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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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...

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Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches
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STK10 missense mutations associated with anti-apoptotic function.

Kazutaka Fukumura1, Yoshihiro Yamashita, Masahito Kawazu

  • 1Department of Medical Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Oncology Reports
|July 12, 2013
PubMed
Summary

Peripheral T-cell lymphoma (PTCL) involves aggressive cancer. STK10 gene mutations, including a common polymorphism, impair its tumor suppressor function, promoting cancer cell survival and growth.

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Area of Science:

  • Molecular Oncology
  • Cancer Genetics
  • Hematologic Malignancies

Background:

  • Peripheral T-cell lymphoma (PTCL) is an aggressive cancer with poor prognosis.
  • Identifying genes involved in PTCL carcinogenesis is crucial for understanding disease development.

Purpose of the Study:

  • To identify genes and mutations associated with carcinogenesis in PTCL.
  • To investigate the functional impact of STK10 gene alterations in PTCL.

Main Methods:

  • High-throughput resequencing of target-captured cDNA from PTCL specimens.
  • Analysis of STK10 mutations, including a specific missense substitution (R634H) and other reported somatic variants.
  • Functional assessment of wild-type and mutant STK10 on NF-κB activity and apoptosis.

Main Results:

  • Identified 19 missense mutations in 18 independent genes in PTCL.
  • A specific STK10 mutation (R634H) was found, decreasing its ability to suppress NF-κB and potentiate apoptosis.
  • This STK10 alteration is also present as a single nucleotide polymorphism (SNP) in databases.
  • Other STK10 somatic mutations (L85P, K277E) exhibited more significant anti-apoptotic effects than R634H.

Conclusions:

  • STK10 functions as a tumor suppressor gene in PTCL.
  • Dysfunctional STK10, due to polymorphisms or somatic mutations, contributes to carcinogenesis by reducing apoptosis.
  • STK10 alterations represent a potential therapeutic target in PTCL.