Cancer slides2013
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Cyclins regulate the cell cycle by signaling when cells should divide and progress through different phases. Internal regulators ensure cells are prepared for mitosis while external regulators control cell division rates in response to contact with other cells or signals. Cancer results from faulty cell cycle control where cells lose the ability to regulate growth and divide uncontrollably, potentially spreading through metastasis to form malignant tumors that displace normal tissue. Causes of cancer include carcinogens, DNA mutations, viruses, heredity, and radiation. Treatments aim to stop cell division through surgery, radiation, or chemotherapy.
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Chpt9.3 cell cycle regulation
The document summarizes key aspects of cell cycle regulation and cancer. It discusses that cells have regulatory checkpoints to monitor the cell cycle. Cancer occurs when there is a failure of regulation, resulting in uncontrolled growth and division that can crowd out normal cells. Cancer cells also demonstrate a lack of contact inhibition and continue dividing even when touching other cells. Cancer is caused by mutations in DNA that control the cell cycle and proteins regulating division.
9.2 Cell Cycle Disrupted
1. The cell cycle, which includes interphase and mitosis, is tightly regulated by checkpoints to ensure errors don't occur.
2. Mutations in genes that control the cell cycle, such as oncogenes and tumor suppressor genes, can disrupt the checkpoints and allow cells to divide uncontrollably, potentially leading to cancer.
3. Viruses, carcinogens, and errors during DNA replication and mitosis can also introduce mutations that disrupt the cell cycle and contribute to cancer development if cells ignore checkpoints and divide excessively.
The Cell Cycle and Cancer
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
Cancer and cell cycle
Cell division must follow the exact steps of mitosis or it can lead to cancer. Cancer cells lose the ability to control their growth and divide uncontrollably, forming tumors that damage surrounding tissues. Cancer cells are able to divide without control by slowing or speeding up the cell cycle and bypassing checkpoints during interphase, mitosis, and cytokinesis. The most common type of skin cancer, melanoma, is caused by DNA damage from UV radiation that causes mutations allowing skin cells to form tumors.
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.
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.
Cell cycle and cancer
The document summarizes key aspects of the cell cycle. It describes the main phases (G1, S, G2, M), as well as checkpoints that regulate progression. Mitosis and cytokinesis are explained. The roles of cyclins, CDKs and CKIs are mentioned. Checkpoints for DNA damage, replication errors and spindle assembly are summarized. The document then briefly discusses how cell cycle dysregulation can lead to cancer, noting examples of proto-oncogenes and tumor suppressor genes that are commonly mutated in cancer.
Cell
This document discusses apoptosis, cancer, and cell death. Apoptosis is programmed cell death that involves caspase activation and the dismantling of cellular proteins. Abnormalities in apoptosis can cause diseases. Cancer arises due to mutations in genes controlling cell growth. Not all mutations cause cancer due to feedback controls and immune surveillance. However, factors like radiation, chemicals, viruses, and heredity can increase mutation rates and cancer risk. Cancer cells have invasive properties that allow them to evade growth limits and spread throughout the body.
Recommended
Chpt9.3 cell cycle regulation
The document summarizes key aspects of cell cycle regulation and cancer. It discusses that cells have regulatory checkpoints to monitor the cell cycle. Cancer occurs when there is a failure of regulation, resulting in uncontrolled growth and division that can crowd out normal cells. Cancer cells also demonstrate a lack of contact inhibition and continue dividing even when touching other cells. Cancer is caused by mutations in DNA that control the cell cycle and proteins regulating division.
9.2 Cell Cycle Disrupted
1. The cell cycle, which includes interphase and mitosis, is tightly regulated by checkpoints to ensure errors don't occur.
2. Mutations in genes that control the cell cycle, such as oncogenes and tumor suppressor genes, can disrupt the checkpoints and allow cells to divide uncontrollably, potentially leading to cancer.
3. Viruses, carcinogens, and errors during DNA replication and mitosis can also introduce mutations that disrupt the cell cycle and contribute to cancer development if cells ignore checkpoints and divide excessively.
The Cell Cycle and Cancer
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
Cancer and cell cycle
Cell division must follow the exact steps of mitosis or it can lead to cancer. Cancer cells lose the ability to control their growth and divide uncontrollably, forming tumors that damage surrounding tissues. Cancer cells are able to divide without control by slowing or speeding up the cell cycle and bypassing checkpoints during interphase, mitosis, and cytokinesis. The most common type of skin cancer, melanoma, is caused by DNA damage from UV radiation that causes mutations allowing skin cells to form tumors.
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.
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.
Cell cycle and cancer
The document summarizes key aspects of the cell cycle. It describes the main phases (G1, S, G2, M), as well as checkpoints that regulate progression. Mitosis and cytokinesis are explained. The roles of cyclins, CDKs and CKIs are mentioned. Checkpoints for DNA damage, replication errors and spindle assembly are summarized. The document then briefly discusses how cell cycle dysregulation can lead to cancer, noting examples of proto-oncogenes and tumor suppressor genes that are commonly mutated in cancer.
Cell
This document discusses apoptosis, cancer, and cell death. Apoptosis is programmed cell death that involves caspase activation and the dismantling of cellular proteins. Abnormalities in apoptosis can cause diseases. Cancer arises due to mutations in genes controlling cell growth. Not all mutations cause cancer due to feedback controls and immune surveillance. However, factors like radiation, chemicals, viruses, and heredity can increase mutation rates and cancer risk. Cancer cells have invasive properties that allow them to evade growth limits and spread throughout the body.
Cancer Biology
Cancer is caused by uncontrolled cell growth and can spread throughout the body. The three main properties of cancer cells are that they grow aggressively, can invade nearby tissues, and may spread (metastasize) to distant areas. Nearly all cancers are caused by genetic abnormalities within cells that affect genes regulating cell growth and death. Some genetic changes are inherited, but many are acquired from environmental exposures like tobacco smoke, radiation, chemicals or infectious agents. Cancer development involves multiple genetic mutations that cause cells to proliferate uncontrollably and evade the immune system.
Cell Cycle
1) The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). Cyclins activate CDKs and drive the cell cycle through different phases like S phase for DNA replication and M phase for mitosis.
2) Tumor suppressor genes like RB1 and p53 regulate the cell cycle and prevent uncontrolled cell division. RB1 regulates the transition from G1 to S phase while p53 acts as a guardian of the genome by inducing cell cycle arrest or apoptosis in response to DNA damage.
3) Oncogenes can mutate normal genes involved in cell cycle regulation, causing uncontrolled cell division and cancer. Growth factors also influence the cell cycle by binding to cell surface receptors and
Basics of cellular aging and
1. Cellular aging results from a progressive decline in the proliferative capacity and lifespan of cells due to accumulation of damage from genetic and environmental factors over time.
2. Key mechanisms of cellular aging include shortening of telomeres, accumulation of aging pigments, free radicals, and changes in gene expression through epigenetic alterations.
3. Apoptosis is a tightly regulated form of programmed cell death where cells activate enzymes to degrade their own nuclear DNA and proteins, then break into fragments that are cleared by phagocytes before potential inflammation from secondary necrosis.
Cell cycle,growth regulation ,molecular basis of cancer by dr.Tasnim
The document discusses cell cycle regulation and carcinogenesis. It can be summarized as follows:
1. The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs), which help cells advance through different stages. External growth factors and internal factors like cyclins and kinases control progression.
2. Carcinogenesis is a multistep process caused by accumulating genetic mutations that alter genes regulating cell growth, apoptosis, and DNA repair. These mutations activate oncogenes and inactivate tumor suppressor genes.
3. For malignant transformation, tumors acquire self-sufficiency in growth signals, insensitivity to growth inhibitors, evasion of apoptosis, limitless replication, angiogenesis, invasion and metastasis
Development of cancer
Cancer is characterized by uncontrolled cell growth and spread. Key points:
- Oncogenes are mutated proto-oncogenes that regulate cell growth. Carcinogens and hereditary factors can cause mutations.
- Cancer cells lack contact inhibition and crowd out healthy cells. They reproduce rapidly, forming tumors.
- Tumors can be benign or malignant, with malignant tumors spreading to other sites (metastasizing).
- Early detection through screening and self-exams improves cancer treatment outcomes. Risk-reducing behaviors include not smoking, limiting alcohol, eating fruits/veggies, wearing sunscreen, and exercising regularly.
Role of Inflammation, Genetics, Epigenetics, and Stem Cells in Tumorigenesis
This is a 2.5 hour presentation on the basic mechanisms of tumorigenesis. It has been used to introduce students to the importance of inflammation, basic concepts/terminology in genetics and epigenetics, and thoughts pertaining to stem cells in tumorigenesis.
Cancer 111
This document discusses the aetiology of neoplasia (tumor development). It identifies several risk factors for cancer development including age, genetics, environment, and lifestyle habits. It describes how various carcinogenic agents like chemicals, radiation, viruses, and hormones can cause DNA damage and genetic mutations over time, leading to cancer initiation and promotion. Specifically, it explains how ionizing radiation, ultraviolet light, viruses, chemicals, and hormones may contribute to cancer development and progression through their effects on DNA and cell proliferation.
Cell aging
- Aging is characterized by a declining ability to respond to stress, increasing homeostatic imbalance, and higher risk of disease. It is a degenerative process with no positive features.
- The main factors that act in the aging process include mitochondrial dysfunction, DNA damage and repair, cell cycle regulation, telomere shortening, and changes in transcription and translation.
- Theories of aging include the molecular gene theory, cellular theories involving free radicals and apoptosis, and evolutionary theories such as antagonistic pleiotropy and mutation accumulation. Apoptosis is programmed cell death while necrosis is unregulated cell death from external factors like toxins.
Lecture 1 cell cycle new
These are Lectures of Basic molecular pharmacology presented by Dr.Omer Yahia In coordination with faculty of pharmacy university of Khartoum, al-Neelen medical research center, GENOM Professional training center and National center of Research (Ministry of science and communication).
Cancer & Oncogenesis (Tumorigenesis)
Cancer arises from uncontrolled cell growth. Malignant tumors can invade other tissues and spread, while benign tumors remain localized. Cancer stem cell hypothesis suggests that cancers originate from mutated adult stem cells that have lost their normal constraints. Tumor cells resemble embryonic cells in their migration and ability to be influenced by their environment - some tumors can be stopped by inducing differentiation of the cancer cells. Cancer development involves a combination of genetic and epigenetic factors, including mutations in oncogenes and tumor suppressor genes as well as epigenetic changes like DNA methylation that regulate these genes.
Physical factors carcino
Physical and chemical factors can cause carcinogenesis. Physical factors include ionizing radiation, ultraviolet radiation, radiofrequency/microwave radiation, electromagnetic fields, asbestos, and nanoparticles. Ionizing radiation can directly damage DNA and induce mutations. UV radiation induces pyrimidine dimers and 6-4 photoproducts in DNA, which can lead to mutations if not repaired. Asbestos fibers can cause DNA damage through reactive oxygen species and inflammation, increasing lung cancer and mesothelioma risk. The document discusses the mechanisms of damage and cancer risks from these physical and chemical carcinogenic factors.
Regulation of DNA synthesis
This document summarizes a lecture on the regulation of DNA synthesis, specifically growth factors and inhibitors. It discusses:
1. Growth factors and inhibitors that control DNA replication within the cell cycle in eukaryotes.
2. Cyclin dependent kinase complexes and MPF that drive the cell into mitosis and prevent re-replication of DNA.
3. The processes of licensing and geminin, which positively and negatively regulate replication through ORC protein complexes, Mcm proteins, and inhibition of Cdt1 by geminin to ensure one round of replication per cell cycle.
Cell cycle dysregulation in cancer
Cell cycle dysregulation is a hallmark of cancer cells. Cancer cells progress relentlessly through rounds of cell division even when it would be more appropriate to pause, exit the cycle, or undergo apoptosis. Progression through the cell cycle is controlled by cyclins and cyclin-dependent kinases and regulated at checkpoints. Three key tumor suppressor genes - RB1, TP53, and CDKN2A - control events in G1 phase and are commonly mutated in cancers. Mutations in these genes allow inappropriate cell cycle progression.
01 Replication and Division of Nuclei and Cells
Cells undergo two types of nuclear division: mitosis and meiosis. Mitosis produces genetically identical daughter cells and allows for growth and tissue repair, while meiosis halves the number of chromosomes to produce gametes for sexual reproduction. Precise nuclear division is important for development, but errors can lead to cancer if mutations cause uncontrolled cell growth and division. Many environmental and inherited factors can increase cancer risks by damaging chromosomes.
8. neoplasia
This document provides an overview of neoplasia (new growth) and cancer. It discusses how cancer is caused by genetic mutations, and how cancer cells acquire properties called cancer hallmarks that allow for abnormalities in cell growth, invasion and metastasis. These properties are driven by mutations in cancer genes like oncogenes and tumor suppressor genes. The document outlines the characteristics of benign and malignant tumors, risk factors for cancer like age, environment and genetics, common precursor lesions, and describes the multistep process of carcinogenesis and the hallmarks of cancer like sustained proliferation and evading growth suppression. Key cancer genes discussed are cyclins/CDKs that regulate the cell cycle, RB which suppresses the cell cycle, and TP53 which
Cancer cell biology
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
12 lectures ppt
The document summarizes key aspects of the cell cycle and cell division. It discusses how cell division results in genetically identical daughter cells through DNA replication and chromosome separation. The mitotic phase alternates with interphase in the cell cycle. Mitosis is divided into prophase, prometaphase, metaphase, anaphase and telophase. Cytokinesis then divides the cytoplasm. The cell cycle is regulated by a molecular control system involving cyclins and cyclin-dependent kinases. Cancer cells exhibit deregulated cell cycle control and proliferation.
Mitosis
Cell division occurs through mitosis and cytokinesis to produce two daughter cells that are identical to the original parent cell. Mitosis involves four phases - prophase, metaphase, anaphase, and telophase - where the genetic material (DNA) is replicated and the chromosomes are separated into two identical sets. Cytokinesis then divides the cytoplasm and organelles to complete the formation of the two new cells from the single original cell. Cell division allows for growth and repair of tissues and is the basic means by which single-celled organisms reproduce asexually.
Neoplasia
Neoplasia refers to new abnormal growth of tissue. A neoplasm is an abnormal mass of tissue that grows in an uncontrolled manner. Neoplasms can be benign (non-cancerous) or malignant (cancerous). The growth of neoplasms is driven by genetic changes that allow the cells to proliferate autonomously. Tumors are monoclonal in origin, arising from a single cell. The hallmarks of neoplasms include persistent and purposeless proliferation, a parasitic nature, progression, and clonal expansion. Tumors are classified based on their tissue of origin and behavior. Malignant tumors can invade surrounding tissues and metastasize to distant sites. The development of neoplasms involves genetic and environmental factors
Cancer character and types
Cancer character and typesMarudhar Kesari Jain College for Women Vaniyambadi - 635 751, Tamil Nadu, INDIA.
Cancer is the uncontrolled growth of abnormal cells anywhere in a body
Causative agents – chemical, toxic compound exposures, ionizing radiation, some pathogens
Most cancer form tumors, but not all tumors are cancerous.
7_Cancer Notes_F11.ppt
1. Cancer cells have lost genetic controls on cell division and are immortal, metastasizing and spreading to other tissues. They have also lost differentiation.
2. The cell cycle is tightly regulated by internal and external signals at checkpoints like G1 to control division. Cancer cells evade these controls.
3. Oncogenes are mutated genes that cause uncontrolled growth, while tumor suppressor genes normally stop division but are inactivated in cancer.
Regulation of the_cell_cycle
The cell cycle is regulated by internal and external factors that control when a cell divides. External factors include cell-cell contact and growth factors, while internal factors include cyclins and kinases that help control the cell cycle. Uncontrolled cell division can lead to cancer as cancer cells divide without regard for growth signals and contact inhibition. Cancer occurs due to mutations in genes that regulate the cell cycle, which can be caused by environmental exposures like radiation, viruses, and carcinogens. Treatment options aim to stop rapidly dividing cells like chemotherapy but may also harm healthy cells.
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Cancer Biology
Cancer is caused by uncontrolled cell growth and can spread throughout the body. The three main properties of cancer cells are that they grow aggressively, can invade nearby tissues, and may spread (metastasize) to distant areas. Nearly all cancers are caused by genetic abnormalities within cells that affect genes regulating cell growth and death. Some genetic changes are inherited, but many are acquired from environmental exposures like tobacco smoke, radiation, chemicals or infectious agents. Cancer development involves multiple genetic mutations that cause cells to proliferate uncontrollably and evade the immune system.
Cell Cycle
1) The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). Cyclins activate CDKs and drive the cell cycle through different phases like S phase for DNA replication and M phase for mitosis.
2) Tumor suppressor genes like RB1 and p53 regulate the cell cycle and prevent uncontrolled cell division. RB1 regulates the transition from G1 to S phase while p53 acts as a guardian of the genome by inducing cell cycle arrest or apoptosis in response to DNA damage.
3) Oncogenes can mutate normal genes involved in cell cycle regulation, causing uncontrolled cell division and cancer. Growth factors also influence the cell cycle by binding to cell surface receptors and
Basics of cellular aging and
1. Cellular aging results from a progressive decline in the proliferative capacity and lifespan of cells due to accumulation of damage from genetic and environmental factors over time.
2. Key mechanisms of cellular aging include shortening of telomeres, accumulation of aging pigments, free radicals, and changes in gene expression through epigenetic alterations.
3. Apoptosis is a tightly regulated form of programmed cell death where cells activate enzymes to degrade their own nuclear DNA and proteins, then break into fragments that are cleared by phagocytes before potential inflammation from secondary necrosis.
Cell cycle,growth regulation ,molecular basis of cancer by dr.Tasnim
The document discusses cell cycle regulation and carcinogenesis. It can be summarized as follows:
1. The cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs), which help cells advance through different stages. External growth factors and internal factors like cyclins and kinases control progression.
2. Carcinogenesis is a multistep process caused by accumulating genetic mutations that alter genes regulating cell growth, apoptosis, and DNA repair. These mutations activate oncogenes and inactivate tumor suppressor genes.
3. For malignant transformation, tumors acquire self-sufficiency in growth signals, insensitivity to growth inhibitors, evasion of apoptosis, limitless replication, angiogenesis, invasion and metastasis
Development of cancer
Cancer is characterized by uncontrolled cell growth and spread. Key points:
- Oncogenes are mutated proto-oncogenes that regulate cell growth. Carcinogens and hereditary factors can cause mutations.
- Cancer cells lack contact inhibition and crowd out healthy cells. They reproduce rapidly, forming tumors.
- Tumors can be benign or malignant, with malignant tumors spreading to other sites (metastasizing).
- Early detection through screening and self-exams improves cancer treatment outcomes. Risk-reducing behaviors include not smoking, limiting alcohol, eating fruits/veggies, wearing sunscreen, and exercising regularly.
Role of Inflammation, Genetics, Epigenetics, and Stem Cells in Tumorigenesis
This is a 2.5 hour presentation on the basic mechanisms of tumorigenesis. It has been used to introduce students to the importance of inflammation, basic concepts/terminology in genetics and epigenetics, and thoughts pertaining to stem cells in tumorigenesis.
Cancer 111
This document discusses the aetiology of neoplasia (tumor development). It identifies several risk factors for cancer development including age, genetics, environment, and lifestyle habits. It describes how various carcinogenic agents like chemicals, radiation, viruses, and hormones can cause DNA damage and genetic mutations over time, leading to cancer initiation and promotion. Specifically, it explains how ionizing radiation, ultraviolet light, viruses, chemicals, and hormones may contribute to cancer development and progression through their effects on DNA and cell proliferation.
Cell aging
- Aging is characterized by a declining ability to respond to stress, increasing homeostatic imbalance, and higher risk of disease. It is a degenerative process with no positive features.
- The main factors that act in the aging process include mitochondrial dysfunction, DNA damage and repair, cell cycle regulation, telomere shortening, and changes in transcription and translation.
- Theories of aging include the molecular gene theory, cellular theories involving free radicals and apoptosis, and evolutionary theories such as antagonistic pleiotropy and mutation accumulation. Apoptosis is programmed cell death while necrosis is unregulated cell death from external factors like toxins.
Lecture 1 cell cycle new
These are Lectures of Basic molecular pharmacology presented by Dr.Omer Yahia In coordination with faculty of pharmacy university of Khartoum, al-Neelen medical research center, GENOM Professional training center and National center of Research (Ministry of science and communication).
Cancer & Oncogenesis (Tumorigenesis)
Cancer arises from uncontrolled cell growth. Malignant tumors can invade other tissues and spread, while benign tumors remain localized. Cancer stem cell hypothesis suggests that cancers originate from mutated adult stem cells that have lost their normal constraints. Tumor cells resemble embryonic cells in their migration and ability to be influenced by their environment - some tumors can be stopped by inducing differentiation of the cancer cells. Cancer development involves a combination of genetic and epigenetic factors, including mutations in oncogenes and tumor suppressor genes as well as epigenetic changes like DNA methylation that regulate these genes.
Physical factors carcino
Physical and chemical factors can cause carcinogenesis. Physical factors include ionizing radiation, ultraviolet radiation, radiofrequency/microwave radiation, electromagnetic fields, asbestos, and nanoparticles. Ionizing radiation can directly damage DNA and induce mutations. UV radiation induces pyrimidine dimers and 6-4 photoproducts in DNA, which can lead to mutations if not repaired. Asbestos fibers can cause DNA damage through reactive oxygen species and inflammation, increasing lung cancer and mesothelioma risk. The document discusses the mechanisms of damage and cancer risks from these physical and chemical carcinogenic factors.
Regulation of DNA synthesis
This document summarizes a lecture on the regulation of DNA synthesis, specifically growth factors and inhibitors. It discusses:
1. Growth factors and inhibitors that control DNA replication within the cell cycle in eukaryotes.
2. Cyclin dependent kinase complexes and MPF that drive the cell into mitosis and prevent re-replication of DNA.
3. The processes of licensing and geminin, which positively and negatively regulate replication through ORC protein complexes, Mcm proteins, and inhibition of Cdt1 by geminin to ensure one round of replication per cell cycle.
Cell cycle dysregulation in cancer
Cell cycle dysregulation is a hallmark of cancer cells. Cancer cells progress relentlessly through rounds of cell division even when it would be more appropriate to pause, exit the cycle, or undergo apoptosis. Progression through the cell cycle is controlled by cyclins and cyclin-dependent kinases and regulated at checkpoints. Three key tumor suppressor genes - RB1, TP53, and CDKN2A - control events in G1 phase and are commonly mutated in cancers. Mutations in these genes allow inappropriate cell cycle progression.
01 Replication and Division of Nuclei and Cells
Cells undergo two types of nuclear division: mitosis and meiosis. Mitosis produces genetically identical daughter cells and allows for growth and tissue repair, while meiosis halves the number of chromosomes to produce gametes for sexual reproduction. Precise nuclear division is important for development, but errors can lead to cancer if mutations cause uncontrolled cell growth and division. Many environmental and inherited factors can increase cancer risks by damaging chromosomes.
8. neoplasia
This document provides an overview of neoplasia (new growth) and cancer. It discusses how cancer is caused by genetic mutations, and how cancer cells acquire properties called cancer hallmarks that allow for abnormalities in cell growth, invasion and metastasis. These properties are driven by mutations in cancer genes like oncogenes and tumor suppressor genes. The document outlines the characteristics of benign and malignant tumors, risk factors for cancer like age, environment and genetics, common precursor lesions, and describes the multistep process of carcinogenesis and the hallmarks of cancer like sustained proliferation and evading growth suppression. Key cancer genes discussed are cyclins/CDKs that regulate the cell cycle, RB which suppresses the cell cycle, and TP53 which
Cancer cell biology
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
12 lectures ppt
The document summarizes key aspects of the cell cycle and cell division. It discusses how cell division results in genetically identical daughter cells through DNA replication and chromosome separation. The mitotic phase alternates with interphase in the cell cycle. Mitosis is divided into prophase, prometaphase, metaphase, anaphase and telophase. Cytokinesis then divides the cytoplasm. The cell cycle is regulated by a molecular control system involving cyclins and cyclin-dependent kinases. Cancer cells exhibit deregulated cell cycle control and proliferation.
Mitosis
Cell division occurs through mitosis and cytokinesis to produce two daughter cells that are identical to the original parent cell. Mitosis involves four phases - prophase, metaphase, anaphase, and telophase - where the genetic material (DNA) is replicated and the chromosomes are separated into two identical sets. Cytokinesis then divides the cytoplasm and organelles to complete the formation of the two new cells from the single original cell. Cell division allows for growth and repair of tissues and is the basic means by which single-celled organisms reproduce asexually.
Neoplasia
Neoplasia refers to new abnormal growth of tissue. A neoplasm is an abnormal mass of tissue that grows in an uncontrolled manner. Neoplasms can be benign (non-cancerous) or malignant (cancerous). The growth of neoplasms is driven by genetic changes that allow the cells to proliferate autonomously. Tumors are monoclonal in origin, arising from a single cell. The hallmarks of neoplasms include persistent and purposeless proliferation, a parasitic nature, progression, and clonal expansion. Tumors are classified based on their tissue of origin and behavior. Malignant tumors can invade surrounding tissues and metastasize to distant sites. The development of neoplasms involves genetic and environmental factors
Cancer character and types
Cancer character and typesMarudhar Kesari Jain College for Women Vaniyambadi - 635 751, Tamil Nadu, INDIA.
Cancer is the uncontrolled growth of abnormal cells anywhere in a body
Causative agents – chemical, toxic compound exposures, ionizing radiation, some pathogens
Most cancer form tumors, but not all tumors are cancerous.
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Cell cycle,growth regulation ,molecular basis of cancer by dr.Tasnim
Cell cycle,growth regulation ,molecular basis of cancer by dr.Tasnim
Role of Inflammation, Genetics, Epigenetics, and Stem Cells in Tumorigenesis
Role of Inflammation, Genetics, Epigenetics, and Stem Cells in Tumorigenesis
Similar to Cancer slides2013
7_Cancer Notes_F11.ppt
1. Cancer cells have lost genetic controls on cell division and are immortal, metastasizing and spreading to other tissues. They have also lost differentiation.
2. The cell cycle is tightly regulated by internal and external signals at checkpoints like G1 to control division. Cancer cells evade these controls.
3. Oncogenes are mutated genes that cause uncontrolled growth, while tumor suppressor genes normally stop division but are inactivated in cancer.
Regulation of the_cell_cycle
The cell cycle is regulated by internal and external factors that control when a cell divides. External factors include cell-cell contact and growth factors, while internal factors include cyclins and kinases that help control the cell cycle. Uncontrolled cell division can lead to cancer as cancer cells divide without regard for growth signals and contact inhibition. Cancer occurs due to mutations in genes that regulate the cell cycle, which can be caused by environmental exposures like radiation, viruses, and carcinogens. Treatment options aim to stop rapidly dividing cells like chemotherapy but may also harm healthy cells.
Cell cycle n its regulation
External and internal factors regulate the cell cycle to control cell division. External factors include cell-cell contact and growth factors that signal cells to divide. Internal factors include cyclins and kinases that help control the cell cycle. Cancer occurs when cell division becomes uncontrolled, potentially forming tumors that are either benign or malignant. Malignant tumors can metastasize by spreading cancerous cells to other parts of the body, making the cancer difficult to treat. Mutations in genes that regulate the cell cycle can cause cancer if they accelerate cell growth or disable cell cycle brakes, which may result from inheritance, exposure to carcinogens like tobacco or radiation, or viruses carrying oncogenes.
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Cells need to divide through the process of mitosis in order to repair and replace damaged or dead cells, to grow and develop, and for sexual reproduction. Mitosis involves the replication of DNA and the division of the cell into two identical daughter cells. The cell cycle is tightly regulated by internal and external factors to ensure proper cell division, growth and function. Deregulation of the cell cycle controls can lead to cancer if cells divide uncontrollably and form tumors that may metastasize and spread to other parts of the body. Treatments for cancer include surgery, chemotherapy, and radiation therapy.
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The cell cycle is regulated by a molecular control system involving cyclins, cyclin-dependent kinases (CdKs), and M-phase promoting factor (MPF). Cyclins and CdKs control progression through the cell cycle by triggering phosphorylation events. MPF triggers mitosis when cyclin levels peak. There are checkpoints at the G1, G2, and M phases to monitor cell growth and DNA replication before allowing division. Cancer cells evade these controls and divide uncontrollably, potentially spreading through metastasis. Treatments target rapidly dividing cells but have side effects due to impacts on normal cells.
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It's given cell cycle also help one in getting idea about what and how is it going on.
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This document discusses anti-cancer therapy and cancer biology. It begins by defining cancer and describing its characteristics, including deregulated cellular processes, uncontrolled proliferation, and potential to metastasize. It then covers topics like the cell cycle, mitosis, mitotic checkpoints, cancer-causing genes, cancer progression, types of cancer, and treatments like surgery, radiation, chemotherapy, and newer targeted therapies. It provides details on mechanisms of chemotherapy drugs and how they work at different phases of the cell cycle to kill cancer cells.
CANCER (Overview).docx
The document discusses cancer epidemiology, etiology, pathophysiology, and carcinogenesis. It notes that the most commonly diagnosed cancers are breast, lung, colorectal, liver, and cervical cancers. Cancer develops through multiple genetic mutations over time from factors like viruses, radiation, chemicals and lifestyle/diet. Carcinogenesis involves initiation of DNA damage, promotion of cell growth, progression to malignancy, and potential metastasis. Cancer development and growth involves deregulated cell proliferation, loss of differentiation, evasion of immune destruction, self-sufficiency in growth signals, insensitivity to anti-growth signals, sustained angiogenesis, and tissue invasion and metastasis.
Biology - Chp 10 - Cell Growth And Reproduction - PowerPoint
The document discusses cell growth and reproduction. It explains that cells divide through the cell cycle to replace old or damaged cells and allow organisms to grow. The cell cycle consists of interphase, where the cell grows and prepares to divide, and mitosis, where the cell nucleus and cytoplasm divide. During mitosis, the genetic material in chromosomes is replicated and then separated, with one set of chromosomes going to each new daughter cell. The cell cycle is tightly regulated by internal and external factors to control cell division and stop growth when needed, such as during wound healing. Cancer occurs when cells lose control over the cell cycle and divide uncontrollably.
cancer how when and what
Cancer is caused by uncontrolled cell growth that can spread to other parts of the body. There are over 100 types of cancer that can affect different parts of the body. The four most common cancers are breast cancer, colon cancer, lung cancer, and prostate cancer. Cancer is treated through surgery, chemotherapy, and radiation therapy depending on the type and stage. Maintaining a healthy lifestyle can help prevent cancer by avoiding risk factors like smoking and excessive sun exposure.
LECTURE 11 CANCER DRUGS, IMMUNOCHEMISTRY and CHEMOCHEMISTRY.docx
LECTURE 11 CANCER: DRUGS, IMMUNOCHEMISTRY and CHEMOCHEMISTRY
A dividing breast cancer cell.
Cancer is the name given to a collection of related diseases. In all types of cancer, some of the body’s cells begin to divide without stopping and spread into surrounding tissues.
Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and divide to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.
When cancer develops, this orderly process breaks down. As cells become more and more abnormal, old or damaged cells survive when they should die, and new cells form when they are not needed. These extra cells can divide without stopping and may form growths called tumors.
Many cancers form solid tumors, which are masses of tissue. Cancers of the blood, such as leukemia, generally do not form solid tumors.
Cancerous tumors are malignant, which means they can spread into, or invade, nearby tissues. In addition, as these tumors grow, some cancer cells can break off and travel to distant places in the body through the blood or the lymph system and form new tumors far from the original tumor.
Unlike malignant tumors, benign tumors do not spread into, or invade, nearby tissues. Benign tumors can sometimes be quite large, however. When removed, they usually don’t grow back, whereas malignant tumors sometimes do. Unlike most benign tumors elsewhere in the body, benign brain tumors can be life threatening.
What are the differences between cancer cells and normal cells?
Cancer cells differ from normal cells in many ways that allow them to grow out of control and become invasive. One important difference is that cancer cells are less specialized than normal cells. That is, whereas normal cells mature into very distinct cell types with specific functions, cancer cells do not. This is one reason that, unlike normal cells, cancer cells continue to divide without stopping.
In addition, cancer cells are able to ignore signals that normally tell cells to stop dividing or that begin a process known as programmed cell death, or apoptosis, which the body uses to get rid of unneeded cells.
Cancer cells may be able to influence the normal cells, molecules, and blood vessels that surround and feed a tumor, an area known as the microenvironment. For instance, cancer cells can induce nearby normal cells to form blood vessels that supply tumors with oxygen and nutrients, which they need to grow. These blood vessels also remove waste products from tumors.
Cancer cells are also often able to evade the immune system, a network of organs, tissues, and specialized cells that protects the body from infections and other conditions. Although the immune system normally removes damaged or abnormal cells from the body, some cancer cells are able to “hide” from the immune system.
Tumors can also use the immune system to stay alive and grow. For example, with.
Cell divison
Cell division occurs through mitosis and binary fission. Mitosis involves nuclear division followed by cytokinesis to produce two identical daughter cells. Binary fission involves bacterial cell replication and division. The cell cycle is tightly regulated by internal and external factors to ensure proper cell growth and division. Disruptions can lead to uncontrolled cell growth and cancer.
TUMOR MARKERS.......................pptx
A tumor marker is a substance found in your blood, urine, or body tissue. The term "tumor markers" may refer to proteins that are made by both healthy
....
Cancer signaling pathway
This document summarizes cancer signaling pathways. It introduces cancer as uncontrolled cell growth that arises from genetic mutations. The main causes of mutations are described as mutagens like radiation, chemicals, viruses, and hereditary factors. The document then discusses signal transduction in cancer, explaining how extracellular signals are converted into cellular responses through ligand-receptor binding and activation of downstream pathways. Common ligands and receptor types involved in cancer signaling are outlined, with a focus on growth factors binding tyrosine kinase receptors to promote proliferation and other responses. References for further information are provided at the end.
cancer cells الخلايا السرطانية الدكتور كرار رأفت علوش < Dr. karrar raafat alwash
Cancer cells are abnormal cells that have undergone genetic mutations causing uncontrolled growth and division. Unlike normal cells, cancer cells do not respond to signals regulating growth and can invade nearby tissues and spread through metastasis. Cancer cells can arise from different tissues and exhibit varied characteristics depending on cancer type. Understanding cancer cell biology and behavior is crucial for developing effective treatments. Ongoing research is providing insights into cancer cell genetics and molecules, enabling personalized treatment approaches targeting cancer cells while sparing healthy cells.
1. Hallmarks of cancer.ppt
The document outlines the eight hallmarks of cancer that enable tumor growth and metastatic spread. These hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, reprogramming energy metabolism, and evading immune destruction. The hallmarks represent biological capabilities that are acquired during the development and progression of cancer and provide an organizing framework for understanding the complexities of the disease.
Cancer
This lecture power point gives the basic and fundamental understanding and management of cancer and its diseases.
And as well as some remedies and recommendations
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Biology - Chp 10 - Cell Growth And Reproduction - PowerPoint
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LECTURE 11 CANCER DRUGS, IMMUNOCHEMISTRY and CHEMOCHEMISTRY.docx
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cancer cells الخلايا السرطانية الدكتور كرار رأفت علوش < Dr. karrar raafat alwash
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Cancer slides2013
- 1. 10-3 Regulating the Cell Cycle Cyclins are proteins that regulate the cell cycle – “Tell” cell when to divide, enter cell cycle phases – Signal spindle formation during Interphase – In addition to cyclins, other proteins also help regulate cycle Internal regulators respond to events inside a cell - check that a cell is prepared for mitosis – spindle fibers, replicated DNA, etc. External regulators are outside signals to speed up/slow down cell division – ie: contact inhibition, wound healing
- 2. Contact Inhibition Most cells will keep dividing until they come in contact with other cells
- 3. What is Cancer? Result of faulty cell cycle – Cells lose ability to control growth – do not respond to regulatory signals – Cells divide out of control – do not spot dividing when come in contact with other cells like normal cells do – Demonstrate bizarre behavior
- 5. What is Cancer? Malignant tumor – Lump resulting from division of cancer cell • Can spread • Displaces normal tissue • Can spread into circulatory system Metastasis – Spread of malignant cells to other tissues Cancers named for where they originate • Non-metastatic, noninvasive tumors are called benign
- 6. What causes Cancer? Causes of cancer – Carcinogens – cancer causing chemicals (tobacco, asbestos) – Mutations in DNA overproduce growth factors (cells keep dividing) OR do not produce suppressors (cells never stop dividing) - a defect in p53 gene – Some viruses – Heredity - genes – Radiation
- 7. Symptoms/Treatments Symptoms vary – Unexplained weight change – Lumps or growths – Abnormal bleeding Treatment – Prevention! (diet, lifestyle, self-examinations) – Surgery/Radiation/Chemotheraphy
- 8. Cancer Treatments GOAL: Stop cells from dividing! – Surgery – remove the cells/tumor – Radiation • High energy radiation disrupts cell division – Chemotherapy • Drugs that disrupt cell division • Anti-mitotic drugs (taxol, vinblastine)