
carcinogenesis
Sign in to saveAlso known as oncogenesis, tumorigenesis
thumb|150px|right|Cancers and tumors are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat. Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally, the balance between proliferation and programmed cell death, in the form of apoptosis,
Research
218,271 papers- Squamous carcinogenesis: potential truncal mutations.Human pathology · 2023
- Arsenic-Induced Carcinogenesis and Immune Dysregulation.International journal of environmental research and public health · 2019
- Plakophilin 1 in carcinogenesis.Molecular carcinogenesis · 2024
- Metals and molecular carcinogenesis.Carcinogenesis · 2020
- Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect.Carcinogenesis · 2017
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Article
27 sectionsContents
- Causes
- Genetic and epigenetic
- DNA damage
- Contribution of field defects
- Genome instability
- Non-mainstream theories
- Cancer cell biology
- Clonal evolution
- Biological properties of cancer cells
- Cancer as a defect in cell interactions
- In fish
- Mechanisms
- Oncogenes
- Proto-oncogenes
- Tumor suppressor genes
- Multiple mutations
- Non-mutagenic carcinogens
- Role of infections
- Bacterial
- Viral
- Helminthiasis
- Epigenetics
- Cancer stem cells
- Clonal evolution
- See also
- References
- Further reading
thumb|150px|right|Cancers and tumors are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat. Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally, the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs. According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by interfering with the programming regulating the processes, upsetting the normal balance between proliferation and cell death. This results in uncontrolled cell division and the evolution of those cells by natural selection in the body. Only certain mutations lead to cancer whereas the majority of mutations do not.
Variants of inherited genes may predispose individuals to cancer. In addition, environmental factors such as carcinogens and radiation cause mutations that may contribute to the development of cancer. Finally random mistakes in normal DNA replication may result in cancer-causing mutations. A series of several mutations to certain classes of genes is usually required before a normal cell will transform into a cancer cell. Recent comprehensive patient-level classification and quantification of driver events in TCGA cohorts revealed that there are on average 12 driver events per tumor, of which 0.6 are point mutations in oncogenes, 1.5 are amplifications of oncogenes, 1.2 are point mutations in tumor suppressors, 2.1 are deletions of tumor suppressors, 1.5 are driver chromosome losses, 1 is a driver chromosome gain, 2 are driver chromosome arm losses, and 1.5 are driver chromosome arm gains. Mutations in genes that regulate cell division, apoptosis (cell death), and DNA repair may result in uncontrolled cell proliferation and cancer.