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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
Oncogenes and tumor suppressor genes as paradigms in oncogenesis
1Medical School, University of Crete, Heraklion, Crete, Greece. spandidos@spandidos.gr
Abstract:
Cancer is the result of genetic and epigenetic changes that occur mainly in stem (precursor) cells of various cell types. Two main categories of genes are involved in the process of carcinogenesis. Oncogenes are activated proto-oncogenes and tumor suppressor genes are inactivated by mutation in the global sense, that is point mutation, deletion, rearrangement, and duplication. Both types of genes are required for normal cell proliferation and differentiation and aberrant expression leads to abnormal cell proliferation. Ras and p53 genes are the paradigms for oncogenes and tumor suppressor genes, respectively, whereas the oncogenes carried by the human papillomaviruses (HPV) comprise the best example of tumor viruses involvement in human cancer.
Insights
Cancer arises from genetic and epigenetic alterations in stem cells, involving oncogenes and tumor suppressor genes. Aberrant gene expression drives abnormal cell proliferation, exemplified by Ras, p53, and human papillomaviruses.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cancer originates from genetic and epigenetic changes in stem (precursor) cells.
- Carcinogenesis involves two primary gene categories: oncogenes and tumor suppressor genes.
- Normal cell proliferation and differentiation depend on these genes; aberrant expression leads to uncontrolled growth.
Purpose of the Study:
- To elucidate the genetic and epigenetic mechanisms underlying cancer development.
- To explain the roles of oncogenes and tumor suppressor genes in carcinogenesis.
- To highlight key examples of oncogenes, tumor suppressor genes, and viral oncogenes in human cancer.
Main Methods:
- Review of genetic and epigenetic alterations in carcinogenesis.
- Analysis of gene mutations (point mutation, deletion, rearrangement, duplication) affecting proto-oncogenes and tumor suppressor genes.
- Examination of specific gene paradigms (Ras, p53) and viral oncogenes (HPV).
Main Results:
- Cancer results from genetic and epigenetic changes primarily in stem cells.
- Oncogenes (activated proto-oncogenes) and tumor suppressor genes (inactivated by mutation) are crucial.
- Ras and p53 are key examples of oncogenes and tumor suppressor genes, respectively.
- Human papillomaviruses (HPV) oncogenes exemplify viral involvement in human cancer.
Conclusions:
- Genetic and epigenetic alterations in stem cells are fundamental to cancer.
- Dysregulation of oncogenes and tumor suppressor genes drives abnormal cell proliferation.
- Specific genes like Ras, p53, and viral oncogenes from HPV are critical in understanding cancer etiology.
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