Related Experiment Video
Updated: Jun 13, 2026
Establishment of Tumor Organoids, Carcinoma-Associated Fibroblasts, and Counterpart Fibroblasts from the Same Esophageal Cancer Patient
Published on: April 3, 2026
Lack of Fas-pathway gene mutations in primary resected esophageal squamous cell carcinoma
Chih-Ling Ko1, Chiou-Ying Yang, Cheng-Yen Chung
1Division of Thoracic Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan.
Background:
The Fas system regulates a number of physiological and pathological processes of cell death. Many types of cancer cells are resistant to Fas-mediated apoptosis by several mechanisms, including mutations of the genes involved in Fas-mediated apoptosis. The present study aimed to detect Fas pathway gene alterations in primary resected esophageal squamous cell carcinoma (ESCC).
Methods:
Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were used to analyze the expression of Fas in 34 archival specimens from patients with primary resected ESCC. We then explored the possibility of mutations in the genes involved in the proximal pathway of Fas mediated apoptosis (Fas, FADD). We analyzed exon 9 (death domain) of the Fas gene and exon 1 (death effective domain) of the FADD gene for gene mutations in these 34 specimens by polymerase chain reaction and DNA sequencing.
Results:
Immunohistochemistry and RT-PCR revealed that Fas was expressed in all primary resected ESCC specimens analyzed. However, we did not detect any structural alterations in exon 9 of the Fas gene or exon 1 of the FADD gene.
Conclusions:
Inhibition of Fas-mediated apoptosis may not be due to gene mutations in the critical exon 9 of the Fas gene and exon 1 of the FADD gene in esophageal squamous cell carcinoma.
Insights
Fas gene mutations in exon 9 and FADD gene mutations in exon 1 do not appear to cause resistance to Fas-mediated apoptosis in esophageal squamous cell carcinoma (ESCC). Further research is needed to understand ESCC cell death resistance mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- The Fas system is crucial for regulating cell death, including apoptosis.
- Cancer cells often develop resistance to Fas-mediated apoptosis through various mechanisms.
- Understanding these resistance mechanisms is vital for developing effective cancer therapies.
Purpose of the Study:
- To investigate alterations in Fas pathway genes within primary esophageal squamous cell carcinoma (ESCC).
- To determine if mutations in key Fas and FADD genes contribute to apoptosis resistance in ESCC.
Main Methods:
- Analyzed 34 ESCC specimens using immunohistochemistry and RT-PCR to assess Fas expression.
- Examined exon 9 of the Fas gene and exon 1 of the FADD gene for mutations using PCR and DNA sequencing.
Main Results:
- Fas expression was detected in all analyzed ESCC specimens.
- No structural alterations were found in the analyzed regions of the Fas and FADD genes.
Conclusions:
- Gene mutations in critical regions of Fas (exon 9) and FADD (exon 1) are unlikely to be the cause of Fas-mediated apoptosis inhibition in ESCC.
- Alternative mechanisms may be responsible for apoptosis resistance in esophageal squamous cell carcinoma.
Related Concept Videos
01:21Barrett Esophagus-I: Introduction
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
01:12Loss of Tumor Suppressor Gene Functions
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...
01:12Loss of Tumor Suppressor Gene Functions
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...
01:23Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...