Cancer Biology
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A brief discussion on cancer biology. Vast topic from eric J Hall summarized. Figures in epigenetic slides were explained.
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Cancer biology
This document provides an overview of cancer biology, covering topics such as the definition of cancer, types of cancers like carcinomas and sarcomas, common cancers by incidence rate, key characteristics of specific cancers like lung cancer and colon cancer, cancer genetics including oncogenes and tumor suppressor genes, hallmarks of cancer, and the process of metastasis. It includes descriptions, risk factors, images and literature references.
Hallmarks of cancer
The document summarizes the hallmarks of cancer, which are the key capabilities that enable tumor growth and metastasis. The hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and evading immune destruction. Genomic instability and mutation, and tumor-promoting inflammation also enable cancer's capabilities by altering DNA and creating an inflammatory microenvironment. Targeting these hallmark capabilities is important for cancer therapeutics.
CANCER STEM CELLS
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Cancer biology
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread to other parts of the body.
## To understand how cancer develops and progresses, researchers first need to investigate the biological differences between normal cells and cancer cells. This work focuses on the mechanisms that underlie fundamental processes such as cell growth, the transformation of normal cells to cancer cells, and the spread, or metastasis, of cancer cells.
Cancer biology b7 4 lecures
Cancer is abnormal and uncontrolled cell growth that can invade tissues and spread to other parts of the body. It is caused by changes in gene expression leading to imbalanced cell proliferation and death. The document defines several key cancer-related terms and describes how cancers are classified based on their origin, morphology, grade, and stage. It also lists several hallmarks of cancer cells, including unlimited growth, self-sufficiency, evasion of cell death, angiogenesis, and metastasis.
Molecular Basis of Cancer
Cancer is caused by uncontrolled cell growth and can spread through invasion and metastasis. There are over 200 types of cancer that can affect different parts of the body. The cellular basis of cancer involves a disruption of the normal balance between new cell growth and cell death. Cancer arises due to mutations in genes controlling cell proliferation, which can be caused by carcinogens, radiation, viruses, or heredity. Oncogenes promote cancer by stimulating cell growth and division, while tumor suppressor genes normally inhibit cell proliferation, and inactivation of both copies allows for uncontrolled growth.
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.
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.
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Cancer biology
This document provides an overview of cancer biology, covering topics such as the definition of cancer, types of cancers like carcinomas and sarcomas, common cancers by incidence rate, key characteristics of specific cancers like lung cancer and colon cancer, cancer genetics including oncogenes and tumor suppressor genes, hallmarks of cancer, and the process of metastasis. It includes descriptions, risk factors, images and literature references.
Hallmarks of cancer
The document summarizes the hallmarks of cancer, which are the key capabilities that enable tumor growth and metastasis. The hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and evading immune destruction. Genomic instability and mutation, and tumor-promoting inflammation also enable cancer's capabilities by altering DNA and creating an inflammatory microenvironment. Targeting these hallmark capabilities is important for cancer therapeutics.
CANCER STEM CELLS
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Cancer biology
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread to other parts of the body.
## To understand how cancer develops and progresses, researchers first need to investigate the biological differences between normal cells and cancer cells. This work focuses on the mechanisms that underlie fundamental processes such as cell growth, the transformation of normal cells to cancer cells, and the spread, or metastasis, of cancer cells.
Cancer biology b7 4 lecures
Cancer is abnormal and uncontrolled cell growth that can invade tissues and spread to other parts of the body. It is caused by changes in gene expression leading to imbalanced cell proliferation and death. The document defines several key cancer-related terms and describes how cancers are classified based on their origin, morphology, grade, and stage. It also lists several hallmarks of cancer cells, including unlimited growth, self-sufficiency, evasion of cell death, angiogenesis, and metastasis.
Molecular Basis of Cancer
Cancer is caused by uncontrolled cell growth and can spread through invasion and metastasis. There are over 200 types of cancer that can affect different parts of the body. The cellular basis of cancer involves a disruption of the normal balance between new cell growth and cell death. Cancer arises due to mutations in genes controlling cell proliferation, which can be caused by carcinogens, radiation, viruses, or heredity. Oncogenes promote cancer by stimulating cell growth and division, while tumor suppressor genes normally inhibit cell proliferation, and inactivation of both copies allows for uncontrolled growth.
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.
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.
Chapter 32 invasion and metastasis
The document summarizes the process of cancer metastasis through the invasion-metastasis cascade. It involves 6 key steps: 1) Localized invasion of primary tumor cells aided by loss of cell adhesion molecules and matrix metalloproteinases. 2) Intravasation of tumor cells into blood vessels assisted by tumor-associated macrophages. 3) Transport of circulating tumor cells protected by platelet emboli. 4) Extravasation of tumor cells from vessels into distant tissues. 5) Formation of dormant micrometastases. 6) Rare colonization of micrometastases into macroscopic tumors limited by the foreign tissue environment. Metastasis suppressor genes and strategies targeting multiple steps simultaneously show promise for preventing cancer spread.
Oncogenes
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Cancer Genetics - Denise Sheer
This document provides an overview of the molecular foundations of cancer. It discusses how cancer arises from genetic and epigenetic aberrations that accumulate in cells and lead to altered gene expression and the acquisition of hallmark capabilities that allow tumors to form and progress. Key points covered include the types of genomic changes like mutations and chromosome defects that occur; the roles of oncogenes and tumor suppressor genes; how cancer risk can be inherited; and the uses of genomics in cancer diagnosis and targeted treatment.
Biology of cancer
The document summarizes a presentation on the biology of cancer. It discusses the characteristics of cancer cells, including uncontrolled proliferation and avoidance of apoptosis. It describes different types of cancer classified by position and tissue of origin. The document outlines some of the known causes of cancer including physical, chemical, and biological agents as well as genetic factors. It discusses important cancer-related genes such as oncogenes like ras that promote cancer when mutated, and tumor suppressor genes like p53 and Rb that normally prevent cancer when functioning properly. The presentation covers topics such as molecular basis of cancer, etiology, normal cells versus cancer cells, and treatments.
TUMOR microenvironment
The document summarizes the role of innate and adaptive immune cells in the tumor microenvironment and their effect on tumor growth. It discusses how the tumor microenvironment can influence immune cells and how immune cells can affect tumor progression. Key cells discussed include macrophages, neutrophils, NK cells, T cells, B cells, dendritic cells, and regulatory T cells. It covers topics like hypoxia, inflammation, immune evasion mechanisms used by tumors, and the pro-tumoral phenotypes that immune cells can adopt in the microenvironment.
Role of apoptosis in cancer progression
it gives you answer to the question that why does cell proceed towards carcinogenesis when there are mechanisms to remove cells unfit for survival?
Multistep Carcinogenesis
Mutistep carcinogenesis refers to the process by which normal cells transform into cancerous cells through the accumulation of multiple genetic mutations over time. These mutations can be caused by environmental or inherited factors and affect genes that regulate cell growth (oncogenes) or cell cycle arrest (tumor suppressor genes). The accumulation of mutations in genes that control processes like apoptosis, cell proliferation, and DNA repair enable cells to proliferate uncontrollably and form malignant tumors.
Oncogenes
This document discusses oncogenes and their role in cancer development. It notes that oncogenes are activated versions of normal cellular genes that regulate cell proliferation, growth, survival and other processes. Oncogenes become activated through genetic mutations, chromosomal translocations, or gene amplification. Some key oncogenes mentioned include Ras, MYC, and BCL2. The document also explains how certain oncogenes contribute to cancer properties like unlimited replication, evading cell death, and stimulating angiogenesis.
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.
Telomeres kiran br
1) Telomeres are protective nucleoprotein structures at the ends of chromosomes that shorten with each cell division due to the end replication problem.
2) Telomerase is an enzyme that adds telomeric repeats to chromosome ends to counteract shortening and allow indefinite cell division.
3) Telomerase activation allows cancer cells to avoid replicative senescence and become immortalized, while preceding telomere shortening provides a mechanism for genetic instability and tumor progression.
Oncogenes
Cancer is characterized by uncontrolled cell growth and spread. At the cellular level, cancer cells proliferate excessively, grow in an uncoordinated manner, and infiltrate surrounding tissues. This uncontrolled growth is caused by genetic disorders that affect genes regulating cell growth. Cancer cells lose control over growth and multiplication and do not self-destruct like normal cells. They crowd out healthy cells. Genetic changes can activate oncogenes or inactivate tumor suppressor genes, disrupting the normal balance between cell proliferation and cell death. A variety of genetic, environmental, and viral factors can cause these genetic changes and contribute to cancer development.
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.
tumor suppressor gene, prb, p53 gene
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
Molecular biologyofca csbrp
Oncogenes encode proteins that promote cell growth and inhibit apoptosis. There are four classes of genes that regulate cell growth: proto-oncogenes, tumor suppressor genes, genes that regulate apoptosis, and genes involved in DNA repair. Oncogenes can be activated by mutations, gene fusions, or amplification and drive cancer progression. The products of oncogenes resemble normal growth factors, growth factor receptors, signal transducers, transcription factors, apoptosis regulators, and chromatin remodelers but endow cells with autonomous growth.
Chapter 3.1 tumor angiogneisis
Tumor growth requires angiogenesis to develop new blood vessels. This process is regulated by a balance of pro-angiogenic and anti-angiogenic factors. Tumors disrupt this balance by inducing hypoxia and secreting factors like VEGF, which activate the "angiogenic switch" and promote new vessel growth. This allows tumors to recruit blood vessels to supply nutrients and remove waste. Anti-angiogenic therapies aim to block this process by targeting VEGF and its receptors. Drugs like bevacizumab and sorafenib inhibit angiogenesis to limit tumor growth and progression.
Cancer - Molecular basis
Molecular Basis of Cancer
- Dr. Prabhash Bhavsar
The document discusses the molecular basis of cancer in three parts. It begins by explaining key terms like neoplasm, benign and malignant tumors. It then discusses the fundamental principles of carcinogenesis including genetic damage targeting growth genes and tumor suppressor genes. Finally, it outlines the seven essential alterations for malignant transformation: self-sufficiency in growth signals, insensitivity to growth inhibitors, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, invasion and metastasis, and defects in DNA repair.
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.
Regulation by Wnt Signaling
The Wnt cascade has emerged as a critical regulator of stem cells. In many tissues, activation of Wnt signaling has also been found to be associated with cancer. Understanding the regulation by Wnt signaling may serve as a paradigm for understanding the dual nature of self-renewal signals.
Genomic instability and Cancer
Genomic instability refers to changes in chromosome structure and number that can lead to cancer. It is caused by failures in DNA replication, damage sensing and repair, and cell cycle checkpoints. There are several types of genetic instability, including chromosomal instability (CIN), microsatellite instability (MIN), and DNA replication errors. CIN results in chromosome gains and losses, while MIN causes repetitive DNA expansions and contractions. Genomic instability can arise from defects in DNA damage response genes like p53 and ATM, problems with DNA replication, fragile sites in the genome, and DNA secondary structures. While genetic instability promotes evolution, it also contributes to pathological conditions like cancer by enabling the accumulation of mutations needed for malignant transformation.
Oncogene activation
This document summarizes key concepts regarding oncogenes:
1. Oncogenes are genes that can trigger cancer development through viral insertion or mutation of normal cellular genes.
2. Early retroviruses like RSV were found to contain viral oncogenes like v-src that caused cancer upon infection.
3. Normal cellular genes called proto-oncogenes were later discovered that are homologous to viral oncogenes and can become activated by mutations to drive cancer. Common mutations include point mutations, gene amplifications, and chromosomal translocations.
neoplasia.pptx
This document defines neoplasia and describes the characteristics and classification of tumors. It discusses the components of tumors, benign and malignant tumor nomenclature, criteria to differentiate benign from malignant neoplasms including clinical features, growth rate, microscopy, invasion and metastasis. It also covers tumor markers, immunohistochemistry and cytology methods.
14 march seminar
Cancer is caused by defects in cell division that result from genetic mutations. Normal cell growth becomes unregulated, as cells multiply uncontrollably and crowd out healthy tissue. If cancer cells invade surrounding areas or spread to other parts of the body through metastasis and angiogenesis, it is considered malignant. Staging and grading of tumors helps determine prognosis and appropriate treatment options like surgery, radiation, chemotherapy, or targeted therapies.
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Chapter 32 invasion and metastasis
The document summarizes the process of cancer metastasis through the invasion-metastasis cascade. It involves 6 key steps: 1) Localized invasion of primary tumor cells aided by loss of cell adhesion molecules and matrix metalloproteinases. 2) Intravasation of tumor cells into blood vessels assisted by tumor-associated macrophages. 3) Transport of circulating tumor cells protected by platelet emboli. 4) Extravasation of tumor cells from vessels into distant tissues. 5) Formation of dormant micrometastases. 6) Rare colonization of micrometastases into macroscopic tumors limited by the foreign tissue environment. Metastasis suppressor genes and strategies targeting multiple steps simultaneously show promise for preventing cancer spread.
Oncogenes
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Cancer Genetics - Denise Sheer
This document provides an overview of the molecular foundations of cancer. It discusses how cancer arises from genetic and epigenetic aberrations that accumulate in cells and lead to altered gene expression and the acquisition of hallmark capabilities that allow tumors to form and progress. Key points covered include the types of genomic changes like mutations and chromosome defects that occur; the roles of oncogenes and tumor suppressor genes; how cancer risk can be inherited; and the uses of genomics in cancer diagnosis and targeted treatment.
Biology of cancer
The document summarizes a presentation on the biology of cancer. It discusses the characteristics of cancer cells, including uncontrolled proliferation and avoidance of apoptosis. It describes different types of cancer classified by position and tissue of origin. The document outlines some of the known causes of cancer including physical, chemical, and biological agents as well as genetic factors. It discusses important cancer-related genes such as oncogenes like ras that promote cancer when mutated, and tumor suppressor genes like p53 and Rb that normally prevent cancer when functioning properly. The presentation covers topics such as molecular basis of cancer, etiology, normal cells versus cancer cells, and treatments.
TUMOR microenvironment
The document summarizes the role of innate and adaptive immune cells in the tumor microenvironment and their effect on tumor growth. It discusses how the tumor microenvironment can influence immune cells and how immune cells can affect tumor progression. Key cells discussed include macrophages, neutrophils, NK cells, T cells, B cells, dendritic cells, and regulatory T cells. It covers topics like hypoxia, inflammation, immune evasion mechanisms used by tumors, and the pro-tumoral phenotypes that immune cells can adopt in the microenvironment.
Role of apoptosis in cancer progression
it gives you answer to the question that why does cell proceed towards carcinogenesis when there are mechanisms to remove cells unfit for survival?
Multistep Carcinogenesis
Mutistep carcinogenesis refers to the process by which normal cells transform into cancerous cells through the accumulation of multiple genetic mutations over time. These mutations can be caused by environmental or inherited factors and affect genes that regulate cell growth (oncogenes) or cell cycle arrest (tumor suppressor genes). The accumulation of mutations in genes that control processes like apoptosis, cell proliferation, and DNA repair enable cells to proliferate uncontrollably and form malignant tumors.
Oncogenes
This document discusses oncogenes and their role in cancer development. It notes that oncogenes are activated versions of normal cellular genes that regulate cell proliferation, growth, survival and other processes. Oncogenes become activated through genetic mutations, chromosomal translocations, or gene amplification. Some key oncogenes mentioned include Ras, MYC, and BCL2. The document also explains how certain oncogenes contribute to cancer properties like unlimited replication, evading cell death, and stimulating angiogenesis.
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.
Telomeres kiran br
1) Telomeres are protective nucleoprotein structures at the ends of chromosomes that shorten with each cell division due to the end replication problem.
2) Telomerase is an enzyme that adds telomeric repeats to chromosome ends to counteract shortening and allow indefinite cell division.
3) Telomerase activation allows cancer cells to avoid replicative senescence and become immortalized, while preceding telomere shortening provides a mechanism for genetic instability and tumor progression.
Oncogenes
Cancer is characterized by uncontrolled cell growth and spread. At the cellular level, cancer cells proliferate excessively, grow in an uncoordinated manner, and infiltrate surrounding tissues. This uncontrolled growth is caused by genetic disorders that affect genes regulating cell growth. Cancer cells lose control over growth and multiplication and do not self-destruct like normal cells. They crowd out healthy cells. Genetic changes can activate oncogenes or inactivate tumor suppressor genes, disrupting the normal balance between cell proliferation and cell death. A variety of genetic, environmental, and viral factors can cause these genetic changes and contribute to cancer development.
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.
tumor suppressor gene, prb, p53 gene
Introduction
History
Tumor suppressor gene- pRB
- RB gene
- Role of RB in regulation of cell cycle
- Tumor associated with RB gene mutation
Tumor suppressor gene- p53
- What is p53 gene?
- Function of p53 gene
- How it regulates cell cycle
- What happen if p53 gene inactivated
- Cancer associated with p53 mutation
- Conclusion
- References
Molecular biologyofca csbrp
Oncogenes encode proteins that promote cell growth and inhibit apoptosis. There are four classes of genes that regulate cell growth: proto-oncogenes, tumor suppressor genes, genes that regulate apoptosis, and genes involved in DNA repair. Oncogenes can be activated by mutations, gene fusions, or amplification and drive cancer progression. The products of oncogenes resemble normal growth factors, growth factor receptors, signal transducers, transcription factors, apoptosis regulators, and chromatin remodelers but endow cells with autonomous growth.
Chapter 3.1 tumor angiogneisis
Tumor growth requires angiogenesis to develop new blood vessels. This process is regulated by a balance of pro-angiogenic and anti-angiogenic factors. Tumors disrupt this balance by inducing hypoxia and secreting factors like VEGF, which activate the "angiogenic switch" and promote new vessel growth. This allows tumors to recruit blood vessels to supply nutrients and remove waste. Anti-angiogenic therapies aim to block this process by targeting VEGF and its receptors. Drugs like bevacizumab and sorafenib inhibit angiogenesis to limit tumor growth and progression.
Cancer - Molecular basis
Molecular Basis of Cancer
- Dr. Prabhash Bhavsar
The document discusses the molecular basis of cancer in three parts. It begins by explaining key terms like neoplasm, benign and malignant tumors. It then discusses the fundamental principles of carcinogenesis including genetic damage targeting growth genes and tumor suppressor genes. Finally, it outlines the seven essential alterations for malignant transformation: self-sufficiency in growth signals, insensitivity to growth inhibitors, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, invasion and metastasis, and defects in DNA repair.
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.
Regulation by Wnt Signaling
The Wnt cascade has emerged as a critical regulator of stem cells. In many tissues, activation of Wnt signaling has also been found to be associated with cancer. Understanding the regulation by Wnt signaling may serve as a paradigm for understanding the dual nature of self-renewal signals.
Genomic instability and Cancer
Genomic instability refers to changes in chromosome structure and number that can lead to cancer. It is caused by failures in DNA replication, damage sensing and repair, and cell cycle checkpoints. There are several types of genetic instability, including chromosomal instability (CIN), microsatellite instability (MIN), and DNA replication errors. CIN results in chromosome gains and losses, while MIN causes repetitive DNA expansions and contractions. Genomic instability can arise from defects in DNA damage response genes like p53 and ATM, problems with DNA replication, fragile sites in the genome, and DNA secondary structures. While genetic instability promotes evolution, it also contributes to pathological conditions like cancer by enabling the accumulation of mutations needed for malignant transformation.
Oncogene activation
This document summarizes key concepts regarding oncogenes:
1. Oncogenes are genes that can trigger cancer development through viral insertion or mutation of normal cellular genes.
2. Early retroviruses like RSV were found to contain viral oncogenes like v-src that caused cancer upon infection.
3. Normal cellular genes called proto-oncogenes were later discovered that are homologous to viral oncogenes and can become activated by mutations to drive cancer. Common mutations include point mutations, gene amplifications, and chromosomal translocations.
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1) Tumor suppressor genes normally apply brakes to cell proliferation through proteins that form checkpoints to prevent uncontrolled growth. Loss of function of these genes allows tumor development.
2) The proteins encoded by tumor suppressor genes regulate cell cycle control, apoptosis, and cell survival/growth through mechanisms like transcription factors, cell cycle inhibitors, and DNA damage response.
3) Famous tumor suppressor genes include RB, p53, APC, and WT1. Mutation of both copies is required for loss of function, leading to cancers like retinoblastoma, Li-Fraumeni syndrome, colon cancer, and Wilms tumor.
Cancer and tumor markers
Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
NEOPLASIA: CARCINOGENESIS
Carcinogenesis is a multistep process involving genetic mutations that cause cells to proliferate uncontrollably. There are four classes of regulatory genes involved: 1) growth promoters like proto-oncogenes that become activated oncogenes, 2) inhibitors like tumor suppressor genes, 3) genes regulating apoptosis, and 4) DNA repair genes. Genetic damage occurs through environmental and spontaneous mutations and fails to be repaired if the DNA damage response is defective. This can result in oncogene activation and tumor suppressor inactivation, leading to autonomous growth, evasion of growth inhibition, apoptosis resistance, limitless replication through telomerase expression, angiogenesis, invasion and metastasis. Cancer progression involves the accumulation of additional mutations that
ch7neoplasia-.pptx
This document provides an overview of neoplasia (new abnormal growth) and cancer. It discusses the history and nomenclature of cancer, the difference between benign and malignant tumors, epidemiology, and the molecular basis and hallmarks of cancer development. Specifically, it describes how cancer arises from genetic mutations that cause cells to grow uncontrollably, evade growth controls, develop new blood vessels, and spread to other areas of the body. The document also examines in more detail the roles of tumor suppressor genes like RB and p53, which normally inhibit cell growth but are inactivated in cancer.
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Cancer Biology
- 1. Cancer Biology Dr. Julfikar Saif Phase A, Oncology BSMMU
- 2. Growth disorder • Hypertrophy • Hyperplasia • Metaplasia • Neoplasia
- 3. Neoplasm • A lesion resulting from autonomous or relatively autonomous growth of cells which persist in the same manner even after the initiating stimuli have been removed
- 4. Cancer • Cancer is a genetic disorder caused by DNA mutations.
- 5. Continue…. • Cancer cells are final transformation product of normal cells by a long process called tumorogenesis or carcinogenesis • They have distinct attributes – Gains ‘’darwininian’’ advantage over normal – Ultimately enables growth
- 7. Cell cycle
- 8. Genetic basis of cancer • Two groups of genes working in balance – Oncogene – Tumor suppressor gene
- 9. Genetic basis of cancer…Oncogene…
- 10. Genetic basis of cancer…Oncogene… • Eg – Proviral insertion- no human cancer – Point mutation- N-ras (melanoma) K-ras (pancreatic) H-ras (colon) neu (neuroblastoma)
- 11. Genetic basis of cancer…Oncogene… • Eg – Gene Amplification- N-myc (neuroblastoma) L-myc (Lung) neu (breast) EGFR (NSCLC) – Translocation – bcr-abl (leukemia) bcl2 (DLBCL) c-myc (burkitt lymphoma)
- 12. Genetic basis of cancer…Cont… • Tumor supressor gene – Act in recessive fashion – Somatic homozygosity • One chromosome of a pair is lost • deletion in remaining chromosome
- 13. Genetic basis of cancer…Cont… • Tumor supressor genes are 3 type – Caretaker genes – Gatekeeper genes – Landscaper genes
- 14. Genetic basis of cancer…Cont… • Caretaker gene – DNA repair and stability gene • ATM (Leukemia, Lymphoma) • XP (Skin) • BRCA1,2 (Breast, Ovary ) • hMSH2,6 hMLH1 hPMS1,2 (Colon)
- 15. Genetic basis of cancer…Cont… • Gate keeper gene – rate limiting for tumor growth – Eg- APC, p53 • Landscaper gene – do not directly affect cellular growth – Produce dysfunctional stromal environments conducive to neoplastic growth – Eg PTEN, JPS, UC etc
- 18. Epigenetics • C.H. Waddington coined the term epigenetics • mean above or in addition to genetics to explain differentiation • How do different adult stem cells know their fate? – Myoblasts can only form muscle cells – Keratinocytes only form skin cells – Hematopoetic cells only become blood cells – But all have identical DNA sequences
- 19. Epigenetics
- 20. Epigenetics
- 21. Epigenetics
- 22. Epigenetics
- 23. Epigenetics
- 24. Epigenetics
- 25. Epigenetics
- 26. Epigenetics
- 27. Epigenetics
- 28. Epigenetics
- 29. Epigenetics
- 30. Hallmark of cancer…Cont… • Sustaining proliferative signal • Maybe hypersensitive to growth factor • Autocrinely acting growth factor • Stimulates surrounding tissue to secrete growth factor • May become independent of growth factor
- 31. Hallmark of cancer…Cont… • Evade growth suppressor – Mutation or dysfunction • RB, p53, APC, WT1, BRCA • LKB1, NF2- contact inhibition • TGF-B
- 32. Hallmark of cancer…Cont… • Resisting cell death – Apoptosis- increasing bcl-2 family and decreasing Bax and Bak or TP53 – Autophagy- disrupting PI3K, mTOR – Necrosis- use released cytokines to induce proneoplastic inflammatory environment, angiogenesis and own growth
- 33. Hallmark of cancer…Cont… • Enabling replicative immortality – Normal cells undergo only limited number of divisions before undergoing senescence or crisis/apoptosis due to telomere shortening – Cancer cells express telomerase (90%<)
- 34. Hallmark of cancer…Cont… • Inducing angiogenesis – Charecterestic malignant vessels – enables further growth and metastases – VEGF promotes Thromspondin inhibit
- 35. Hallmark of cancer…Cont… • Activating invasion and metastasis – Decreased adhesion molecules eg E- cadherin – Collective/amoeboid invasion – epithelial–mesenchymal transition
- 36. Hallmark of cancer…Cont… • Reprogramming energy metabolism – Anaerobic glycolysis • Evading immune destruction – Evade survailance – Disable components of immune system
- 37. Miscellaneous • BRCA1, BRCA2 – Functionally, BRCA1 acts as a sensor of DNA damage and replication stress and mediates homologous recombination through BRCA2 – rely on error-prone nonhomologous end-joining (NHEJ)
- 39. Cont… • T-cell checkpoint concept