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Related Concept Videos

Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Mutations01:39

Mutations

Overview
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

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Updated: Jun 22, 2026

Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation
07:17

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Published on: August 23, 2024

WT1 mutations in T-ALL.

Valeria Tosello1, Marc R Mansour, Kelly Barnes

  • 1Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.

Blood
|June 5, 2009
PubMed
Summary
This summary is machine-generated.

Recurrent WT1 gene mutations are identified in T-cell acute lymphoblastic leukemia (T-ALL). These mutations, primarily frameshift types, are common in pediatric and adult T-ALL and do not appear to impact prognosis.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Mechanisms of T-cell acute lymphoblastic leukemia (T-ALL) progression and relapse remain unclear.
  • Understanding genetic alterations is crucial for T-ALL treatment strategies.

Purpose of the Study:

  • To identify recurrent genetic alterations in T-ALL using paired diagnostic and relapsed samples.
  • To investigate the role of WT1 gene mutations in T-ALL pathogenesis and prognosis.

Main Methods:

  • Single nucleotide polymorphism (SNP) array analysis of paired diagnostic and relapsed T-ALL samples.
  • Mutation analysis of the WT1 tumor suppressor gene.
  • Correlation of WT1 mutations with oncogenic transcription factor rearrangements and patient survival.

Main Results:

  • Relapsed T-ALL frequently loses chromosomal markers from diagnosis, suggesting emergence from a distinct ancestral clone.
  • WT1 mutations were identified in 13.2% of pediatric and 11.7% of adult T-ALL cases.
  • WT1 mutations are predominantly heterozygous frameshift mutations, often found with TLX1, TLX3, and HOXA oncogene rearrangements, and do not affect prognosis.

Conclusions:

  • WT1 mutations represent a recurrent genetic alteration in T-ALL.
  • WT1 mutations are associated with specific oncogenic transcription factor rearrangements.
  • WT1 mutations do not appear to influence survival outcomes in T-ALL patients.