Related Experiment Video
Updated: Jan 13, 2026

An Efficient Method for Extracting Human Fallopian Tube Epithelia for Single-cell Analyses
Published on: March 28, 2025
P53 Mutation Induces Epithelial-to-Mesenchymal Transition (EMT) Associated with Stem Cell Properties and
Kholoud Alwosaibai1,2,3, Barbara C Vanderhyden2,3,4, Fatimah A Alsaffar5
1Biomedical Research Department, Research Center, King Fahad Specialist Hospital-Dammam, Eastern Health Cluster, Dammam 32253, Saudi Arabia.
None:
Background/Objectives: Type II ovarian cancer, including high-grade serous carcinoma (HGSC), is genetically unstable and exhibits frequent mutations in the tumor suppressor genes. Mutations of TP53 and BRCA1 genes have been associated with HGSC, which has been suggested as a subtype that arises from the fallopian tube lesion called serous tubal intraepithelial carcinoma (STIC). Although TP53 and BRCA1 genes are well-known tumor suppressor genes, the actual effects of TP53 and BRCA1 mutations in enhancing the development of ovarian cancer initiated from STIC are poorly understood. Methods: In this study, we knocked out Trp53 and Brca-1 in epithelial cell clones derived from mice fallopian tube tissues (known as oviducts) and investigated the potential involvement of these two mutations in inducing cancer stem-like cells as cancer-initiating cells. Results: We have shown that the knockout of Trp53 induced oviduct cells to undergo EMT and acquire stem cell characteristics. Conclusions:Trp53 mutation may induce the early stage of precursor lesions formation at the distal end of the oviducts.
Related Concept Videos
Abnormal Proliferation
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Negative Regulator Molecules
Induced Pluripotent Stem Cells
Somatic...

