Proto oncogene to onco gene cell signaling
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This document discusses how proto-oncogenes can become cancer-causing oncogenes through mutations or alterations. Proto-oncogenes are normal genes involved in cell growth, but mutations can cause them to produce excess growth proteins. There are two main ways mutations can occur: point mutations involving a single DNA base change, and chromosomal rearrangements like translocations. Point mutations can change amino acids, while rearrangements can fuse genes or place a gene near a strong promoter. Other alterations include deletions removing gene controls, translocations moving a gene to a new location with different expression, and gene amplification through extra DNA replication. Overall, various mutations and alterations can disrupt normal gene expression and regulation, transforming proto-oncogenes into onc
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Oncogenes
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Oncogenes
Cancer is caused by mutations in genes that regulate cell growth and proliferation. These mutations can activate proto-oncogenes into oncogenes or inactivate tumor suppressor genes. Oncogenes promote cell growth while tumor suppressor genes normally inhibit cell proliferation. Common mechanisms of proto-oncogene activation include chromosomal translocations, gene amplifications, and point mutations. Disruptions to cell cycle checkpoints, apoptosis, telomere maintenance and DNA repair pathways can also contribute to cancer development by allowing abnormal cell growth and survival.
tumor suppressor gene, prb, p53 gene
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
Oncogene
Oncogenes are mutated proto-oncogenes that can cause normal cells to become cancerous. Proto-oncogenes regulate cell growth and differentiation and are involved in signal transduction and mitogenic signals. They can become oncogenes through point mutations, increased expression from gene amplification, or chromosomal translocations. The first confirmed oncogene, src, was discovered in 1970. Oncogenes are classified into groups based on their functions, such as secreted growth factors, cell surface receptors, intracellular transducers, and regulators of the cell cycle. The challenge is developing cancer treatments that kill cancer cells without harming healthy cells.
Tumour supressor gene
Tumor suppressor genes regulate cell growth and division. When functioning properly, they inhibit tumor formation but when mutated or inactivated, they lose this ability. Examples include p53, Rb, APC, BRCA1, BRCA2. p53 is mutated in 50% of cancers and regulates DNA repair/cell cycle arrest or apoptosis. Li-Fraumeni syndrome results from germline p53 mutations increasing cancer risk. The APC gene regulates beta-catenin to control cell growth. Mutations in tumor suppressor genes are often required for tumor development according to the two-hit hypothesis as seen with retinoblastoma caused by Rb mutations.
ONCOGENE AND TUMOUR SUPPRESSOR GENE
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
Proto oncogenes
Proto-oncogenes are normal cellular genes that encode proteins involved in cell proliferation. When mutated, they become oncogenes that encode constitutively active oncoproteins driving increased cell growth. Proto-oncogenes can encode growth factors, growth factor receptors, signal transducers, transcription factors, or cell cycle regulators. Common mutations include RAS mutations in pancreatic cancer, BRAF mutations in melanoma, PI3K mutations in breast cancer, and MYC translocations in Burkitt's lymphoma. These mutations result in constitutive activation of signaling pathways that drive uncontrolled cell proliferation.
Dna repair
DNA repair mechanisms identify and correct damage to DNA that occurs due to normal cellular processes and environmental factors. There are two main types of DNA damage: endogenous damage caused by normal cellular processes and exogenous damage caused by external agents like UV radiation and chemicals. The main repair mechanisms are base excision repair, nucleotide excision repair, direct repair via photolyases, and error-prone repair systems like SOS repair. Together, these pathways maintain genome integrity by repairing different types of DNA lesions.
Recommended
Oncogenes
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Oncogenes
Cancer is caused by mutations in genes that regulate cell growth and proliferation. These mutations can activate proto-oncogenes into oncogenes or inactivate tumor suppressor genes. Oncogenes promote cell growth while tumor suppressor genes normally inhibit cell proliferation. Common mechanisms of proto-oncogene activation include chromosomal translocations, gene amplifications, and point mutations. Disruptions to cell cycle checkpoints, apoptosis, telomere maintenance and DNA repair pathways can also contribute to cancer development by allowing abnormal cell growth and survival.
tumor suppressor gene, prb, p53 gene
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
Oncogene
Oncogenes are mutated proto-oncogenes that can cause normal cells to become cancerous. Proto-oncogenes regulate cell growth and differentiation and are involved in signal transduction and mitogenic signals. They can become oncogenes through point mutations, increased expression from gene amplification, or chromosomal translocations. The first confirmed oncogene, src, was discovered in 1970. Oncogenes are classified into groups based on their functions, such as secreted growth factors, cell surface receptors, intracellular transducers, and regulators of the cell cycle. The challenge is developing cancer treatments that kill cancer cells without harming healthy cells.
Tumour supressor gene
Tumor suppressor genes regulate cell growth and division. When functioning properly, they inhibit tumor formation but when mutated or inactivated, they lose this ability. Examples include p53, Rb, APC, BRCA1, BRCA2. p53 is mutated in 50% of cancers and regulates DNA repair/cell cycle arrest or apoptosis. Li-Fraumeni syndrome results from germline p53 mutations increasing cancer risk. The APC gene regulates beta-catenin to control cell growth. Mutations in tumor suppressor genes are often required for tumor development according to the two-hit hypothesis as seen with retinoblastoma caused by Rb mutations.
ONCOGENE AND TUMOUR SUPPRESSOR GENE
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
Proto oncogenes
Proto-oncogenes are normal cellular genes that encode proteins involved in cell proliferation. When mutated, they become oncogenes that encode constitutively active oncoproteins driving increased cell growth. Proto-oncogenes can encode growth factors, growth factor receptors, signal transducers, transcription factors, or cell cycle regulators. Common mutations include RAS mutations in pancreatic cancer, BRAF mutations in melanoma, PI3K mutations in breast cancer, and MYC translocations in Burkitt's lymphoma. These mutations result in constitutive activation of signaling pathways that drive uncontrolled cell proliferation.
Dna repair
DNA repair mechanisms identify and correct damage to DNA that occurs due to normal cellular processes and environmental factors. There are two main types of DNA damage: endogenous damage caused by normal cellular processes and exogenous damage caused by external agents like UV radiation and chemicals. The main repair mechanisms are base excision repair, nucleotide excision repair, direct repair via photolyases, and error-prone repair systems like SOS repair. Together, these pathways maintain genome integrity by repairing different types of DNA lesions.
Oncogenes
This document discusses oncogenes and their role in cancer development. It notes that oncogenes are activated versions of normal cellular genes that regulate cell proliferation, growth, survival and other processes. Oncogenes become activated through genetic mutations, chromosomal translocations, or gene amplification. Some key oncogenes mentioned include Ras, MYC, and BCL2. The document also explains how certain oncogenes contribute to cancer properties like unlimited replication, evading cell death, and stimulating angiogenesis.
Oncogene
Oncogenes are genes that have the potential to cause cancer. They were originally normal proto-oncogenes that became activated through mutations or increased expression. The first confirmed oncogene, SRC, was discovered in 1970 in a chicken retrovirus. Proto-oncogenes stimulate cell division, inhibit differentiation, and prevent apoptosis. They can become oncogenes through point mutations, gene amplification, or chromosomal translocations. When activated, oncogenes result in uncontrolled cell growth and proliferation signals, leading to cancer. Maintaining a healthy lifestyle may help lower the risk of cancer-causing mutations in proto-oncogenes.
tumor suppressor gene, prb, p53
This document summarizes two important tumor suppressor genes - PRB and P53. It provides background on tumor suppressor genes, noting that they function through loss of function to regulate cell cycle and suppress uncontrolled cell proliferation. For PRB, it describes its role in retinoblastoma cancer and cell cycle regulation. For P53, it discusses its role as the "guardian of the genome" in DNA repair and apoptosis, as well as its structure and functions in halting the cell cycle when damage is detected.
Tumour suppressor genes
1. Cancer develops through genetic changes in cells, including mutations in oncogenes and tumor suppressor genes.
2. Tumor suppressor genes normally inhibit cell proliferation and promote apoptosis but their inactivation allows for uncontrolled cell growth.
3. Examples of important tumor suppressor genes discussed include RB, p53, PTEN, BRCA1, and BRCA2. Their protein products regulate processes like cell cycle arrest, DNA repair, and apoptosis.
Sos repair
SOS response was discovered by Miroslav Radman. It's a part of DNA repair system- synthesizes enzymes required for DNA repair. Cellular response to UV damage.
Gene transfer methods @ujjwasirohi
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Site directed mutagenesis
Site-directed mutagenesis is a technique used to introduce specific changes to the DNA sequence of a gene by altering the nucleotide sequence. It allows researchers to study the impact of mutations by changing individual bases, deleting bases, or inserting new bases. There are different methods of site-directed mutagenesis including oligonucleotide-based methods and PCR-based methods. Site-directed mutagenesis has applications in research, production of desired proteins, and development of engineered proteins for commercial uses like detergents.
Oncogene and Proto-oncogene
Proto-oncogenes are normal genes that can become oncogenes following mutations. They encode proteins involved in cell growth, proliferation, differentiation and apoptosis. Examples include HER2, Wnt, Myc, Ras and genes in the Ras signaling pathway. Mutations in proto-oncogenes convert them into oncogenes, driving uncontrolled cell growth and tumor development. Common mutations are point mutations, which result in overactive gene products by altering transcription or protein function. For example, point mutations in Ras genes are found in many cancers and keep the Ras protein constantly active.
Mitochondrial genome
Mitochondria contain their own circular genome that is 16.5kb in size and located in the mitochondrial matrix. The mitochondrial genome contains 37 genes that encode 13 proteins, 22 tRNAs, and 2 rRNAs. These genes help produce enzymes and proteins that are crucial for oxidative phosphorylation and energy production in mitochondria. The control region of mitochondrial DNA contains signals that regulate mitochondrial DNA and RNA synthesis.
ONCOGENES
Oncogenes, tumor suppressor genes, and DNA repair genes all play roles in cancer development. Oncogenes are mutated proto-oncogenes that encode proteins regulating cell growth and proliferation. Their mutation results in uncontrolled cell stimulation and growth. Tumor suppressor genes normally inhibit cell growth and proliferation; their inactivation or deletion allows uncontrolled cell division. DNA repair genes ensure accurate DNA replication; mutations in these genes increase mutations in other genes like proto-oncogenes and tumor suppressor genes, promoting tumorigenesis.
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Cancer genetics
Genetic changes play a key role in cancer development. Cancer arises due to mutations in genes that regulate cell growth, such as oncogenes and tumor suppressor genes. Oncogenes promote cell growth when activated by mutations, while tumor suppressor genes normally inhibit cell growth but require two mutations to be inactivated. Many cancers are caused by the accumulation of both germline and somatic mutations in genes over time. Certain inherited genetic syndromes predispose individuals to specific cancer types if high-risk genes are mutated.
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Dna repair mechanisms
DNA repair mechanisms in prokaryotes involve direct repair, excision repair, and mismatch repair. Direct repair converts damaged nucleotides directly back to their original structure using enzymes like photolyase. Excision repair removes damaged sections of DNA through base excision repair which removes single damaged bases using glycosylases and AP endonucleases, or nucleotide excision repair which removes short oligonucleotides. Mismatch repair recognizes and fixes errors made during DNA replication by distinguishing the parental DNA strands and excising the newly synthesized strand containing mistakes.
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Oncogene and tumor suppressor gene
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The document discusses oncogenes and tumor suppressor genes. It defines proto-oncogenes as genes involved in cell growth that can become activated oncogenes through mutations. Oncogenes are classified into five groups. Tumor suppressor genes normally inhibit tumor formation but mutations inactivate this function in a two-hit model. Examples discussed include HER2/neu, Ras, Myc, Rb, p53, BRCA1, BRCA2, and APC.
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Genetic recombination involves the exchange of genetic material between chromosomes or DNA molecules. It occurs through two main types - homologous recombination, which exchanges DNA between similar sequences, and non-homologous recombination between dissimilar sequences. Recombination is important for genetic diversity, DNA repair, and proper chromosome segregation during cell division. It can happen during both mitosis and meiosis, but only meiotic recombination shuffles genes from parents to offspring. There are also different mechanisms of recombination, including site-specific, transposition, and various DNA repair pathways that facilitate genetic exchange.
Oncogene.pptx
Cancerous studies are essential in this decades and for that primarily we need to know "What is oncogenes".
Factors controlling growth, Oncogenesis
Oncogenesis is the process by which normal cells are transformed into cancer cells. It can occur through changes to cell cycle checkpoints, oncogenes, proto-oncogenes, and tumor suppressor genes. Oncogenes become activated through mutations, gene amplification, or chromosomal rearrangements and cause uncontrolled cell growth. Various factors can damage DNA and cause mutations, such as genome instability, environmental exposures, and viruses. Proper regulation of growth factors, growth factor receptors, signal transducers, transcription factors, and programmed cell death is required to control cell growth and prevent oncogenesis.
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Oncogenes
This document discusses oncogenes and their role in cancer development. It notes that oncogenes are activated versions of normal cellular genes that regulate cell proliferation, growth, survival and other processes. Oncogenes become activated through genetic mutations, chromosomal translocations, or gene amplification. Some key oncogenes mentioned include Ras, MYC, and BCL2. The document also explains how certain oncogenes contribute to cancer properties like unlimited replication, evading cell death, and stimulating angiogenesis.
Oncogene
Oncogenes are genes that have the potential to cause cancer. They were originally normal proto-oncogenes that became activated through mutations or increased expression. The first confirmed oncogene, SRC, was discovered in 1970 in a chicken retrovirus. Proto-oncogenes stimulate cell division, inhibit differentiation, and prevent apoptosis. They can become oncogenes through point mutations, gene amplification, or chromosomal translocations. When activated, oncogenes result in uncontrolled cell growth and proliferation signals, leading to cancer. Maintaining a healthy lifestyle may help lower the risk of cancer-causing mutations in proto-oncogenes.
tumor suppressor gene, prb, p53
This document summarizes two important tumor suppressor genes - PRB and P53. It provides background on tumor suppressor genes, noting that they function through loss of function to regulate cell cycle and suppress uncontrolled cell proliferation. For PRB, it describes its role in retinoblastoma cancer and cell cycle regulation. For P53, it discusses its role as the "guardian of the genome" in DNA repair and apoptosis, as well as its structure and functions in halting the cell cycle when damage is detected.
Tumour suppressor genes
1. Cancer develops through genetic changes in cells, including mutations in oncogenes and tumor suppressor genes.
2. Tumor suppressor genes normally inhibit cell proliferation and promote apoptosis but their inactivation allows for uncontrolled cell growth.
3. Examples of important tumor suppressor genes discussed include RB, p53, PTEN, BRCA1, and BRCA2. Their protein products regulate processes like cell cycle arrest, DNA repair, and apoptosis.
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SOS response was discovered by Miroslav Radman. It's a part of DNA repair system- synthesizes enzymes required for DNA repair. Cellular response to UV damage.
Gene transfer methods @ujjwasirohi
gene transfer methods
transformation methods
ELECTROPORATION,PEG, MICROINJECTION, MACROINJECTION, LIPOSOME MEDIATED, BIOLISTIC GUN, AGROBACTERIUM MEDIATED
Site directed mutagenesis
Site-directed mutagenesis is a technique used to introduce specific changes to the DNA sequence of a gene by altering the nucleotide sequence. It allows researchers to study the impact of mutations by changing individual bases, deleting bases, or inserting new bases. There are different methods of site-directed mutagenesis including oligonucleotide-based methods and PCR-based methods. Site-directed mutagenesis has applications in research, production of desired proteins, and development of engineered proteins for commercial uses like detergents.
Oncogene and Proto-oncogene
Proto-oncogenes are normal genes that can become oncogenes following mutations. They encode proteins involved in cell growth, proliferation, differentiation and apoptosis. Examples include HER2, Wnt, Myc, Ras and genes in the Ras signaling pathway. Mutations in proto-oncogenes convert them into oncogenes, driving uncontrolled cell growth and tumor development. Common mutations are point mutations, which result in overactive gene products by altering transcription or protein function. For example, point mutations in Ras genes are found in many cancers and keep the Ras protein constantly active.
Mitochondrial genome
Mitochondria contain their own circular genome that is 16.5kb in size and located in the mitochondrial matrix. The mitochondrial genome contains 37 genes that encode 13 proteins, 22 tRNAs, and 2 rRNAs. These genes help produce enzymes and proteins that are crucial for oxidative phosphorylation and energy production in mitochondria. The control region of mitochondrial DNA contains signals that regulate mitochondrial DNA and RNA synthesis.
ONCOGENES
Oncogenes, tumor suppressor genes, and DNA repair genes all play roles in cancer development. Oncogenes are mutated proto-oncogenes that encode proteins regulating cell growth and proliferation. Their mutation results in uncontrolled cell stimulation and growth. Tumor suppressor genes normally inhibit cell growth and proliferation; their inactivation or deletion allows uncontrolled cell division. DNA repair genes ensure accurate DNA replication; mutations in these genes increase mutations in other genes like proto-oncogenes and tumor suppressor genes, promoting tumorigenesis.
Polyadenylation
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Transposable elements in Maize And Drosophila
Transposable elements are mobile DNA sequences found in genomes of all organisms. Barbara McClintock discovered transposable elements called Ac and Ds in maize that cause color patterns in corn kernels. Her discovery showed that genes can move within genomes. Experiments with Drosophila revealed another transposable element called P elements that cause hybrid dysgenesis. Transposable elements can provide genetic variation and flexibility that influences evolution.
Cancer genetics
Genetic changes play a key role in cancer development. Cancer arises due to mutations in genes that regulate cell growth, such as oncogenes and tumor suppressor genes. Oncogenes promote cell growth when activated by mutations, while tumor suppressor genes normally inhibit cell growth but require two mutations to be inactivated. Many cancers are caused by the accumulation of both germline and somatic mutations in genes over time. Certain inherited genetic syndromes predispose individuals to specific cancer types if high-risk genes are mutated.
Transfection
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Dna repair mechanisms
DNA repair mechanisms in prokaryotes involve direct repair, excision repair, and mismatch repair. Direct repair converts damaged nucleotides directly back to their original structure using enzymes like photolyase. Excision repair removes damaged sections of DNA through base excision repair which removes single damaged bases using glycosylases and AP endonucleases, or nucleotide excision repair which removes short oligonucleotides. Mismatch repair recognizes and fixes errors made during DNA replication by distinguishing the parental DNA strands and excising the newly synthesized strand containing mistakes.
Mutagens, types of mutations
This document discusses mutagens and types of mutations. It defines mutagens as physical, chemical, or biological agents that cause mutations by altering genes or gene expression. It describes several types of mutagens including radiation, chemicals, viruses and bacteria. It also categorizes different types of mutations including point mutations, frameshift mutations, transitions, transversions, missense mutations and more. Several examples of diseases caused by specific mutations are provided such as sickle cell anemia, cystic fibrosis, and others.
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The document discusses oncogenes and tumor suppressor genes. It defines proto-oncogenes as genes involved in cell growth that can become activated oncogenes through mutations. Oncogenes are classified into five groups. Tumor suppressor genes normally inhibit tumor formation but mutations inactivate this function in a two-hit model. Examples discussed include HER2/neu, Ras, Myc, Rb, p53, BRCA1, BRCA2, and APC.
RNA SPLICING
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Topoisomerase
Topoisomerases are enzymes that alter the supercoiling of DNA by transiently cutting one or both strands of DNA. There are two main types of topoisomerases. Type 1 enzymes remove supercoils by breaking a single DNA strand, while Type 2 enzymes break both strands simultaneously. The regulation of DNA supercoiling by topoisomerases is essential for DNA transcription and replication to occur as it allows unwinding of the DNA helix. Bacteria contain DNA gyrase as their Type 2 topoisomerase, while eukaryotes contain multiple topoisomerase enzymes that can introduce or remove both positive and negative supercoils. Topoisomerases are important drug targets, with inhibitors of bacterial gyrase
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AnswerCellular oncogene formation Carcinogenesis, tumorogenesis .pdf
Answer:
Cellular oncogene formation: Carcinogenesis, tumorogenesis or oncogenesis are developed from
normal cells into a lethal cancer due to the following mechanisms inside the cell.
1. Point mutation: This mutation induces alteration in cellular DNA sequence through
synonymous nucleotide substitution result in normal gene becomes protooncogene finally
become oncogene due to chromosomal DNA replication. For example normal Ras protein
synthesizing gene become mutant Ras oncogene due to point mutation.
2. Gene amplification: This is the process of abnormal amplification of DNA in chromosomes
and generates protooncogenes into oncogenes due to numerous replications of chromosomal
DNA in succession. Example is presence of MYC gene family in lung and breast cancer cells
due to amplied DNA homogeneously.
3. Chromosomal translocation: BCR-ABL leukemia is the due to chromosomal translocation and
meticulous translocation of chromosmomal regions leading to coding of a fusion protein from an
oncogene. Ex. Philadelphia chromosome
4. DNA rearrangement: Insertions, deletions, transposition & inversion of nitrogen bases of
nucleotide sequences in DNA rearrangement generates cellular oncogenes. These rearrangements
are due to exposure of cells to carcinogenic agent
5. Insertional mutagenesis: This type of oncogene development is mainly due to retrovirus as
explained
below
For example:
The genetic changes are expected to alter the activity of the gene product --> loss of
heterozygosity ---> abnormal phenotype
Mutations result in genetic drift, which in turn results in the loss of heterozygosity. This loss of
one parental copy of nucleotide gene bases may lead to the lethal and dangerous consequences of
the living being in the following of life. This loss or drift may result in the occurrence of cancer
(breast cancer) hereditary retinoblastoma, because there may be nonexistence of the functional
tumor suppressor gene in the lost region. One parental copy only can be noticed at that lost
region there by hemizygosity.
But however there is one more functional gene copy inside the genome copy thereby offspring
can get resistance proteins synthesis against the mutation induced cancer.
If both copies are bad or one copy is become badly due to mutation the remaining gene copy
responsible for the tumor growth (the tumor suppressor gene example p53) can be denaturated by
another point mutation, result in complete suppression of gene to protect the body.
A lot of catastrophic events and consequences may occur with loss of heterozygosity (LOH).
Genetic drift results in loss of heterozygosity which may reduce and limit longevity of asexual
organisms in a population there by low population size.
During intermittent cancer development, usually inactivation of the TSG induced due to the two
somatic mutations acting on respective 2 alleles. In contrast, during the familial cancer
development merely one somatic mutation is considerably enough to generate inactivation of
TSG (p.
Oncogenes and tumour suppressor genes
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Oncogenes
This document discusses oncogenes, which are genes that can cause cancer. It defines oncogenes as genes that were originally proto-oncogenes, which are normal genes involved in cell growth that become mutated and cause uncontrolled cell division. The document covers several topics related to oncogenes, including the classes of genes involved in cancer development (proto-oncogenes, tumor suppressor genes, apoptosis genes), the mechanisms by which proto-oncogenes become activated, the properties of cancer cells, and the role of carcinogens and oncogenic retroviruses in cancer development. It also provides examples of specific oncogenes and tumor suppressor genes.
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Mutistep carcinogenesis refers to the process by which normal cells transform into cancerous cells through the accumulation of multiple genetic mutations over time. These mutations can be caused by environmental or inherited factors and affect genes that regulate cell growth (oncogenes) or cell cycle arrest (tumor suppressor genes). The accumulation of mutations in genes that control processes like apoptosis, cell proliferation, and DNA repair enable cells to proliferate uncontrollably and form malignant tumors.
Mutations
Mutations are permanent changes to the nucleotide sequence of genetic material. There are two main types of mutations: chromosomal mutations which involve changes in chromosome structure like deletions, inversions, or duplications, and gene mutations which alter single nucleotides and can be substitutions, insertions, or deletions. Mutations can occur spontaneously during DNA replication or be caused by mutagens like radiation or chemicals. While many mutations are harmful, some can provide benefits for organisms and increase their chances of survival.
ALTERED GENE FUNCTION.pptx
Mutations can occur through various mechanisms that alter the DNA sequence, including substitutions, insertions, deletions, duplications, frameshifts, and loss of heterozygosity. These mutations can change amino acid sequences and cause proteins to malfunction or not function at all. Specific types of mutations include substitutions, in which a single nucleotide is exchanged; deletions, in which a DNA segment is removed; duplications, where a DNA segment is copied multiple times; and translocations, where a DNA segment is moved to a new location. These genetic alterations can contribute to diseases if they impact important genes.
Cancer
Genetics plays a key role in cancer development. Cancer results from mutations in proto-oncogenes, tumor suppressor genes, miRNA genes, and mutator genes. Proto-oncogenes promote cell growth but become oncogenes when mutated. Tumor suppressor genes normally inhibit cell growth but are inactivated by mutations in cancer. The cell cycle is tightly regulated by checkpoints but deregulation can lead to uncontrolled cell division in cancer. Cancers can be caused by inherited genetic mutations or environmental exposures like radiation and carcinogens. The development of cancer typically involves multiple genetic alterations accumulating over time.
Tumor suppressor
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Mutations of na
Mutations are changes in the genetic sequence that can have differing consequences. There are two types of mutations: gene mutations that affect a single gene, and chromosomal mutations that involve changes to whole chromosomes. Mutations can be caused by errors in DNA replication, recombination, chemical or radiation damage to DNA, or defects in DNA repair. Gene mutations can lead to genetic disorders by changing a gene's instructions for making a protein and causing the protein to malfunction or be missing entirely. Most mutations are neutral, but some that dramatically alter protein structure or function can be harmful. Mutations are a source of genetic variability in a species.
Gene regulation
assignment (ppt.) on Gene Regulation: its mechanism,levels and types (gene regulation in prokaryotes and eukaryotes)
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Oncogene
Oncogenes are mutated genes that cause the transformation of normal cells into cancer cells. Proto-oncogenes are normal genes involved in cell growth and proliferation that can become oncogenes when mutated. Oncogenes can be activated by viruses carrying oncogenic genes or through mutations in normal cellular genes, such as point mutations, chromosomal rearrangements, and gene amplifications. Examples of oncogene activation discussed include the viral oncogene v-src carried by Rous sarcoma virus and mutations in the RAS and MYC proto-oncogenes. Oncogenes encode oncoproteins that promote uncontrolled cell growth and division leading to cancer.
mutagenesis and genetic disorders
Mutagenesis is the process of inducing heritable changes in an organism's genetic material through physical or chemical mutagens. Directed mutagenesis specifically alters the DNA sequence to change amino acid coding. There are several types of mutagenesis including directed, random, insertional, and PCR mutagenesis which can be used to study gene function and induce mutations. Common genetic disorders that result from mutations include cystic fibrosis caused by defects in the CFTR gene, sickle cell disease from hemoglobin mutations, and Down syndrome from an extra copy of chromosome 21.
Training on Cancer for Medical Representatives of Pharma Company
The document discusses cancer and the cell cycle. It explains that cancer is uncontrolled cell growth and defines the stages of the normal cell cycle. It then describes how abnormalities can cause cells to continuously divide, leading to cancer. Some of the factors that control cancer development include natural factors, risk factors, and carcinogens. The document outlines the molecular basis of cancer, including oncogenes, tumor suppressor genes, and mechanisms of oncogene activation. It provides examples of oncogenes that can affect growth factors, growth factor receptors, and cytoplasmic proteins.
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Mitotic cell division (2)
The document summarizes the stages of mitotic cell division. It discusses the cell cycle stages of interphase (G1, S, G2 phases) and mitosis (prophase, metaphase, anaphase, telophase). Key events at each mitosis stage are described, such as chromosome condensation in prophase and separation of sister chromatids in anaphase. The significance of mitosis in growth, development, regeneration and asexual reproduction is highlighted. Potential errors in mitosis that can lead to chromosomal abnormalities are also briefly mentioned.
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Dairy science
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Tuberculosis (TB) is an infectious disease that usually affects the lungs. It is caused by the Mycobacterium tuberculosis bacterium and is spread through inhaling droplets from the coughs or sneezes of an infected individual. TB has been present for thousands of years but saw increased cases in the 18th-19th centuries before Robert Koch discovered the bacterial cause in 1882. Proper treatment can cure most TB cases, but drug-resistant strains have emerged, like multidrug-resistant TB, which is difficult to treat.
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The cell cycle is regulated by cyclically operating reaction sequences that trigger and coordinate key events. It is driven by a built-in clock that is adjusted by external stimuli. There are checkpoints at the G1, G2, and M phases to regulate the cell cycle. Cyclin-dependent kinases (CDKs) drive progression through the cell cycle by phosphorylating other proteins when activated by cyclins. CDK-cyclin complexes are major control switches that cause the cell to progress from G1 to G2.
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An introduction to fermentation process
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Proto oncogene to onco gene cell signaling
- 1. WELCOME
- 3. Proto oncogenes are normal genes involved in the cell growth and division. Mutation to a proto oncogene can lead to it to become a cancer-causing oncogene by producing growth stimulating protein that are in excess level. A tumour suppressor gene or anti oncogene is a gene that protect a cell from path to cancer. When this gene is mutated to cause a loss or reduction in its function, the cell can progress to cancer. INTRODUCTION
- 4. An oncogene formed by mechanism encodes an onco protein. Oncogene, that are slightly differs from the normal protein encoded by the corresponding proto oncogene. Normally the oncogenes are not expressed. They arise, the gain of function mutations that convert proto oncogene to oncogene and act dominantly. Mutation is only one of the two alleles is sufficient for induction of cancer.
- 7. HOW DOSE A PROTO ONCOGENE BECOME AN ONCOGENE ? Due to different type of DNA alteration. It is classified into two broad categories, Point mutation Chromosomal Rearrangement
- 8. 1.POINT MUTATION To the substitution of one base for another, resulting in a change in that particular amino acids. Commonly produce a protein that has lost its ability to the regulating by external signalling. In point mutation translate into a changed amino acid that has different biochemical properties than the amino acid the DNA sequence originally encoded for. This change in amino acid can mimic phosphorylation or inhibit binding of negative regulatory molecules, resulting in a constituently active protein.
- 9. 2.CHROMOSOMAL REARRANGEMENT/TRANSLOCATION It produce oncogene in several way I. Fusion of one chromosome to another, result in a strong promoter being placed upstream of a gene that would normally be either absent or present in very low quality. The effect of increasing the intracellular concentration. II. By fusion protein, or proteins that are the product of two separate gene that have been joined.
- 10. ALTERATIONS CHANGING PROTO ONCOGENE INTO ONCOGENE The alterations distinguishing oncogenes from proto oncogene fall into several clearly defined classes involving: 1 Sequence substitution in the gene/coding or its control region. 2 Onco gene created by deletions. 3 Translocations and oncogene formation. 4 Amplification in oncogene production.
- 11. SEQUENCE SUBSTITUTION IN THE GENE/CODING OR ITS CONTROL REGION Mutation altering coding segments, promoter or enhancer are among the most common alterations Eg:Oncogene forms the ras gene associated with human bladder carcinoma ras gene. The alteration cause amino acid substitution in corresponding position in the G protein encoded in the gene.
- 12. Mutation leads to substitution of valine of glycine at position 12 in the amino acid sequence of the encoded or protein. Eg:Human lung cancer ras gene. Leucine for glutamine at position 61 in the encoded G protein.
- 13. ONCOGENE CREATED BY DELETION Deletion of sequences from either control or coding regions eg: myc gene Three exon separated by two introns .Its oncogenic form, first exon and intron and the control sequences in advance of the gene are missing . Deletion of first exon, which is normally copied into the myc mRNA but not translated into a protein sequence, may alter RNA processing to increase the amount of mRNA available to ribosomes in the cytoplasm . Removal of the promoter region of the myc gene does not prevent transcription .
- 14. TRNSLOCATION AND ONCOGENE FORMATION Translocation of gene to a new position in the chromosomes often places the gene in a control environment that is distinctly different from its previous location , may be absent in the new environment causing them to be more active. The gene in its new location become more active by influence of highly active promoter or enhancer of another gene. This translocation may result in uncontrolled cell division.
- 15. Many translocation responsible for gene movement, result of gross exchanger in which whole chromosome segment separate. Some translocation brakes occur in two chromosomes, setting up a reciprocal exchange between chromosome involved eg:1 Leukaemia 2 Burkitt’s lymphoma Reciprocal exchange of chromosome 8 and 14
- 16. AMPLIFICATION IN ONCOGENE PRODUCTION Gene amplification results from over replication of restricted segments of the DNA. The long chromosomes of eukaryotic cells contain multiple sites from which DNA replication of a sub part of the DNA molecule known as replicon.
- 17. Normally each replicon is activated only once during an S period. So that the entire DNA molecule is duplicated only once . Rarely one or more replicons may be activated more than one during an S phase causing amplification, leading to cancer.
- 20. ONCOGENE FORMATION WITHOUT ALTERATION IN GENE SEQUENCES In some instance normal genes are converted to oncogenes without changes in the coding or control sequence of the gene itself . This process term insertional activation.
- 21. THANK YOU