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Related Concept Videos

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.
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...
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...

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Related Experiment Video

Updated: Jul 10, 2026

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
06:59

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter

Published on: March 31, 2022

Caspase-8 Mutation Promotes HNSCC Development and Resistance to Anti-PD-1.

Z Cui1,2, H Wu2, L C Woerner1

  • 1Department of Otolaryngology-Head and Neck Surgery, University of California-San Francisco, San Francisco, CA, USA.

Journal of Dental Research
|July 9, 2026
PubMed
Summary
This summary is machine-generated.

Caspase-8 mutations promote head and neck cancer development and resistance to anti-PD-1 immunotherapy. These mutations may serve as biomarkers for predicting poor response to cancer treatment.

Keywords:
T-Lymphoctesanimaldendritic cellsdisease modelsimmunotherapymiceprogrammed cell death 1 receptortransgenic

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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Heterozygous mutations in caspase-8 occur in 10% of head and neck squamous cell carcinomas (HNSCCs), potentially blocking apoptosis.
  • The in vivo role of caspase-8 mutations in HNSCC development and response to immune checkpoint blockade remains unclear.

Purpose of the Study:

  • To investigate the in vivo role of caspase-8 mutations in HNSCC development.
  • To determine the impact of caspase-8 mutations on response to anti-PD-1 immunotherapy.

Main Methods:

  • Generated mice with heterozygous, epithelium-specific knock-in of a caspase-8 mutation (D305G).
  • Assessed HNSCC development and anti-PD-1 response following carcinogen treatment (4NQO).
  • Engineered murine oral cancer cell line (MOC1) for heterozygous caspase-8 mutations and assessed tumor response to anti-PD-1.

Main Results:

  • Caspase-8 mutant mice developed more tongue tumors and advanced carcinomas after 4NQO treatment.
  • Tumors with caspase-8 mutations showed increased resistance to anti-PD-1 therapy.
  • Caspase-8 mutant tumors exhibited reduced CD8+ T cells and impaired immune cell recruitment during PD-1 blockade.

Conclusions:

  • Caspase-8 mutation promotes carcinogen-induced HNSCC development.
  • Caspase-8 mutation confers resistance to anti-PD-1 immunotherapy by altering the tumor immune microenvironment.
  • Caspase-8 mutations warrant investigation as biomarkers for predicting immunotherapy response in HNSCC patients.