Brca 1 (breast cancer susceptibility gene-1)
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BRCA-1 is a tumor suppressor gene that regulates cell division and helps repair DNA damage; it exists in two copies inherited from each parent, and variations can render it ineffective, allowing cells with damaged DNA to divide uncontrollably and potentially develop into cancerous cells.
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Li fraumeni Syndrome
Li-Fraumeni syndrome is a rare inherited disorder caused by mutations in the TP53 tumor suppressor gene. It increases the risk of developing several cancers, especially soft tissue sarcomas, osteosarcomas, breast cancer, brain tumors, and adrenocortical carcinoma. The syndrome was first described in 1969 based on studies of families with multiple early-onset cancers. Diagnosis is based on pathogenic variants found in TP53 genetic testing and meeting criteria such as having sarcoma before age 45 and a first-degree relative with cancer before age 45. There is no cure, but some cancers may be treated similarly to other patients while research studies how best to manage cancers associated with Li-Fraumeni syndrome.
5. tumor suppressor genes dr. sinhasan, mdzah
Tumour suppressor genes regulate cell growth and help prevent tumor formation. When both copies of a tumour suppressor gene are inactivated due to mutations or deletions, cancer can develop. Some important tumour suppressor genes include Rb, p53, APC, and WT1. Rb regulates the cell cycle and its inactivation leads to retinoblastoma and other cancers. p53 is called the "guardian of the genome" as it arrests the cell cycle if DNA is damaged and initiates apoptosis; its mutation is common in many cancer types. APC inactivation causes colon polyps and cancer. Loss of tumour suppressor gene function allows abnormal cell growth and proliferation that can form tumors if unchecked.
P53 in hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is the most common form of liver cancer. Mutations in the p53 tumor suppressor gene occur in 25-30% of HCC cases and play an important role in HCC development. p53 helps regulate the cell cycle and induces apoptosis in damaged cells but is inactivated by mutations in HCC. Chronic liver damage from conditions like hepatitis and cirrhosis can also lead to genetic alterations like p53 mutations that promote uncontrolled cell growth and HCC. Targeting the interaction between p53 and its negative regulator MDM2 may help reactivate p53's tumor suppressor functions in HCC cases with wild type p53.
Role of progesterone receptor in bc
Progesterone receptor (PR) plays an important role in breast cancer progression and response to hormone therapy. PR exists as two isoforms, PR-A and PR-B, which act as transcription factors. PR signaling can occur through both nuclear and non-nuclear pathways. While PR expression correlates with better outcomes from hormone therapy, loss of PR is a mechanism of resistance. Targeting the PR pathway through drugs like anti-RANKL agents may be a preventative strategy, while newer endocrine therapies aim to overcome resistance.
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.
Tumor Suppressor Gene
Tumor suppressor genes help repair damaged DNA and inhibit cell proliferation and cancer growth. They fall into two categories: caretaker genes that maintain genome integrity through DNA repair, and gatekeeper genes that inhibit proliferation or promote death of cells with damaged DNA. Key tumor suppressor genes include p53, Rb, APC, WT1, NF1, VHL, p15, p16, BRCA1, BRCA2, and PTEN. Mutation of both copies of a tumor suppressor gene, as with the two-hit hypothesis for retinoblastoma, can lead to uncontrolled cell growth and cancer development.
Factor influencing the diseases conditions
This document discusses factors that influence diseases and conditions. It identifies four main components of factors: predisposing factors which increase susceptibility; enabling factors which facilitate manifestation; precipitating factors associated with disease onset; and reinforcing factors which aggravate disease presence. It also discusses important host factors like sex, age, nutritional status, and genetic makeup that influence exposure, susceptibility, or response to agents. Age is linked to increased risk of various diseases, and children under 5 are most vulnerable to infectious diseases due to immature immune systems. Sex also influences disease susceptibility. Nutritional status and genetic makeup further determine disease risk.
Breast cancer
Breast cancer originates from breast tissue, most commonly from the inner lining of milk ducts or lobules. The breast is made up of a network of mammary ducts that lead to lobes containing lobules, which secrete milk stimulated by hormones. There are several types of breast cancer classified based on the location of origin within the breast tissue and whether they have spread. Factors like family history and genetic mutations can increase breast cancer risk, while lifestyle factors like obesity, alcohol use, and lack of physical activity can also impact risk. Treatment may involve surgery, chemotherapy, radiation therapy, and hormonal therapy depending on the cancer type, stage, and receptor status.
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Li-Fraumeni syndrome is a rare inherited disorder caused by mutations in the TP53 tumor suppressor gene. It increases the risk of developing several cancers, especially soft tissue sarcomas, osteosarcomas, breast cancer, brain tumors, and adrenocortical carcinoma. The syndrome was first described in 1969 based on studies of families with multiple early-onset cancers. Diagnosis is based on pathogenic variants found in TP53 genetic testing and meeting criteria such as having sarcoma before age 45 and a first-degree relative with cancer before age 45. There is no cure, but some cancers may be treated similarly to other patients while research studies how best to manage cancers associated with Li-Fraumeni syndrome.
5. tumor suppressor genes dr. sinhasan, mdzah
Tumour suppressor genes regulate cell growth and help prevent tumor formation. When both copies of a tumour suppressor gene are inactivated due to mutations or deletions, cancer can develop. Some important tumour suppressor genes include Rb, p53, APC, and WT1. Rb regulates the cell cycle and its inactivation leads to retinoblastoma and other cancers. p53 is called the "guardian of the genome" as it arrests the cell cycle if DNA is damaged and initiates apoptosis; its mutation is common in many cancer types. APC inactivation causes colon polyps and cancer. Loss of tumour suppressor gene function allows abnormal cell growth and proliferation that can form tumors if unchecked.
P53 in hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is the most common form of liver cancer. Mutations in the p53 tumor suppressor gene occur in 25-30% of HCC cases and play an important role in HCC development. p53 helps regulate the cell cycle and induces apoptosis in damaged cells but is inactivated by mutations in HCC. Chronic liver damage from conditions like hepatitis and cirrhosis can also lead to genetic alterations like p53 mutations that promote uncontrolled cell growth and HCC. Targeting the interaction between p53 and its negative regulator MDM2 may help reactivate p53's tumor suppressor functions in HCC cases with wild type p53.
Role of progesterone receptor in bc
Progesterone receptor (PR) plays an important role in breast cancer progression and response to hormone therapy. PR exists as two isoforms, PR-A and PR-B, which act as transcription factors. PR signaling can occur through both nuclear and non-nuclear pathways. While PR expression correlates with better outcomes from hormone therapy, loss of PR is a mechanism of resistance. Targeting the PR pathway through drugs like anti-RANKL agents may be a preventative strategy, while newer endocrine therapies aim to overcome resistance.
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.
Tumor Suppressor Gene
Tumor suppressor genes help repair damaged DNA and inhibit cell proliferation and cancer growth. They fall into two categories: caretaker genes that maintain genome integrity through DNA repair, and gatekeeper genes that inhibit proliferation or promote death of cells with damaged DNA. Key tumor suppressor genes include p53, Rb, APC, WT1, NF1, VHL, p15, p16, BRCA1, BRCA2, and PTEN. Mutation of both copies of a tumor suppressor gene, as with the two-hit hypothesis for retinoblastoma, can lead to uncontrolled cell growth and cancer development.
Factor influencing the diseases conditions
This document discusses factors that influence diseases and conditions. It identifies four main components of factors: predisposing factors which increase susceptibility; enabling factors which facilitate manifestation; precipitating factors associated with disease onset; and reinforcing factors which aggravate disease presence. It also discusses important host factors like sex, age, nutritional status, and genetic makeup that influence exposure, susceptibility, or response to agents. Age is linked to increased risk of various diseases, and children under 5 are most vulnerable to infectious diseases due to immature immune systems. Sex also influences disease susceptibility. Nutritional status and genetic makeup further determine disease risk.
Breast cancer
Breast cancer originates from breast tissue, most commonly from the inner lining of milk ducts or lobules. The breast is made up of a network of mammary ducts that lead to lobes containing lobules, which secrete milk stimulated by hormones. There are several types of breast cancer classified based on the location of origin within the breast tissue and whether they have spread. Factors like family history and genetic mutations can increase breast cancer risk, while lifestyle factors like obesity, alcohol use, and lack of physical activity can also impact risk. Treatment may involve surgery, chemotherapy, radiation therapy, and hormonal therapy depending on the cancer type, stage, and receptor status.
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This document discusses hereditary cancer predisposition. It notes that cancer arises from gene mutations, which can be either germline mutations present in eggs or sperm that are heritable, or somatic mutations in non-germline tissues that are not heritable. While all cancer has a genetic basis, not all cancer is inherited. It highlights BRCA1 and BRCA2 as genes commonly associated with hereditary breast and ovarian cancer risk, especially in Ashkenazi Jewish populations. Management options for related cancer risks include surveillance, chemoprevention, and prophylactic surgery. Genetic testing for predisposition involves multiple steps including counseling, consent, testing, and disclosure of results.
Tumor suppressor genes
describe the tumor suppressor genes and examples for downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
P53
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
Fxs 35
Fragile X Syndrome is caused by mutations in the FMR1 gene located on the X chromosome. The most common mutation is a CGG triplet expansion in the 5' untranslated region of the FMR1 gene, which causes hypermethylation and silencing of the gene. This results in reduced or absent production of the fragile X mental retardation protein (FMRP) and leads to excessive mGluR signaling in synapses. Several drug treatments aim to reduce mGluR activity and correct the imbalance, such as mGluR antagonists and drugs that increase GABA or AMPA receptor activity. While data from animal studies of Fragile X Syndrome support the mGluR theory and effectiveness of related drug treatments
Fragile X Syndrome Mutation by Methylation Sensitive PCR
This document discusses the diagnosis of Fragile X syndrome through methylation-sensitive PCR (MS-PCR) testing. It provides background information on the characteristics, inheritance, and FMR1 gene mutation associated with Fragile X syndrome. It then describes the MS-PCR diagnostic method, which analyzes both the methylation status of the FMR1 promoter region and the number of CGG repeats to determine if a sample is normal, a premutation, or has a full mutation associated with Fragile X syndrome. The document concludes by validating the MS-PCR method against the gold standard Southern blot technique.
P53
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
Fragile X Syndrome
Fragile X Syndrome (FXS) is caused by a mutation on the X chromosome involving expansion of the CGG repeat in the FMR1 gene. This leads to hypermethylation and reduced production of the Fragile X Mental Retardation Protein (FMRP). Lack of FMRP results in excessive mGluR signaling and protein synthesis at synapses. FXS is characterized by intellectual disability, autism-like behaviors, and various physical features. Testing involves genetic tests like PCR and Southern blot. Treatment focuses on mGluR antagonists to reduce excessive signaling, with several drugs in clinical trials showing promise based on preclinical findings in animal models of FXS.
Fragile x Syndrome
Fragile X syndrome is caused by the expansion of the CGG trinucleotide repeat on the X chromosome, which results in failure to express the FMR1 protein needed for normal neural development. It is the most common inherited cause of intellectual disability and can also cause autism spectrum disorder. While there is no cure, treatment focuses on behavioral therapy and special education.
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.
Fxs 43
Fragile X Syndrome (FXS) is the most common inherited form of intellectual disability (ID). It is caused by an expansion of CGG repeats on the X chromosome, which can lead to reduced or absent production of the FMRP protein. In males, a full mutation with over 200 CGG repeats typically causes ID, autism, and physical characteristics. In females, the effects are usually more mild. The premutation, between 55-200 repeats, increases risks for disorders like fragile X-associated tremor/ataxia syndrome in older individuals and premature ovarian insufficiency in females. Understanding the molecular basis of FXS continues to provide insights into psychiatry and opportunities for targeted treatments.
Oncogenes
Genes contain DNA instructions that direct cell growth and function. Cancer arises when genes mutate and cells grow out of control. Most cancers are caused by multiple acquired gene mutations over a person's lifetime from environmental exposures or random errors during cell division. Inherited gene mutations can also increase cancer risk if they reduce the body's ability to repair other DNA damage before it transforms cells into cancers. The more a single gene mutation impacts normal gene function, the greater the risk of associated diseases like cancer appearing in carriers of that mutation.
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.
Fragile x syndrome
Fragile X syndrome is caused by a mutation on the FMR1 gene that prevents production of the FMRP protein. Males are more commonly affected and exhibit characteristics like prominent ears, long face, delayed speech, enlarged testes, and autism-like behaviors. Females may show fewer symptoms, with about half having normal intelligence. While there is no single cure, early intervention through education, therapy and medication can help those with Fragile X develop their skills and capabilities.
Fragile X Syndrome
Fragile X syndrome is caused by mutations in the FMR1 gene located on the X chromosome. There are three main types of mutations - normal, premutation, and full mutation - defined by the number of CGG repeats in the FMR1 gene. A full mutation with over 200 CGG repeats causes methylation and silencing of the FMR1 gene, resulting in little or no production of the FMRP protein and causing the symptoms of fragile X syndrome. The document discusses the history, genetics, diagnosis, and effects of fragile X syndrome. It also presents a case study examining the results of prenatal testing for a pregnant woman.
Genetics of cancer
This document summarizes key information about tumor suppressor genes. It discusses retinoblastoma, the first tumor suppressor gene identified. It was found that deletion of the RB gene causes retinoblastoma cancer. The document also describes several other important tumor suppressor genes, such as p53, PTEN, Rb, and INK4. It explains how mutations or deletions in these genes can lead to uncontrolled cell growth and cancer development by disrupting cell cycle regulation and apoptosis.
Chromosomal brekage syndrome
Chromosomal breakage syndromes are a group of rare, inherited disorders characterized by defects in DNA repair that lead to increased cancer risk. The major types discussed were ataxia telangiectasia, Fanconi anemia, Bloom syndrome, and xeroderma pigmentosum. These syndromes are caused by mutations that disrupt critical DNA repair pathways, leading to genomic instability and improper DNA repair. Common features include cancer predisposition, developmental defects, and skin abnormalities like pigmentation changes. Diagnosis involves genetic testing, cytogenetic analysis of chromosome breaks and rearrangements, and assessing clinical manifestations.
Chromosomal breakage syndrome
Chromosomal breakage syndromes are conditions caused by improper DNA repair that lead to genomic instability. They include Louis-Bar syndrome, Fanconi anemia, Bloom syndrome, and Xeroderma pigmentosum. These syndromes are caused by mutations in genes responsible for DNA repair, resulting in an increased risk of cancer due to a failure to repair DNA damage. Common symptoms include bone marrow failure, skin abnormalities like dark spots, neurological issues, and premature aging. Management focuses on protecting skin from sun exposure and treating associated health problems.
FRAGILE X SYNDROME ( FXS ) an inherited cause of mental retardation.
Fragile X syndrome is a genetic condition and the most common inherited cause of intellectual disability. It is caused by a mutation on the X chromosome that results in reduced production of the FMRP protein, important for neural development. Signs may include prominent ears, long face, joint flexibility, and cognitive impairment. Diagnosis is made through genetic testing. While there is no cure, treatment aims to manage symptoms through education, therapy and medication. Ongoing research studies new drugs that target underlying mechanisms.
Fragile x syndrome
Fragile X syndrome is a genetic disorder caused by a mutation on the X chromosome involving expansion of the CGG repeat region in the FMR1 gene. This results in reduced or absent FMRP protein which is important for neural development. Symptoms can include intellectual disabilities, autism-like behaviors, large testes in males, and physical features like prominent ears and flat feet. It is typically diagnosed through genetic testing. While there is no cure, early intervention including therapies can help maximize learning and development.
Fs54 fragile x syndrome..inheritance
- Fragile X syndrome is caused by a change in the FMR-1 gene on the X chromosome that disrupts production of the FMRP protein. It is characterized by learning difficulties, behavioral issues, and particular physical features.
- It affects around 1 in 4,000 males and between 1 in 5,000 to 1 in 8,000 females. The condition can range from mild to severe intellectual disability.
- The number of CGG repeats in the FMR-1 gene determines its classification as normal, premutation, or full mutation, and the associated effects. Males with a full mutation are most severely affected while female carriers may be unaffected or mildly affected.
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.
TUMOR SUPRESSOR GENES
A CLEAR EXPLANATION OF TUMOR SUPRESSOR GENES AND explanation of different examples and cancers about them
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Ganz 2 13-13
This document discusses hereditary cancer predisposition. It notes that cancer arises from gene mutations, which can be either germline mutations present in eggs or sperm that are heritable, or somatic mutations in non-germline tissues that are not heritable. While all cancer has a genetic basis, not all cancer is inherited. It highlights BRCA1 and BRCA2 as genes commonly associated with hereditary breast and ovarian cancer risk, especially in Ashkenazi Jewish populations. Management options for related cancer risks include surveillance, chemoprevention, and prophylactic surgery. Genetic testing for predisposition involves multiple steps including counseling, consent, testing, and disclosure of results.
Tumor suppressor genes
describe the tumor suppressor genes and examples for downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
P53
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
Fxs 35
Fragile X Syndrome is caused by mutations in the FMR1 gene located on the X chromosome. The most common mutation is a CGG triplet expansion in the 5' untranslated region of the FMR1 gene, which causes hypermethylation and silencing of the gene. This results in reduced or absent production of the fragile X mental retardation protein (FMRP) and leads to excessive mGluR signaling in synapses. Several drug treatments aim to reduce mGluR activity and correct the imbalance, such as mGluR antagonists and drugs that increase GABA or AMPA receptor activity. While data from animal studies of Fragile X Syndrome support the mGluR theory and effectiveness of related drug treatments
Fragile X Syndrome Mutation by Methylation Sensitive PCR
This document discusses the diagnosis of Fragile X syndrome through methylation-sensitive PCR (MS-PCR) testing. It provides background information on the characteristics, inheritance, and FMR1 gene mutation associated with Fragile X syndrome. It then describes the MS-PCR diagnostic method, which analyzes both the methylation status of the FMR1 promoter region and the number of CGG repeats to determine if a sample is normal, a premutation, or has a full mutation associated with Fragile X syndrome. The document concludes by validating the MS-PCR method against the gold standard Southern blot technique.
P53
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
Fragile X Syndrome
Fragile X Syndrome (FXS) is caused by a mutation on the X chromosome involving expansion of the CGG repeat in the FMR1 gene. This leads to hypermethylation and reduced production of the Fragile X Mental Retardation Protein (FMRP). Lack of FMRP results in excessive mGluR signaling and protein synthesis at synapses. FXS is characterized by intellectual disability, autism-like behaviors, and various physical features. Testing involves genetic tests like PCR and Southern blot. Treatment focuses on mGluR antagonists to reduce excessive signaling, with several drugs in clinical trials showing promise based on preclinical findings in animal models of FXS.
Fragile x Syndrome
Fragile X syndrome is caused by the expansion of the CGG trinucleotide repeat on the X chromosome, which results in failure to express the FMR1 protein needed for normal neural development. It is the most common inherited cause of intellectual disability and can also cause autism spectrum disorder. While there is no cure, treatment focuses on behavioral therapy and special education.
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.
Fxs 43
Fragile X Syndrome (FXS) is the most common inherited form of intellectual disability (ID). It is caused by an expansion of CGG repeats on the X chromosome, which can lead to reduced or absent production of the FMRP protein. In males, a full mutation with over 200 CGG repeats typically causes ID, autism, and physical characteristics. In females, the effects are usually more mild. The premutation, between 55-200 repeats, increases risks for disorders like fragile X-associated tremor/ataxia syndrome in older individuals and premature ovarian insufficiency in females. Understanding the molecular basis of FXS continues to provide insights into psychiatry and opportunities for targeted treatments.
Oncogenes
Genes contain DNA instructions that direct cell growth and function. Cancer arises when genes mutate and cells grow out of control. Most cancers are caused by multiple acquired gene mutations over a person's lifetime from environmental exposures or random errors during cell division. Inherited gene mutations can also increase cancer risk if they reduce the body's ability to repair other DNA damage before it transforms cells into cancers. The more a single gene mutation impacts normal gene function, the greater the risk of associated diseases like cancer appearing in carriers of that mutation.
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.
Fragile x syndrome
Fragile X syndrome is caused by a mutation on the FMR1 gene that prevents production of the FMRP protein. Males are more commonly affected and exhibit characteristics like prominent ears, long face, delayed speech, enlarged testes, and autism-like behaviors. Females may show fewer symptoms, with about half having normal intelligence. While there is no single cure, early intervention through education, therapy and medication can help those with Fragile X develop their skills and capabilities.
Fragile X Syndrome
Fragile X syndrome is caused by mutations in the FMR1 gene located on the X chromosome. There are three main types of mutations - normal, premutation, and full mutation - defined by the number of CGG repeats in the FMR1 gene. A full mutation with over 200 CGG repeats causes methylation and silencing of the FMR1 gene, resulting in little or no production of the FMRP protein and causing the symptoms of fragile X syndrome. The document discusses the history, genetics, diagnosis, and effects of fragile X syndrome. It also presents a case study examining the results of prenatal testing for a pregnant woman.
Genetics of cancer
This document summarizes key information about tumor suppressor genes. It discusses retinoblastoma, the first tumor suppressor gene identified. It was found that deletion of the RB gene causes retinoblastoma cancer. The document also describes several other important tumor suppressor genes, such as p53, PTEN, Rb, and INK4. It explains how mutations or deletions in these genes can lead to uncontrolled cell growth and cancer development by disrupting cell cycle regulation and apoptosis.
Chromosomal brekage syndrome
Chromosomal breakage syndromes are a group of rare, inherited disorders characterized by defects in DNA repair that lead to increased cancer risk. The major types discussed were ataxia telangiectasia, Fanconi anemia, Bloom syndrome, and xeroderma pigmentosum. These syndromes are caused by mutations that disrupt critical DNA repair pathways, leading to genomic instability and improper DNA repair. Common features include cancer predisposition, developmental defects, and skin abnormalities like pigmentation changes. Diagnosis involves genetic testing, cytogenetic analysis of chromosome breaks and rearrangements, and assessing clinical manifestations.
Chromosomal breakage syndrome
Chromosomal breakage syndromes are conditions caused by improper DNA repair that lead to genomic instability. They include Louis-Bar syndrome, Fanconi anemia, Bloom syndrome, and Xeroderma pigmentosum. These syndromes are caused by mutations in genes responsible for DNA repair, resulting in an increased risk of cancer due to a failure to repair DNA damage. Common symptoms include bone marrow failure, skin abnormalities like dark spots, neurological issues, and premature aging. Management focuses on protecting skin from sun exposure and treating associated health problems.
FRAGILE X SYNDROME ( FXS ) an inherited cause of mental retardation.
Fragile X syndrome is a genetic condition and the most common inherited cause of intellectual disability. It is caused by a mutation on the X chromosome that results in reduced production of the FMRP protein, important for neural development. Signs may include prominent ears, long face, joint flexibility, and cognitive impairment. Diagnosis is made through genetic testing. While there is no cure, treatment aims to manage symptoms through education, therapy and medication. Ongoing research studies new drugs that target underlying mechanisms.
Fragile x syndrome
Fragile X syndrome is a genetic disorder caused by a mutation on the X chromosome involving expansion of the CGG repeat region in the FMR1 gene. This results in reduced or absent FMRP protein which is important for neural development. Symptoms can include intellectual disabilities, autism-like behaviors, large testes in males, and physical features like prominent ears and flat feet. It is typically diagnosed through genetic testing. While there is no cure, early intervention including therapies can help maximize learning and development.
Fs54 fragile x syndrome..inheritance
- Fragile X syndrome is caused by a change in the FMR-1 gene on the X chromosome that disrupts production of the FMRP protein. It is characterized by learning difficulties, behavioral issues, and particular physical features.
- It affects around 1 in 4,000 males and between 1 in 5,000 to 1 in 8,000 females. The condition can range from mild to severe intellectual disability.
- The number of CGG repeats in the FMR-1 gene determines its classification as normal, premutation, or full mutation, and the associated effects. Males with a full mutation are most severely affected while female carriers may be unaffected or mildly affected.
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Fragile X Syndrome Mutation by Methylation Sensitive PCR
Fragile X Syndrome Mutation by Methylation Sensitive PCR
FRAGILE X SYNDROME ( FXS ) an inherited cause of mental retardation.
FRAGILE X SYNDROME ( FXS ) an inherited cause of mental retardation.
Similar to Brca 1 (breast cancer susceptibility gene-1)
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.
TUMOR SUPRESSOR GENES
A CLEAR EXPLANATION OF TUMOR SUPRESSOR GENES AND explanation of different examples and cancers about them
Tumor Suppressor Genes.pptx
This document summarizes tumor suppressor genes. It begins by defining tumors and genes. Tumor suppressor genes code for proteins that act as brakes on cell division. When mutated, they can no longer slow cell growth, allowing cancer to develop. There are three main types of tumor suppressor gene functions: slowing cell division, repairing DNA damage, and inducing cell death. Famous tumor suppressor genes include RB, p53, BRCA1, and BRCA2. Mutations in these genes are associated with increased cancer risks. Understanding tumor suppressor genes helps explain why cancer therapies don't always provide a cure.
4.Tumour Suppressor genes
Tumor suppressor genes are genes that normally restrain cell growth but whose loss or inactivation can lead to cancer. Two key tumor suppressor genes are RB, which was discovered through studies of retinoblastoma, and p53, which is the most commonly mutated gene in human cancers. Other important tumor suppressor genes include APC, which codes for a protein that inhibits the Wnt signaling pathway and is linked to colon cancer when mutated. Loss of tumor suppressor gene function can cause genetic instability in cells, allowing the accumulation of mutations that drive cancer development.
Basics of Cancer.pptx
This document provides information about the basics of cancer treatment. It defines cancer as abnormal cells that divide uncontrollably and are able to invade other tissues and spread. It describes the main characteristics of tumors. It also covers the types of genes linked to cancer development including tumor suppressor genes and oncogenes. The document discusses the different modalities used to treat cancer, including surgery, chemotherapy, radiation therapy, hormonal therapy, and targeted therapy. It provides details on the various classes and examples of chemotherapy drugs and hormonal therapies used to treat breast and prostate cancer.
Cancer.pptx
Cancer is caused by genetic mutations that cause cells to grow uncontrollably and spread. There are two major classes of cancer genes - oncogenes which stimulate cell growth, and tumor suppressor genes which normally limit cell growth. Cancer can be caused by genetic, infectious, chemical, or physical factors that cause these mutations. Treatment involves surgery, radiation, chemotherapy, hormone therapy, or targeted therapy depending on the cancer type and stage. Chemotherapy uses drugs to destroy cancer cells and works through several mechanisms including alkylating DNA, interfering with cell division, damaging DNA, or stopping cell division.
Cancer Basics.pptx
Cancer is caused by genetic mutations that cause cells to grow uncontrollably and spread. There are two major classes of cancer genes - oncogenes which stimulate cell growth, and tumor suppressor genes which normally limit cell growth. Cancer can be caused by genetic, infectious, or environmental factors. Treatment may involve surgery, radiation, chemotherapy, hormone therapy, or targeted therapy. Chemotherapy uses drugs to destroy cancer cells and works in different phases of the cell cycle. Common drug classes include alkylating agents, antimetabolites, anti-tumor antibiotics, topoisomerase inhibitors, mitotic inhibitors, and corticosteroids.
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.
Cancer genetics and diagnosis
This document discusses cancer genetics and diagnosis. It begins by defining cancer and tumors, explaining that cancer is characterized by uncontrolled cell growth that causes malignant tumors. It then explains that cancer arises from mutations in DNA, particularly in cancer genes like tumor suppressor genes and oncogenes. Tumor suppressor genes normally prevent cell growth but mutations cause loss of function, while oncogenes promote cell growth but mutations result in constant activity. Some cancers are caused by viruses like HPV. Cancer diagnosis is usually based on finding lumps or masses, not genetics. Treatments include surgery, radiation, chemotherapy, anti-angiogenesis drugs, and differentiation therapies.
Cancer by online teaching ot
in this slide we will discuss about normal cellular pathways types and reason of many types of cancer
Tumour supressor genes
p53 and pRB structure function and mechanism of action together with strategy of cancer treatment by p53 and pRB
Da 2
Cancer is caused by uncontrolled cell growth and can spread through the body. There are many types of cancer and symptoms vary by type. Treatments include chemotherapy, radiation, and surgery. Cancer treatments work by manipulating DNA, blocking cell metabolism and growth, disrupting cell division, altering hormone balance, and restricting amino acid supply to cancer cells.
Tumor suppressor genes
Tumor suppressor genes normally control cell growth and division and prevent cancer by repairing DNA damage or inducing apoptosis of damaged cells. Some key tumor suppressor genes discussed are RB, which is mutated in retinoblastoma; p53, which is mutated in many cancers and Li-Fraumeni syndrome; TGF-β, which inhibits cell proliferation and is mutated in several cancers; and APC, which is mutated in colon cancer and causes β-catenin to accumulate and promote cell growth. Other important tumor suppressor genes include BRCA1/2, VHL, WT1/2, and NF1/2. Mutation or loss of these genes allows for uncontrolled cell growth and tumor formation.
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
Cancer-an overview by Prof Viyatprajna Acharya, KIMS, Bhubaneswar
This presentation is targeted for MBBS, MD and BDS students that describes briefly about aetiopathogenesis, tumour markers, anti cancer agents, apoptosis
Cellular and molecular basis pathogenesis of cancer
This document discusses neoplasia and cancer. It defines a neoplasm as abnormal tissue growth that exceeds normal limits. Cancer is the term for malignant tumors. The molecular basis of cancer involves genetic damage to proto-oncogenes, tumor suppressor genes, apoptosis genes, and DNA repair genes. Essential alterations for cancer include self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, defects in DNA repair, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize. Cancer development is a multistep process involving genetic alterations that affect cell cycle regulation, growth signals, tumor suppressor pathways, apoptosis, and DNA repair.
The Genetic Basis of Cancer
Introduction to Cancer
Stem cells and cancer cells
major pathways that lead to formation of tumors.
Tumor Supressors
Colon cancer to prove Knudson hypothesis.
The modern treatments available to treat cancer.
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 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
The Relationship Between Telomerase and Tumor
Tumor is a kind of disease that faces various difficulties for treating because our immune system can not recognize it, and the tumor cell is a permanently dividing cell. Telomerase is essential for the immortalization of tumor cells so that it can serve as a good target for antineoplastic agents.
Similar to Brca 1 (breast cancer susceptibility gene-1) (20)
Cancer-an overview by Prof Viyatprajna Acharya, KIMS, Bhubaneswar
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Cellular and molecular basis pathogenesis of cancer
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Brca 1 (breast cancer susceptibility gene-1)
- 1. BRCA-1(breast cancer susceptibility gene-1): BRCA-1 belongstoa classof genescalled"tumorsuppressorgenes" which are involved in regulating how fast the cell divides. BRCA-1 helpsrepaircome formsof mutationsinthe DNA as if the DNA is damaged BRCA-1 keeps the cell from dividing until the mutation is repaired. There are 2 copies of the BRCA-1 gene in the cells. One inherits one copy from each parent. Unfortunately, there are hundreds of variations of BRCA-1.
- 2. Some regulate the cell cycle more effectivelythanthe others. In other words, some people are born withbetterregulatingandrepairmechanisms thanothers.Andinsome cases mutations may render BRCA-1 gene ineffective.Whenthishappens,cellswithdamagedDNA are allowedtodivide and may cause the cells to be less specialized and develop into cancerous cells.