Carcinogenesis(penfriend841)
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Carcinogenesis is the process by which normal cells are transformed into cancerous cells. It involves genetic changes that affect cell proliferation, differentiation, and interaction. Carcinogenesis is influenced by factors like family history, age, environment, lifestyle, and viruses. The process involves initiation of DNA damage, promotion of cell growth, progression of the cancer, and potential metastasis. Staging of cancer describes the extent of spread from Stage 0 carcinoma in situ to Stage IV cancer that has metastasized to distant organs. Diagnosis involves tumor markers, imaging, and biopsy to evaluate extent of disease. Nursing care focuses on preventing infection, managing skin integrity issues from radiation, nutritional support, and other side effects of cancer treatment.
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Carcinogenesis and pathogenesis
The document discusses carcinogenesis and cancer. It begins with an overview of cell anatomy and the cell cycle, including the phases of interphase and mitosis. It then discusses how abnormalities in cell cycle regulation and checkpoints can lead to uncontrolled cell growth and carcinogenesis. Factors involved in carcinogenesis include oncogenes, tumor suppressor genes, and DNA damage. The document outlines several theories of carcinogenesis and describes the multistage process. It also covers the characteristics, metastatic process, and classification of malignant tumors.
Carcinogen
This document discusses carcinogens and cancer. It defines cancer as abnormal cell growth that can invade other tissues and spread to other parts of the body. Carcinogens are substances that can cause cancer. Chemical carcinogens include aromatic hydrocarbons, aromatic amines, and chemicals containing epoxide, organohalogen, and nitroso groups. Carcinogens can damage DNA directly or require metabolic activation. Factors that influence cancer development include dose of exposure, lifestyle factors like smoking, and inherited conditions. Engineering controls, personal protective equipment, hygiene practices, and proper waste disposal can reduce exposure to carcinogens.
Carcinogenesis
Carcinogenesis is the process by which normal cells are transformed into cancer cells. It involves genetic and epigenetic changes that disrupt the normal balance between cell proliferation and cell death. According to the somatic mutation theory, mutations in DNA and epimutations lead to uncontrolled cell division by disrupting the programming that regulates these processes. The development of cancer involves changes to oncogenes and tumor suppressor genes that promote uncontrolled growth. The process of carcinogenesis can be divided into initiation, promotion, and progression stages and is triggered by factors like retroviruses, oncogenes, and carcinogens.
Carcinogenesis
1) Carcinogenesis is a multistep process involving initiation, promotion, and progression. Initiation involves genetic mutations from environmental factors like smoking. Promotion involves clonal expansion driven by growth factors in a reversible stage. Progression results in irreversible aneuploidy and cellular anaplasia.
2) The multihit hypothesis proposes cancer develops through accumulation of multiple genetic mutations in oncogenes and tumor suppressor genes, requiring 4-5 mutations for malignancy.
3) Cancers arise from a single cell of origin (monoclonal) that accumulates mutations over time, leading to intratumor heterogeneity as subclones evolve. Evidence for monoclonal origin includes single enzyme/immunoglob
Carcinogenesis
CARCINOGENESIS
By- Dr. Chirag Patil
chiragpatil1275@gmail.com
M.D.S in Oral & Maxillofacial Surgery
The Cell Cycle and Cancer
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
Cancer Treatment
The document discusses various cancer treatment options including surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy, and synthetic lethality. Surgery aims to remove the tumor while chemotherapy uses drugs to kill cancer cells. Radiation therapy uses radiation to damage cancer cell DNA. Hormonal therapy slows cancer growth by blocking hormones. Targeted therapy blocks cancer growth pathways. Synthetic lethality kills cancer cells by combining deficiencies in two repair genes. Treatment choice depends on cancer type, stage, and patient health.
Molecular basis of Cancer
Cancer arises from mutations in genes that regulate cell growth and division. These mutations can cause cells to grow uncontrollably and form tumors. There are two main types of cancer genes - oncogenes which promote cell growth when mutated, and tumor suppressor genes which normally inhibit cell growth but cannot when mutated in both copies of the gene. Most cancers are caused by multiple mutations that accumulate over time due to environmental exposures, random errors in cell division, or inherited genetic syndromes.
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Carcinogenesis and pathogenesis
The document discusses carcinogenesis and cancer. It begins with an overview of cell anatomy and the cell cycle, including the phases of interphase and mitosis. It then discusses how abnormalities in cell cycle regulation and checkpoints can lead to uncontrolled cell growth and carcinogenesis. Factors involved in carcinogenesis include oncogenes, tumor suppressor genes, and DNA damage. The document outlines several theories of carcinogenesis and describes the multistage process. It also covers the characteristics, metastatic process, and classification of malignant tumors.
Carcinogen
This document discusses carcinogens and cancer. It defines cancer as abnormal cell growth that can invade other tissues and spread to other parts of the body. Carcinogens are substances that can cause cancer. Chemical carcinogens include aromatic hydrocarbons, aromatic amines, and chemicals containing epoxide, organohalogen, and nitroso groups. Carcinogens can damage DNA directly or require metabolic activation. Factors that influence cancer development include dose of exposure, lifestyle factors like smoking, and inherited conditions. Engineering controls, personal protective equipment, hygiene practices, and proper waste disposal can reduce exposure to carcinogens.
Carcinogenesis
Carcinogenesis is the process by which normal cells are transformed into cancer cells. It involves genetic and epigenetic changes that disrupt the normal balance between cell proliferation and cell death. According to the somatic mutation theory, mutations in DNA and epimutations lead to uncontrolled cell division by disrupting the programming that regulates these processes. The development of cancer involves changes to oncogenes and tumor suppressor genes that promote uncontrolled growth. The process of carcinogenesis can be divided into initiation, promotion, and progression stages and is triggered by factors like retroviruses, oncogenes, and carcinogens.
Carcinogenesis
1) Carcinogenesis is a multistep process involving initiation, promotion, and progression. Initiation involves genetic mutations from environmental factors like smoking. Promotion involves clonal expansion driven by growth factors in a reversible stage. Progression results in irreversible aneuploidy and cellular anaplasia.
2) The multihit hypothesis proposes cancer develops through accumulation of multiple genetic mutations in oncogenes and tumor suppressor genes, requiring 4-5 mutations for malignancy.
3) Cancers arise from a single cell of origin (monoclonal) that accumulates mutations over time, leading to intratumor heterogeneity as subclones evolve. Evidence for monoclonal origin includes single enzyme/immunoglob
Carcinogenesis
CARCINOGENESIS
By- Dr. Chirag Patil
chiragpatil1275@gmail.com
M.D.S in Oral & Maxillofacial Surgery
The Cell Cycle and Cancer
1. The document discusses the cell cycle, cancer, and mutations. It describes the different phases of the cell cycle including interphase and mitosis.
2. It notes that mutations most commonly occur during the S phase of interphase when DNA is being replicated. Cancer occurs when cells lose control mechanisms and divide uncontrollably due to genetic mutations.
3. Mutations can be point mutations like substitutions, or larger chromosomal mutations involving deletions, duplications, inversions or translocations of DNA. These genetic changes can cause cancer when they affect genes regulating cell growth and division.
Cancer Treatment
The document discusses various cancer treatment options including surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy, and synthetic lethality. Surgery aims to remove the tumor while chemotherapy uses drugs to kill cancer cells. Radiation therapy uses radiation to damage cancer cell DNA. Hormonal therapy slows cancer growth by blocking hormones. Targeted therapy blocks cancer growth pathways. Synthetic lethality kills cancer cells by combining deficiencies in two repair genes. Treatment choice depends on cancer type, stage, and patient health.
Molecular basis of Cancer
Cancer arises from mutations in genes that regulate cell growth and division. These mutations can cause cells to grow uncontrollably and form tumors. There are two main types of cancer genes - oncogenes which promote cell growth when mutated, and tumor suppressor genes which normally inhibit cell growth but cannot when mutated in both copies of the gene. Most cancers are caused by multiple mutations that accumulate over time due to environmental exposures, random errors in cell division, or inherited genetic syndromes.
Cancer carcinogens
This document discusses various carcinogenic agents and their mechanisms of action. It describes direct-acting carcinogens that damage DNA directly and indirect-acting carcinogens that require metabolic activation before becoming carcinogenic. It also discusses initiation and promotion in chemical carcinogenesis. Radiation carcinogenesis from ionizing radiation, ultraviolet light, and viral oncogenesis are also covered, noting specific cancer risks from different exposures.
Cancer cell biology
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
Carcinogenesis
UNDERSTANDING OF CHEMICAL CARCINOGENESIS: CURRENT AND FUTURE PERSPECTIVES
Carcinogenesis refers to the process by which a normal cell is transformed into a malignant cell and repeatedly divides to become a cancer
Chemicals which initiate this process is called chemical carcinogens
Chemicals which increase the effectiveness of carcinogens is called co-carcinogens
CLASSIFICATION OF CHEMICAL CARCINOGENS
MECHANISM OF ACTION
STAGES OF CARCINOGENESIS
ROLE OF PROTO-ONCOGENES AND TUMOR SUPPRESSOR GENES
ACTIVATION OF PROTO ONCOGENES
INACTIVATION OF TUMOR SUPPRESSOR GENE
OXIDATIVE STRESS IN CARCINOGENESIS
ROS can be produced from both endogenous and exogenous sources
Attack both purine and pyrimidine bases, as well as the deoxyribose backbone
Induces DNA damage which includes single or double-strand breakage, deoxyribose modification, and DNA cross-link
If DNA damage is not properly repaired it may result in mutation which leads to cancer
BIOMARKERS
REGULATORY BACKGROUND
OECD guidelines
451- Carcinogenecity studies
453- Combined chronic toxicity/carcinogenecity
ICH guidelines
S1A- Guideline on the need for carcinogenicity studies of
pharmaceuticals
S1B- Testing for carcinogenicity of pharmaceuticals
S1C- Dose selection for carcinogenicity studies of pharmaceuticals
Targeted Therapies in Cancer
This document discusses targeted cancer therapies, which work by interfering with specific molecular targets involved in cancer growth and progression, unlike traditional chemotherapy which acts on all rapidly dividing cells. It provides examples of molecular targets for small molecule drugs and monoclonal antibodies, including growth factor receptors and fusion proteins. The document also discusses methods of target identification, categories of targeted therapies, examples of FDA-approved targeted drugs, limitations and side effects of targeted therapies, and concludes by emphasizing the importance and promise of targeted therapies while noting challenges that remain.
Molecular Genetics and Cancer Biology
This document provides an overview of molecular genetics and cancer biology concepts. It begins with an introduction to basic molecular genetics topics like DNA, genes, chromosomes, and gene expression. It then discusses how normal cells can become cancerous through genetic mutations that disrupt processes like tumor suppressor genes, oncogenes, the cell cycle, and DNA repair. The document emphasizes how understanding molecular genetics advances has helped improve diagnosis and treatment of cancers like prostate and bladder cancer, but also highlights ongoing challenges. It provides context on cancer rates and the need for continued research.
Principles of chemotherapy ppt
Chemotherapy involves the use of cytotoxic drugs to treat cancer. The goals of chemotherapy are to cure cancer, improve survival rates, or relieve symptoms. Key principles of chemotherapy include: (1) using drug combinations to increase efficacy and decrease resistance, (2) treating micrometastatic disease early on, and (3) dose intensity being important for response. Adjuvant chemotherapy after surgery or radiation has improved survival rates for several cancers like breast cancer and osteosarcoma by targeting remaining micrometastatic disease.
Signal Transduction in cancer
This document discusses cell signaling pathways and cell death. It describes the RAS pathway which involves RAS, RAF, MEK and ERK proteins and is mutated in 30% of cancers. Mutations in the PI3K/AKT/mTOR pathways are associated with several cancer types. Inhibitors target proteins in these pathways like PI3K, AKT and mTOR. Apoptosis is described as a programmed cell death pathway involving cell shrinkage, chromatin condensation and formation of apoptotic bodies. Caspases are cysteine proteases that cleave proteins during apoptosis. Cells can also evade apoptosis through expression of anti-apoptotic and pro-apoptotic BCL2 family proteins.
Staging an tumor markers
This document discusses tumor staging and biomarkers for oral cancer. It introduces the TNM staging system and its components for assessing tumor size, lymph node involvement, and metastasis. It also addresses limitations of staging and types of biomarkers that can be used, including commonly used ones like CD44, interleukin levels, and tissue polypeptide antigen. Biomarkers can help with screening, diagnosis, prognosis, and monitoring treatment response for oral cancer.
Hormones and cancer final ppt
Hormones play an important role in certain cancers like breast, prostate, and ovarian cancer. Hormones stimulate the growth of cancerous cells in hormone-dependent cancers. Risk factors for breast cancer include factors affecting hormone levels like early menarche, late menopause, hormone replacement therapy, and oral contraceptive use. Prostate cancer risk is influenced by ethnicity and androgen receptor genes. Hormonal therapies target hormone levels and receptors to slow cancer growth by using medications like anti-androgens and GnRH agonists.
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.
Cancer types and properties
This document discusses cancer types, properties, symptoms, prevention, screening, and treatment. It defines cancer as abnormal cell growth with the potential to invade other parts of the body. The six hallmarks of cancer are described as uncontrolled cell growth, growth despite growth-inhibiting signals, evading cell death, unlimited cell division potential, inducing blood vessel growth, and spreading to other tissues. Common cancer symptoms depend on the location and can include lumps, bleeding, weight loss, and fever. Prevention methods include vaccines, medication like aspirin and tamoxifen, and diet low in processed meat. Screening considers test accuracy, potential harms, treatment options, and cost. Cancer treatment includes chemotherapy, radiation, palliative care
Overview and classification of chemotherapeutic agents and theory
This document provides an overview of chemotherapy. It discusses key figures in the development of chemotherapy like Paul Ehrlich and Sidney Farber. It describes different classes of chemotherapeutic agents including alkylating agents, antimetabolites, antitubulins, topoisomerase inhibitors, antibiotics, and their mechanisms and uses for treating various cancers. Side effects of different drug classes are also outlined.
Cancer Staging
Cancer staging classifies how far a cancer has spread and is an important factor in determining treatment. The TNM system stages most cancers based on tumor size (T), lymph node involvement (N), and metastasis (M). A pathological stage is assigned after surgery. Staging helps doctors determine prognosis and the most appropriate treatment for a patient's individual cancer.
targeted therapy
This document discusses principles of targeted cancer therapy and summarizes several studies. It describes how targeted therapies inhibit specific biological targets expressed by tumor cells, such as the epidermal growth factor receptor (EGFR). The document reviews EGFR inhibitors gefitinib and erlotinib, noting their efficacy in certain patient subgroups. It also discusses acquired resistance to these drugs via secondary mutations and the use of EGFR monoclonal antibodies like cetuximab. Further, it summarizes studies of anti-angiogenic therapy with bevacizumab and describes models used to study angiogenesis.
Cell biology and cancer
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.
diagnosis of cancer
There are several methods used to diagnose cancer including radiological, cytological, histological, and molecular diagnoses. Radiological exams like x-rays, CT scans, MRIs are non-invasive methods to detect cancers early. Cytological diagnosis involves examining cells through fine needle aspiration of tumors. Histological diagnosis requires biopsying tissue via various methods to examine under a microscope. Molecular diagnosis and tumor markers in blood can also help detect cancers and minimal residual disease. Making an accurate cancer diagnosis often requires using multiple diagnostic methods and sometimes getting a second opinion.
Etiology of Cancer
Cancer is caused by various genetic, environmental, and lifestyle factors. The document discusses the major etiological factors of cancer such as tobacco use (25-30% of cancers), certain viral infections, chronic inflammation, chemical and physical carcinogens, dietary components, and obesity. It provides details on how each of these factors can damage DNA and promote uncontrolled cell growth and tumor development. The key message is that lifestyle modifications like quitting tobacco, eating healthy, and staying physically active can prevent up to 65% of cancers.
4. molecular basis of cancer dr. sinhasan, mdzah
This document discusses the multistep process of carcinogenesis. It involves nonlethal genetic damage through DNA damaging agents or inherited mutations that affect genes regulating DNA repair, cell growth, and apoptosis. This can lead to mutations in somatic cells and alterations in genes controlling growth and apoptosis. If DNA repair fails, altered gene expression and loss of regulatory genes can cause clonal expansion and additional mutations, resulting in tumor heterogeneity. Tumors are monoclonal, arising from a single mutated precursor cell.
Oncology and surgical practice
Oncology and surgical practice are becoming more integrated, as surgeons are often responsible for initially diagnosing and managing solid tumors. A thorough understanding of cancer epidemiology, etiology, staging, and natural history is required to determine the optimal surgical therapy for each patient. Tumor cells acquire several characteristics before becoming fully malignant, including establishing independence from normal growth controls, achieving immortality and angiogenesis, and developing the abilities to invade other tissues and disseminate throughout the body. Both genetic and environmental factors contribute to cancer development in complex ways. A combination of inherited predispositions and exposures to carcinogenic chemicals, viruses, radiation, and other external factors drive the transformation of normal cells into malignant tumors.
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.
Carcinogenesis , invasion & metastasis
This document summarizes key concepts about carcinogenesis, invasion, and metastasis. It discusses how cancer arises from stem cells and malignant cells grow uncontrollably by evading the body's defenses. Cancer development is driven by genetic changes that result in overexpression of oncogenes and loss of tumor suppressor genes. The process of invasion and metastasis is multistep, involving angiogenesis, loss of cell adhesion, proteolysis, and spread through natural pathways. Some cancers may exist asymptomatically for many years without detection. The goal of treatment is quality of life rather than an undefined concept of cure, as asymptomatic coexistence is possible.
carcinogenesis-
Cancer is characterized by abnormal, uncontrolled cell growth caused by mutations in DNA. Carcinogenesis, the process by which normal cells become cancerous, occurs in multiple stages: initiation, promotion, and progression. Initiation involves genetic mutations from exposure to carcinogens. Promotion causes slow, gradual growth through prolonged exposure. Progression allows the growth to become clinically detectable tumors through continuous proliferation and escape from host defenses. Multiple mutations are required before a normal cell becomes cancerous.
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Cancer carcinogens
This document discusses various carcinogenic agents and their mechanisms of action. It describes direct-acting carcinogens that damage DNA directly and indirect-acting carcinogens that require metabolic activation before becoming carcinogenic. It also discusses initiation and promotion in chemical carcinogenesis. Radiation carcinogenesis from ionizing radiation, ultraviolet light, and viral oncogenesis are also covered, noting specific cancer risks from different exposures.
Cancer cell biology
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
Carcinogenesis
UNDERSTANDING OF CHEMICAL CARCINOGENESIS: CURRENT AND FUTURE PERSPECTIVES
Carcinogenesis refers to the process by which a normal cell is transformed into a malignant cell and repeatedly divides to become a cancer
Chemicals which initiate this process is called chemical carcinogens
Chemicals which increase the effectiveness of carcinogens is called co-carcinogens
CLASSIFICATION OF CHEMICAL CARCINOGENS
MECHANISM OF ACTION
STAGES OF CARCINOGENESIS
ROLE OF PROTO-ONCOGENES AND TUMOR SUPPRESSOR GENES
ACTIVATION OF PROTO ONCOGENES
INACTIVATION OF TUMOR SUPPRESSOR GENE
OXIDATIVE STRESS IN CARCINOGENESIS
ROS can be produced from both endogenous and exogenous sources
Attack both purine and pyrimidine bases, as well as the deoxyribose backbone
Induces DNA damage which includes single or double-strand breakage, deoxyribose modification, and DNA cross-link
If DNA damage is not properly repaired it may result in mutation which leads to cancer
BIOMARKERS
REGULATORY BACKGROUND
OECD guidelines
451- Carcinogenecity studies
453- Combined chronic toxicity/carcinogenecity
ICH guidelines
S1A- Guideline on the need for carcinogenicity studies of
pharmaceuticals
S1B- Testing for carcinogenicity of pharmaceuticals
S1C- Dose selection for carcinogenicity studies of pharmaceuticals
Targeted Therapies in Cancer
This document discusses targeted cancer therapies, which work by interfering with specific molecular targets involved in cancer growth and progression, unlike traditional chemotherapy which acts on all rapidly dividing cells. It provides examples of molecular targets for small molecule drugs and monoclonal antibodies, including growth factor receptors and fusion proteins. The document also discusses methods of target identification, categories of targeted therapies, examples of FDA-approved targeted drugs, limitations and side effects of targeted therapies, and concludes by emphasizing the importance and promise of targeted therapies while noting challenges that remain.
Molecular Genetics and Cancer Biology
This document provides an overview of molecular genetics and cancer biology concepts. It begins with an introduction to basic molecular genetics topics like DNA, genes, chromosomes, and gene expression. It then discusses how normal cells can become cancerous through genetic mutations that disrupt processes like tumor suppressor genes, oncogenes, the cell cycle, and DNA repair. The document emphasizes how understanding molecular genetics advances has helped improve diagnosis and treatment of cancers like prostate and bladder cancer, but also highlights ongoing challenges. It provides context on cancer rates and the need for continued research.
Principles of chemotherapy ppt
Chemotherapy involves the use of cytotoxic drugs to treat cancer. The goals of chemotherapy are to cure cancer, improve survival rates, or relieve symptoms. Key principles of chemotherapy include: (1) using drug combinations to increase efficacy and decrease resistance, (2) treating micrometastatic disease early on, and (3) dose intensity being important for response. Adjuvant chemotherapy after surgery or radiation has improved survival rates for several cancers like breast cancer and osteosarcoma by targeting remaining micrometastatic disease.
Signal Transduction in cancer
This document discusses cell signaling pathways and cell death. It describes the RAS pathway which involves RAS, RAF, MEK and ERK proteins and is mutated in 30% of cancers. Mutations in the PI3K/AKT/mTOR pathways are associated with several cancer types. Inhibitors target proteins in these pathways like PI3K, AKT and mTOR. Apoptosis is described as a programmed cell death pathway involving cell shrinkage, chromatin condensation and formation of apoptotic bodies. Caspases are cysteine proteases that cleave proteins during apoptosis. Cells can also evade apoptosis through expression of anti-apoptotic and pro-apoptotic BCL2 family proteins.
Staging an tumor markers
This document discusses tumor staging and biomarkers for oral cancer. It introduces the TNM staging system and its components for assessing tumor size, lymph node involvement, and metastasis. It also addresses limitations of staging and types of biomarkers that can be used, including commonly used ones like CD44, interleukin levels, and tissue polypeptide antigen. Biomarkers can help with screening, diagnosis, prognosis, and monitoring treatment response for oral cancer.
Hormones and cancer final ppt
Hormones play an important role in certain cancers like breast, prostate, and ovarian cancer. Hormones stimulate the growth of cancerous cells in hormone-dependent cancers. Risk factors for breast cancer include factors affecting hormone levels like early menarche, late menopause, hormone replacement therapy, and oral contraceptive use. Prostate cancer risk is influenced by ethnicity and androgen receptor genes. Hormonal therapies target hormone levels and receptors to slow cancer growth by using medications like anti-androgens and GnRH agonists.
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.
Cancer types and properties
This document discusses cancer types, properties, symptoms, prevention, screening, and treatment. It defines cancer as abnormal cell growth with the potential to invade other parts of the body. The six hallmarks of cancer are described as uncontrolled cell growth, growth despite growth-inhibiting signals, evading cell death, unlimited cell division potential, inducing blood vessel growth, and spreading to other tissues. Common cancer symptoms depend on the location and can include lumps, bleeding, weight loss, and fever. Prevention methods include vaccines, medication like aspirin and tamoxifen, and diet low in processed meat. Screening considers test accuracy, potential harms, treatment options, and cost. Cancer treatment includes chemotherapy, radiation, palliative care
Overview and classification of chemotherapeutic agents and theory
This document provides an overview of chemotherapy. It discusses key figures in the development of chemotherapy like Paul Ehrlich and Sidney Farber. It describes different classes of chemotherapeutic agents including alkylating agents, antimetabolites, antitubulins, topoisomerase inhibitors, antibiotics, and their mechanisms and uses for treating various cancers. Side effects of different drug classes are also outlined.
Cancer Staging
Cancer staging classifies how far a cancer has spread and is an important factor in determining treatment. The TNM system stages most cancers based on tumor size (T), lymph node involvement (N), and metastasis (M). A pathological stage is assigned after surgery. Staging helps doctors determine prognosis and the most appropriate treatment for a patient's individual cancer.
targeted therapy
This document discusses principles of targeted cancer therapy and summarizes several studies. It describes how targeted therapies inhibit specific biological targets expressed by tumor cells, such as the epidermal growth factor receptor (EGFR). The document reviews EGFR inhibitors gefitinib and erlotinib, noting their efficacy in certain patient subgroups. It also discusses acquired resistance to these drugs via secondary mutations and the use of EGFR monoclonal antibodies like cetuximab. Further, it summarizes studies of anti-angiogenic therapy with bevacizumab and describes models used to study angiogenesis.
Cell biology and cancer
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.
diagnosis of cancer
There are several methods used to diagnose cancer including radiological, cytological, histological, and molecular diagnoses. Radiological exams like x-rays, CT scans, MRIs are non-invasive methods to detect cancers early. Cytological diagnosis involves examining cells through fine needle aspiration of tumors. Histological diagnosis requires biopsying tissue via various methods to examine under a microscope. Molecular diagnosis and tumor markers in blood can also help detect cancers and minimal residual disease. Making an accurate cancer diagnosis often requires using multiple diagnostic methods and sometimes getting a second opinion.
Etiology of Cancer
Cancer is caused by various genetic, environmental, and lifestyle factors. The document discusses the major etiological factors of cancer such as tobacco use (25-30% of cancers), certain viral infections, chronic inflammation, chemical and physical carcinogens, dietary components, and obesity. It provides details on how each of these factors can damage DNA and promote uncontrolled cell growth and tumor development. The key message is that lifestyle modifications like quitting tobacco, eating healthy, and staying physically active can prevent up to 65% of cancers.
4. molecular basis of cancer dr. sinhasan, mdzah
This document discusses the multistep process of carcinogenesis. It involves nonlethal genetic damage through DNA damaging agents or inherited mutations that affect genes regulating DNA repair, cell growth, and apoptosis. This can lead to mutations in somatic cells and alterations in genes controlling growth and apoptosis. If DNA repair fails, altered gene expression and loss of regulatory genes can cause clonal expansion and additional mutations, resulting in tumor heterogeneity. Tumors are monoclonal, arising from a single mutated precursor cell.
Oncology and surgical practice
Oncology and surgical practice are becoming more integrated, as surgeons are often responsible for initially diagnosing and managing solid tumors. A thorough understanding of cancer epidemiology, etiology, staging, and natural history is required to determine the optimal surgical therapy for each patient. Tumor cells acquire several characteristics before becoming fully malignant, including establishing independence from normal growth controls, achieving immortality and angiogenesis, and developing the abilities to invade other tissues and disseminate throughout the body. Both genetic and environmental factors contribute to cancer development in complex ways. A combination of inherited predispositions and exposures to carcinogenic chemicals, viruses, radiation, and other external factors drive the transformation of normal cells into malignant tumors.
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.
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This document summarizes key concepts about carcinogenesis, invasion, and metastasis. It discusses how cancer arises from stem cells and malignant cells grow uncontrollably by evading the body's defenses. Cancer development is driven by genetic changes that result in overexpression of oncogenes and loss of tumor suppressor genes. The process of invasion and metastasis is multistep, involving angiogenesis, loss of cell adhesion, proteolysis, and spread through natural pathways. Some cancers may exist asymptomatically for many years without detection. The goal of treatment is quality of life rather than an undefined concept of cure, as asymptomatic coexistence is possible.
carcinogenesis-
Cancer is characterized by abnormal, uncontrolled cell growth caused by mutations in DNA. Carcinogenesis, the process by which normal cells become cancerous, occurs in multiple stages: initiation, promotion, and progression. Initiation involves genetic mutations from exposure to carcinogens. Promotion causes slow, gradual growth through prolonged exposure. Progression allows the growth to become clinically detectable tumors through continuous proliferation and escape from host defenses. Multiple mutations are required before a normal cell becomes cancerous.
ASTHMA
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Carcinogenesis
Carcinogenesis refers to the process by which a normal cell is transformed into a malignant cell and repeatedly divides to become a cancer
Chemicals which initiate this process is called chemical carcinogens
Chemicals which increase the effectiveness of carcinogens is called co-carcinogens
REGULATORY BACKGROUND
ROLE OF PROTO-ONCOGENES AND TUMOR SUPPRESSOR GENES
ACTIVATION OF PROTO ONCOGENES
OXIDATIVE STRESS IN CARCINOGENESIS
OECD guidelines
451- Carcinogenecity studies
453- Combined chronic toxicity/carcinogenecity
ICH guidelines
S1A- Guideline on the need for carcinogenicity studies of
pharmaceuticals
S1B- Testing for carcinogenicity of pharmaceuticals
S1C- Dose selection for carcinogenicity studies of pharmaceuticals
Neoplasia & Carcinogenesis
Neoplasia refers to abnormal cell growth or tumors. There are two main types of neoplasia - benign and malignant. Benign tumors remain localized and are non-invasive, while malignant tumors can invade surrounding tissues and spread to distant sites through lymphatic vessels or blood vessels in a process called metastasis. The development of cancer is a multistep process that involves genetic mutations that activate oncogenes and inactivate tumor suppressor genes, resulting in uncontrolled cell growth and division. Key hallmarks of cancer include self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize.
Hepatotoxicity
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- 1. A Presentation on CARCINOGENESIS Presented By : Sejuti Mazumder 3rd year, B.Sc nursing (C.O.N.R.G.K.M.C.H) Submitted To : Sujata Das Senior Lecturer (C.O.N.R.G.K.M.C.H)
- 2. Definition The process by which normal cells are transformed into CANCER or malignant cells . Result of a disturbance in : - control of cell proliferation -cell differentiation - relationship of cells to each other and to their surrounding
- 3. Genetic basis of Carcinogenesis Proto-oncogene ( Accelerator ) Cell Division Gene products Differentiation (GF,GFR, DNA binding Ageing Death proteins ) Tumour Sup , gene (Breaks)
- 4. Etiological Factors 1. Family History 2. Genetic predisposition 3. Age 4. Environmental Factors 5. Occupational exposure 6. Life style factors 7. Viruses & Bacteria 8. Drugs & Medical treatment 9. Humonal agent
- 5. Process of Carcinogenesis INITIATION PROMOTION PROGRESSION METASTASIS 1.Occurs in genetic 1.cancer cell form tumor . 1.cells show capacity to 1.movement of cancar cell level. 2.promoting of agent beyond invade or metasize to from primary to remote site. 2.Permit malignant atency period. Surrounding tissues. 2.cells loss adherence property transformation. 2.tumor develops own 3.DNA chain break. blood supply. 4.Gene mutation 3.Angiogenesis happen. activate proto- 4.TAF also happen. oncogenes.
- 6. Mechanism of Invasion and Metastasis Invasion and metastasis is a multi-stepped process : Angiogenesis – Tumour acquires an additional blood supply Homotypic cell adhesion lost – Normal cell adhesion is due to desmosomes, negative cell surface charge and calcium dependent adhesion molecules-cadherins. Adhesion of tumour cells to the BM & extracellular matrices- Mediated by a receptor ligand mechanism known as laminin & integrin. Proteolysis- Cells penetrate through the basement membrane and extracellular matrix. Cells move through the connective tissue matrix and invade natural anatomic pathways of spread such as lymphatics, blood vessels and serosalined cavities.
- 7. Staging of Cancer Stage 0 or Carcinoma Stage I Stage IA Stage IB Stage II Stage IIA Stage IIB Stage III Stage IV Stage IVA Stage IVB
- 8. Stage 0 or Carcinoma 1. Carcinoma-in-situ Carcinoma-in-situ (CIS) is a pre-cancerous condition. Under the microscope, cells with CIS show some degree of change but the epithelial basement membrane is not breached. 2.Classification of carcinomas Carcinomas from different origins are classified into six broad subgroups: -Adrenocortical carcinoma which affect the adrenal glands -Thyroid carcinoma which affects the thyroid gland -Nasopharyngeal carcinoma which affects the nose and pharynx -Malignant melanoma which describes skin cancer -Skin carcinoma other than melanoma -Other carcinomas including those affecting the salivary gland, colon, appendix, lung and bronchus, cervix, and urinary bladder
- 9. Stage-1 Cancer involves the primary site but has not spread to nearly tissues. 1. STAGE IA-A very small amount of cancer –visible under a microscope –is found deeper in the tissues. 1. STAGE IB- A larger amount of cancer is the tissues.
- 10. STAGE-II Cancer has spread to nearly areas but it still inside the primary site. Stage IIA – Cancer has spread beyond the primary site. Stage IIB – Cancer has spread to other tissue around the primary site. STAGE – III Cancer has spread throughout the nearby area.
- 11. Stage IV Cancer has spread to other parts of the body Stage IV A – Cancer has spread to organs close to the pelvic area. Stage IV B – Cancer has spread to distant organs such as the lungs.
- 12. TNM Staging Letter Stands for Description T tumour Indicates the sizes of primary tumour and the degree of spread into nearby tissues.( local version) N Lymph node indicates whether or not the cancer has spread to nearby lymph nodes, the size of the nodes that contain cancer and how many lymph nodes contain cancer. M Metastasis indicates whether or not cancer has spread (metastasized) to distant organs .
- 13. TNM Staging
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