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A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication.[1]
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Tumor suppressor gene - Wikipedia
pedia, the free encyclopedia Gene that inhibits expression of the tumorigenic phenotype The cell cycle. Many tumor suppressors work to regulate the cycle at specific checkpoints in order to pr. <span>A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication.[1] If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is mutated, it results in a loss or reduction in its function. In combination with other genetic




TSGs can be grouped into the following categories: caretaker genes, gatekeeper genes, and more recently landscaper genes.

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Tumor suppressor gene - Wikipedia
this could allow the cell to grow abnormally. The loss of function for these genes may be even more significant in the development of human cancers, compared to the activation of oncogenes.[2] <span>TSGs can be grouped into the following categories: caretaker genes, gatekeeper genes, and more recently landscaper genes. Caretaker genes ensure stability of the genome via DNA repair and subsequently when mutated allow mutations to accumulate.[3] Meanwhile, gatekeeper genes directly regulate cell growth b




Caretaker genes ensure stability of the genome via DNA repair and subsequently when mutated allow mutations to accumulate. [3]
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Tumor suppressor gene - Wikipedia
velopment of human cancers, compared to the activation of oncogenes.[2] TSGs can be grouped into the following categories: caretaker genes, gatekeeper genes, and more recently landscaper genes. <span>Caretaker genes ensure stability of the genome via DNA repair and subsequently when mutated allow mutations to accumulate.[3] Meanwhile, gatekeeper genes directly regulate cell growth by either inhibiting cell cycle progression or inducing apoptosis.[3] Lastly landscaper genes regulate growth by contributing t




Meanwhile, gatekeeper genes directly regulate cell growth by either inhibiting cell cycle progression or inducing apoptosis.[3]
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Tumor suppressor gene - Wikipedia
etaker genes, gatekeeper genes, and more recently landscaper genes. Caretaker genes ensure stability of the genome via DNA repair and subsequently when mutated allow mutations to accumulate.[3] <span>Meanwhile, gatekeeper genes directly regulate cell growth by either inhibiting cell cycle progression or inducing apoptosis.[3] Lastly landscaper genes regulate growth by contributing to the surrounding environment, when mutated can cause an environment that promotes unregulated proliferation.[4] The classificat




Lastly landscaper genes regulate growth by contributing to the surrounding environment, when mutated can cause an environment that promotes unregulated proliferation.[4]
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Tumor suppressor gene - Wikipedia
r and subsequently when mutated allow mutations to accumulate.[3] Meanwhile, gatekeeper genes directly regulate cell growth by either inhibiting cell cycle progression or inducing apoptosis.[3] <span>Lastly landscaper genes regulate growth by contributing to the surrounding environment, when mutated can cause an environment that promotes unregulated proliferation.[4] The classification schemes are evolving as medical advances are being made from fields including molecular biology, genetics, and epigenetics. History[edit] The discovery of oncogenes a




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Unlike oncogenes, tumor suppressor genes generally follow the two-hit hypothesis, which states both alleles that code for a particular protein must be affected before an effect is manifested.[7]

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Tumor suppressor gene - Wikipedia
for the Rb gene. This deletion caused increased tumor growth in retinoblastoma, suggesting that loss or inactivation of a tumor suppressor gene can increase tumorigenicity.[6] Two-hit hypothesis<span>[edit] Unlike oncogenes, tumor suppressor genes generally follow the two-hit hypothesis, which states both alleles that code for a particular protein must be affected before an effect is manifested.[7] If only one allele for the gene is damaged, the other can still produce enough of the correct protein to retain the appropriate function. In other words, mutant tumor suppressor alleles




If only one allele for the gene is damaged, the other can still produce enough of the correct protein to retain the appropriate function.
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Tumor suppressor gene - Wikipedia
nlike oncogenes, tumor suppressor genes generally follow the two-hit hypothesis, which states both alleles that code for a particular protein must be affected before an effect is manifested.[7] <span>If only one allele for the gene is damaged, the other can still produce enough of the correct protein to retain the appropriate function. In other words, mutant tumor suppressor alleles are usually recessive, whereas mutant oncogene alleles are typically dominant. Models of tumor suppression Illustration of two-hit hypoth




In other words, mutant tumor suppressor alleles are usually recessive, whereas mutant oncogene alleles are typically dominant.
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Tumor suppressor gene - Wikipedia
ein must be affected before an effect is manifested.[7] If only one allele for the gene is damaged, the other can still produce enough of the correct protein to retain the appropriate function. <span>In other words, mutant tumor suppressor alleles are usually recessive, whereas mutant oncogene alleles are typically dominant. Models of tumor suppression Illustration of two-hit hypothesis Proposed by A.G. Knudson for cases of retinoblastoma.[7] He observed that 40% of U.S cases were caused by a mutation in th




hen located in a gene promoter, DNA methylation typically acts to repress gene transcription.
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DNA methylation - Wikipedia
DNA sequence. DNA methylation is a biological process by which methyl groups are added to the DNA molecule. Methylation can change the activity of a DNA segment without changing the sequence. W<span>hen located in a gene promoter, DNA methylation typically acts to repress gene transcription. In mammals, DNA methylation is essential for normal development and is associated with a number of key processes including genomic imprinting, X-chromosome inactivation, repression of t




As of 2016, two nucleobases have been found on which natural, enzymatic DNA methylation takes place: adenine and cytosine.
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DNA methylation - Wikipedia
for normal development and is associated with a number of key processes including genomic imprinting, X-chromosome inactivation, repression of transposable elements, aging, and carcinogenesis. <span>As of 2016, two nucleobases have been found on which natural, enzymatic DNA methylation takes place: adenine and cytosine. The modified bases are N6-methyladenine[1], 5-methylcytosine[2] and N4-methylcytosine.[3] Unmodified base Adenine, A Cytosine, C Modified forms N6-Methyladenine, 6mA 5-Methylcytosine, 5




DNA methylation is a biological process by which methyl groups are added to the DNA molecule.
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DNA methylation - Wikipedia
al process Representation of a DNA molecule that is methylated. The two white spheres represent methyl groups. They are bound to two cytosine nucleotide molecules that make up the DNA sequence. <span>DNA methylation is a biological process by which methyl groups are added to the DNA molecule. Methylation can change the activity of a DNA segment without changing the sequence. When located in a gene promoter, DNA methylation typically acts to repress gene transcription. In mam




Methylation can change the activity of a DNA segment without changing the sequence.
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DNA methylation - Wikipedia
t methyl groups. They are bound to two cytosine nucleotide molecules that make up the DNA sequence. DNA methylation is a biological process by which methyl groups are added to the DNA molecule. <span>Methylation can change the activity of a DNA segment without changing the sequence. When located in a gene promoter, DNA methylation typically acts to repress gene transcription. In mammals, DNA methylation is essential for normal development and is associated with a n