML) were analyzed.
  • Polymerase chain reaction (PCR) amplified Exon 3 of the Kip1/p27 gene.
  • Single strand conformational polymorphism and heterodouplex analysis detected DNA sequence alterations, followed by sequencing.

Main Results:

  • Kip1/p27 gene mutations were identified in 2/3 T-ALL, 6/12 AML, and 1/34 B-ALL cases.
  • Mutation status significantly correlated with leukemia type (P=0.0037) and risk group (P=0.00021).
  • A significant difference in white blood cell count was observed between mutated and non-mutated groups (P=0.019).

Conclusions:

  • Kip1/p27 mutations are present in childhood leukemia, particularly T-ALL and AML.
  • These mutations show a significant association with leukemia type and risk stratification.
  • Kip1/p27 mutations warrant further investigation as a prognostic marker for childhood leukemia treatment.

More Related Videos

Analysis of Cell Cycle Position in Mammalian Cells12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.