Related Experiment Video
Updated: Jul 28, 2026
07:50
Establishment of a Clinic-based Biorepository
Published on: May 29, 2017
Malignant Transformation in Sinonasal Papillomas Is Closely Associated With Aberrant p53 Expression
1Department of Pathology, University of Pittsburgh Medical Center
Molecular Diagnosis : a Journal Devoted to the Understanding of Human Disease Through the Clinical Application of Molecular Biology
|March 30, 1999
Summary
p53 gene mutations are linked to malignant transformation in sinonasal papillomas. Analyzing these mutations in archival tissues aids in evaluating potentially cancerous lesions.
Area of Science:
- Oncology
- Molecular Biology
- Pathology
Background:
- Sinonasal papillomas are typically benign growths in the nasal cavity.
- Malignant transformation of these papillomas is infrequent and poorly understood.
- The p53 gene plays a crucial role in tumor suppression.
Purpose of the Study:
- To investigate the molecular mechanisms behind the malignant transformation of sinonasal papillomas.
- To examine p53 protein expression and gene mutations in these lesions.
Main Methods:
- Immunohistochemistry was used to assess p53 protein overexpression in 11 sinonasal papillomas (7 with carcinoma) and 3 squamous cell carcinomas.
- Topographic genotyping and polymerase chain reaction amplification were employed to analyze mutations in exons 5-8 of the p53 gene.
Main Results:
- Aberrant p53 gene function was detected in all 7 papillomas with associated carcinoma and all 3 squamous cell carcinomas.
- Several cases showed point mutations leading to missense codons.
- One case had a nonsense mutation and was immunonegative for p53 protein.
Conclusions:
- p53 gene mutations are strongly associated with the malignant transformation of sinonasal papillomas.
- Genotyping of archival tissues is a valuable method for assessing malignant or potentially malignant sinonasal lesions.
More Related Videos
07:00Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas
Published on: February 28, 2019
09:37Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
Related Concept Videos
02:23Abnormal 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...
02:07Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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...
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...
01:12Loss 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...
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...
03:03mTOR Signaling and Cancer Progression
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
01:19Interactions Between Signaling Pathways
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
02:23Abnormal 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...