Tumors can affect the host locally, hormonally, and systemically. Locally, tumors can cause compression, obstruction, tissue destruction, and bleeding. Hormonally, tumors may cause paraneoplastic syndromes like hypoglycemia or hypercalcemia. Systemically, tumors can cause cachexia, fever, and anorexia. The immune system responds to tumors through cellular immunity using cytotoxic T cells and NK cells, and humoral immunity with antibody production. However, tumors evade immune responses through antigen loss, immunosuppression, and apoptosis of cytotoxic T cells. Immunotherapy uses active methods like vaccines or passive methods like antibodies to stimulate anti-tumor immunity.
Neoplasia refers to abnormal cell growth. Benign tumors grow slowly, are self-limited and non-invasive, while malignant tumors grow rapidly, invade surrounding tissues, and can metastasize to distant sites. The mechanism of neoplasia involves loss of differentiation, increased growth rate, local invasion, and metastasis in malignant tumors compared to benign tumors. Nomenclature of tumors is based on the cell of origin and suffix, such as carcinoma for epithelial tumors and sarcoma for mesenchymal tumors.
This document discusses the histopathology of carcinogenesis. It begins with an overview of carcinogenesis as a complex, multistep process influenced by multiple intrinsic and extrinsic factors. It then defines key terms in the lexicon of neoplasia, including hyperplasia, metaplasia, anaplasia, and dysplasia. Molecular factors in carcinogenesis are described, such as alterations in proto-oncogenes and cancer suppressor genes that regulate cell growth and proliferation. Morphological factors like pathological hyperplasia, preneoplasia, adenomas, and carcinomas are also outlined.
Principles of cancer cheotherapy by Dr Deenadayalan MD.,DM(Onco),Madurai.Dr DEENADAYALAN T
- Chemotherapy involves using cytotoxic drugs to destroy cancer cells. The goal is to cure cancer when possible or palliate symptoms when cure is not achievable.
- Cancer cells differ from normal cells in characteristics like increased growth factor secretion and loss of tumor suppressor genes. Tumor growth depends on factors like growth fraction and cell cycle time.
- Combination chemotherapy aims to increase efficacy by using drugs with different mechanisms of action and resistance profiles. Dose-dense regimens prevent tumor repopulation between treatment cycles.
- Factors influencing response to chemotherapy include tumor type and size, drug resistance, and patient characteristics like organ function and performance status. Measuring treatment response relies on changes in tumor size, cell
Cancer develops through a multi-step process involving genetic mutations that disrupt the normal cell cycle and allow uncontrolled cell growth. The cell cycle is regulated by various proto-oncogenes and tumor suppressor genes. Mutations in these genes, such as activating mutations in proto-oncogenes or loss of function mutations in tumor suppressor genes, can cause cells to ignore growth controls and proliferate unchecked. This can eventually lead to the development of malignant tumors. Common tumor suppressor genes include RB1, TP53, BRCA1, and BRCA2, which are involved in processes like cell cycle regulation and DNA repair. Mutations in these genes increase cancer risk.
Cell cycle- Dr Deenadayalan,Medical Oncologst,MauraiDr DEENADAYALAN T
This document provides information about the cell cycle and its regulation. It discusses the key phases of the cell cycle - prophase, metaphase, anaphase and telophase. It describes the cell cycle regulators including cyclins, cyclin dependent kinases, and cyclin dependent kinase inhibitors. It also discusses cell cycle checkpoints and alterations in cell cycle control proteins that can lead to cancer. Finally, it briefly mentions cell cycle phase specific and non-specific agents used in cancer treatment.
Tumor markers are proteins or mutated proteins that can indicate the presence of cancer. They are useful for screening, diagnosis, monitoring treatment and detecting recurrence, though none are sufficiently sensitive and specific for screening alone. Tumor markers associated with cell proliferation, differentiation, metastasis and other tumor events can provide information about cancer. While not diagnostic, they are helpful for treatment monitoring given their limitations. Proper use requires understanding their sensitivity, specificity and potential causes of false positives.
This document discusses neoplasia and chemical carcinogenesis. It identifies two types of major chemical carcinogens: directly acting carcinogens like alkylating and acylating agents, and procarcinogens that require metabolic activation. It also lists several paraneoplastic syndromes associated with different types of cancers, such as ACTH and ADH secretion in small cell lung cancer. Finally, it categorizes nine different types of tumor antigens.
This document discusses neoplasia and cancer. It defines benign and malignant tumors, with malignant tumors being cancerous and having the potential to kill the host if untreated through invasion or metastasis. Cancer development is described as a multistep process involving initiation through genetic mutations, promotion of cell growth, and progression to a malignant phenotype. Risk factors for cancer like tobacco use, nutrition, and genetic factors are examined. The roles of oncogenes and tumor suppressor genes in carcinogenesis are explained.
Neoplasia refers to abnormal cell growth. Benign tumors grow slowly, are self-limited and non-invasive, while malignant tumors grow rapidly, invade surrounding tissues, and can metastasize to distant sites. The mechanism of neoplasia involves loss of differentiation, increased growth rate, local invasion, and metastasis in malignant tumors compared to benign tumors. Nomenclature of tumors is based on the cell of origin and suffix, such as carcinoma for epithelial tumors and sarcoma for mesenchymal tumors.
This document discusses the histopathology of carcinogenesis. It begins with an overview of carcinogenesis as a complex, multistep process influenced by multiple intrinsic and extrinsic factors. It then defines key terms in the lexicon of neoplasia, including hyperplasia, metaplasia, anaplasia, and dysplasia. Molecular factors in carcinogenesis are described, such as alterations in proto-oncogenes and cancer suppressor genes that regulate cell growth and proliferation. Morphological factors like pathological hyperplasia, preneoplasia, adenomas, and carcinomas are also outlined.
Principles of cancer cheotherapy by Dr Deenadayalan MD.,DM(Onco),Madurai.Dr DEENADAYALAN T
- Chemotherapy involves using cytotoxic drugs to destroy cancer cells. The goal is to cure cancer when possible or palliate symptoms when cure is not achievable.
- Cancer cells differ from normal cells in characteristics like increased growth factor secretion and loss of tumor suppressor genes. Tumor growth depends on factors like growth fraction and cell cycle time.
- Combination chemotherapy aims to increase efficacy by using drugs with different mechanisms of action and resistance profiles. Dose-dense regimens prevent tumor repopulation between treatment cycles.
- Factors influencing response to chemotherapy include tumor type and size, drug resistance, and patient characteristics like organ function and performance status. Measuring treatment response relies on changes in tumor size, cell
Cancer develops through a multi-step process involving genetic mutations that disrupt the normal cell cycle and allow uncontrolled cell growth. The cell cycle is regulated by various proto-oncogenes and tumor suppressor genes. Mutations in these genes, such as activating mutations in proto-oncogenes or loss of function mutations in tumor suppressor genes, can cause cells to ignore growth controls and proliferate unchecked. This can eventually lead to the development of malignant tumors. Common tumor suppressor genes include RB1, TP53, BRCA1, and BRCA2, which are involved in processes like cell cycle regulation and DNA repair. Mutations in these genes increase cancer risk.
Cell cycle- Dr Deenadayalan,Medical Oncologst,MauraiDr DEENADAYALAN T
This document provides information about the cell cycle and its regulation. It discusses the key phases of the cell cycle - prophase, metaphase, anaphase and telophase. It describes the cell cycle regulators including cyclins, cyclin dependent kinases, and cyclin dependent kinase inhibitors. It also discusses cell cycle checkpoints and alterations in cell cycle control proteins that can lead to cancer. Finally, it briefly mentions cell cycle phase specific and non-specific agents used in cancer treatment.
Tumor markers are proteins or mutated proteins that can indicate the presence of cancer. They are useful for screening, diagnosis, monitoring treatment and detecting recurrence, though none are sufficiently sensitive and specific for screening alone. Tumor markers associated with cell proliferation, differentiation, metastasis and other tumor events can provide information about cancer. While not diagnostic, they are helpful for treatment monitoring given their limitations. Proper use requires understanding their sensitivity, specificity and potential causes of false positives.
This document discusses neoplasia and chemical carcinogenesis. It identifies two types of major chemical carcinogens: directly acting carcinogens like alkylating and acylating agents, and procarcinogens that require metabolic activation. It also lists several paraneoplastic syndromes associated with different types of cancers, such as ACTH and ADH secretion in small cell lung cancer. Finally, it categorizes nine different types of tumor antigens.
This document discusses neoplasia and cancer. It defines benign and malignant tumors, with malignant tumors being cancerous and having the potential to kill the host if untreated through invasion or metastasis. Cancer development is described as a multistep process involving initiation through genetic mutations, promotion of cell growth, and progression to a malignant phenotype. Risk factors for cancer like tobacco use, nutrition, and genetic factors are examined. The roles of oncogenes and tumor suppressor genes in carcinogenesis are explained.
The document discusses tumour biology and classification. It defines benign and malignant tumours, with benign tumours being localized growths that are non-invasive and slow-growing, while malignant tumours infiltrate surrounding tissues, metastasize, and are poorly differentiated. Tumours are classified based on their tissue of origin, with epithelial tumours called carcinomas and mesenchymal tumours called sarcomas. Grading and staging of malignant tumours is also discussed, with grade relating to differentiation and stage relating to tumour size, lymph node involvement, and metastasis. Various benign and malignant tumour types and their microscopic features are presented with images.
This document discusses tumor pathogenesis and the general development of tumors. It describes how tumors progress through initiation, promotion and progression stages due to the effects of various growth factors, genes, mutagens and epigenetic factors. The main causes of cancer are identified as smoking, dietary imbalances, and chronic infections leading to inflammation. Benign and malignant tumors are defined, and the characteristics of neoplasms, including loss of growth control, unlimited division, invasion and metastasis, are outlined.
Bone marrow transplantation replaces unhealthy blood-forming cells with healthy ones. There are three main types of bone marrow transplants: autologous uses the patient's own cells, allogeneic uses a donor's cells, and syngeneic uses an identical twin's cells. A bone marrow transplant is carried out to treat life-threatening blood, immune, or genetic disorders like leukemia or myeloma. The transplantation process involves conditioning the patient with chemotherapy or radiation, collecting stem cells from the donor, infusing the donor's stem cells, and an engraftment period where the new stem cells establish in the bone marrow. Potential adverse effects include infections, gastrointestinal issues, and temporary hair loss.
This document provides an overview of general principles in cancer chemotherapy. It discusses that chemotherapy uses cytotoxic drugs to destroy malignant cells. Drugs can be cell cycle specific, killing dividing cells, or nonspecific, killing resting and dividing cells. Combination chemotherapy using multiple drugs with different mechanisms of action is now common to achieve total tumor cell kill. Careful scheduling of cell cycle specific and nonspecific drugs is important. Tumors can become resistant to repeated use of single drugs through selection of less responsive cells or mutations altering drug targets. The goal of chemotherapy is complete remission through use of maximum tolerated drug doses in combination regimens.
Cancer is defined as abnormal cell growth that can spread to other parts of the body. There are two main types of tumors - benign tumors which do not spread, and malignant tumors which can metastasize. The cell cycle is the series of events cells go through during cell division, including interphase (G1, S, G2 phases) and mitosis. Mitosis involves the replication and separation of chromosomes, followed by cytokinesis where the cell cytoplasm divides forming two daughter cells. Metastasis occurs through a multi-step process where cancer cells break away from the primary tumor and travel through the bloodstream to form secondary tumors elsewhere in the body.
- Stephen Paget's "Seed and Soil" hypothesis from 1889 proposed that tumor cells ("seeds") need to find a supportive microenvironment ("soil") to grow in. The molecular characteristics of the tumor microenvironment ("soil") are less understood than those of the tumor cells ("seeds").
- The tumor microenvironment consists of various cell types like fibroblasts, immune cells, and endothelial cells as well as the extracellular matrix. It plays an important role in regulating normal cell behavior but can shift to a growth-promoting state and support tumor development.
- Chronic inflammation can override the protective constraints of the microenvironment and promote a growth-supporting state through cells like tumor-associated macrophages that secrete factors influencing angiogenesis,
1. Metastasis is a multi-step process by which tumor cells spread from a primary tumor to distant sites in the body and form secondary tumors.
2. The document discusses factors that drive tumor cell invasion and metastasis, including hypoxia, inflammation, escaping apoptosis and senescence, self-renewal ability, and coupling tumorigenesis with metastasis initiation and progression.
3. It also describes the key steps in metastasis including intravasation, survival in circulation, arrest and extravasation in distant organs, and growth of metastases.
This document discusses cancer invasion and metastasis. It begins by introducing the concepts of invasion and metastasis, where cancer spreads from the primary site to distant tissues. It then discusses the somatic evolution of cancer and the multiple genetic alterations required for malignancy. The document covers clinical and pathological correlations with metastasis risk, and the "seed and soil" hypothesis of why cancers metastasize to certain organs. It outlines the basic steps in the metastatic cascade, including invasion, intravasation, arrest and extravasation at distant sites. Finally, it discusses the implications of the traditional progression model, including the rarity of metastatic cells and prevention of metastasis through early detection and treatment.
This document provides an overview of cancer and chemotherapy. It discusses that cancer is caused by deregulation of cell proliferation and apoptotic mechanisms. Cancer develops through multiple mutations that cause uncontrolled growth. Chemotherapy aims to kill rapidly dividing cells and works through several classes of drugs including alkylating agents, antimetabolites, anthracyclins, plant alkaloids, and cytotoxic antibiotics. These drugs have various mechanisms of action but commonly cause side effects by also killing normal cells. Chemotherapy regimens typically combine multiple drugs to reduce resistance.
Principles of chemotherapy(types, indications and complications)ashirwad karigoudar
This document provides an overview of the principles of chemotherapy. It discusses the historical origins of chemotherapy beginning in the 1960s when combination chemotherapy was found to cure childhood leukemias and lymphomas. It also addresses the main obstacles of toxicity and drug resistance. The document then covers the clinical applications of chemotherapy including primary induction, neoadjuvant, adjuvant, and site-directed treatments. It concludes by discussing principles of cancer kinetics, drug resistance biology, and methods for assessing clinical response.
The document discusses the role of immunohistochemistry (IHC) in head and neck pathology. IHC uses antibodies to identify antigens in tissues and can help diagnose cancers and determine tumor type. It plays an important role in pathology subspecialties like oncology, neuropathology, and hematopathology. The document provides details on the principle of IHC, various tissue and tumor markers used in IHC, and how IHC can help diagnose lesions in the head and neck region like oral cancers, salivary gland tumors, melanomas, sarcomas, and lymphomas.
This document outlines various laboratory methods for diagnosing neoplasia, including morphological, immunohistochemistry, molecular, and flow cytometry techniques. Morphological methods include cytological examinations like fine needle aspiration cytology, exfoliative cytology, and abrasive cytology. Immunohistochemistry and molecular techniques help identify tumor origin and prognostic markers. Flow cytometry allows rapid quantification of individual cell characteristics to classify tumors. Together, an integrated approach using multiple diagnostic methods provides the most accurate assessment of cancer.
Principles of cancer chemotherapy: a deep insight, by RxVichuZ!!RxVichuZ
This presentation deals with PRINCIPLES OF CANCER CHEMOTHERAPY.
The following headings are included:
A. PRINCIPLES OF ONCOLOGY
B. CELL-CYCLE
C. PRINCIPLES OF CANCER CHEMOTHERAPY
Precise details have been provided.
Do go through!!
Introduction
Etiology of cancer
Genetic and molecular basis of cancer
The cell cycle
Pathology of cancer
Tumor origin
Tumor characteristics
Invasion and metastasis
Diagnosis and staging
Screening
Diagnosis
Staging and workup
The document describes various types of rodent liver lesions including neoplastic lesions such as hepatocellular adenomas and carcinomas, cholangiomas and cholangiocarcinomas, hepatoblastomas, hepatocholangiomas and hepatocholangiocarcinomas, Ito cell tumors, histiocytic sarcomas, hemangiomas and hemangiosarcomas, as well as lymphomas, erythroleukemia, and mononuclear cell leukemia. Photomicrographs are provided to illustrate characteristics such as nodular growth patterns, cellular pleomorphism, and infiltrative properties of these rodent liver tumors and cancers.
Cancer metastasis is the process where cancer cells spread from the primary tumor to distant sites in the body. There are 5 major steps in metastasis: 1) invasion of surrounding tissue, 2) release into circulation, 3) survival in circulation, 4) arrest in capillaries of distant organs, 5) penetration of vessel walls and growth. Metastasis can occur through the bloodstream (hematogenous), lymphatic system, or body cavities. Cancer cells degrade the extracellular matrix using enzymes to migrate, and can die from detachment, damage in vessels, or immune system attack. Some cancers have preferential metastatic sites thought to be due to anatomical proximity or a compatible tissue environment.
This document discusses principles of oncology including cell number control, growth disorders, cancer classification, tumor spread and metastasis, stages of cancer, and an overview of carcinogenesis. It defines key terms like neoplasia, benign and malignant tumors, dysplasia, carcinoma and sarcoma. It also summarizes the hallmarks of cancer including self-sufficiency in growth signals, evasion of apoptosis, unlimited replicative potential, sustained angiogenesis, and genetic instability.
This document discusses cancer and chemotherapy. It begins by defining cancer as abnormal cells that do not stop dividing. It then lists the top causes of cancer deaths in the United States for males and females. Next, it identifies nine avoidable risk factors that cause one third of cancer deaths, such as smoking and obesity. The document goes on to explain what chemotherapy is and describes how chemotherapy drugs work to destroy cancer cells. It provides examples of different types of chemotherapy drugs and their mechanisms of action. Finally, it discusses some complications of cancer and chemotherapy treatment, including pain, nausea, and mouth sores.
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 definitions and explanations of key cancer-related terms:
- Cancer is characterized by uncontrolled cell growth and spread. Benign tumors are not invasive while malignant tumors continue growing and spreading. Metastasis occurs when cancer cells spread from the original tumor to other parts of the body.
- Carcinomas arise from epithelial tissues, sarcomas from connective tissues, and leukemia from blood-forming tissues in the bone marrow. Carcinogens are agents that can cause cancer. Tumor antigens include those from mutated genes and overexpressed proteins. Immunotherapy harnesses the immune system to fight cancer using approaches like monoclonal antibody treatment, adoptive cell transfer, and cancer vaccines.
Tumor immunology studies the immune response to tumors and tumor evasion of the immune system. Cancers arise due to genetic mutations and environmental factors that cause dysregulated cell growth. The immune system surveils for tumors but tumors can evade detection through mechanisms like antigen modulation or immunosuppression. Cancer immunotherapy aims to boost anti-tumor immunity through cytokines, monoclonal antibodies, and vaccines to prevent tumor escape. Promising areas of research include vaccines targeting neoantigens and immune checkpoint therapies.
The document discusses tumour biology and classification. It defines benign and malignant tumours, with benign tumours being localized growths that are non-invasive and slow-growing, while malignant tumours infiltrate surrounding tissues, metastasize, and are poorly differentiated. Tumours are classified based on their tissue of origin, with epithelial tumours called carcinomas and mesenchymal tumours called sarcomas. Grading and staging of malignant tumours is also discussed, with grade relating to differentiation and stage relating to tumour size, lymph node involvement, and metastasis. Various benign and malignant tumour types and their microscopic features are presented with images.
This document discusses tumor pathogenesis and the general development of tumors. It describes how tumors progress through initiation, promotion and progression stages due to the effects of various growth factors, genes, mutagens and epigenetic factors. The main causes of cancer are identified as smoking, dietary imbalances, and chronic infections leading to inflammation. Benign and malignant tumors are defined, and the characteristics of neoplasms, including loss of growth control, unlimited division, invasion and metastasis, are outlined.
Bone marrow transplantation replaces unhealthy blood-forming cells with healthy ones. There are three main types of bone marrow transplants: autologous uses the patient's own cells, allogeneic uses a donor's cells, and syngeneic uses an identical twin's cells. A bone marrow transplant is carried out to treat life-threatening blood, immune, or genetic disorders like leukemia or myeloma. The transplantation process involves conditioning the patient with chemotherapy or radiation, collecting stem cells from the donor, infusing the donor's stem cells, and an engraftment period where the new stem cells establish in the bone marrow. Potential adverse effects include infections, gastrointestinal issues, and temporary hair loss.
This document provides an overview of general principles in cancer chemotherapy. It discusses that chemotherapy uses cytotoxic drugs to destroy malignant cells. Drugs can be cell cycle specific, killing dividing cells, or nonspecific, killing resting and dividing cells. Combination chemotherapy using multiple drugs with different mechanisms of action is now common to achieve total tumor cell kill. Careful scheduling of cell cycle specific and nonspecific drugs is important. Tumors can become resistant to repeated use of single drugs through selection of less responsive cells or mutations altering drug targets. The goal of chemotherapy is complete remission through use of maximum tolerated drug doses in combination regimens.
Cancer is defined as abnormal cell growth that can spread to other parts of the body. There are two main types of tumors - benign tumors which do not spread, and malignant tumors which can metastasize. The cell cycle is the series of events cells go through during cell division, including interphase (G1, S, G2 phases) and mitosis. Mitosis involves the replication and separation of chromosomes, followed by cytokinesis where the cell cytoplasm divides forming two daughter cells. Metastasis occurs through a multi-step process where cancer cells break away from the primary tumor and travel through the bloodstream to form secondary tumors elsewhere in the body.
- Stephen Paget's "Seed and Soil" hypothesis from 1889 proposed that tumor cells ("seeds") need to find a supportive microenvironment ("soil") to grow in. The molecular characteristics of the tumor microenvironment ("soil") are less understood than those of the tumor cells ("seeds").
- The tumor microenvironment consists of various cell types like fibroblasts, immune cells, and endothelial cells as well as the extracellular matrix. It plays an important role in regulating normal cell behavior but can shift to a growth-promoting state and support tumor development.
- Chronic inflammation can override the protective constraints of the microenvironment and promote a growth-supporting state through cells like tumor-associated macrophages that secrete factors influencing angiogenesis,
1. Metastasis is a multi-step process by which tumor cells spread from a primary tumor to distant sites in the body and form secondary tumors.
2. The document discusses factors that drive tumor cell invasion and metastasis, including hypoxia, inflammation, escaping apoptosis and senescence, self-renewal ability, and coupling tumorigenesis with metastasis initiation and progression.
3. It also describes the key steps in metastasis including intravasation, survival in circulation, arrest and extravasation in distant organs, and growth of metastases.
This document discusses cancer invasion and metastasis. It begins by introducing the concepts of invasion and metastasis, where cancer spreads from the primary site to distant tissues. It then discusses the somatic evolution of cancer and the multiple genetic alterations required for malignancy. The document covers clinical and pathological correlations with metastasis risk, and the "seed and soil" hypothesis of why cancers metastasize to certain organs. It outlines the basic steps in the metastatic cascade, including invasion, intravasation, arrest and extravasation at distant sites. Finally, it discusses the implications of the traditional progression model, including the rarity of metastatic cells and prevention of metastasis through early detection and treatment.
This document provides an overview of cancer and chemotherapy. It discusses that cancer is caused by deregulation of cell proliferation and apoptotic mechanisms. Cancer develops through multiple mutations that cause uncontrolled growth. Chemotherapy aims to kill rapidly dividing cells and works through several classes of drugs including alkylating agents, antimetabolites, anthracyclins, plant alkaloids, and cytotoxic antibiotics. These drugs have various mechanisms of action but commonly cause side effects by also killing normal cells. Chemotherapy regimens typically combine multiple drugs to reduce resistance.
Principles of chemotherapy(types, indications and complications)ashirwad karigoudar
This document provides an overview of the principles of chemotherapy. It discusses the historical origins of chemotherapy beginning in the 1960s when combination chemotherapy was found to cure childhood leukemias and lymphomas. It also addresses the main obstacles of toxicity and drug resistance. The document then covers the clinical applications of chemotherapy including primary induction, neoadjuvant, adjuvant, and site-directed treatments. It concludes by discussing principles of cancer kinetics, drug resistance biology, and methods for assessing clinical response.
The document discusses the role of immunohistochemistry (IHC) in head and neck pathology. IHC uses antibodies to identify antigens in tissues and can help diagnose cancers and determine tumor type. It plays an important role in pathology subspecialties like oncology, neuropathology, and hematopathology. The document provides details on the principle of IHC, various tissue and tumor markers used in IHC, and how IHC can help diagnose lesions in the head and neck region like oral cancers, salivary gland tumors, melanomas, sarcomas, and lymphomas.
This document outlines various laboratory methods for diagnosing neoplasia, including morphological, immunohistochemistry, molecular, and flow cytometry techniques. Morphological methods include cytological examinations like fine needle aspiration cytology, exfoliative cytology, and abrasive cytology. Immunohistochemistry and molecular techniques help identify tumor origin and prognostic markers. Flow cytometry allows rapid quantification of individual cell characteristics to classify tumors. Together, an integrated approach using multiple diagnostic methods provides the most accurate assessment of cancer.
Principles of cancer chemotherapy: a deep insight, by RxVichuZ!!RxVichuZ
This presentation deals with PRINCIPLES OF CANCER CHEMOTHERAPY.
The following headings are included:
A. PRINCIPLES OF ONCOLOGY
B. CELL-CYCLE
C. PRINCIPLES OF CANCER CHEMOTHERAPY
Precise details have been provided.
Do go through!!
Introduction
Etiology of cancer
Genetic and molecular basis of cancer
The cell cycle
Pathology of cancer
Tumor origin
Tumor characteristics
Invasion and metastasis
Diagnosis and staging
Screening
Diagnosis
Staging and workup
The document describes various types of rodent liver lesions including neoplastic lesions such as hepatocellular adenomas and carcinomas, cholangiomas and cholangiocarcinomas, hepatoblastomas, hepatocholangiomas and hepatocholangiocarcinomas, Ito cell tumors, histiocytic sarcomas, hemangiomas and hemangiosarcomas, as well as lymphomas, erythroleukemia, and mononuclear cell leukemia. Photomicrographs are provided to illustrate characteristics such as nodular growth patterns, cellular pleomorphism, and infiltrative properties of these rodent liver tumors and cancers.
Cancer metastasis is the process where cancer cells spread from the primary tumor to distant sites in the body. There are 5 major steps in metastasis: 1) invasion of surrounding tissue, 2) release into circulation, 3) survival in circulation, 4) arrest in capillaries of distant organs, 5) penetration of vessel walls and growth. Metastasis can occur through the bloodstream (hematogenous), lymphatic system, or body cavities. Cancer cells degrade the extracellular matrix using enzymes to migrate, and can die from detachment, damage in vessels, or immune system attack. Some cancers have preferential metastatic sites thought to be due to anatomical proximity or a compatible tissue environment.
This document discusses principles of oncology including cell number control, growth disorders, cancer classification, tumor spread and metastasis, stages of cancer, and an overview of carcinogenesis. It defines key terms like neoplasia, benign and malignant tumors, dysplasia, carcinoma and sarcoma. It also summarizes the hallmarks of cancer including self-sufficiency in growth signals, evasion of apoptosis, unlimited replicative potential, sustained angiogenesis, and genetic instability.
This document discusses cancer and chemotherapy. It begins by defining cancer as abnormal cells that do not stop dividing. It then lists the top causes of cancer deaths in the United States for males and females. Next, it identifies nine avoidable risk factors that cause one third of cancer deaths, such as smoking and obesity. The document goes on to explain what chemotherapy is and describes how chemotherapy drugs work to destroy cancer cells. It provides examples of different types of chemotherapy drugs and their mechanisms of action. Finally, it discusses some complications of cancer and chemotherapy treatment, including pain, nausea, and mouth sores.
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 definitions and explanations of key cancer-related terms:
- Cancer is characterized by uncontrolled cell growth and spread. Benign tumors are not invasive while malignant tumors continue growing and spreading. Metastasis occurs when cancer cells spread from the original tumor to other parts of the body.
- Carcinomas arise from epithelial tissues, sarcomas from connective tissues, and leukemia from blood-forming tissues in the bone marrow. Carcinogens are agents that can cause cancer. Tumor antigens include those from mutated genes and overexpressed proteins. Immunotherapy harnesses the immune system to fight cancer using approaches like monoclonal antibody treatment, adoptive cell transfer, and cancer vaccines.
Tumor immunology studies the immune response to tumors and tumor evasion of the immune system. Cancers arise due to genetic mutations and environmental factors that cause dysregulated cell growth. The immune system surveils for tumors but tumors can evade detection through mechanisms like antigen modulation or immunosuppression. Cancer immunotherapy aims to boost anti-tumor immunity through cytokines, monoclonal antibodies, and vaccines to prevent tumor escape. Promising areas of research include vaccines targeting neoantigens and immune checkpoint therapies.
This document discusses tumor immunity and the immune system's response to tumors. It begins with an introduction and outlines the aim and objectives. It then covers basic concepts of tumor immunity including tumor antigens and anti-tumor effector mechanisms. It discusses immunosurveillance and immunoediting of cancer and how tumors can evade the immune system. It also touches on laboratory investigation, cancer vaccine development, cancer immunotherapy, and conclusions. The overall goal is to explain how the immune system responds to tumors and the complex relationship between immunity and tumor development.
This document summarizes tumor immunology and immunotherapy for cancer treatment. It discusses how the immune system interacts with tumors and identifies tumor antigens. It also describes tumor evasion mechanisms that allow cancers to avoid immune detection and destruction. Current immunotherapeutic strategies discussed include antibody therapy, cytokine therapy, adoptive T cell therapy, vaccination, and combination approaches. The document reviews obstacles to effective cancer immunotherapy like self-tolerance and suppressive cells in the tumor microenvironment.
CANCER: A REVIEW: WORLD'S SECOND MOST FEARED DIAGNOSISCharu Pundir
It is a basic review presentation on cancer, world's second most dreadful disease followed by cardiovascular events, involving basic defination, pathophysiology, screening methods, types of tumor, tumor origin, cancer cell lines, treatment, recent advancements made in the field and diagnosis.
Cancer can both weaken the immune system and be fought by the immune system. It can weaken immunity by spreading to bone marrow and reducing blood cell production, or through side effects of treatments like chemotherapy and radiation. However, parts of the immune system also recognize cancer cells as abnormal and try to kill them. New immunotherapies aim to boost this response by using antibodies, cytokines, vaccines, and other methods to help the immune system better eliminate cancer cells. A balanced relationship exists between cancer and immunity.
This document discusses anti-neoplastic drugs, including their objectives, classification, mechanisms of action, and toxicities. It begins with an introduction to normal and malignant cells. It then covers classification of anti-neoplastic drugs, their goals in cancer treatment, common mechanisms of action like preventing DNA synthesis, and general toxicities like bone marrow suppression. Specific drug classes are also summarized, including antimetabolites, antibiotics, alkylating agents, and microtubule inhibitors.
This document discusses tumor immunology and immunotherapy. It provides evidence that the immune system can recognize and react against tumors. It describes tumor-associated antigens that can be recognized by the immune system. However, tumors also have mechanisms for escaping immune surveillance, such as not expressing immunogenic antigens or secreting immunosuppressive molecules. The document discusses various tumor-associated antigens and oncofetal antigens. It also outlines approaches for tumor immunotherapy, including using cytokines and immunopotentiating agents to enhance anti-tumor immunity.
This document defines various tumor markers and their clinical applications. It discusses commonly ordered tumor markers such as alpha-fetoprotein, cancer antigen 125, carcinoembryonic antigen, human chorionic gonadotropin, and prostate-specific antigen. These markers can be used for cancer diagnosis, prognosis, and monitoring treatment effectiveness. However, tumor marker levels are not specific to cancer and can be elevated in certain non-cancerous conditions. Enzymes were among the first tumor markers identified but provide only nonspecific indications of malignancy.
This document provides an overview of oncology and cancer. It begins by defining key terms like oncology and describing the characteristics of normal cells. It then discusses how cancer develops, defining cancer and describing the pathophysiology and carcinogenesis. It differentiates between benign and malignant tumors and identifies various carcinogens. The document continues by describing the classification, diagnosis, symptoms and treatment of cancer. It provides information on the nursing role in various cancer treatment modalities.
ROLE OF IMMUNE CELLS IN CANCER AND TARGETING IMMUNE CELLS FOR CANCER THERAPYSIVASWAROOP YARASI
Immune cells like macrophages, neutrophils, natural killer cells, T cells, B cells, and cytokines in the tumor microenvironment can either promote or inhibit cancer progression. Adoptive cell immunotherapy uses tumor-infiltrating lymphocytes, cytotoxic T lymphocytes, or chimeric antigen receptor T/NK cells to target cancers. Clinical trials are exploring these immunotherapies for various solid tumors and hematological malignancies, though challenges remain for treating solid tumors due to the immunosuppressive tumor microenvironment.
Cancer is caused by uncontrolled cell growth that can spread to other parts of the body. There are over 100 types of cancer that can affect different parts of the body. The four most common cancers are breast cancer, colon cancer, lung cancer, and prostate cancer. Cancer is treated through surgery, chemotherapy, and radiation therapy depending on the type and stage. Maintaining a healthy lifestyle can help prevent cancer by avoiding risk factors like smoking and excessive sun exposure.
The document discusses immuno-oncology and the relationship between cancer and the immune system. It provides an overview of topics that will be covered in an upcoming webinar, including advances in immuno-oncology for different cancer types and combination immunotherapy approaches. The document then reviews key topics in more depth, including how immuno-oncology focuses on improving the body's immune response against cancer and recent immunotherapy approvals. It also discusses how cancer can evade the immune system and strategies for cancer immunotherapy, such as manipulating co-stimulatory signals, enhancing antigen presenting cells, and using cytokines, monoclonal antibodies, and cancer vaccines.
The document outlines the eight hallmarks of cancer that enable tumor growth and metastatic spread. These hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, reprogramming energy metabolism, and evading immune destruction. The hallmarks represent biological capabilities that are acquired during the development and progression of cancer and provide an organizing framework for understanding the complexities of the disease.
Tumor antigens & cancer immunotherapy.pptxRagavi32
Tumor antigens are proteins, glycoproteins, glycolipids, or carbohydrates expressed uniquely on tumor cells. There are two types: tumor specific antigens produced from mutations and tumor associated antigens normally expressed during development but reactivated in cancer. The immune system mounts responses against these antigens via antibodies and cytotoxic T cells to eliminate tumor cells. However, tumors can evolve to escape immune destruction by losing antigen expression or inhibiting immune responses. Immunotherapies aim to enhance antigen presentation, co-stimulation, and pro-inflammatory cytokines to strengthen anti-tumor immunity.
Trends in local anesthetic injection techniquesDr Ramesh R
This document discusses several new technologies for administering local anesthetic injections to children in a painless manner, including computer-controlled syringes, vibrating devices attached to syringes, jet injections using high pressure, and a potential future option using nanorobots instilled onto the gums. The goal is to reduce pain experienced during dental procedures to avoid damaging children's future responses to needed dental care.
This document provides an overview of model analysis for mixed dentition. It defines study models and their objectives. Various types of model analyses are described, including those for mixed dentition like Moyer's analysis, which uses measurements of erupted mandibular incisors to estimate the sizes of unerupted canines and premolars. The goals and procedures of mixed dentition analysis are outlined, such as determining if there is enough space for permanent teeth. Factors considered include tooth sizes, arch perimeter, and expected changes during development.
This document provides guidelines for publishing manuscripts in medical/dental journals. It discusses various types of manuscripts like case reports, case series, research articles, and systematic reviews. It explains guidelines for each type like CARE guidelines for case reports and CONSORT guidelines for clinical trials. It also discusses the peer review process, impact factor, indexing/abstracting of journals, and tips for manuscript acceptance. Overall, the document serves as a useful reference for authors to understand the publishing process and guidelines for improving the quality of their manuscripts.
Clear aligners are a revolutionary orthodontic treatment method that uses custom-made, removable, clear plastic aligners to gradually move teeth into the desired position. The treatment utilizes CAD/CAM technology to digitally plan and guide tooth movements through sequential aligner trays worn for two weeks each. Clear aligners are a viable treatment option for less complex malocclusions and offer advantages like aesthetics, comfort, and reduced treatment time compared to traditional braces. However, clear aligners also have limitations in the types of tooth movements that can be accurately achieved. Careful patient selection and use of ancillary devices may be needed to optimize clinical outcomes.
The document discusses the principles of minimal intervention dentistry (MID). It begins with the history and definitions of MID, highlighting key figures like GV Black, Hyatt, and Mount who advanced the concept. The document outlines the philosophy of MID, including the golden triangle of reduction, recognition, and repair. It discusses the caries process and various methods for caries detection and risk assessment, emphasizing early detection. The document then covers the minimal intervention approach, including caries removal techniques, cavity designs, and restorative materials used in MID. It concludes by noting the dental public health significance and articles supporting MID.
The document discusses radiography techniques used in pediatric dentistry. It begins with an introduction and definitions of key terms like radiation and dental radiographs. The history of radiography is then outlined, noting important discoveries and advancements over time. Common radiographic techniques for pediatric patients are described, including bitewing, periapical, and panoramic radiographs. Guidelines for obtaining quality radiographs and selecting appropriate techniques based on a patient's age are also provided.
This document provides an overview of questionnaire surveys and their design. It discusses key aspects of developing and conducting a questionnaire survey such as defining objectives, conceptualizing variables, exploring concepts through focus groups and interviews, designing the questionnaire, and testing methods. The document also covers factors that affect questionnaire surveys, advantages and disadvantages, psychology of asking questions, and ensuring validity and reliability. The overall summary is that this document outlines best practices for designing and implementing a rigorous questionnaire survey from start to finish.
This document describes and compares various obturation techniques that can be used for filling root canals in primary teeth. It begins by defining obturation and describing the goal of creating a fluid-tight seal to prevent reinfection. It then provides details on 12 different techniques: endodontic pressure syringe, Lentulo spiral, mechanical syringe, incremental filling technique, Jiffy tube, tuberculin syringe, reamer technique, insulin syringe technique, disposable injection technique, NaviTip, bi-directional spiral, and Pastinject. For each technique, it discusses advantages such as ease of use and ability to fully fill canals, as well as disadvantages like difficulty with placement and increased risk of voids
This document provides information about nasoalveolar molding (NAM) for treating cleft lip and palate. It defines cleft lip and cleft palate, and describes presurgical NAM which reshapes the alveolar and nasal segments before surgical repair. The key steps of NAM include taking an impression, fabricating an acrylic molding plate with a nasal stent, inserting the plate and using tape for retention, and making weekly adjustments to reshape the tissues over 3-5 months before surgery. The goals of NAM are to decrease the cleft deformity and improve symmetry, with benefits such as reducing the need for future bone grafts or surgeries.
Local anesthesia & details of surgical instruments in pedodonticsDr Ramesh R
The document discusses details of surgical instruments used in pediatric dentistry, focusing on needles and local anesthesia. It provides a brief history of local anesthesia development. It then describes the composition of local anesthetic solutions, including the anesthetic agent, vasoconstrictor, reducing agent, preservative, fungicide, isotonic agent, and vehicle. It also classifies local anesthetics and discusses their metabolism. Finally, it discusses various needles, syringes, and cartridges used to administer local anesthesia, emphasizing factors important for pediatric patients such as needle gauge and length.
This document provides anticipatory guidance for various stages of child development from infancy through adolescence. It begins with definitions of anticipatory guidance and caries risk assessment. It then covers topics like prenatal counseling, development of oral tissues, oral hygiene, teething, diet and nutrition, fluoride needs, non-nutritive habits, speech development, and more. Guidelines are provided for different age groups from 6-12 months to adolescence. The document aims to educate parents and caregivers to promote optimal oral health at each stage of development.
Management of maxillary canine impactionDr Ramesh R
The document provides information on comprehensive management of impacted canine teeth. It discusses the prevalence, classification, diagnosis and various treatment options for impacted canines. Some key points:
- Impacted canines occur in approximately 2% of the population and are most commonly impacted in the maxilla.
- Classification systems are based on the position of the impacted canine crown relative to the dental arch and occlusal plane.
- Diagnosis involves clinical examination, radiographs such as panoramic and CBCT images to determine the location and relationship of the impacted tooth.
- Treatment options include interceptive removal of primary canines, surgical exposure with or without orthodontic alignment, autotransplantation, and prosthetic
This document provides information on banding instruments and procedures in pediatric dentistry. It discusses the history of bands, various band materials and sizes, advantages and disadvantages of bands, ideal band material requirements, instruments used for banding, and banding techniques. The key points are:
- Bands are thin metal rings placed on teeth, typically molars, to secure orthodontic appliances. Accurate band placement is important for fitting appliances.
- Stainless steel is commonly used due to properties like resistance to tarnish and springiness. Band sizes vary based on tooth type.
- Banding provides strong attachment but risks caries if cement seals fail. Autoclaving is the most reliable steril
This document provides an overview of bacterial genetics. It discusses the structure and function of bacterial genetic material, including DNA and RNA. It describes protein synthesis through transcription and translation. It also covers extrachromosomal genetic elements in bacteria, bacterial variation, mutation, and gene transfer. The key topics covered include the lac operon and its role in regulating lactose metabolism, different types of mutations and their effects, and the mechanisms of genetic variation and antibiotic resistance in bacteria.
This document discusses various spaces in the mandible that can become infected from dental infections, including the submental, sublingual, submandibular, masseteric, pterygomandibular, and temporal spaces. It describes the anatomy and boundaries of each space, potential causes of infection, clinical signs and symptoms, and surgical approaches for incision and drainage. Infections can spread between spaces if not properly treated.
This document discusses platelet rich plasma (PRP), which contains concentrated platelets and growth factors that stimulate bone and soft tissue healing. PRP works by secreting growth factors like PDGF, TGF, VEGF and EGF from platelet alpha granules after injury. These growth factors recruit cells and stimulate regeneration. Clinical studies found PRP increased bone mineral density and accelerated bone maturation compared to autogenous bone grafts. For soft tissue healing, PRP reduced scarring and improved pigmentation compared to thrombin. PRP is used to enhance healing in various surgical specialties, though bovine thrombin used to activate PRP carries risks. Contraindications include coagulation defects or hypersensitivity to bovine proteins.
Platelet rich fibrin (PRF) is an autologous platelet concentrate that can be used to deliver growth factors to bone defects for regeneration. It has advantages over platelet rich plasma as it requires no biochemical handling or additives like bovine thrombin. PRF is prepared by centrifuging blood samples without anticoagulant. This results in a fibrin clot containing platelets and growth factors between the acellular plasma and red blood cell layers. PRF can be used with bone grafts or as a membrane to promote wound healing, bone growth, and graft stabilization. The case report describes using PRF mixed with a bone graft to regenerate an intra-bony defect in a patient, which resulted in reduction of pocket
Tetanus is a medical condition caused by a toxin produced by Clostridium tetani bacteria. It is characterized by prolonged contraction of skeletal muscle fibers. The toxin enters the body through breaks in the skin like wounds, burns, or puncture wounds. Incubation periods can last up to months but symptoms usually appear within 2 weeks. Generalized tetanus is the most common type and causes painful muscle spasms, lockjaw, and stiffness. It can be life-threatening if not properly treated with a tetanus immunoglobulin and antibiotic like metronidazole.
This document discusses various topics related to antimicrobial agents including classification, mechanisms of action, uses, and adverse effects. It describes different classes of antibiotics such as beta-lactams, sulfonamides, fluoroquinolones, and their characteristics. It provides information on classification based on source and mechanism of action. Common uses and adverse effects of these antibiotics are also summarized. The document also includes several multiple choice questions related to antimicrobial therapy.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
3. INTRODUCTION
• In simple terms Neoplasia is defined as a mass of tissue formed as a
result of abnormal, excessive, uncoordinated, autonomous and
purposeless proliferation of cells.
• Whether benign or malignant these tumors exert some effects on
the host tissue with difference only in the severity of those effects
between benign and malignant conditions.
• On the contrary the body exhibit some responses to the tumor tissue
as well.
• In this seminar, these effects of tumor growth on the body and the
body’s response to the growth are being discussed
5. EFFECT OF TUMOR ON HOST
LOCAL
EFFECTS
Compression
Mechanical
obstruction
Tissue destruction
Infarction
Ulceration
hemorrhage
HORMONAL
EFFECTS
Hypoglycemia
Hyperthyroidism
Hypercalcemia
Cushing’s syndrome
Polycythemia
SYSTEMIC
EFFECTS
Cancer cachexia
Fever
Anorexia
Paraneoplastic
syndrome
6. LOCAL EFFECTS
• COMPRESSION
Eg pituitary adenoma leads to severe endocrinopathy
small benign tumor of Ampulla of Vater leads to biliary
obstruction
• MECHANICAL OBSTRUCTION
eg benign and malignant tumors of gut produce
mechanical obstruction of intestine
7. • TISSUE DESTRUCTION
malignant tumors infiltrate and destroy
the vital structures
• INFARCTION, ULCERATION, HEMORRHAGE
caused more by malignant tumors
secondary bacterial infection may supervene.
eg large tumors in mobile organs like Ovarian tumors may
undergo torsion and produce infarction and hemorrhage.
8. HORMONAL EFFECTS
• Common in benign tumors
eg Adenoma of islet of Langerhans cause fatal hypoglycemia
thyroid adenoma causes hyperthyroidism
parathyroid adenoma causes hypercalcemia and osteoporosis
9. SYSTEMIC EFFECTS
I CANCER CACHEXIA
• Kakos means bad
• Hexia is condition
• Its also called wasting syndrome
10. • In cancer patients there is progressive loss of body weight leading to
lean body mass accompanied by profound weakness, anorexia and
anemia- CACHEXIA
• It’s a combination of asthenia( weakness) and anorexia
• Seen in end stage of cancer
• Positive risk factor for death
• More seen in upper GIT and pancreatic cancer
• Exact mechanism is not known but not due to increased nutritional
demands of the tumor
11. • Thought to be related to cytokine production by tumor cells
TNF alpha ( cachectin )
Excess mobilisation of suppress appetite
fat from tissue storage
CACHEXIA
12. • OTHER FACTORS
proteolysis inducing factors
lipid mobilising factors
( increase the catabolism of muscle and adipose tissue)
Lipid mobilising factor is suspected to be inducing protein degradation in
skeletal muscle by upregulation of ubiquitin- proteasome pathway and
lipolysis in adipocytes.
TREATMENT
• Improve appetite using appetite stimulants to ensure adequate intake of
nutrients.
• Removal of tumor is the definitive treatment.
13.
14. FEVER
• Fever of unexplained origin may be presenting feature in some
malignancies such as Hodgkin’s disease, adenocarcinoma kidney,
osteogenic sarcoma etc
• Exact mechanism is unknown
• The tumor cells themselves must be elaborating pyrogens
15. ANOREXIA
• Common problem in cancer patients
• Due to abnormalities in taste and central control of appetite
• Calorie expenditure and BMR often remains high despite of reduced
food intake
• In cancer cachexia there is equal loss of fat and muscle.
16. PARANEOPLASTIC SYNDROME
• These are a group of conditions developing in patients with
advanced cancer
• 10-15 % of advanced cancer patients develop one or more of the
syndromes included in the PNS
• Rarely it will happen as an early manifestation of a latent cancer.
17. HOST RESPONSE AGAINST TUMORS
CELLULAR IMMUNITY
• CTL (cytotoxic T lymphocytes)
• NK cells
• Macrophages
HUMORAL IMMUNITY
• Antibody production by the host against host tumor cells or their
constituents for tumor antigens
18. • Body’s immune system can recognize tumor cells as non - self and
attempt to destroy them and limit the spread of cancer.
• Following observations provides basis for this concept.
1. Certain cancers evoke significant lymphocytic infiltrates composed
of immunocompetent cells
2. Rarely a cancer may spontaneously regress partially or completely
under the influence of host defence mechanism.
3. It is highly unusual to have primary and secondary tumors in the
spleen due to its ability to destroy the growth and proliferation of
the tumor cells.
4. Immune surviellance exists is substantiated by increased frequency
of cancers in immunodeficient host eg: in AIDS patients
19. HOST IMMUNE RESPONSE EVASION BY TUMOR CELLS
• Selective outgrowth of antigen- negative variants
• Loss or reduced expression of histocompatibility antigens
• Lack of costimulation
• Immunosuppression
• Antigen masking
• Apoptosis of cytotoxic T cells
20. TYPES OF GENES THAT CONTROL CANCER
• Four types
1. Growth – promoting proto oncogenes
2. Growth – inhibiting tumor suppressor genes
3. Genes that regulate programmed cell death( apoptosis)
4. Genes involved in DNA repair
21. Immunology of cancer can be discussed under the following
• TUMOR ANTIGENS
• ANTITUMOR IMMUNE RESPONSES
• IMMUNOTHERAPY
22. TUMOR ANTIGENS
• In order for the immune system to react against a tumor, the latter
must have antigens that are recognized as foreign.
• A number of alterations in gene expression occur in cells during
tumorigenesis.
• Tumorigenesis may lead to expression of new antigens (neoantigens)
or alteration in existing antigens that are found on normal cells.
23. Classification of tumor antigens
Two categories
BASED ON THEIR PATTERNS OF EXPRESSION
• TUMOR SPECIFIC ANTIGENS- present only on tumor cells and
not on any normal cells and are unique or specific for a particular
tumor.
• TUMOR ASSOCIATED ANTIGENS – Present on tumor cells and
also on some normal cells from where the tumor originated.
24. • It is now known that TSAs and TAAs can both be present on normal
cells and categorisation into TSA and TAA does not hold true.
• Thus presently distinction of tumor antigens is based on their
recognition by the host immune cells , ie CD8+T cells , and by the
molecular structure of the tumor antigens.
• Current classification is as follows:
25. Based on their molecular structure and source
• Oncoproteins from mutated oncogenes.
• Protein products of tumor suppressor genes.
• Over expressed cellular proteins.
• Abnormally expressed cellular proteins.
• Tumor antigens produced from viral oncoproteins.
• Tumor antigens from randomly mutated genes.
• Oncofetal antigens.
• Altered glycolipids and glycoproteins.
• Cell type- specific differentiation antigens.
26. ONCOPROTEINS FROM MUTATED GENES AND TUMOR
SUPPRESSOR GENE
• Derived from the products of mutant proto oncogenes , tumor
suppressor genes, or other mutated genes. ( beta – catenin, RAS, p53
and CDK4 genes)
• Synthesized in the cytoplasm of tumor cells.
• Enter the class I MHC antigen processing pathway and be recognized
by CD8+ Tcells.
• They may enter class II MHC pathway and be recognized as CD4+ T
cells also.
27. OVEREXPRESSED PROTEINS
• Tumor antigens may be normal cellular proteins that are excessively
expressed in tumor cells and elicit immune responses.
• Eg: Tyrosinase, is expressed on MELANOMAS.
HER2/neu protein overexpressed in breast cancer.
ABNORMALLY EXPRESSED PROTEINS
• Cellular proteins present on some cells is abnormally expressed on
the surface of tumor cells of cancer.
• Eg: MAGE expressed on surface of melanoma, cancers of lungs,
liver, stomach etc
other examples are GAGE , BAGE, RAGE(renal tumor antigen)
28. ONCOFETAL ANTIGENS
• proteins that are expressed at high levels on cancer cells and in normal developing
fetal but not adult tissues.
• They are excellent markers in tumor diagnosis.
• Carcino- embryonic antigens(CEA)
Normally expressed during fetal life on fetal gut. Seen in GIT, pancreas, biliary
system and cancer breast
• Alpha feto protein( AFP)
Normally expressed in fetal life. Seen in hepatocellular carcinoma.
ANTIGENS PRODUCED BY ONCOGENIC VIRUSES
• Oncogenic viruses such as HPV, EBV, HBV produce proteins that are recognized
as foreign by the immune system.
• Viral oncoproteins of HPV in cervical cancer and EBNA proteins of EBV in
Burkitt’s lymphoma
29. ALTERED CELL SURFACE GLYCOLIPIDS AND GLYCOPROTEINS
• Expression of higher than normal levels and/or abnormal forms of surface
glycoproteins and glycolipids.
• Diagnostic markers and targets for therapy.
• These altered molecules include gangliosides, blood group antigens and
mucins.
• These include CA-125 – expressed on ovarian carcinomas
• CA-19-9 = expressed on carcinoma in pancreas & biliary tract
• MUC-1 = expressed on breast carcinomas.
30. CELL TYPE SPECIFIC DIFFERENTIATION ANTIGENS
• Tumors express molecules that are normally present on the cells of
origin
• Important in identifying the tissue of origin of the tumor
• These antigens are called differentiation antigens because they are
specific for particular lineages or differentiation stages of various cell
types.
31.
32. TUMOR IMMUNOLOGY
• Cancer immunology is a branch of immunology that studies
interactions between the immune system and cancer cells.
• It is a field of research that aims to discover cancer
immunotherapies to treat and retard progression of the disease
• The immune response, including the recognition of cancer-
specific antigens , forms the basis of targeted therapy (such
as vaccines and antibody therapies) and tumor marker-
based diagnostic tests.
33. EVIDENCE FOR TUMOR IMMUNITY
• Regression of metastasis after removal of primary tumor
• Infiltraton of tumor by lymphocytes and macrophages
• Lymphocyte proliferation in draining sites of cancer
• Direct demonstration of tumor specific T cells and
antibodies in patients.
• Increased cancer risk after immunosuppression and
immunodeficiency
34. Immunosurveillance
• Formulated in 1957 by Burnet and Thomas.
• proposed that lymphocytes act as sentinels in recognizing and
eliminating continuously arising, nascent transformed cells.
• Cancer immunosurveillance appears to be an important host
protection process that decreases cancer rates through inhibition
of carcinogenesis and maintaining of regular cellular homeostasis.
35. CANCER IMMUNOEDITING
Describe the effects of immune system
in preventing tumor formation
In sculpting the immunologic properties of tumors to select tumor
cells that escape immune elimination.
Many tumors do elicit an immune response due to tumor antigens
Many tumors evade host immune response through several
mechanisms.
three main phases: elimination, equilibrium and escape.
36. Elimination
• first phase of elimination involves the initiation of an
antitumor immune response.
Cells of the innate immune system recognize the presence of a growing tumor, when it
begins the local tissue damage.
recruiting cells of the innate immune system (e.g. natural killer
cells, macrophages and dendritic cells ) to the tumor site.
• second phase of elimination, newly synthesized IFN-gamma
induces tumor death.
production of chemokines CXCL10, CXCL 9 and CXCL 11. These chemokines play an
important role in promoting tumor death by blocking the formation of new blood
vessels.
37. • third phase, natural killer cells and macrophages transactivate one
another via the reciprocal production of IFN-gamma and IL 12.
This again promotes more tumor killing by these cells via apoptosis
• final phase of elimination, tumor-specific CD4+ and CD8+ T cells
home to the tumor site and the cytotoxic T lymphocytes then destroy
the antigen-bearing tumor cells which remain at the site.
38. Equilibrium and escape
• Tumor cell variants which have survived the elimination phase enter
the equilibrium phase. In this phase, lymphocytes and IFN gamma
exert a selection pressure on tumor cells which are genetically
unstable and rapidly mutating.
• Tumor cell variants which have acquired resistance to elimination
then enter the escape phase.
• In the escape phase, tumor cells continue to grow and expand in an
uncontrolled manner and may eventually lead to malignancies
39. CANCER IMMUNOLOGY AND IMMUNOTHERAPY
• Immunotherapy has been used as a novel means of treating cancer.
Both active and passive means of stimulating the non-specific and
specific immune systems have been employed, in some cases with
significant success.
40. • ACTIVE IMMUNOTHERAPY
In this, the host actively participates in mounting an immune response
• Specific activation is achieved by using vaccines:
i) Hepatitis B vaccine
ii) Human Papilloma virus (HPV) vaccine
• Nonspecific activation is achieved by immunization with:
i) Bacillus Calmette-Guerin (BCG)
ii) Corynebacterium parvum
These activate macrophages to be tumoricidal.
41. • PASSIVE IMMUNOTHERAPY
This involves transfer of preformed antibodies, immune cells and
other factors into the hosts.
Specific:
i) Antibodies against tumor antigens (e.g. Her2/Neu for treatment of
breast cancer)
ii) Antibodies against IL-2R for Human T lymphotropic virus (HTLV-
1)-induced adult T cell leukemia
iii) Antibodies against CD20 expressed on non Hodgkin’s B cell
lymphoma.
iv) Antibodies conjugated to toxins, radioisotopes and anti-cancer
drugs have also been used. These enter the cells and inhibit protein
synthesis.
42. • Nonspecific:
i) Adoptive Transfer of lymphocytes:
Lymphokine-activated killer (LAK) cells which are IL-2 activated T and NK cells.
Tumor-infiltrating lymphocytes (TIL)
ii) Dendritic cells pulsed with tumor antigens may induce tumor-specific T cell
responses.
iii) Cytokines
• IL-2: Activates T cells/NK cells expressing IL-2 receptors. This is used in the
treatment of renal cell carcinoma and melanoma
• IFN-alpha: This induces MHC expression on tumors and used in the treatment of
hairy B cell leukemias
• IFN-gamma: This increases class II MHC expression; used in the treatment of
ovarian cancers.
• TNF-alpha: This kills tumor cells.
• iv) Cytokine gene transfected tumor cells may also be used which can activate T or
LAK cell-mediated anti-tumor immunity.
43. REFERENCE
• OXFORD TEXTBOOK OF PATHOLOGY- Mc GEE VOL 1
• TEXT BOOK OF PATHOLOGY- HARSHMOHAN, 4th EDITION
• WIKIPEDIA
Editor's Notes
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Set of sign and symptoms that is consequence of cancer in body not due to local presence of cancer cells