Tumorigenesis
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«Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cell are transformed into cancer cell. 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 disrupting 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 cell 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.[1] A series of several mutations to certain classes of genes is usually required before a normal cell will transform into a cancer cell.[2][3][4][5] On average, for example, 15 "driver mutations" and 60 "passenger" mutations are found in colon cancer.[2] Mutations in genes that regulate cell division, apoptosis (cell death), and DNA repair may result in uncontrolled cell proliferation and cancer.
Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes that regulate cell growth and differentiation must be altered.[6] Genetic and epigenetic changes can occur at many levels, from gain or loss of entire chromosomes, to a mutation affecting a single DNA nucleotide, or to silencing or activating a microRNA that controls expression of 100 to 500 genes.[7][8] There are two broad categories of genes that are affected by these changes. Oncogenes may be normal genes that are expressed at inappropriately high levels, or altered genes that have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cell. Tumor suppressor genes are genes that inhibit cell division, survival, or other properties of cancer cell. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Finally Oncovirinae, virus that contain an oncogene, are categorized as oncogenic because they trigger the growth of tumorous tissues in the host. This process is also referred to as viral transformation.» (wikipedia)
Summary on Tumorigenesis
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Pathways of Tumorigenesis
Tumorigenesis Biolinks
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-1.2Perhaps, ALA may increase Tumorigenesis(BioMindmap Proof Quality is Negative.) (BioMindmap had flagged this statement.)
Evidence Sources
Biolinks for Tumorigenesis are extracted by users from 31 related publications.-
2006Publications Review
- Organism: In vitro
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2010
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2016Systematic Review
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2019Systematic Review
- Organism: Humans
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2001
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2001
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2006Systematic Review
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2007Rodents
- Organism: Mouse / Rat (Rodents)
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2008
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- From this research we know that
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-1.2Perhaps, ALA may increase Tumorigenesis(BioMindmap Proof Quality is Negative.) (BioMindmap had flagged this statement.)
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2009Rodents
- Organism: Mouse / Rat (Rodents)
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2010
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2013
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2013
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2014
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2016
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- From this research we know that
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-1.2Perhaps, ALA may increase Tumorigenesis(BioMindmap Proof Quality is Negative.) (BioMindmap had flagged this statement.)
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2017
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2018
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2018
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2020Human Cells
- Organism: In vitro
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- From this research we know that
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-1.2Perhaps, ALA may increase Tumorigenesis(BioMindmap Proof Quality is Negative.) (BioMindmap had flagged this statement.)
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2014Rodents
- Organism: Mouse / Rat (Rodents)
- Notable Magnitude of Effect.
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