Expression of survivin, CDK4, Ki-67 and clinical significance in pediatric acute leukemia

Related Experiment Video

Updated: Jul 17, 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

Liuqing Zhang1, Jing Liu, Hanhua Lin

  • 1Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban
|January 16, 2007
PubMed

Insights

Survivin, CDK4, and Ki-67 proteins are overexpressed in pediatric acute leukemia (AL), indicating their role in cancer cell proliferation and apoptosis. These findings highlight potential therapeutic targets for childhood leukemia.

Area of Science:

  • Oncology
  • Pediatric Hematology

Background:

  • Pediatric acute leukemia (AL) remains a significant health concern.
  • Understanding the molecular mechanisms driving AL is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the expression levels of Survivin, CDK4, and Ki-67 in pediatric AL.
  • To determine the clinical significance of these proteins in childhood leukemia.

Main Methods:

  • Immunohistochemical assay was used to detect Survivin, CDK4, and Ki-67 protein expression.
  • The study included 37 children diagnosed with AL and 10 healthy children as controls.

Main Results:

  • Survivin, CDK4, and Ki-67 were overexpressed in pediatric AL patients compared to controls (P<0.05).
  • Positive correlations were observed between Survivin expression and both CDK4 (P=0.007) and Ki-67 (P=0.008).

Conclusions:

  • Survivin, CDK4, and Ki-67 proteins are significantly upregulated in pediatric acute leukemia.
  • These proteins are implicated in the regulation of apoptosis and proliferation in pediatric AL, suggesting their potential as therapeutic targets.

More Related Videos

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up09:01

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up

Published on: March 26, 2018

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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...