This document provides an overview of cancer and its genetic basis. It defines cancer as a genetic disorder where normal cell growth control is lost. Cancer arises due to mutations in genes regulating cell proliferation, development, and other functions. These mutated genes, called oncogenes, promote uncontrolled cell growth. The document discusses various cancer risk factors and causes, including genetic predisposition, carcinogens, viruses, and lifestyle factors. It also describes the roles of oncogenes and tumor suppressor genes in cancer development.
This document summarizes key concepts about cell biology and cancer. It states that cancer results from genetic changes related to cell division, growth control, genetic instability, and other cellular processes. These genetic changes disable normal controls that prevent uncontrolled cell growth and invasion. The abnormalities usually result from mutations in genes regulating cell division. Cancer development involves mutations in tumor suppressor genes and oncogenes. If cancer cells spread to other parts of the body, it can form new tumors in a process called metastasis.
Cancer is disease where cells grows out of control and invade, erode and destroy normal tissues
Normal body cells grow, divide and die in orderly fashion
Cancer cell does not obey this path
Cancer cells don't die (Immortality). They just continue to grow and divide in disorderly fashion
This makes it hard for the body to work the way it should
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.
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Introduction to cancer biology nerdy scientiststazib rahaman
This document discusses cancer initiation, promotion, and progression. It defines initiation as the creation of abnormal DNA from carcinogens. Promoters then stimulate replication of these neoplastic cells and tumor development. Enhancers increase the likelihood that nearby genes will be transcribed. Gene amplification and point mutations can further cancer progression. The document also summarizes a study finding COVID-19 infection is associated with severe outcomes in cancer patients, especially those undergoing immunosuppressive therapy, recommending screening and decreased immunosuppressive treatment during the pandemic.
The document discusses cancer including what it is, different types like carcinomas and sarcomas, how cancers are named based on their location, the process of normal cell growth becoming uncontrolled cancerous growth, how cancers are detected through screening tests, what can cause cancers like viruses, chemicals, radiation, and heredity, and ways to prevent cancers through behaviors like not smoking, limiting sun exposure, and diet.
Introduction
Tumours
Types of Tumours
Formation of Tumours
How cancer cell differ from normal cells
Classification of cancer
The causes of cancer
Viruses and Cancer
Cancer and Gene: A. Oncogene
B. Tumours suppressor gene
Detection and Diagnosis
Therapy of cancer
How can cancer are prevented
Conclusion
References
This document summarizes key concepts about cell biology and cancer. It states that cancer results from genetic changes related to cell division, growth control, genetic instability, and other cellular processes. These genetic changes disable normal controls that prevent uncontrolled cell growth and invasion. The abnormalities usually result from mutations in genes regulating cell division. Cancer development involves mutations in tumor suppressor genes and oncogenes. If cancer cells spread to other parts of the body, it can form new tumors in a process called metastasis.
Cancer is disease where cells grows out of control and invade, erode and destroy normal tissues
Normal body cells grow, divide and die in orderly fashion
Cancer cell does not obey this path
Cancer cells don't die (Immortality). They just continue to grow and divide in disorderly fashion
This makes it hard for the body to work the way it should
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.
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Introduction to cancer biology nerdy scientiststazib rahaman
This document discusses cancer initiation, promotion, and progression. It defines initiation as the creation of abnormal DNA from carcinogens. Promoters then stimulate replication of these neoplastic cells and tumor development. Enhancers increase the likelihood that nearby genes will be transcribed. Gene amplification and point mutations can further cancer progression. The document also summarizes a study finding COVID-19 infection is associated with severe outcomes in cancer patients, especially those undergoing immunosuppressive therapy, recommending screening and decreased immunosuppressive treatment during the pandemic.
The document discusses cancer including what it is, different types like carcinomas and sarcomas, how cancers are named based on their location, the process of normal cell growth becoming uncontrolled cancerous growth, how cancers are detected through screening tests, what can cause cancers like viruses, chemicals, radiation, and heredity, and ways to prevent cancers through behaviors like not smoking, limiting sun exposure, and diet.
Introduction
Tumours
Types of Tumours
Formation of Tumours
How cancer cell differ from normal cells
Classification of cancer
The causes of cancer
Viruses and Cancer
Cancer and Gene: A. Oncogene
B. Tumours suppressor gene
Detection and Diagnosis
Therapy of cancer
How can cancer are prevented
Conclusion
References
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.
This document discusses neoplasia and the molecular basis of cancer. It covers the clinical effects and spread of cancer, including tumor-host relationships and pathological diagnosis. Cancer causes local and systemic effects on the host through fever, weight loss, endocrine/neurologic/hematologic syndromes, and more. Cancer spreads locally through direct extension or metastatically through the blood or lymphatic system. The molecular basis of cancer involves genetic mutations in oncogenes and tumor suppressor genes that deregulate cell growth, proliferation, and apoptosis. Important oncogenes and tumor suppressors are described.
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.
Comprehensive Notes on the Molecular Basis of Cancermeducationdotnet
This document summarizes key aspects of cancer growth and spread. It notes that most benign tumors grow slowly over months to years, while cancers generally grow faster and can metastasize. Cancer stem cells have been identified in some cancers and may sustain tumor growth. Cancers infiltrate and invade surrounding tissue, unlike benign tumors which develop capsules. Metastasis, the growth of secondary tumors in distant sites, is a hallmark of malignancy. Cancers can metastasize through seeding in body cavities, lymphatic spread, or hematogenous spread through the bloodstream.
Radiation can cause both deterministic and stochastic effects. Deterministic effects have a threshold dose and increase in severity with higher doses, while stochastic effects like cancer have no threshold and risk increases with any dose but severity is independent of dose. Studies of radiation exposures from radium dial painters, atomic bomb survivors, and medical treatments provide data showing radiation is a carcinogen and mutagen, and the risk of cancer increases linearly with dose without a threshold. The lifetime cancer risk from radiation is estimated to be 10% per sievert of exposure at high doses.
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.
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.
This document provides information about cancer including definitions, types, signs and symptoms, causes, incidence and mortality rates, and prevention. It defines cancer as uncontrolled growth and spread of abnormal cells. The main types discussed are carcinomas, leukemia, and lymphomas. Signs and symptoms include changes in bowel or bladder habits, unusual bleeding or lumps. Causes mentioned include lifestyle factors like smoking and diet, environmental exposures, and family history or inherited gene mutations. Statistics provided include global cancer incidence and mortality rates by region and for some common cancers. Prevention strategies discussed are avoiding tobacco, eating more plant-based foods, limiting alcohol, wearing sun protection, and regular exercise.
This document discusses the etiology of cancer. It classifies etiological factors into extrinsic (chemical, physical, biological) and intrinsic (genetic, hormonal, immune) factors. Extrinsic factors predominate in causing adult cancers while intrinsic factors are more common in pediatric cancers. Major extrinsic factors include chemicals, radiation, infections, and tobacco. Chemicals can directly or indirectly damage DNA. Radiation can directly or indirectly ionize DNA. Certain viruses and bacteria are associated with specific cancer types. The interaction between multiple genetic and environmental factors usually leads to cancer development.
This document discusses cancer, including the types, causes, symptoms, diagnosis, and treatment. It notes that cancer prevalence is increasing worldwide and especially in developing countries. In India, the major causes of cancer are dietary habits, tobacco, alcohol, radiation, and other pollutants. Recent studies discussed found that lifestyle changes can reduce prostate cancer risk, research aims to suppress brain cancer therapy resistance, and fish oil may reduce breast cancer risk. The conclusion emphasizes controlling cancer risk factors, increasing awareness, and focusing on diet and lifestyle to prevent cancer.
The document discusses different types of cancer including carcinomas, sarcomas, lymphomas, and leukemia. Carcinomas make up 85% of cancers and arise from epithelial cells in organs like the skin, breast, prostate, lung and colon. Sarcomas arise from connective tissues and make up 2% of cancers. Lymphomas affect lymphatic and blood tissues and are 4% of cancers, while leukemia affects white blood cells and is also 4% of cancers. Common cancers in males are lung, prostate, colorectal, stomach and brain, while in females they are breast, colorectal, lung, cervical, brain and ovarian. Causes of cancer include environment, diet, infections, radiation, chemicals
There are many types of cancer treatment that depend on the type and stage of cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplants, and precision medicine. Surgery attempts to remove the entire tumor mass and sometimes lymph nodes, while radiation therapy uses radiation to damage cancer cell DNA. Chemotherapy uses cytotoxic drugs to kill rapidly dividing cells, and can be used with other treatments. Targeted therapy and immunotherapy target specific molecular differences in cancer cells. Hormone therapy slows the growth of cancers that use hormones, and stem cell transplants restore blood-forming stem cells after other treatments destroy them. Precision medicine selects individualized treatments based on the genetics of a patient's cancer.
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.
The document discusses the hallmarks of cancer as proposed by Hanahan and Weinberg. It identifies the eight hallmarks as sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and avoiding immune destruction. It also discusses two enabling characteristics - genome instability and mutation, and tumor-promoting inflammation. Finally, it summarizes how several of these hallmarks, including sustaining proliferative signaling, activating invasion and metastasis, resisting cell death, and genome instability and mutation have been identified in breast cancer and contribute to its heterogeneity and treatment resistance.
Rhabdomyosarcoma is the most common soft tissue sarcoma in children. It arises from skeletal muscle and can occur anywhere in the body. The prognosis depends on the histology, stage, and primary site. Treatment involves surgery, chemotherapy, and radiation therapy. For orbital tumors, biopsy followed by chemotherapy and lower-dose radiation of 45 Gy achieves high cure rates over 90%. For parameningeal head and neck tumors, chemotherapy and higher radiation dose of 50.4 Gy is used due to risk of meningeal spread.
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.
Hallmarks of Cancer - Classical vs Metabolic approachSreepadmanabh M
The document summarizes the "Hallmarks of Cancer" proposed by Douglas Hanahan and Robert Weinberg in 2000. It identified six common traits or hallmarks that allow normal cells to transform into cancer cells: (1) self-sufficiency in growth signals, (2) insensitivity to anti-growth signals, (3) evading apoptosis, (4) limitless replicative potential, (5) sustained angiogenesis, and (6) tissue invasion and metastasis. In 2011, Hanahan proposed four additional hallmarks: deregulated metabolism, immune evasion, severe chromosomal abnormalities, and chronic inflammation inducing cancer. The document discusses evidence that a metabolic approach may provide further insights into understanding cancer.
In this file, you can ref resume materials for supervisor such as resume tips, resume samples, cover letter samples, types of interview questions, supervisor situational interview, supervisor behavioral interview…
Edison F. Gatdula is applying for a position as an IT Specialist. He has a Bachelor's degree in Information Management and experience as a Technical Support Staff, MIS Staff, and current position as an IT Specialist. His skills include knowledge of network cabling, devices, software and hardware installation, computer troubleshooting, backups, Microsoft and Linux operating systems, and basic programming languages.
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.
This document discusses neoplasia and the molecular basis of cancer. It covers the clinical effects and spread of cancer, including tumor-host relationships and pathological diagnosis. Cancer causes local and systemic effects on the host through fever, weight loss, endocrine/neurologic/hematologic syndromes, and more. Cancer spreads locally through direct extension or metastatically through the blood or lymphatic system. The molecular basis of cancer involves genetic mutations in oncogenes and tumor suppressor genes that deregulate cell growth, proliferation, and apoptosis. Important oncogenes and tumor suppressors are described.
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.
Comprehensive Notes on the Molecular Basis of Cancermeducationdotnet
This document summarizes key aspects of cancer growth and spread. It notes that most benign tumors grow slowly over months to years, while cancers generally grow faster and can metastasize. Cancer stem cells have been identified in some cancers and may sustain tumor growth. Cancers infiltrate and invade surrounding tissue, unlike benign tumors which develop capsules. Metastasis, the growth of secondary tumors in distant sites, is a hallmark of malignancy. Cancers can metastasize through seeding in body cavities, lymphatic spread, or hematogenous spread through the bloodstream.
Radiation can cause both deterministic and stochastic effects. Deterministic effects have a threshold dose and increase in severity with higher doses, while stochastic effects like cancer have no threshold and risk increases with any dose but severity is independent of dose. Studies of radiation exposures from radium dial painters, atomic bomb survivors, and medical treatments provide data showing radiation is a carcinogen and mutagen, and the risk of cancer increases linearly with dose without a threshold. The lifetime cancer risk from radiation is estimated to be 10% per sievert of exposure at high doses.
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.
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.
This document provides information about cancer including definitions, types, signs and symptoms, causes, incidence and mortality rates, and prevention. It defines cancer as uncontrolled growth and spread of abnormal cells. The main types discussed are carcinomas, leukemia, and lymphomas. Signs and symptoms include changes in bowel or bladder habits, unusual bleeding or lumps. Causes mentioned include lifestyle factors like smoking and diet, environmental exposures, and family history or inherited gene mutations. Statistics provided include global cancer incidence and mortality rates by region and for some common cancers. Prevention strategies discussed are avoiding tobacco, eating more plant-based foods, limiting alcohol, wearing sun protection, and regular exercise.
This document discusses the etiology of cancer. It classifies etiological factors into extrinsic (chemical, physical, biological) and intrinsic (genetic, hormonal, immune) factors. Extrinsic factors predominate in causing adult cancers while intrinsic factors are more common in pediatric cancers. Major extrinsic factors include chemicals, radiation, infections, and tobacco. Chemicals can directly or indirectly damage DNA. Radiation can directly or indirectly ionize DNA. Certain viruses and bacteria are associated with specific cancer types. The interaction between multiple genetic and environmental factors usually leads to cancer development.
This document discusses cancer, including the types, causes, symptoms, diagnosis, and treatment. It notes that cancer prevalence is increasing worldwide and especially in developing countries. In India, the major causes of cancer are dietary habits, tobacco, alcohol, radiation, and other pollutants. Recent studies discussed found that lifestyle changes can reduce prostate cancer risk, research aims to suppress brain cancer therapy resistance, and fish oil may reduce breast cancer risk. The conclusion emphasizes controlling cancer risk factors, increasing awareness, and focusing on diet and lifestyle to prevent cancer.
The document discusses different types of cancer including carcinomas, sarcomas, lymphomas, and leukemia. Carcinomas make up 85% of cancers and arise from epithelial cells in organs like the skin, breast, prostate, lung and colon. Sarcomas arise from connective tissues and make up 2% of cancers. Lymphomas affect lymphatic and blood tissues and are 4% of cancers, while leukemia affects white blood cells and is also 4% of cancers. Common cancers in males are lung, prostate, colorectal, stomach and brain, while in females they are breast, colorectal, lung, cervical, brain and ovarian. Causes of cancer include environment, diet, infections, radiation, chemicals
There are many types of cancer treatment that depend on the type and stage of cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplants, and precision medicine. Surgery attempts to remove the entire tumor mass and sometimes lymph nodes, while radiation therapy uses radiation to damage cancer cell DNA. Chemotherapy uses cytotoxic drugs to kill rapidly dividing cells, and can be used with other treatments. Targeted therapy and immunotherapy target specific molecular differences in cancer cells. Hormone therapy slows the growth of cancers that use hormones, and stem cell transplants restore blood-forming stem cells after other treatments destroy them. Precision medicine selects individualized treatments based on the genetics of a patient's cancer.
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.
The document discusses the hallmarks of cancer as proposed by Hanahan and Weinberg. It identifies the eight hallmarks as sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and avoiding immune destruction. It also discusses two enabling characteristics - genome instability and mutation, and tumor-promoting inflammation. Finally, it summarizes how several of these hallmarks, including sustaining proliferative signaling, activating invasion and metastasis, resisting cell death, and genome instability and mutation have been identified in breast cancer and contribute to its heterogeneity and treatment resistance.
Rhabdomyosarcoma is the most common soft tissue sarcoma in children. It arises from skeletal muscle and can occur anywhere in the body. The prognosis depends on the histology, stage, and primary site. Treatment involves surgery, chemotherapy, and radiation therapy. For orbital tumors, biopsy followed by chemotherapy and lower-dose radiation of 45 Gy achieves high cure rates over 90%. For parameningeal head and neck tumors, chemotherapy and higher radiation dose of 50.4 Gy is used due to risk of meningeal spread.
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.
Hallmarks of Cancer - Classical vs Metabolic approachSreepadmanabh M
The document summarizes the "Hallmarks of Cancer" proposed by Douglas Hanahan and Robert Weinberg in 2000. It identified six common traits or hallmarks that allow normal cells to transform into cancer cells: (1) self-sufficiency in growth signals, (2) insensitivity to anti-growth signals, (3) evading apoptosis, (4) limitless replicative potential, (5) sustained angiogenesis, and (6) tissue invasion and metastasis. In 2011, Hanahan proposed four additional hallmarks: deregulated metabolism, immune evasion, severe chromosomal abnormalities, and chronic inflammation inducing cancer. The document discusses evidence that a metabolic approach may provide further insights into understanding cancer.
In this file, you can ref resume materials for supervisor such as resume tips, resume samples, cover letter samples, types of interview questions, supervisor situational interview, supervisor behavioral interview…
Edison F. Gatdula is applying for a position as an IT Specialist. He has a Bachelor's degree in Information Management and experience as a Technical Support Staff, MIS Staff, and current position as an IT Specialist. His skills include knowledge of network cabling, devices, software and hardware installation, computer troubleshooting, backups, Microsoft and Linux operating systems, and basic programming languages.
Megan Davies has experience as a manufacturing engineering assistant and cashier/assistant manager. She has a Bachelor's Degree in Mechanical Engineering from UC Berkeley with a GPA of 3.8. Her relevant skills include Microsoft Office, CAD, technical drawing, programming, and analytics software like CheckPoint and CircuitCam. She is seeking new opportunities and can start immediately.
The document describes the condition of tires with LEFT indicating normal wear on the outside and RIGHT indicating normal wear on the inside. Tapered, cracked, or chipped tires or tires with only one wheel worn are in need of replacement.
Tribute to John Hill, Prolific Wargame Designer of Across A Deadly Field, Squad Leader and Johnny Reb. John was also a military analyst and hobbyist of garden railroading.
Visit John Hill's Tribute Site at http://acrossadeadlyfield.com
Learn to build a legitimate online business http;//legitimateonlineopportunity.com
The document outlines a manifesto put forth by an organization called the BRIGHTS that calls for the consolidation of power and control over society. It asserts that only the BRIGHTS, by virtue of their superior intellect and wisdom, are fit to rule. It lays out 48 principles that would establish the BRIGHTS philosophy as the sole basis for law and governance. This includes denying the existence of God or absolute moral truths, granting the BRIGHTS unlimited powers and controlling all aspects of society, from education to history to speech. The intended goal is for the BRIGHTS to become the unquestioned rulers and for their ideology to be universally accepted without opposition.
This document provides suggested key dates throughout the year for pro-life and constitutional educational events as alternatives to solely focusing on January 22nd. It lists various dates and provides brief descriptions of how each date could be used to emphasize pro-life messages and teach about the history of movements protecting human rights. Examples include King's birthday to reject racist arguments for abortion, and anniversary dates of important court cases and battles to draw connections to the protection of human life.
This document outlines a political strategy to undermine support for the Democratic Party by highlighting areas where the party's platform contradicts principles like the Constitution, Martin Luther King Jr.'s vision of equality and justice, and protection of innocent life. It argues the Democratic agenda promotes division, destruction, and moral degradation. The strategy aims to educate voters on real policy differences between parties and show how the Democratic agenda expands government beyond its lawful powers. It seeks to appeal to voters' intelligence and values to reject the Democratic platform in favor of principles like liberty, rule of law, and virtue.
Grounded theory is a research methodology that involves collecting and analyzing qualitative data to generate an abstract theoretical understanding of the main themes in the data. Rather than testing an existing theory, grounded theory is intended to generate new theories grounded in data. The data collection and analysis occur in iterative cycles, with subsequent data collection informed by emerging theoretical insights from ongoing analysis. This process continues until theoretical saturation is reached and no new theoretical insights emerge. Grounded theory was developed in the 1960s as an alternative to strict theory verification approaches and emphasizes inductive theory building through comparative analysis of qualitative data.
Religious Dimensions Common to Human Rights Abuses with Abortion as a Case StudyAl Lemmo
This document provides an overview of a presentation on religious dimensions common to human rights abuses, using abortion as a case study. The presentation introduces a model for understanding conflicts as involving three "abortions" - theological, mental, and physical. It examines abortion as an example of rejecting the philosophy of intrinsicism in favor of "abortionism." The document outlines principles of conflict resolution and discusses opposing perspectives on defining the abortion conflict, with the goal of building understanding and stopping human rights abuses.
Cancer is one of the most common diseases worldwide and arises due to mutations in genes. There are over 100 types of cancer that can affect different parts of the body. Cancerous cells divide uncontrollably and crowd out normal cells. Factors that can cause mutations include carcinogens like tobacco, certain viruses, radiation, and genetic predisposition. Early diagnosis improves survival rates and treatments are improving, seeking to remove less healthy tissue and combine therapies.
Types of Cancer its intro and difference between normal and cancerous cell.pptxSachinKumar945617
This document discusses cancer, including its characteristics, types, causes, and spread. Cancer is defined as abnormal cell growth that can invade other tissues. The main types of cancer are carcinomas, sarcomas, leukemia, lymphomas, and multiple myeloma. Carcinomas make up most cancers and affect epithelial tissues. Sarcomas develop in bone and soft tissues. Leukemia originates in bone marrow and causes abnormal blood cells. Lymphomas involve lymphocytes. Multiple myeloma affects plasma cells. Cancers can spread via the lymphatic system or bloodstream to other parts of the body. Common causes of cancer include carcinogens like tobacco, viruses, radiation, and genetic mutations.
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.
1. Neoplasia refers to abnormal and uncontrolled cell growth that can be benign or malignant. Benign tumors are slow-growing and localized, while malignant tumors proliferate rapidly and can spread throughout the body.
2. Tumors are classified based on their cell of origin - carcinomas arise from epithelial cells, sarcomas from mesenchymal cells. Special tumor categories include teratomas (derived from multiple germ layers), mixed tumors (containing two cell types), and blastomas (embryonic cell tumors more common in children).
3. Characteristics used to distinguish benign from malignant tumors include rate of growth, degree of differentiation, invasion of surrounding tissues, and metastasis. Malignant tumors
This document provides information about cancer (malignant tumors) including:
- Definitions of key terms like neoplasm, benign vs malignant tumors, and metastasis.
- Cancer is abnormal cell growth that is uncontrolled, able to invade other tissues, and spread to other parts of the body.
- Cancers are classified by site of origin, cell type, grade, and stage. The stage considers tumor size, node involvement, and metastasis.
- Cancers are caused by genetic, environmental, and lifestyle factors and can be treated through surgery, radiation, chemotherapy, biotherapy, and hormonal therapy depending on the cancer type and stage.
Cancer causes cell to divide uncontrollably. Cancer is the second-leading cause of death in the world. But survival rates are improving for many types of cancer, thanks to improvements in cancer screening, treatment and prevention. Cancer is caused by changes (mutations) to the DNA within cells.
Tumors can be benign or malignant. Benign tumors are not cancerous, grow slowly, and rarely spread. Malignant tumors or cancers are life-threatening as they grow quickly, invade nearby tissue, and can spread through metastasis to other parts of the body. Cancers develop through multi-stage processes involving genetic mutations that disrupt normal cell growth and division over many years. Cancers are classified based on their tissue of origin, grade, stage, and other characteristics to determine prognosis and treatment. The major categories are carcinomas, sarcomas, leukemias, lymphomas, and mixed or unknown types.
Neoplasia & carcinogenesis.pptx dr.jawahar singh.pptx 1jawahar singh
This document summarizes a presentation on neoplasia and carcinogenesis. It begins with definitions of neoplasia and discusses the nomenclature and classification of neoplasms as benign or malignant. The key differences between benign and malignant tumors are described. The document then covers the molecular basis of cancer, outlining a multistep process of carcinogenesis involving oncogenes, tumor suppressor genes, DNA repair genes, and genes regulating apoptosis. It describes the hallmarks of cancer and discusses epidemiology, etiology, tumor immunity, and clinical aspects of neoplasia.
This document provides information about cancer cell research. It defines cancer and tumors, discusses the causes and types of cancer, and describes cancer treatments. Specifically, it explains that cancer is uncontrolled cell growth that can be caused by genetic or environmental factors. It classifies cancers by the type of cell they arise from and outlines some key differences between cancer cells and normal cells, such as their uncontrolled growth and loss of communication with other cells. The document also summarizes the process of cancer metastasis where cancer spreads from one part of the body to another through the bloodstream or lymphatic system. Finally, it lists several common treatment approaches for cancer including surgery, chemotherapy, and radiation therapy.
Neoplasia refers to abnormal cell growth. Cancer occurs when cells grow uncontrollably and spread. Benign tumors are noncancerous growths that do not spread, while malignant tumors are cancers that can invade nearby tissues and spread to distant sites via metastasis. The characteristics that distinguish benign and malignant tumors are differentiation, growth rate, local invasion, and metastasis. Carcinogenesis can be caused by chemical, radiation, and microbial agents. Chemical carcinogens can act as initiators or promoters of cancer development. Radiation exposure can cause DNA damage leading to cancer-causing mutations. Viruses and bacteria can also directly or indirectly cause chronic inflammation and mutations that lead to cancer. Genetic mutations in oncogenes, tumor suppress
This document discusses neoplasms and tumors. It begins by defining neoplasia and neoplasms, and distinguishes between benign and malignant tumors. It then describes the two basic components of tumors - the parenchyma comprising proliferating tumor cells, and the supportive stroma. Several special categories of tumors are discussed such as mixed tumors, teratomas, and blastomas. The document also covers tumor characteristics such as rate of growth, clinical and microscopic features, local invasion and metastasis. It provides details on classification of tumors based on cell type and discusses the mechanisms of invasion and metastasis.
This document discusses tumors and cancer classification. It defines benign and malignant tumors, with malignant tumors being able to invade surrounding tissues and metastasize. Tumor genesis is described as a multi-step process involving genetic alterations that transform normal cells into cancerous cells. Cancers are classified by their site of origin, tissue type, grade which describes cell differentiation, and stage which describes tumor size, node involvement and metastasis. The main types of cancer are carcinoma, sarcoma, leukemia, lymphoma and mixed types.
This document provides an overview of cancer. It defines cancer as abnormal and uncontrolled cell growth that can form tumors. There are over 200 types of cancer that can start in any body tissue. Cancer arises due to genetic mutations that disrupt the normal balance between cell growth and death. Tumors are classified as either benign (non-cancerous) or malignant (cancerous). Malignant tumors can spread to other parts of the body through a process called metastasis. The main types of cancer are carcinomas, sarcomas, lymphomas, and leukemias. Diagnosis and treatment methods are also discussed.
Cancer is caused by genetic mutations that alter key cellular processes like growth, survival and senescence. These mutations are passed down to daughter cells, allowing cancer cells to grow uncontrollably. The accumulation of mutations gives cancers abilities like self-sufficient growth, evading cell death and spreading to other areas. Benign tumors are well-differentiated, localized and do not invade other tissues or metastasize. Malignant tumors are poorly differentiated, grow and spread rapidly, invade locally and metastasize to distant sites. The ability to metastasize defines a tumor as cancerous.
This document provides an overview of nursing management for patients with cancer. It begins with objectives for a lecture on cancer nursing management. The outline then covers definitions of cancer-related terminology, risk factors, pathophysiology, symptoms, diagnostic tests, and management approaches including various treatment types and nursing interventions. Key points covered include defining cancer and differentiating between benign and malignant tumors, discussing common risk factors and the multi-step process of carcinogenesis, and comparing characteristics of benign versus malignant cells and tumors.
Cancer is predominantly a disease of middle age and elderly. Environment and genetics influence cancer risk. The global cancer burden is estimated at 10 million new cases per year, predicted to rise to 15 million by 2020. Cancer is the second most common cause of death in developed countries. The major cancers vary by sex, with lung cancer most common in men and breast cancer in women. Cancer risk depends on factors like age, sex, geography, occupation, diet, and smoking. Cancer spreads locally, through lymphatics, blood vessels, body cavities, and along epithelial surfaces. Premalignant conditions include changes in benign tumors, intraepithelial neoplasia, and malignancies from chronic inflammation.
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This presentation by Yong Lim, Professor of Economic Law at Seoul National University School of Law, was made during the discussion “Artificial Intelligence, Data and Competition” held at the 143rd meeting of the OECD Competition Committee on 12 June 2024. More papers and presentations on the topic can be found at oe.cd/aicomp.
This presentation was uploaded with the author’s consent.
Suzanne Lagerweij - Influence Without Power - Why Empathy is Your Best Friend...Suzanne Lagerweij
This is a workshop about communication and collaboration. We will experience how we can analyze the reasons for resistance to change (exercise 1) and practice how to improve our conversation style and be more in control and effective in the way we communicate (exercise 2).
This session will use Dave Gray’s Empathy Mapping, Argyris’ Ladder of Inference and The Four Rs from Agile Conversations (Squirrel and Fredrick).
Abstract:
Let’s talk about powerful conversations! We all know how to lead a constructive conversation, right? Then why is it so difficult to have those conversations with people at work, especially those in powerful positions that show resistance to change?
Learning to control and direct conversations takes understanding and practice.
We can combine our innate empathy with our analytical skills to gain a deeper understanding of complex situations at work. Join this session to learn how to prepare for difficult conversations and how to improve our agile conversations in order to be more influential without power. We will use Dave Gray’s Empathy Mapping, Argyris’ Ladder of Inference and The Four Rs from Agile Conversations (Squirrel and Fredrick).
In the session you will experience how preparing and reflecting on your conversation can help you be more influential at work. You will learn how to communicate more effectively with the people needed to achieve positive change. You will leave with a self-revised version of a difficult conversation and a practical model to use when you get back to work.
Come learn more on how to become a real influencer!
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This presentation was uploaded with the author’s consent.
This presentation by OECD, OECD Secretariat, was made during the discussion “Pro-competitive Industrial Policy” held at the 143rd meeting of the OECD Competition Committee on 12 June 2024. More papers and presentations on the topic can be found at oe.cd/pcip.
This presentation was uploaded with the author’s consent.
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This presentation was uploaded with the author’s consent.
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Moreover, having well-defined career goals fosters a sense of purpose and direction, enhancing job satisfaction and overall productivity. It encourages continuous learning and adaptation, as professionals remain attuned to industry trends and evolving job market demands. Career goals also facilitate better time management and resource allocation, as individuals prioritize tasks and opportunities that advance their professional growth. In addition, articulating career goals can aid in networking and mentorship, as it allows individuals to communicate their aspirations clearly to potential mentors, colleagues, and employers, thereby opening doors to valuable guidance and support. Ultimately, career goals are integral to personal and professional development, driving individuals toward sustained success and fulfillment in their chosen fields.
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Insight: In a landscape where traditional narrative structures are giving way to fragmented and non-linear forms of storytelling, there lies immense potential for creativity and exploration.
'Collapsing Narratives: Exploring Non-Linearity' is a micro report from Rosie Wells.
Rosie Wells is an Arts & Cultural Strategist uniquely positioned at the intersection of grassroots and mainstream storytelling.
Their work is focused on developing meaningful and lasting connections that can drive social change.
Please download this presentation to enjoy the hyperlinks!
This presentation by Nathaniel Lane, Associate Professor in Economics at Oxford University, was made during the discussion “Pro-competitive Industrial Policy” held at the 143rd meeting of the OECD Competition Committee on 12 June 2024. More papers and presentations on the topic can be found at oe.cd/pcip.
This presentation was uploaded with the author’s consent.
Mastering the Concepts Tested in the Databricks Certified Data Engineer Assoc...SkillCertProExams
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XP 2024 presentation: A New Look to Leadershipsamililja
Presentation slides from XP2024 conference, Bolzano IT. The slides describe a new view to leadership and combines it with anthro-complexity (aka cynefin).
This presentation by OECD, OECD Secretariat, was made during the discussion “Artificial Intelligence, Data and Competition” held at the 143rd meeting of the OECD Competition Committee on 12 June 2024. More papers and presentations on the topic can be found at oe.cd/aicomp.
This presentation was uploaded with the author’s consent.
2. CONTENTS
Introduction
3
Definition
5
Basic molecular genetics
10
Classification
12
Causes and Risk factors
19
Genetic nature of cancer
29
Oncogenes
40
Tumor and suppressor genes
50
3. INTRODUCTION
Despite decades of intensive biomedical
research, cancer remains a significant
cause of morbidity and mortality
worldwide, account for more than 20% of
all deaths
Cancer is a complex disease that result
from the same basic process of
uncontrolled growth: cells divide and
multiply as the body needs them. When
these cells continue multiplying when the
body doesn't need them, the result is a
4. INTRODUCTION
A mass that invades neighbouring tissues
and may metastasize to more distant sites
The growth is autonomous increasingly
malignant, if untreated ,invariably fatal
Tumor formation is a multistep process
involving many of genetic changes in the
evolving tumor cell population
These growths are considered either
benign or malignant, tumours are
classified by site, tissue type and degree
of malignancy
Most cancer are disorders of later life, but
some affect childhood
5. CANCER
Cancer is a genetic disorder in which
the normal control of cell growth is
lost. The basic mechanism in all cancer
is mutation, either in the germ line or
much more frequently, in somatic cells.
Cancer is multi-factorial diseases,
much remains to be learned about the
genetic processes of carcinogenesis
and about the environmental factors
that alter DNA and thus lead to
malignancy
6. CANCER
What is Cancer?
Uncontrolled growth and spread of abnormal
cells
Neoplasms
Malignant tumors
Benign tumors
Cellular Change/Mutation Theories
Spontaneous errors
External agents
Oncogenes
7. CELLS GROW, REPLICATE
AND REPAIR BODY
ORGANS.
THE GENETIC
MATERIAL (DNA/RNA)
AND YOUR IMMUNE
SYSTEM REGULATE
THIS PROCESS.
Cells represent the
smallest,
functional unit of
our existence
which contains
cytoplasm and a
nucleus (i.e.
metabolism,
reproduction, day
to day functions)
Cells have a
specialized
function
depending on their
Healthy Cells
8. The division (mitosis) of normal cells is precisely controlled
Cancerous cells divide repeatedly out of control, they crowd out other
normal cells and function abnormally.
They can also destroy the correct functioning of major organs.
9.
10. BASIC MOLECULAR GENETICS
Somatic cell is any biological cell forming the
body of an organism
Germ cells are cells that give rise to gametes
Gametes : is a cell that fuses with another cell
during fertilization (conception)
in organisms that sexually reproduce, witch
carry half the genetic information of an
individual.
Stem cells are cells that can divide through
mitosis and differentiate into diverse
specialized cell types.
11. DIFFERENT TYPES OF CELLS
Blood cells
Muscle cells
(smooth,
striated,
cardiac)
Nerve cells
Bone cells
Cartilage cells
Liver (hepa)
12. THE CELL CYCLE AND CANCER
Neoplasm- abnormal growth of cells
Benign neoplasms are not cancerous
Encapsulated; Do not invade
neighboring tissue or spread
Malignant neoplasms are cancerous
Not encapsulated; Readily invade
neighboring tissues
May also detach and lodge in distant
places – metastasis
13. TUMORS
Benign Tumors
(noncancerous)
Enclosed in a
fibrous shell or
capsule.
Take up space
Concerned if they
interfere with
surrounding
tissues or vessels
or impede the
function of the
body.
• Malignant Tumors
(cancerous)
• Not usually
contained –
metastasis
• Invade and emit claw
like protrusions that
disrupt the RNA and
DNA of normal cells
(these cancerous cells
act like a virus).
14. CLASSIFICATION OF CANCER
Cancers may be classified by their
primary site of origin or by their
histological or tissue types
Classification by tissue types
The international standard for the
classification and nomenclature of
histologies is the International
Classification of Diseases for Oncology
15. Based on tissue types cancers may be classified
into six major categories:
1. Carcinoma
Originates from the epithelial layer of cells that form
the lining of external parts of the body or the
internal linings of organs within the body.
Carcinomas, malignancies of epithelial tissue,
account for 80 to 90% of all cancer cases.
Carcinomas usually affect organs or glands capable
of secretion including breast, lungs, bladder, colon
and prostate.
Carcinomas are of two types – adenocarcinoma and
squamous cell carcinoma. Adenocarcinoma
develops in an organ or gland and squamous cell
carcinoma originates in squamous epithelium.
Adenocarcinomas may affect mucus membranes
and are first seen as a thickened plaque-like white
mucosa. These are rapidly spreading cancers.
16. 2. Sarcoma
Originate in connective and supportive
tissues including muscles, bones, cartilage
and fat. Bone cancer is one of the sarcomas
termed osteosarcoma. It affects the young
most commonly.
Other examples include chondrosarcoma (of
the cartilage), leiomyosarcoma (smooth
muscles)
3. Myeloma
These originate in the plasma cells of bone
marrow. Plasma cells are capable of
producing various antibodies in response to
17. 4. Leukemia
This a group of cancers that are grouped within blood
cancers. These cancers affect the bone marrow which is
the site for blood cell production. When cancerous, the
bone marrow begins to produce excessive immature
white blood cells that fail to perform their usual actions
and the patient is often prone to infection.
Types of leukemia include:
Acute myelocytic leukemia (AML) – these are
malignancy of the myeloid and granulocytic white blood
cell series seen in childhood.
Chronic myelocytic leukemia (CML) – this is seen in
adulthood.
Acute Lymphatic, lymphocytic, or lymphoblastic
leukemia (ALL) – these are malignancy of the lymphoid
and lymphocytic blood cell series seen in childhood and
young adults.
Chronic Lymphatic, lymphocytic, or lymphoblastic
leukemia (CLL) – this is seen in the elderly.
Polycythemia Vera or erythremia – this is cancer of
18. 5. Lymphoma
These are cancers of the lymphatic system.
Unlike the leukemias, which affect the blood
and are called “liquid cancers”, lymphomas
are “solid cancers”. These may affect lymph
nodes at specific sites like stomach, brain,
intestines etc. These lymphomas are
referred to as extranodal lymphomas.
Lymphomas may be of two types –
Hodgkin’s lymphoma and Non-Hodgkin’s
lymphomas. In Hodgkin lymphoma there is
characteristic presence of Reed-Sternberg
cells in the tissue samples which are not
present in Non-Hodgkin lymphoma.
19. 6. Mixed types
These have two or more components of
the cancer. Some of the examples
include mixed mesodermal tumor,
carcinosarcoma, adenosquamous
carcinoma and teratocarcinoma.
Blastomas are another type that
involves embryonic tissues.
20. CLASSIFICATION BY GRADE
Cancers can also be classified according to grade. The
abnormality of the cells with respect to surrounding
normal tissues determines the grade of the cancer.
Increasing abnormality increases the grade, from 1–4.
Cells that are well differentiated closely resemble
normal specialized cells and belong to low grade
tumors. Cells that are undifferentiated are highly
abnormal with respect to surrounding tissues. These
are high grade tumors.
Grade 1 – well differentiated cells with slight
abnormality
Grade 2 – cells are moderately differentiated and
slightly more abnormal
Grade 3 – cells are poorly differentiated and very
abnormal
Grade 4 – cells are immature and primitive and
undifferentiated
21. CLASSIFICATION BY STAGE
Cancers are also classified individually according to their stage.
There are several types of staging methods. The most
commonly used method uses classification in terms of tumor
size (T), the degree of regional spread or node involvement (N),
and distant metastasis (M). This is called the TNM staging.
For example, T0 signifies no evidence of tumor, T 1 to 4 signifies
increasing tumor size and involvement and Tis signifies
carcinoma in situ or limited to surface cells. Similarly N0
signifies no nodal involvement and N 1 to 4 signifies increasing
degrees of lymph node involvement. Nx signifies that node
involvement cannot be assessed. Metastasis is further classified
into two – M0 signifies no evidence of distant spread while M1
signifies evidence of distant spread.
Stages may be divided according to the TNM staging
classification. Stage 0 indicates cancer being in situ or limited to
surface cells while stage I indicates cancer being limited to the
tissue of origin. Stage II indicates limited local spread, Stage III
indicates extensive local and regional spread while stage IV is
advanced cancer with distant spread and metastasis.
22. CLASSIFICATION BY SITE OF ORIGIN
By primary site of origin, cancers may be
of specific types like breast cancer, lung
cancer, prostate cancer, liver cancer renal
cell carcinoma (kidney cancer), oral
cancer, brain cancer etc.
26. HOW CAN NORMAL CELL BECOME CANCER CELL
?
1. Genetic instability
2. Autonomous growth
3. Insensitivity to internal and external
antiproliferative signals
4. Resistance to apoptosis and other forms of
induced cell suicide
5. Unlimited cell division potential
6. The ability to induce new blood vessel
formation , a process termed angiogenesis.
7. Locally invasive behavior, which uniquely
distinguishes malignant from benign
neoplasms.
8. Evasion of the immune system.
27. RISK FACTORS (MULTI-FACTORIAL)
Exposure to Cancer-causing agents
Cellular Mutations (what agents cause this?
Environment & Lifestyle agents)
Genetics & Hormone exposure (i.e. breast
cancer)
Occupation and Environment Factors
Social and Psychological Factors
Chemicals in Food
Viral (i.e. herpes, HPV, mononucleosis) create an
opportunistic environment
Medical Factors
Risks for Cancer-Lifestyle
Smoking among greatest
Nutrition/exercise
30. CAUSES OF CANCER
Randomly acquired through errors in DNA
replication
Inherited and thus present in all cells from
birth. The heritability of cancers are usually
affected by complex interactions between
carcinogens and the host genome
Carcinogens such as tobacco smoke,
radiation, chemical or infectious agents
31. WHAT CAUSES CANCER
Biological Factors
Genetic predisposition
Reproductive and hormonal risks
Hereditary predisposition – Some families
are more susceptible to getting certain cancers.
Remember you can’t inherit cancer its just that
you maybe more susceptible to getting it.
32. WHAT CAUSES CANCER
Occupational and Environmental
Factors
Asbestos, nickel, chromate
Radioactive substances
Ionising radiation – X Rays, UV light
Viral Factors
Herpes-related virus and human
papillomavirus
Chemicals in Food
Sodium nitrate
Clostridium botulism
33. WHAT CAUSES CANCER
Social and Psychological Factors
Stress
Decrease negative emotions
There is connection between stress,
immune system and cancer, that is
changing the direction of research: it now
appears that cancer cells make proteins
that actually tell the immune system to let
them alone and even to help them grow.
cancer can weaken the immune system
and allowing tumor to grow
34. WHAT CAUSES CANCER
Medical Factors
Diethylstilbestrol (DES)
Chemotherapy
Any agent that causes cancer is called a
carcinogen and is described as
carcinogenic
35.
36. GENETIC NATURE OF CANCER
Nearly all cancers are caused by abnormalities
in the genetic material of the transformed cell
In order for a normal cell to transform into a
cancer cell, genes regulate cell growth and
differentiation must be altered. When normal
regulation is altered, uncontrolled growth is
initiated
Genetic changes can occur at many levels, from
gain or loss of entire chromosomes to a
mutation affecting a single DNA nucleotide
New aspects of the genetics of cancer
pathogenesis, such as DNA methylation and
37. Cancer is a genetic disorder in which the normal
control of cell growth is lost, the basic mechanism
in all cancer is mutation. Carcinogenic agents are
involved through causing mutation
The mutation affects gene responsible for cell
proliferation, cell development and other cellular
activities
Initiation of cancer; cells undergoing a series of
genetic mutation or alteration which result in their
instability to respond normally to
intracellular/extracellular signals that control
proliferation, differentiation and death
38. Germline mutations are responsible for 5% of
cancer cases, this is also called familial cancer.
These mutations are present in every cell of the
body and are passed from parent to child
Sporadic cancer or somatic mutation are
caused by tobacco, over-exposure to UV
radiation, and other toxins and chemicals.
These mutations are not in every cell of the body
and are not passed from parent to child
39. CHARACTERISTICS OF CANCER CELLS
Lack differentiation (control)
Have abnormal nuclei
Form tumors
Mitosis controlled by contact with
neighboring cells – contact inhibition
Cancer cells have lost contact
inhibition
41. Cancer arises from the mutation of a normal gene.
A factor which brings about a mutation is called a
mutagen.
It is thought that several mutations need to occur
to give rise to cancer
Mutated genes that cause cancer
are called oncogenes.
Any agent that causes cancer is called a
carcinogen and is described as carcinogenic.
Cancerous cells do not self destruct and continue
to divide rapidly producing millions of new
cancerous cells.
42.
43.
44.
45.
46.
47.
48. ONCOGENES
Oncogenes are known by three letter abbreviation
which reflect their origin or the type of tumor with
which they are associated
Cancer-promoting oncogenes: if oncogene is
altered or over expressed, either as a result of
mutation in the gene itself or by altered external
control, the cell in which the change occurred can
undergo uncontrolled growth, eventually malignant.
Most oncogenes are mutated forms of normal genes ,
called proto-oncogenes
Two oncogenes that have been found to be over
expressed in a variety of cancers include :
c-MYC (regulator gene that codes for a transcription
factor)
49. Mutations in DNA can lead to changes in protein
function or expression that increase the potential
for cancer initiation, progression, or metastasis.
Tumor suppressor genes regulate and control
cellular growth.
Oncogenes promote cell growth.
Types of Proto-oncogenes:
Cellular oncogenes(c-oncogenes): proto-
oncogene which have been mutate in any
individual
Normal oncogenes(n-oncogenes): proto-
oncogenes that have not been found to mutate
50. CHARACTERISTIC OF CELLULAR PROTO-ONCOGENE
These are typical cellular genes with typical
control sequences. As eukaryotic genes:
Most have introns
They are always at same place in genome
No LTR sequences
They show normal Mendelian inheritance because
they are normal genes, essential to the function
of the cell
Cellular oncogenes are expressed by the cell at
some period of life of the cell, they are usually
proteins that are involved in growth control
Cellular oncogenes are highly conserved
51. ACTIVATION OF PROTO-ONCOGENES
Point mutations
Deletions, or insertions that leads to hyperactive
product
Deletion, or insertions in the promoter region of a
proto-oncogene that lead to increased transcription
Gene amplification events leading to extra chromosomal
copies of proto-oncogene lead to normal protein
greatly overproduced. Amplified segment of DNA are
often detected as two types of cytogenetic change,
double minute and homogeneously staining regions
Chromosomal translocation
Relocation of a proto-oncogene to a new
chromosomal site that leads to higher expression
Fusion between a proto-oncogene and a second gene,
which produces a fusion protein with oncogenic
52.
53.
54.
55. TYPES OF ONCOGENES
Oncogene can be classified to their cellular
location and function of their encoded
oncoproteins in the signal transduction pathway:
Growth factors
Growth factor receptors
GTP binding proteins
Post receptor tyrosine kinase
Cytoplasmic oncogenes
Nuclear oncogenes
Apoptotic oncogenes
56.
57.
58. TUMOR SUPPRESSOR GENES
Tumor suppressor genes (antioncogene)
Normal genes regulate cellular growth and play a critical
role in the normal processes of the cell cycle.
These genes are also important for DNA repair and
cell signaling ”tell cells when to die(apoptosis or
programmed cell death)”
The product of tumor suppressor genes normally
block abnormal growth and malignant transformation
The absence of tumor suppressor gene function may
lead to dysregulation of normal growth control and
malignancy
In contrast of mutations in proto-oncogene, which are
dominant in their action, most mutation in tumor
59. Many oncogenes and tumor suppressors
exert their effects by interfering with cell
cycle checkpoints and apoptotic pathways,
allowing cancer cells to divide continuously
and accumulate.
Loss of the ability to respond appropriately
to damaged DNA is particularly dangerous,
because it fosters genetic instability, a key
attribute of cancer cells.
Loss of DNA damage checkpoint controls
results in an increased mutation rate,
accelerating the mutation of cancer-
associate genes, thus contributing to
carcinogenesis and disease progression.
60. TUMOR SUPPRESSOR GENE
Genes that control cell division some suppressor
genes help control cell growth and reproduction
e.g. retinoblastoma gene (RB1). Abnormalities of
the RB1 gene can lead to a type of eye
cancer(retinoblastoma) in infants as well as to
other cancers
DNA repair genes these are genes that fix any
mistakes made when DNA is replicated. Mistakes
that aren’t fixed become mutations, which may
eventually lead to cancer e.g. Gene responsible for
‘hereditary nonpolyposis colon cancer’. When
genes don’t repair the errors in DNA, HNPCC can
result
61.
62.
63. Inherited Abnormalities of some tumor
suppressor genes
Have been found in several cancers that tend to run in
families
Mutations in p53, RB1, and the genes involved in HNPCC
A defective APC gene causes familial polyposis a
condition in which people develop hundreds or thousands
of colon polyps, some of which may eventually may
acquire several sporadic mutations and turn into colon
cancer
Abnormalities of the BRCA genes account for 5% to 10%
of breast cancer
Non-inherited mutations of tumor suppressor
genes
Acquired mutations of the p53 gene appear to be
involved in a wide range of cancers including lung,
64.
65.
66. Loss of tumor suppressor gene function
can occur primarily by :
(1) homozygous deletion
(2) loss of one allele and mutational
inactivation of the second allele
(3) mutational events involving both alleles
(4) loss of one allele and inactivation of the
second allele by DNA methylation
Proto-oncogenes can be converted to
oncogenes by :
(1) mutation of the proto-oncogene resulting in an
activated form of the gene
(2) gene amplification
(3) chromosomal rearrangement.
67. TELOMERE & TELOMERASE
Telomeres contain stretches of terminal,
noncoding, repetitive DNA that cap the
ends of each chromosome, thereby
stabilizing them.
Telomere DNA repeats are progressively
lost as cells divide and as a result of
oxidative DNA damage at the telomeres.
68. Normal cells monitor their telomere
lengths and permanently exit the cell
cycle (cellular senescence) or commit
suicide (apoptosis) in response to
telomere shortening. This tumor-
suppressive telomere length
checkpoint involves TP53 and pRB.
Loss of telomere length checkpoints
can lead to critical telomere shortening
that initiates chromosomal instability,
thus contributing to carcinogenesis.
69. A majority of cancers and premalignant
lesions have abnormally short
telomeres.
Most cancers express the enzyme
telomerase, which restabilizes the
telomeres and allows unlimited cell
division potential (“immortalization”),
thus telomerase represents an
attractive therapeutic target.
70. METASTASIS
The process by which a tumor cell leaves the
primary tumor, travels to a distant site via the
circulatory system, and establishes a secondary
tumor
Approximately 30% of newly diagnosed patients
with solid tumours present with metastases
Forms of cancer metastasis
71. PATHWAYS OF SPREAD
(1) Seeding of the body cavities and
surfaces
When a malignant neoplasm penetrates
into a natural ‘open field’ e.g. peritoneal
cavity
(2) Lymphatic Spread
Most common pathway for the initial
dissemination of carcinomas
Tends to follow the natural routes of
lymphatic drainage
(3) Haematogenous Spread
Typical of sarcomas
More readily via venous (than arterial)
72. 5 MAJOR STEPS IN METASTASIS
1. Invasion and infiltration of surrounding
normal host tissue with penetration of
small lymphatic or vascular channels;
2. Release of neoplastic cells, either or
single cells or small clumps, into the
circulation;
3. Survival in the circulation;
4. Arrest in the capillary beds of distant
organs;
5. Penetration of the lymphatic or blood
vessel walls followed by growth of the
73.
74. ANGIOGENESIS
The formation of new blood vessels out of pre-
existing capillaries.
INVOLVES : Sprouting
Splitting
Remodeling of the existing vessels
Small localized
tumor
Angiogenesis
Tumor that can grow and spread
75. CELLULAR MECHANISMS OF TUMOUR
ANGIOGENESIS
(1) host vascular network
expands by budding of
endothelial sprouts or
formation of bridges
(angiogenesis);
(2) tumour vessels remodel
and expand by the
insertion of interstitial
tissue columns into the
lumen of pre-existing
vessels
(intussusceptions); and
(3) endothelial cell
precursors (angioblasts)
home from the bone
marrow or peripheral
blood into tumours and
contribute to the
endothelial lining of
tumour vessels
(vasculogenesis)
(4) Lymphatic vessels
around tumours drain the
interstitial fluid and
provide a gateway for
78. CANCER TREATMENT
Chemotherapy treatment
uses medicine to weaken and destroy
cancer cells in the body, including cells at
the original cancer site and any cancer
cells that may have spread to another part
of the body.
Chemotherapy treatment
or "chemo," is a systemic therapy, which
means it affects the whole body by going
through the bloodstream.
In some cases, chemotherapy is given
79. CANCER TREATMENT
Radiation therapy (also called
radiotherapy)
high-energy rays are used to damage
cancer cells and stop them from growing
and dividing.
Radiation therapy is a local treatment; it
affects cancer cells only in the treated
area. Radiation can come from a machine
(external radiation).
It can also come from an implant (a small
container of radioactive material) placed
directly into or near the tumor (internal
radiation). Some patients receive both
82. CANCER PREVENTION
Healthy lifestyle
Exercise and proper breathing
Balanced diet
Complete rest and sleep
Water (8 to 10 glasses daily)
Eating Fruit on an empty stomach
83.
84.
85. FACING CANCER
Detecting Cancer
Magnetic Resonance Imaging (MRI)
Computerized Axial Tomography scanning
(CAT scan)
Prostatic ultrasound (rectal probe)
Self-exam and check-ups
86. FACING CANCER
New Hope in Cancer Treatments
Surgery to remove tumor
Chemotherapy
Researching genes and cell mutations
Talking with Your Doctor about Cancer
Ask questions about type, treatment,
clinical trials
Ask about surgery
Ask why one treatment is preferred
Get all your options