DESH BANDHU GANGWAR presentation on Somatic hypermutation
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Somatic hypermutation (SHM) introduces mutations in antibody genes in B cells, increasing antibody diversity. SHM occurs at a rate 10,000 times higher than the normal mutation rate. These mutations mainly occur in hypervariable regions of antibody genes and result from nucleotide substitutions. Molecules involved in SHM include activation-induced cytidine deaminase and uracil N-glycosylase, which initiate mutations, and mismatch repair proteins, which normally eliminate mutations but instead increase the mutation rate during SHM. Future directions include using SHM to evolve proteins in mammalian cells by integrating target genes in B cells and selecting cells with desired phenotypes.
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Somatic hypermutation
Somatic hypermutation (SHM) introduces mutations in antibody genes in B cells, increasing antibody diversity and affinity for antigens. SHM occurs through the actions of activation-induced cytidine deaminase and other molecules at a rate of 10-3 mutations per base pair, compared to the typical spontaneous mutation rate of 10-8 per base pair. These mutations mainly occur in hypervariable regions of antibody genes and result from nucleotide substitutions. SHM leads to affinity maturation of B cells and increased antibody affinity for antigens. Future directions include using the SHM process to evolve proteins in mammalian cells.
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This document discusses how proto-oncogenes can become oncogenes through mutations or increased expression. Proto-oncogenes code for proteins that promote cell growth or survival, but mutations can cause them to stimulate excessive proliferation. Several factors are involved in activating proto-oncogenes, including point mutations, viruses, gene amplification, and chromosomal rearrangements. Chromosomal translocations can activate proto-oncogenes or create fusion genes with transforming activity. Examples discussed include mutations in RET and Ras proto-oncogenes, and the BCR-ABL fusion gene created by a translocation in chronic myelogenous leukemia.
Hallmarks of cancer
This document discusses the molecular basis of cancer and the hallmarks of cancer. It describes 8 fundamental changes that cancers display, including excessive autonomous growth, evading growth inhibitory signals, and avoiding apoptosis. It explains how proto-oncogenes become oncogenes through mutations like point mutations, deletions, and translocations. Oncogenes cause abnormal cell proliferation through cell signaling pathways like MAPK/ERK and JAK-STAT pathways. Oncogenes encode for oncoproteins that can be growth factors, receptors, signaling proteins, transcription factors, or cell cycle regulators. Mutations in these genes and proteins allow cancer cells to proliferate uncontrollably.
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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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The document discusses several key concepts regarding the molecular basis of cancer including:
1. Cancer is caused by mutations in proto-oncogenes, tumor suppressor genes, DNA repair genes, and apoptotic genes.
2. Self-sufficiency in growth signals is achieved through mutations in proto-oncogenes encoding growth factors, growth factor receptors, signal transducing proteins, and cell cycle regulators.
3. Examples of targeted cancer therapies include monoclonal antibodies, tyrosine kinase inhibitors, hormones, and hormonal agents.
Tumor supressor genes
Tumor suppressor genes normally inhibit cell growth but can be inactivated through mutations, leading to cancer. The retinoblastoma (RB) gene was the first tumor suppressor gene discovered. According to Knudson's two-hit hypothesis, both copies of the RB gene must be inactivated for retinoblastoma to develop, either through two spontaneous mutations or one inherited mutation plus another acquired mutation. The RB protein regulates the cell cycle by binding to the E2F transcription factor and preventing cell cycle progression. RB can be inactivated through mutations in the gene, overexpression of cyclin-dependent kinases, or viral oncoproteins like HPV E7 binding RB instead of E2F. Cancers associated with
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Rituximab added to CHOP chemotherapy for elderly patients with diffuse large B-cell lymphoma significantly improves outcomes including complete response rates, decreases treatment failure and relapse rates, and improves event-free and overall survival compared to CHOP alone, without significantly increasing toxicity. These benefits are sustained over long-term follow up of 10 years. The addition of rituximab improves progression-free and disease-free survival in patients who initially had a complete remission.
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Somatic hypermutation
Somatic hypermutation (SHM) introduces mutations in antibody genes in B cells, increasing antibody diversity and affinity for antigens. SHM occurs through the actions of activation-induced cytidine deaminase and other molecules at a rate of 10-3 mutations per base pair, compared to the typical spontaneous mutation rate of 10-8 per base pair. These mutations mainly occur in hypervariable regions of antibody genes and result from nucleotide substitutions. SHM leads to affinity maturation of B cells and increased antibody affinity for antigens. Future directions include using the SHM process to evolve proteins in mammalian cells.
Oncogenes
This document discusses how proto-oncogenes can become oncogenes through mutations or increased expression. Proto-oncogenes code for proteins that promote cell growth or survival, but mutations can cause them to stimulate excessive proliferation. Several factors are involved in activating proto-oncogenes, including point mutations, viruses, gene amplification, and chromosomal rearrangements. Chromosomal translocations can activate proto-oncogenes or create fusion genes with transforming activity. Examples discussed include mutations in RET and Ras proto-oncogenes, and the BCR-ABL fusion gene created by a translocation in chronic myelogenous leukemia.
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3. Examples of targeted cancer therapies include monoclonal antibodies, tyrosine kinase inhibitors, hormones, and hormonal agents.
Tumor supressor genes
Tumor suppressor genes normally inhibit cell growth but can be inactivated through mutations, leading to cancer. The retinoblastoma (RB) gene was the first tumor suppressor gene discovered. According to Knudson's two-hit hypothesis, both copies of the RB gene must be inactivated for retinoblastoma to develop, either through two spontaneous mutations or one inherited mutation plus another acquired mutation. The RB protein regulates the cell cycle by binding to the E2F transcription factor and preventing cell cycle progression. RB can be inactivated through mutations in the gene, overexpression of cyclin-dependent kinases, or viral oncoproteins like HPV E7 binding RB instead of E2F. Cancers associated with
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it gives you answer to the question that why does cell proceed towards carcinogenesis when there are mechanisms to remove cells unfit for survival?
oncogenes and tumour supressor genes
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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.
Oncogenes
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Gene Mutation - Genetics
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ONCOGENES
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Ras presentation complete
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Introduction
Definition
History
Two hit hypothesis
Functions
Mutation in tumor suppressor genes
What is mutation
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Acquired mutation of TSGs
What is Oncogenes?
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Stop and go signal
Examples of TSGs:
RB-The retinoblastoma gene
P53 protein
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Conclusion
References
Tumor suppressorgenes
1) Tumor suppressor genes normally apply brakes to cell proliferation through proteins that form checkpoints to prevent uncontrolled growth. Loss of function of these genes allows tumor development.
2) The proteins encoded by tumor suppressor genes regulate cell cycle control, apoptosis, and cell survival/growth through mechanisms like transcription factors, cell cycle inhibitors, and DNA damage response.
3) Famous tumor suppressor genes include RB, p53, APC, and WT1. Mutation of both copies is required for loss of function, leading to cancers like retinoblastoma, Li-Fraumeni syndrome, colon cancer, and Wilms tumor.
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.
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Role of p53 gene
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Onocogene and tumor suppressor genes
This document discusses oncogenes and tumor suppressor genes, which are critical cancer genes. It defines oncogenes as mutant, overactive, or overexpressed versions of normal proto-oncogenes, which promote cell growth. Tumor suppressor genes normally inhibit growth or promote cell death. Activation of oncogenes or inactivation of tumor suppressor genes can cause cancer. Examples of important oncogenes discussed include SRC, RAS, and MYC. Key tumor suppressor genes mentioned are P53, RB, and BRCA1/2. The document outlines several mechanisms by which these genes can become mutated and dysfunctional, ultimately leading to uncontrolled cell growth and cancer.
Somatic hypermutation and affinity maturation
This document discusses affinity maturation, which is the process by which B-cells produce antibodies with increased affinity for antigens during an immune response. It occurs through two main processes: somatic hypermutation and clonal selection. Somatic hypermutation introduces mutations in antibody genes, and clonal selection competitively favors B-cells that produce antibodies with higher antigen affinity. Affinity maturation enhances the antibody response and is critical for vaccine-induced immunity.
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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.
Role of apoptosis in cancer progression
it gives you answer to the question that why does cell proceed towards carcinogenesis when there are mechanisms to remove cells unfit for survival?
oncogenes and tumour supressor genes
This document discusses proto-oncogenes, oncogenes, and tumor suppressor genes. Proto-oncogenes are normal genes that regulate cell growth, while oncogenes are mutated proto-oncogenes that contribute to uncontrolled cell growth. The discovery of oncogenes began with Rous sarcoma virus, which was found to contain the viral oncogene v-src. The tumor suppressor gene p53 plays a key role in DNA repair and apoptosis, preventing cancer formation. When mutated, p53 cannot regulate the cell cycle properly, allowing damaged DNA to be passed on and tumors to form.
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.
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.
Gene Mutation - Genetics
A gene mutation is an alteration in DNA sequence that can change a single nucleotide or larger gene segments. The main types of mutations are point mutations, frameshift mutations, and repeat expansions. Point mutations include silent, missense, and nonsense mutations. Missense mutations can be conservative or non-conservative. Frameshift mutations alter the reading frame. Repeat expansions increase repeated DNA sequences. Specific diseases caused by gene mutations discussed include cystic fibrosis, cancer, and sickle cell anemia.
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.
Cancer signal-transduction
This document discusses signal transduction and how it relates to cancer. It describes how growth factors and receptors contribute to normal signal transduction and how this process is deregulated in cancer. It explains that growth factors regulate growth, proliferation and survival, which are all altered in cancer. Several growth factors and receptors that can contribute to oncogenesis are identified. It also summarizes several key intracellular signaling pathways, like MAPK pathways, that are activated by growth factors and can result in the cancer phenotype if altered.
genetic variations and its role in health/ pharmacology
Here is the reference for the above topic. I have collected the maximum information that i got from the internet. If any one need the complete information comment here.
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.
Mutation causing loss of cell cycle
Introduction
Oncogenes and Tumor Suppressor Genes
Overexpression of cyclin D1
Loss of p16 Function
Loss of signalling Contributes to abnormal cell proliferation and malignancy
Summary
Questions
Oncogene and tumor suppressor gene
Oncogene And Tumor Suppressor Gene
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.
Ras presentation complete
The Ras pathway allows cells to respond to external signals by controlling processes like proliferation, survival, and apoptosis. When growth factors bind to receptor tyrosine kinases, it activates Ras which can then activate the MAPK, PI3K, and other pathways to regulate gene expression and cell behavior. Mutations that cause Ras to be constantly active are implicated in many cancers. Inhibiting Ras function through drugs like farnesyltransferase inhibitors may block its ability to drive uncontrolled cell growth.
tumor suppressor gene by
Introduction
Definition
History
Two hit hypothesis
Functions
Mutation in tumor suppressor genes
What is mutation
Inherited mutation of TSGs
Acquired mutation of TSGs
What is Oncogenes?
TSGs and Oncogenes : Brakes and accelerators
Stop and go signal
Examples of TSGs:
RB-The retinoblastoma gene
P53 protein
TSGs &cell suicide
Conclusion
References
Tumor suppressorgenes
1) Tumor suppressor genes normally apply brakes to cell proliferation through proteins that form checkpoints to prevent uncontrolled growth. Loss of function of these genes allows tumor development.
2) The proteins encoded by tumor suppressor genes regulate cell cycle control, apoptosis, and cell survival/growth through mechanisms like transcription factors, cell cycle inhibitors, and DNA damage response.
3) Famous tumor suppressor genes include RB, p53, APC, and WT1. Mutation of both copies is required for loss of function, leading to cancers like retinoblastoma, Li-Fraumeni syndrome, colon cancer, and Wilms tumor.
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.
Hallmarks of cancer
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Microbiology:Tumor Suppressor Genes
This document discusses tumor suppressor genes. It begins by explaining that cancer is caused by genetic mutations, and describes the characteristic properties of cancer cells that result from these genetic changes. It then discusses two classes of genes affected in cancer - oncogenes and tumor suppressor genes. Oncogenes contribute to tumor development, while tumor suppressors support tumor development when their function is lost. The rest of the document provides details on specific tumor suppressor genes like RB, p53, PTEN, NF1, and BRCA1/2; their functions in inhibiting cell growth and proliferation; and the genetic and epigenetic mechanisms by which their inactivation can lead to cancer development.
Role of p53 gene
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Onocogene and tumor suppressor genes
This document discusses oncogenes and tumor suppressor genes, which are critical cancer genes. It defines oncogenes as mutant, overactive, or overexpressed versions of normal proto-oncogenes, which promote cell growth. Tumor suppressor genes normally inhibit growth or promote cell death. Activation of oncogenes or inactivation of tumor suppressor genes can cause cancer. Examples of important oncogenes discussed include SRC, RAS, and MYC. Key tumor suppressor genes mentioned are P53, RB, and BRCA1/2. The document outlines several mechanisms by which these genes can become mutated and dysfunctional, ultimately leading to uncontrolled cell growth and cancer.
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- 1. SOMATIC HYPERMUTATIONSOMATIC HYPERMUTATIONDeshBandhu 10/pbt/006
- 2. Contents 1-Introduction 2-Molecules involve in SHM 3-Model of SHM 4-Future Directions
- 3. Introduction somatic hypermutation (SHM) is a diversity generating, regulated cellular mechanism displayed by the adaptive immune response. Somatic Hypermutation adds diversity in already Rearranged Gene Segments. Somatic hypermutation occurs at a frequency of 10¯3/base pair/ generation, than the spontaneous mutation rate about 10⁻8/bp/generation.
- 4. This Rate is higher hence the name, hypermutation. These mutations occur mostly at “hotspots” in the DNA, known as hypervariable regions. These regions correspond to the complementarity determining regions, the sites involved in antigen recognition on the antibody.
- 5. These mutation result from nucleotide substitution rather than addition or deletion. They influence the process of affinity maturation of B cells. Affinity maturation leads to increase the affinity of antibodies for a particular antigen.
- 8. Molecules involved in SHM IgM antibodies expressing V regions that have undergone SHM, as well as IgG and IgA antibodies with no somatic mutations. Activation-induced cytidinedeaminase: A B cell-specific protein required for SHM. Uracil N-glycosylase: Removing uracil generated by AID deamination.
- 9. Mismatch repair proteins: Mismatch repair (MMR) normally maintains genomic integrity. MMR eliminates mutations that arise spontaneously in the genome. Error-prone DNA polymerases: increase mutation rate.
- 10. Model of somatic hypermutation
- 12. SHM Plateform
- 13. To Produce New Fluorescent Proteins Tsien’s group has cloned a red fluorescent protein (RFP) into human B-cells and allowed them to make variants that could then be isolated based on their colors by flow-cytometry.
- 14. Questions??