This document provides information about the basics of cancer treatment. It defines cancer as abnormal cells that divide uncontrollably and are able to invade other tissues and spread. It describes the main characteristics of tumors. It also covers the types of genes linked to cancer development including tumor suppressor genes and oncogenes. The document discusses the different modalities used to treat cancer, including surgery, chemotherapy, radiation therapy, hormonal therapy, and targeted therapy. It provides details on the various classes and examples of chemotherapy drugs and hormonal therapies used to treat breast and prostate cancer.
Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
cancer pharmaco therapeutics - 3.3 1.pptxmathihadassa
Cancer develops through a multistage process of genetic mutations that alter the normal control of cellular growth and proliferation. The initial step is initiation by carcinogens, which cause DNA damage and mutations in proto-oncogenes and tumor suppressor genes. This gives cells a selective growth advantage. Promotion makes the environment favor growth of these mutated cells. Finally, progression leads to increased proliferation and metastasis. Oncogenes stimulate growth while tumor suppressors inhibit it. Loss of control over these genes, through acquired or inherited mutations, drives carcinogenesis.
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can increase the risk of mutations accumulating. Once cancer develops, ongoing clonal evolution drives progression to more advanced stages.
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can also increase cancer risk by damaging DNA or altering gene expression through epigenetic changes. The progression of cancer involves a chain reaction of accumulating errors that allow cancer cells to evade controls on growth and spread.
- German chemist Paul Ehrlich coined the term "chemotherapy" to refer to treatment of disease with chemical drugs. By the 1950s, the term was primarily used to refer to drugs used to treat cancer.
- Chemotherapy involves using drugs to treat cancer and typically involves drugs that interfere with cell division, such as methotrexate or fluorouracil.
- The choice of chemotherapy depends on factors like the location and stage of the tumor and the patient's health. While it can cure some cancers, it is most effective against cancer before metastasis.
German chemist Paul Ehrlich coined the term "chemotherapy" to refer to treatment of disease with drugs or chemicals. By the 1950s, the term was primarily used to refer to drugs used to treat cancer. Chemotherapy involves the use of drugs to treat cancers caused by uncontrolled cell proliferation, invasion, and metastasis due to chromosomal abnormalities and oncogene expression. Common chemotherapy drugs act by interfering with cell division, DNA/RNA synthesis, and microtubule formation. Combination chemotherapy using multiple agents with different mechanisms of action has improved treatment outcomes but can also lead to drug resistance developing over time. Factors such as tumor type, stage, location, and patient health determine optimal chemotherapy approaches.
Cancer is characterized by uncontrolled cellular growth and proliferation that can spread to other parts of the body. It is caused by both external factors like chemicals, radiation, viruses and internal factors such as genetic mutations. Cancer development is driven by changes in oncogenes and tumor suppressor genes. Tumor markers are substances produced by cancer cells or the body in response to cancer that can be detected in bodily fluids or tissues and used to diagnose certain cancer types. Some common tumor markers are CEA for colon cancer, AFP for liver cancer, and PSA for prostate cancer.
Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
cancer pharmaco therapeutics - 3.3 1.pptxmathihadassa
Cancer develops through a multistage process of genetic mutations that alter the normal control of cellular growth and proliferation. The initial step is initiation by carcinogens, which cause DNA damage and mutations in proto-oncogenes and tumor suppressor genes. This gives cells a selective growth advantage. Promotion makes the environment favor growth of these mutated cells. Finally, progression leads to increased proliferation and metastasis. Oncogenes stimulate growth while tumor suppressors inhibit it. Loss of control over these genes, through acquired or inherited mutations, drives carcinogenesis.
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can increase the risk of mutations accumulating. Once cancer develops, ongoing clonal evolution drives progression to more advanced stages.
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can also increase cancer risk by damaging DNA or altering gene expression through epigenetic changes. The progression of cancer involves a chain reaction of accumulating errors that allow cancer cells to evade controls on growth and spread.
- German chemist Paul Ehrlich coined the term "chemotherapy" to refer to treatment of disease with chemical drugs. By the 1950s, the term was primarily used to refer to drugs used to treat cancer.
- Chemotherapy involves using drugs to treat cancer and typically involves drugs that interfere with cell division, such as methotrexate or fluorouracil.
- The choice of chemotherapy depends on factors like the location and stage of the tumor and the patient's health. While it can cure some cancers, it is most effective against cancer before metastasis.
German chemist Paul Ehrlich coined the term "chemotherapy" to refer to treatment of disease with drugs or chemicals. By the 1950s, the term was primarily used to refer to drugs used to treat cancer. Chemotherapy involves the use of drugs to treat cancers caused by uncontrolled cell proliferation, invasion, and metastasis due to chromosomal abnormalities and oncogene expression. Common chemotherapy drugs act by interfering with cell division, DNA/RNA synthesis, and microtubule formation. Combination chemotherapy using multiple agents with different mechanisms of action has improved treatment outcomes but can also lead to drug resistance developing over time. Factors such as tumor type, stage, location, and patient health determine optimal chemotherapy approaches.
Cancer is characterized by uncontrolled cellular growth and proliferation that can spread to other parts of the body. It is caused by both external factors like chemicals, radiation, viruses and internal factors such as genetic mutations. Cancer development is driven by changes in oncogenes and tumor suppressor genes. Tumor markers are substances produced by cancer cells or the body in response to cancer that can be detected in bodily fluids or tissues and used to diagnose certain cancer types. Some common tumor markers are CEA for colon cancer, AFP for liver cancer, and PSA for prostate cancer.
Cancer arises from mutations that affect cell division and death rates, leading to uncontrolled cell growth. The cell cycle is controlled by cyclins and CDKs, which are activated by growth factors binding to cell receptors. Cancer is caused by genetic mutations that cause cells to proliferate indefinitely, evade growth suppression, and metastasize. Common mutations occur in proto-oncogenes, tumor suppressor genes, DNA repair genes, and apoptosis genes. Multiple genetic alterations are typically required for cancer to develop and progress.
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.
Genetic changes play a key role in cancer development. Cancer arises due to mutations in genes that regulate cell growth, such as oncogenes and tumor suppressor genes. Oncogenes promote cell growth when activated by mutations, while tumor suppressor genes normally inhibit cell growth but require two mutations to be inactivated. Many cancers are caused by the accumulation of both germline and somatic mutations in genes over time. Certain inherited genetic syndromes predispose individuals to specific cancer types if high-risk genes are mutated.
Cancer arises due to mutations that affect cell cycle regulation and apoptosis, leading to uncontrolled cell growth and proliferation. The key events involved are mutations in proto-oncogenes, tumor suppressor genes, DNA repair genes, and cell cycle control genes. This disrupts normal cell cycle checkpoints and apoptosis. Cancer cells show characteristics like immortality, self-sufficiency in growth signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. The major causes of cancer are inherited mutations and exposure to environmental and viral carcinogens which induce somatic mutations.
Anticancer Drugs
Brief of Cancer
Cancer starts when cells in a part of the body start to grow out of control. Cancer cell growth is different from normal cell growth. Instead of dying, cancer cells continue to grow and form new, abnormal cells. Cancer cells can also invade (grow into) other tissues, something that normal cells can’t do. Growing out of control and invading other tissues are what makes a cell a cancer cell.
Cells become cancer cells because of DNA damage. DNA is in every cell and it directs all its actions. In a normal cell, when DNA is damaged the cell either repairs the damage or dies. In cancer cells, the damaged DNA is not repaired, but the cell doesn’t die like it should. Instead, the cell goes on making new cells that the body doesn’t need. These new cells all have the same damaged DNA as the first abnormal cell does.
People can inherit abnormal DNA (it’s passed on from their parents), but most often DNA damage is caused by mistakes that happen while the normal cell is reproducing or by something in the environment. Sometimes the cause of the DNA damage may be something obvious like cigarette smoking or sun exposure.
In most cases, the cancer cells form a tumor. Over time, the tumors can replace normal tissue, crowd it, or push it aside. Some cancers, like leukemia, rarely form tumors.
"Drivers" of Cancer
The genetic changes that contribute to cancer tend to affect three main types of genes…. proto-oncogenes, tumor suppressor genes and DNA repair genes. These changes are sometimes called “drivers” of cancer.
Proto-oncogenes are involved in normal cell growth and division. However, when these genes are altered in certain ways or are more active than normal, they may become cancer-causing genes (or oncogenes), allowing cells to grow and survive when they should not.
Tumor suppressor genes are also involved in controlling cell growth and division. Cells with certain alterations in tumor suppressor genes may divide in an uncontrolled manner.
DNA repair genes are involved in fixing damaged DNA. Cells with mutations in these genes tend to develop additional mutations in other genes. Together, these mutations may cause the cells to become cancerous.
How cancer spreads?
Cancer cells often travel to other parts of the body where they can grow and form new tumors. This happens when the cancer cells get into the body’s bloodstream or lymph vessels. The process of cancer spreading is called metastasis.
The document discusses chemotherapy, describing its objectives of curing or palliating cancer, how dosages are determined, factors that affect response, classifications of chemotherapeutic agents, administration methods, responses to treatment, and common side effects like bone marrow suppression, digestive issues, nausea and vomiting. It also covers strategies to manage side effects like growth factors and antiemetics.
This presentation is targeted for MBBS, MD and BDS students that describes briefly about aetiopathogenesis, tumour markers, anti cancer agents, apoptosis
Cancer is caused by changes in gene expression that lead to uncontrolled cell growth and proliferation. Cancerous cells can develop from any type of tissue and form tumors that may invade nearby tissues and metastasize to distant sites. There are many potential causes of cancer including physical, chemical, and biological carcinogens as well as lifestyle factors like diet, exercise, and viral infections. Cancer develops through multiple changes that allow cells to evade growth control mechanisms and proliferate indefinitely.
This document discusses fundamentals of cancer including what cancer is, causes of cancer, types of cancer, and hallmarks of cancer. Specifically, it states that cancer is caused by changes in gene expression leading to uncontrolled cell growth and proliferation. The main causes of cancer discussed are physical carcinogens like radiation, chemical carcinogens, and viral infections. The two main types of cancer are leukemias/lymphomas and solid tumors which can be carcinomas or sarcomas. Hallmarks of cancer include self-sufficient growth signals, evading cell death, unlimited replication, induced angiogenesis, and metastasis.
The document summarizes a presentation on the biology of cancer. It discusses the characteristics of cancer cells, including uncontrolled proliferation and avoidance of apoptosis. It describes different types of cancer classified by position and tissue of origin. The document outlines some of the known causes of cancer including physical, chemical, and biological agents as well as genetic factors. It discusses important cancer-related genes such as oncogenes like ras that promote cancer when mutated, and tumor suppressor genes like p53 and Rb that normally prevent cancer when functioning properly. The presentation covers topics such as molecular basis of cancer, etiology, normal cells versus cancer cells, and treatments.
This document provides an overview of anticancer drugs and chemotherapy. It discusses the general approach to cancer therapy, including killing cancer cells and modifying their growth. The main modalities of cancer treatment are described as chemotherapy, surgery, and radiation. The goals of chemotherapy are cure, prolonged remission, or palliation. Common anticancer drug classes are also summarized, including their mechanisms of action, examples, and toxicities.
Cancer is caused by uncontrolled cell growth and can spread through the body. There are many types of cancer and symptoms vary by type. Treatments include chemotherapy, radiation, and surgery. Cancer treatments work by manipulating DNA, blocking cell metabolism and growth, disrupting cell division, altering hormone balance, and restricting amino acid supply to cancer cells.
This document provides information about cancer genetics and cell biology. It defines cancer as uncontrolled cell growth and classifies tumors as benign or malignant. The main cancer types - carcinomas, sarcomas, and leukemias/lymphomas - are described based on their cell of origin. Key concepts in cancer development are discussed, including the roles of oncogenes, tumor suppressor genes, DNA repair genes, and failures in cell cycle control. Cancer results from mutations that disable normal controls on cell growth and division.
Carcinogenesis is the process by which normal cells are transformed into cancer cells due to mutations in DNA that disrupt the orderly processes regulating cell proliferation and death. This results in uncontrolled cell division. A series of mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that discourage cell growth are required before a normal cell transforms into a cancer cell. The ras oncogene and p53 tumor suppressor gene are examples that are commonly mutated in cancer. Grading of cancers provides information on prognosis and treatment by assessing how differentiated the cancer cells are from normal cells.
This document provides an overview of cancer, including solid and hematologic tumors. It discusses how cancer arises from DNA damage that disrupts normal cell proliferation and apoptosis. Key concepts covered include oncogenes, which promote cell growth; tumor suppressor genes, which inhibit growth; and the roles of environmental carcinogens, genetic mutations, and molecular changes like proto-oncogene activation in cancer development. The roles of important tumor suppressors like p53 and oncogenes like MYC and HER1/HER2 are described. Finally, the normal cell cycle is contrasted with neoplastic cell proliferation.
This document provides an overview of cancer, including solid and hematologic tumors. It discusses how cancer arises from DNA damage that disrupts normal cell proliferation and apoptosis. Key concepts covered include oncogenes, which promote cell growth; tumor suppressor genes, which inhibit growth; and the roles of environmental carcinogens, genetic mutations, and molecular changes like proto-oncogene activation in cancer development. The roles of important tumor suppressors like p53 and oncogenes like MYC and HER1/HER2 are described. Finally, the normal cell cycle is contrasted with how it becomes deregulated in cancer cells.
The document discusses the biochemistry of cancer, including:
- The characteristics and mechanisms of cancer cells, such as uncontrolled growth, evading growth suppression signals, and increased glucose consumption.
- The stages of cancer development: initiation by mutagens/carcinogens, promotion of growth by other factors, and progression to malignancy.
- How the immune system can recognize cancer cells but may be insufficient to eliminate them, and how cancer treatments can weaken the immune system.
- The roles of tumor suppressor genes, which normally regulate cell division and DNA repair, and proto-oncogenes, which become oncogenes when mutated and promote cancer.
This document discusses tumor suppressor genes. It begins by explaining that cancer is caused by genetic mutations, and describes the characteristic properties of cancer cells that result from these genetic changes. It then discusses two classes of genes affected in cancer - oncogenes and tumor suppressor genes. Oncogenes contribute to tumor development, while tumor suppressors support tumor development when their function is lost. The rest of the document provides details on specific tumor suppressor genes like RB, p53, PTEN, NF1, and BRCA1/2; their functions in inhibiting cell growth and proliferation; and the genetic and epigenetic mechanisms by which their inactivation can lead to cancer development.
Carcinogenesis is a multistep process involving genetic mutations that cause cells to proliferate uncontrollably. There are four classes of regulatory genes involved: 1) growth promoters like proto-oncogenes that become activated oncogenes, 2) inhibitors like tumor suppressor genes, 3) genes regulating apoptosis, and 4) DNA repair genes. Genetic damage occurs through environmental and spontaneous mutations and fails to be repaired if the DNA damage response is defective. This can result in oncogene activation and tumor suppressor inactivation, leading to autonomous growth, evasion of growth inhibition, apoptosis resistance, limitless replication through telomerase expression, angiogenesis, invasion and metastasis. Cancer progression involves the accumulation of additional mutations that
The document discusses targeted therapy and its role in treating cancer. It defines targeted therapy as using drugs or substances to recognize and kill cancer cells without harming normal cells. It provides examples of targeted therapy drugs, including Gleevec/Imatinib which treats chronic myeloid leukemia, Velcade/Bortezomib which treats multiple myelomas, and Sutent which treats kidney cancer. The document also discusses how these drugs work, such as by inhibiting tyrosine kinases or blocking protein breakdown in cancer cells.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Cancer arises from mutations that affect cell division and death rates, leading to uncontrolled cell growth. The cell cycle is controlled by cyclins and CDKs, which are activated by growth factors binding to cell receptors. Cancer is caused by genetic mutations that cause cells to proliferate indefinitely, evade growth suppression, and metastasize. Common mutations occur in proto-oncogenes, tumor suppressor genes, DNA repair genes, and apoptosis genes. Multiple genetic alterations are typically required for cancer to develop and progress.
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.
Genetic changes play a key role in cancer development. Cancer arises due to mutations in genes that regulate cell growth, such as oncogenes and tumor suppressor genes. Oncogenes promote cell growth when activated by mutations, while tumor suppressor genes normally inhibit cell growth but require two mutations to be inactivated. Many cancers are caused by the accumulation of both germline and somatic mutations in genes over time. Certain inherited genetic syndromes predispose individuals to specific cancer types if high-risk genes are mutated.
Cancer arises due to mutations that affect cell cycle regulation and apoptosis, leading to uncontrolled cell growth and proliferation. The key events involved are mutations in proto-oncogenes, tumor suppressor genes, DNA repair genes, and cell cycle control genes. This disrupts normal cell cycle checkpoints and apoptosis. Cancer cells show characteristics like immortality, self-sufficiency in growth signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. The major causes of cancer are inherited mutations and exposure to environmental and viral carcinogens which induce somatic mutations.
Anticancer Drugs
Brief of Cancer
Cancer starts when cells in a part of the body start to grow out of control. Cancer cell growth is different from normal cell growth. Instead of dying, cancer cells continue to grow and form new, abnormal cells. Cancer cells can also invade (grow into) other tissues, something that normal cells can’t do. Growing out of control and invading other tissues are what makes a cell a cancer cell.
Cells become cancer cells because of DNA damage. DNA is in every cell and it directs all its actions. In a normal cell, when DNA is damaged the cell either repairs the damage or dies. In cancer cells, the damaged DNA is not repaired, but the cell doesn’t die like it should. Instead, the cell goes on making new cells that the body doesn’t need. These new cells all have the same damaged DNA as the first abnormal cell does.
People can inherit abnormal DNA (it’s passed on from their parents), but most often DNA damage is caused by mistakes that happen while the normal cell is reproducing or by something in the environment. Sometimes the cause of the DNA damage may be something obvious like cigarette smoking or sun exposure.
In most cases, the cancer cells form a tumor. Over time, the tumors can replace normal tissue, crowd it, or push it aside. Some cancers, like leukemia, rarely form tumors.
"Drivers" of Cancer
The genetic changes that contribute to cancer tend to affect three main types of genes…. proto-oncogenes, tumor suppressor genes and DNA repair genes. These changes are sometimes called “drivers” of cancer.
Proto-oncogenes are involved in normal cell growth and division. However, when these genes are altered in certain ways or are more active than normal, they may become cancer-causing genes (or oncogenes), allowing cells to grow and survive when they should not.
Tumor suppressor genes are also involved in controlling cell growth and division. Cells with certain alterations in tumor suppressor genes may divide in an uncontrolled manner.
DNA repair genes are involved in fixing damaged DNA. Cells with mutations in these genes tend to develop additional mutations in other genes. Together, these mutations may cause the cells to become cancerous.
How cancer spreads?
Cancer cells often travel to other parts of the body where they can grow and form new tumors. This happens when the cancer cells get into the body’s bloodstream or lymph vessels. The process of cancer spreading is called metastasis.
The document discusses chemotherapy, describing its objectives of curing or palliating cancer, how dosages are determined, factors that affect response, classifications of chemotherapeutic agents, administration methods, responses to treatment, and common side effects like bone marrow suppression, digestive issues, nausea and vomiting. It also covers strategies to manage side effects like growth factors and antiemetics.
This presentation is targeted for MBBS, MD and BDS students that describes briefly about aetiopathogenesis, tumour markers, anti cancer agents, apoptosis
Cancer is caused by changes in gene expression that lead to uncontrolled cell growth and proliferation. Cancerous cells can develop from any type of tissue and form tumors that may invade nearby tissues and metastasize to distant sites. There are many potential causes of cancer including physical, chemical, and biological carcinogens as well as lifestyle factors like diet, exercise, and viral infections. Cancer develops through multiple changes that allow cells to evade growth control mechanisms and proliferate indefinitely.
This document discusses fundamentals of cancer including what cancer is, causes of cancer, types of cancer, and hallmarks of cancer. Specifically, it states that cancer is caused by changes in gene expression leading to uncontrolled cell growth and proliferation. The main causes of cancer discussed are physical carcinogens like radiation, chemical carcinogens, and viral infections. The two main types of cancer are leukemias/lymphomas and solid tumors which can be carcinomas or sarcomas. Hallmarks of cancer include self-sufficient growth signals, evading cell death, unlimited replication, induced angiogenesis, and metastasis.
The document summarizes a presentation on the biology of cancer. It discusses the characteristics of cancer cells, including uncontrolled proliferation and avoidance of apoptosis. It describes different types of cancer classified by position and tissue of origin. The document outlines some of the known causes of cancer including physical, chemical, and biological agents as well as genetic factors. It discusses important cancer-related genes such as oncogenes like ras that promote cancer when mutated, and tumor suppressor genes like p53 and Rb that normally prevent cancer when functioning properly. The presentation covers topics such as molecular basis of cancer, etiology, normal cells versus cancer cells, and treatments.
This document provides an overview of anticancer drugs and chemotherapy. It discusses the general approach to cancer therapy, including killing cancer cells and modifying their growth. The main modalities of cancer treatment are described as chemotherapy, surgery, and radiation. The goals of chemotherapy are cure, prolonged remission, or palliation. Common anticancer drug classes are also summarized, including their mechanisms of action, examples, and toxicities.
Cancer is caused by uncontrolled cell growth and can spread through the body. There are many types of cancer and symptoms vary by type. Treatments include chemotherapy, radiation, and surgery. Cancer treatments work by manipulating DNA, blocking cell metabolism and growth, disrupting cell division, altering hormone balance, and restricting amino acid supply to cancer cells.
This document provides information about cancer genetics and cell biology. It defines cancer as uncontrolled cell growth and classifies tumors as benign or malignant. The main cancer types - carcinomas, sarcomas, and leukemias/lymphomas - are described based on their cell of origin. Key concepts in cancer development are discussed, including the roles of oncogenes, tumor suppressor genes, DNA repair genes, and failures in cell cycle control. Cancer results from mutations that disable normal controls on cell growth and division.
Carcinogenesis is the process by which normal cells are transformed into cancer cells due to mutations in DNA that disrupt the orderly processes regulating cell proliferation and death. This results in uncontrolled cell division. A series of mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that discourage cell growth are required before a normal cell transforms into a cancer cell. The ras oncogene and p53 tumor suppressor gene are examples that are commonly mutated in cancer. Grading of cancers provides information on prognosis and treatment by assessing how differentiated the cancer cells are from normal cells.
This document provides an overview of cancer, including solid and hematologic tumors. It discusses how cancer arises from DNA damage that disrupts normal cell proliferation and apoptosis. Key concepts covered include oncogenes, which promote cell growth; tumor suppressor genes, which inhibit growth; and the roles of environmental carcinogens, genetic mutations, and molecular changes like proto-oncogene activation in cancer development. The roles of important tumor suppressors like p53 and oncogenes like MYC and HER1/HER2 are described. Finally, the normal cell cycle is contrasted with neoplastic cell proliferation.
This document provides an overview of cancer, including solid and hematologic tumors. It discusses how cancer arises from DNA damage that disrupts normal cell proliferation and apoptosis. Key concepts covered include oncogenes, which promote cell growth; tumor suppressor genes, which inhibit growth; and the roles of environmental carcinogens, genetic mutations, and molecular changes like proto-oncogene activation in cancer development. The roles of important tumor suppressors like p53 and oncogenes like MYC and HER1/HER2 are described. Finally, the normal cell cycle is contrasted with how it becomes deregulated in cancer cells.
The document discusses the biochemistry of cancer, including:
- The characteristics and mechanisms of cancer cells, such as uncontrolled growth, evading growth suppression signals, and increased glucose consumption.
- The stages of cancer development: initiation by mutagens/carcinogens, promotion of growth by other factors, and progression to malignancy.
- How the immune system can recognize cancer cells but may be insufficient to eliminate them, and how cancer treatments can weaken the immune system.
- The roles of tumor suppressor genes, which normally regulate cell division and DNA repair, and proto-oncogenes, which become oncogenes when mutated and promote cancer.
This document discusses tumor suppressor genes. It begins by explaining that cancer is caused by genetic mutations, and describes the characteristic properties of cancer cells that result from these genetic changes. It then discusses two classes of genes affected in cancer - oncogenes and tumor suppressor genes. Oncogenes contribute to tumor development, while tumor suppressors support tumor development when their function is lost. The rest of the document provides details on specific tumor suppressor genes like RB, p53, PTEN, NF1, and BRCA1/2; their functions in inhibiting cell growth and proliferation; and the genetic and epigenetic mechanisms by which their inactivation can lead to cancer development.
Carcinogenesis is a multistep process involving genetic mutations that cause cells to proliferate uncontrollably. There are four classes of regulatory genes involved: 1) growth promoters like proto-oncogenes that become activated oncogenes, 2) inhibitors like tumor suppressor genes, 3) genes regulating apoptosis, and 4) DNA repair genes. Genetic damage occurs through environmental and spontaneous mutations and fails to be repaired if the DNA damage response is defective. This can result in oncogene activation and tumor suppressor inactivation, leading to autonomous growth, evasion of growth inhibition, apoptosis resistance, limitless replication through telomerase expression, angiogenesis, invasion and metastasis. Cancer progression involves the accumulation of additional mutations that
The document discusses targeted therapy and its role in treating cancer. It defines targeted therapy as using drugs or substances to recognize and kill cancer cells without harming normal cells. It provides examples of targeted therapy drugs, including Gleevec/Imatinib which treats chronic myeloid leukemia, Velcade/Bortezomib which treats multiple myelomas, and Sutent which treats kidney cancer. The document also discusses how these drugs work, such as by inhibiting tyrosine kinases or blocking protein breakdown in cancer cells.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
-------------------------------------------------------------------------------
Find out more about ISO training and certification services
Training: ISO/IEC 27001 Information Security Management System - EN | PECB
ISO/IEC 42001 Artificial Intelligence Management System - EN | PECB
General Data Protection Regulation (GDPR) - Training Courses - EN | PECB
Webinars: https://pecb.com/webinars
Article: https://pecb.com/article
-------------------------------------------------------------------------------
For more information about PECB:
Website: https://pecb.com/
LinkedIn: https://www.linkedin.com/company/pecb/
Facebook: https://www.facebook.com/PECBInternational/
Slideshare: http://www.slideshare.net/PECBCERTIFICATION
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
हिंदी वर्णमाला पीपीटी, hindi alphabet PPT presentation, hindi varnamala PPT, Hindi Varnamala pdf, हिंदी स्वर, हिंदी व्यंजन, sikhiye hindi varnmala, dr. mulla adam ali, hindi language and literature, hindi alphabet with drawing, hindi alphabet pdf, hindi varnamala for childrens, hindi language, hindi varnamala practice for kids, https://www.drmullaadamali.com
2. Defining Cancer
Cancer is caused by the failure of genetic mechanisms that control the
growth and proliferation of cells.
In cancer, a single transformed cell grows to become a primary tumor,
accumulates more mutations and becomes more aggressive, then
metastasizes to another tissue and forms a secondary tumor
Cancer is a term used for diseases in which abnormal cells divide and
escape the body control.
These cells are able to:
1-Invade surrounding tissues
2-Send distant metastases.
3- Lost their functions
3. Tumor Characteristics
• Invade and destroy the surrounding tissue.
• The cells are genetically unstable
• Loss of normal cell architecture results in cells
that are atypical of their origin.
• Lose the ability to perform their usual functions.
• Metastasize, and consequently, recurrences are
common after removal or destruction of the
primary tumor.
• The most aggressive cancer cells display all of
these features. Alterations are caused by
mutations that affect growth factor receptors
and signal transduction genes, cell cycle
regulatory genes, DNA repair genes, or genes
controlling apoptosis. Depending on whether
the affected gene normally stimulates or inhibits
proliferation, the mutated gene is called an
oncogene or a tumor-suppressor gene.
4. The first step in this process is initiation, which requires
exposure of normal cells to carcinogenic substances.
Substances that may act as carcinogens or initiators
include chemical, physical, and biologic agents
Two major classes of genes are involved in
carcinogenesis: oncogenes and tumor suppressor genes
Cancer arises from the mutation of a normal gene.
Mutated genes that cause cancer are called oncogenes
Etiology of Cancer
5. Causes of Cancer
Genetic predisposition-
– Rb, p53, APC, CDKN2A, BRCA1, BRCA2
Infectious agents
– Viral
HPV – cervical cancer
Hepatitis – liver cancer
EBV - Lymphoma
–Bacterial
H. pylori – stomach cancer
6. Types of genes linked to cancer
Many of the genes that contribute to cancer development fall into broad
categories:
Tumor suppressor genes: These are protective genes. Normally, they limit cell
growth by:
-Monitoring how quickly cells divide into new cells
-Repairing mismatched DNA
-Controlling when a cell dies
When a tumor suppressor gene mutates, cells grow uncontrollably. And they may
eventually form a tumor.
Examples of tumor suppressor genes include, BRCA1, BRCA2 and p53 or TP53.
Germline mutations in BRCA1 or BRCA2 genes increase a woman’s risk of
developing hereditary breast or ovarian cancers and a man’s risk of developing
hereditary prostate or breast cancers. They also increase the risk of pancreatic
cancer and melanoma in women and men.
The most commonly mutated gene in people with cancer is p53 or TP53. More than
50% of cancers involve a missing or damaged p53 gene. Most p53 gene mutations
are acquired. Germline p53 mutations are rare, but patients who carry them are at
a higher risk of developing many different types of cancer.
7. Types of genes linked to cancer
Oncogenes. These turn a healthy cell into a cancerous cell. Mutations in these genes are not
known to be inherited.
Two common oncogenes are:
HER2, a specialized protein that controls cancer growth and spread. It is found in some cancer
cells. For example, breast and ovarian cancer cells.
The RAS family of genes, which makes proteins involved in cell communication pathways, cell
growth, and cell death.
DNA repair genes. These fix mistakes made when DNA is copied. Many of them function as
tumor suppressor genes.
• BRCA1,
• BRCA2, and
• p53 are all DNA repair genes.
If a person has an error in a DNA repair gene, mistakes remain uncorrected. Then, the mistakes
become mutations. These mutations mayeventually lead to cancer, particularly mutations in
tumor suppressor genes or oncogenes. Mutations in DNA repair genes may be inherited or
acquired. Lynch syndrome is an example of the inherited kind.
• BRCA1,
• BRCA2, and
• p53 mutations and their associated syndromes are also inherited.
8. Different Treatment Modalities
• Cancer can be treated by surgery, chemotherapy, radiation therapy, hormonal therapy,
targeted therapy (including immunotherapy such as monoclonal antibody therapy) and
synthetic lethality, most commonly as a series of separate treatments (e.g. chemotherapy
before surgery). The choice of therapy depends upon the location and grade of the tumor
and the stage of the disease, as well as the general state of the patient (performance status).
• systemic therapy (drug therapy - cytotoxic agents, hormones, biologics) distributes widely
through the body - normal and malignant tissues
• local therapy (surgery, radiation) is directed to a defined area of documented or presumed
disease
9. Types of Chemo Drugs
Chemo drugs can be grouped by how they work, their chemical structure, and their
relationships to other drugs. Some drugs work in more than one way and may belong to
more than one group.
Alkylating agents
Alkylating agents keep the cell from reproducing (making copies of itself) by damaging its
DNA. These drugs work in all phases of the cell cycle and are used to treat many different
cancers, including cancers of the lung, breast, and ovary as well as leukemia, lymphoma,
Hodgkin disease, multiple myeloma, and sarcoma.
Because these drugs damage DNA, they can affect the cells of the bone marrow which
make new blood cells. In rare cases, this can lead to leukemia. The risk of leukemia from
alkylating agents is “dose-dependent,” meaning that the risk is small with lower doses but
goes up as the total amount of the drug used gets higher. The risk of leukemia after getting
alkylating agents is highest about 5 to 10 years after treatment.
Examples of alkylating agents include:
Altretamine, Bendamustine, Busulfan, Carboplatin, Carmustine, Chlorambucil, Cisplatin,
Cyclophosphamide, Dacarbazine, Ifosfamide, Lomustine, Mechlorethamine, Melphalan,
Oxaliplatin, Temozolomide, Thiotepa, Trabectedin
10. Nitrosoureas
Nitrosoureas are a group of alkylating agents that have a special action.
The other alkylating agents listed above cannot travel into the brain,
but nitrosoureas are able to do so. They can enter the brain because
they are able to cross through the area known as the blood-brain
barrier, a special area that keeps most drugs out of the brain. This
action makes these drugs useful in treating certain types of brain
tumors.
Examples of nitrosoureas include:
• Carmustine
• Lomustine
• Streptozocin
Types of Chemo Drugs
11. Antimetabolites
Antimetabolites interfere with DNA and RNA by acting as a substitute for
the normal building blocks of RNA and DNA. When this happens, the
DNA cannot make copies of itself, and a cell cannot reproduce. They are
commonly used to treat leukemias, cancers of the breast, ovary, and the
intestinal tract, as well as other types of cancer.
Examples of antimetabolites include: Azacitidine, 5-fluorouracil (5-FU),
6-mercaptopurine (6-MP), Capecitabine (Xeloda), Cladribine,
Clofarabine, Cytarabine (Ara-C), Decitabine, Floxuridine, Fludarabine,
Gemcitabine (Gemzar), Hydroxyurea, Methotrexate, Nelarabine,
Pemetrexed (Alimta), Pentostatin, Pralatrexate, Thioguanine,
Trifluridine/tipiracil combination
Types of Chemo Drugs
12. Anti-tumor antibiotics
These drugs are not like the antibiotics used to treat infections. They work by changing the DNA
inside cancer cells to keep them from growing and multiplying.
Anthracyclines: Anthracyclines are anti-tumor antibiotics that interfere with enzymes involved in
copying DNA during the cell cycle. They bind with DNA so it cannot make copies of itself, and a cell
cannot reproduce. (Enzymes are proteins that start, help, or speed up the rate of chemical reactions
in cells.) They are widely used for a variety of cancers.
Examples of anthracyclines include: Daunorubicin, Doxorubicin (Adriamycin), Doxorubicin liposomal,
Epirubicin, Idarubicin, Valrubicin
A major concern when giving these drugs is that they can permanently damage the heart if given in
high doses. For this reason, lifetime dose limits (also called cumulative dose) are often placed on
these drugs.
Anti-tumor antibiotics that are not anthracyclines include: Bleomycin, Dactinomycin, Mitomycin-C,
Mitoxantrone (also acts as a topoisomerase II inhibitor)
Topoisomerase inhibitors
These drugs are also called plant alkaloids. They interfere with enzymes called topoisomerases, which
help separate the strands of DNA so they can be copied. (Enzymes are proteins that cause chemical
reactions in living cells.) Topoisomerase inhibitors are used to treat certain leukemias, as well as lung,
ovarian, gastrointestinal, colorectal, and pancreatic cancers.
Topoisomerase inhibitors are grouped according to which type of enzyme they affect:
Topoisomerase I inhibitors (also called camptothecins) include: Irinotecan, Irinotecan liposomal,
Topotecan, Topoisomerase II inhibitors (also called epipodophyllotoxins) include: Etoposide (VP-16),
Mitoxantrone (also acts as an anti-tumor antibiotic), Teniposide, Topoisomerase II inhibitors can
increase the risk of a second cancer.
Types of Chemo Drugs
13. Mitotic inhibitors
Mitotic inhibitors are also called plant alkaloids. They are compounds
derived from natural products, such as plants. They work by stopping
cells from dividing to form new cells, but can damage cells in all phases
by keeping enzymes from making proteins needed for cell reproduction.
Examples of mitotic inhibitors include the taxanes and vinca alkaloids.
Taxanes include- Cabazitaxel, Docetaxel, Nab-paclitaxel, Paclitaxel
Vinca alkaloids include- Vinblastine, Vincristine, Vincristine liposomal,
Vinorelbine
They are used to treat many different types of cancer including breast,
lung, myelomas, lymphomas, and leukemias. These drugs may cause
nerve damage, which can limit the amount that can be given.
Types of Chemo Drugs
14. Corticosteroids:
Corticosteroids, often simply called steroids, are natural hormones and
hormone-like drugs that are useful in the treatment of many types of
cancer, as well as other illnesses. When these drugs are used as part of
cancer treatment, they are considered chemotherapy drugs.
Examples of corticosteroids include:
Prednisone, Methylprednisolone, Dexamethasone
Steroids are also commonly used to help prevent nausea and vomiting
caused by chemo. They are used before some types of chemo to help
prevent severe allergic reactions, too.
Types of Chemo Drugs
15. Other chemotherapy drugs
Some chemotherapy drugs act in slightly different ways and do
not fit well into any of the other categories. Here are some
examples:
• All-trans-retinoic acid
• Arsenic trioxide
• Asparaginase
• Eribulin
• Hydroxyurea
• Ixabepilone
• Mitotane
• Omacetaxine
• Pegaspargase
• Procarbazine
• Romidepsin
• Vorinostat
Types of Chemo Drugs
16. Hormonal Therapy
Hormonal therapy is a treatment that uses medicines o block or lower
the amount of hormones in the body to slow down or stop the
growth of cancer.
It involves the manipulation of the endocrine system through
exogenous or external administration of specific hormones,
particularly steroid hormones, or drugs which inhibit the production
or activity of such hormones (hormone antagonists). Because steroid
hormones are powerful drivers of gene expression in certain cancer
cells, changing the levels or activity of certain hormones can cause
certain cancers to cease growing, or even undergo cell death.
Surgical removal of endocrine organs, such as orchiectomy and
oophorectomy can also be employed as a form of hormonal therapy.
17. • Breast cancer hormone therapy
• The female hormones oestrogen and progesterone affect some
breast cancers. Doctors describe these cancers as oestrogen receptor
positive (ER+) or progesterone receptor positive (PR+) or both.
Hormone treatment for breast cancer works by stopping these
hormones getting to the breast cancer cells.
• Tamoxifen
• Tamoxifen works by blocking the oestrogen receptors. It stops
oestrogen from telling the cancer cells to grow.
• Tamoxifen is one of most common hormone therapies for breast
cancer. Women who are still having periods (are pre menopausal) and
women who have had their menopause (are post menopausal)
can take tamoxifen.
• Hormone therapy (tamoxifen or raloxifene) might be offered to
people at high risk of breast cancer. This is called chemoprevention.
This is not suitable for everyone.
18. • Breast cancer hormone therapy
• Aromatase Inhibitors
• You might have an aromatase inhibitor if you have been through the
menopause.
• After menopause, your ovaries stop producing oestrogen. But your
body still makes a small amount by changing other hormones (called
androgens) into oestrogen. Aromatase is the enzyme that makes this
change happen. Aromatase inhibitors block aromatase so that it can’t
change androgens into oestrogen.
• There are a few different types of aromatase inhibitor. We have
detailed information about aromatase inhibitors, including
anastrozole (Arimidex), exemestane (Aromasin) and letrozole
(Femara).
19. • Breast cancer hormone therapy
• Luteinising hormone releasing hormone (LHRH) agonists or LH
blockers
• A gland in the brain called the pituitary gland produces luteinising
hormone (LH) which controls the amount of hormones made by the
ovaries.
• LH blockers are drugs that stop the production of luteinising hormone.
They do this by blocking the signal from the pituitary gland to the
ovaries. So, the ovaries stop making oestrogen or progesterone.
• You will only have this treatment if you have not had your menopause
yet. After menopause, your ovaries don’t produce hormones, so this
type of drug won’t help.
• One type used for breast cancer is goserelin (Zoladex).
• Fulvestrant
• Fulvestrant (Faslodex) stops oestrogen getting to the cancer cells by
blocking oestrogen receptors and reducing the number of receptors
the cancer cells have. You might have this in combination with other
cancer drugs.
20. • Prostate cancer hormone therapy
• Prostate cancer depends on testosterone to grow. Hormone therapy blocks
or lowers the amount of testosterone in the body.
• This can lower the risk of an early prostate cancer coming back when you
have it with other treatments. Or, it can shrink an advanced prostate cancer
or slow its growth.
Luteinising hormone releasing hormone (LHRH) agonists or LH blockers
• A gland in the brain called the pituitary gland produces luteinising hormone
(LH). This controls the amount of testosterone made by the testicles.
• LH blockers are drugs that stop the production of luteinising hormone. They
do this by blocking the signal from the pituitary gland to the testicles. So the
testicles stop making testosterone.
• Types for prostate cancer include goserelin (Zoladex), leuprorelin (Prostap)
and triptorelin (Decapetyl).
Anti androgens
• Prostate cancer cells have areas called receptors. Testosterone attaches to
these receptors and that can encourage the cells to divide so that the cancer
grows.
• Anti androgen drugs work by attaching themselves to these receptors. This
stops testosterone from reaching the prostate cancer cells.
• There are different types of anti androgens including bicalutamide (Casodex),
cyproterone acetate (Cyprostat) and flutamide (Drogenil).
21. • Prostate cancer hormone therapy
Gonadotrophin releasing hormone (GnRH) blocker
• Gonadotrophin releasing hormone (GnRH) blockers stop messages
from a part of the brain called the hypothalamus that tell the
pituitary gland to produce luteinising hormone.
• Luteinising hormone tells the testicles to produce testosterone. So,
blocking GnRH stops the testicles producing testosterone. The drug
degarelix (Firmagon) is a GnRH blocker.
Other hormone therapies
• There are other newer hormonal treatments for prostate cancer.
These therapies include:
• enzalutamide
• abiraterone
• darolutamide
22. • Womb/uterus cancer hormone therapy
The female hormones oestrogen and progesterone affect the growth
and activity of the cells that line the womb. Doctors use progesterone
treatment to help shrink larger womb cancers or to treat womb
cancers that have come back.
There are different types of progesterone that you might have
including medroxyprogesterone acetate (Provera) and megestrol
(Megace).
23. Immunotherapy
A type of therapy that uses substances to stimulate or suppress the
immune system to help the body fight cancer, infection, and other
diseases. Some types of immunotherapy only target certain cells of the
immune system. Others affect the immune system in a general way.
Types of immunotherapy include cytokines, vaccines, bacillus
Calmette-Guerin (BCG), and some monoclonal antibodies.
25. Monoclonal Antibodies (MAB)
• Antibodies are found naturally in our blood and
help us to fight infection. MAB therapies mimic
natural antibodies but are made in a laboratory.
Monoclonal just means all one type. So each
MAB is a lot of copies of one type of antibody.
• A MAB works by recognising and finding specific
proteins on cells. Some work on cancer cells,
others target proteins on cells of the immune
system.
• Each MAB recognises one particular protein.
They work in different ways depending on the
protein they are targeting.
• MABs work as an immunotherapy in different
ways. Some MABs work in more than one way.
They can:
• trigger the immune system to attack and kill
cancer cells
• act on cells to help the immune system attack
cancer cells
26. MAB
• Some MABs trigger the immune system to attack and kill cancer cells
• Some MABs attach themselves to cancer cells, making it easier for the cells
of the immune system to find them. This process is called antibody-
dependent cell-mediated cytotoxicity or ADCC.
• Monoclonal antibodies (MABs) which trigger the immune system to treat
cancer
-An injected monoclonal antibody seeks out cancer cell proteins.
-The monoclonal antibody bind to the proteins.
-The antibodies signal to immune cells.
-The immune cells arrive and punch holes in the cancer cell. The cancer cell
dies.
Examples of MABS that work in this way include:
• rituximab (Mabthera) – a treatment for chronic lymphocytic leukaemia (CLL)
and some types of non Hodgkin lymphoma
• cetuximab (Erbitux) – a treatment for advanced bowel cancer and head and
neck cancer
• trastuzumab (Herceptin) – used to treat breast cancer and stomach cancer
27. Checkpoint Inhibitors
Other MABs work by acting on cells of the immune system. For example, a
type of immunotherapy called checkpoint inhibitors. Checkpoint inhibitors
block proteins that stop the immune system attacking cancer cells.
Checkpoint inhibitors block different proteins, including:
• CTLA-4 (cytotoxic T lymphocyte associated protein 4): Ipilumab
• PD-1 (programmed cell death protein 1)
• PD-L1 (programmed death ligand 1)
So you might hear these drugs named after these checkpoint proteins – for
example, CTLA-4 inhibitors, PD-1 inhibitors and PD-L1 inhibitors.
Examples of checkpoint inhibitors include:
• CTLA-4 inhibitors: Ipilimumab (Yervoy)
• PD-1 inhibitors: nivolumab (Opdivo), pembrolizumab (Keytruda)
• PD-L1 inhibitors: atezolizumab, avelumab, durvalumab
Nivolumab and pembrolizumab are used to treat several different types of
cancer.
28. Checkpoint Inhibitors
• T cells have proteins on them that turn on an immune response and other
proteins that turn it off. These are called checkpoint proteins.
• Some checkpoint proteins help tell T cells to become active, for example
when an infection is present. But if T cells are active for too long, or react to
things they shouldn’t, they can start to destroy healthy cells and tissues. So
other checkpoints help tell T cells to switch off.
• Some cancer cells make high levels of proteins. These can switch off T cells,
when they should really be attacking the cancer cells. So the cancer cells are
pushing a stop button on the immune system. And the T cells can no longer
recognise and kill cancer cells.
• Drugs that block checkpoint proteins are called checkpoint inhibitors. They
stop the proteins on the cancer cells from pushing the stop button. This
turns the immune system back on and the T cells are able to find and attack
the cancer cells.
29. Cytokines
Cytokines are a group of proteins in the body that play an important part
in boosting the immune system. Interferon and interleukin are types of
cytokines found in the body. Scientists have developed man made
versions of these to treat cancer.
The man made version of interleukin is called aldesleukin
Interferon and aldesleukin work in several ways, including:
• interfering with the way cancer cells grow and multiply
• stimulating the immune system and encouraging killer T cells and
other cells to attack cancer cells
• encouraging cancer cells to produce chemicals that attract immune
system cells to them
30. Targeted Therapy
A type of treatment that uses drugs or other substances to identify and
attack specific types of cancer cells with less harm to normal cells.
Some targeted therapies block the action of certain enzymes, proteins,
or other molecules involved in the growth and spread of cancer cells.
Other types of targeted therapies help the immune system kill cancer
cells or deliver toxic substances directly to cancer cells and kill them.
Targeted therapy may have fewer side effects than other types of
cancer treatment. Most targeted therapies are either small molecule
drugs or monoclonal antibodies.
31. Targeted Therapy
• As a form of molecular medicine, targeted therapy blocks the growth
of cancer cells by interfering with specific targeted molecules needed
for carcinogenesis and tumor growth.
• Because most agents for targeted therapy are biopharmaceuticals,
the term biologic therapy is sometimes synonymous with targeted
therapy when used in the context of cancer therapy (and thus
distinguished from chemotherapy, that is, cytotoxic therapy).
However, the modalities can be combined; antibody-drug conjugates
combine biologic and cytotoxic mechanisms into one targeted
therapy.
• Many targeted therapies are examples of immunotherapy (using
immune mechanisms for therapeutic goals) developed by the field of
cancer immunology. Thus, as immunomodulators, they are one type
of biological response modifiers.
• The main categories of targeted therapy are currently small
molecules and monoclonal antibodies.
32. Types of Targeted Therapy
• There are many different types of targeted cancer drugs. These are
grouped together depending on how they work. Some drugs belong
to more than one group because they work in more than one way.
For example, a drug that works by blocking cancer cell growth may
also be a monoclonal antibody.
• Some of these targeted drugs might also be called immunotherapies
or biological therapies.
• monoclonal antibodies
• cancer growth blockers
• drugs that block cancer blood vessel growth
• PARP inhibitors
33. MAB
• MABs work in different ways and some work in more than one way. They may do
one of the following:
• Block signals telling cancer cells to divide: Cancer cells often make large
amounts of molecules called growth factor receptors. These sit on the cell
surface and send signals to help the cell survive and divide. Some MABs stop
growth factor receptors from working properly, either by blocking the signal or
the receptor itself. So the cancer cell no longer receives the signals it needs.
• Carry cancer drugs or radiation to cancer cells: Some MABs have drugs or
radioactive substances attached to them. The MAB finds the cancer cells and
delivers the drug or radioactive substance directly to them. These are called
conjugated MABs.
• Help your immune system find and kill cancer cells: Some MABS have an effect
on the immune system. The immune system is then in a better position to kill
cancer cells. Because MABs work in different ways, some of these drugs are also
a type of immunotherapy. They do this by blocking proteins that stop the
immune system working (checkpoint inhibitors) or attaching to cancer cells,
making it easier for the cells of the immune system to find them (a process called
antibody-dependent cell-mediated cytotoxicity, or ADCC)
• Block signals telling cancer cells to develop a blood supply (anti angiogenic
drugs): Some cancer cells make a protein called vascular endothelial growth
factor (VEGF). The VEGF protein attaches to receptors on cells that line the walls
of blood vessels within the tumour. This triggers the blood vessels to grow so the
cancer can then grow. Some MABs block vascular endothelial growth factor
(VEGF) from attaching to the receptors on the cells that line the blood vessels.
These MABs are called anti angiogenic drugs.
34. Cancer Growth Blockers
• Growth factors are chemicals produced by the body that control cell
growth. There are many different types of growth factors and they all
work in different ways.
• Growth factors work by binding to receptors on the cell surface. This
sends a signal to the inside of the cell, which sets off a chain of
complicated chemical reactions.
• There are a number of different growth factors. These include:
• epidermal growth factor (EGF) – controls cell growth
• vascular endothelial growth factor (VEGF) – controls blood vessel
development
• platelet derived endothelial growth factor (PDGF) – controls blood vessel
development and cell growth
• fibroblast growth factor (FGF) – controls cell growth
• Each growth factor works by attaching to the corresponding receptor
on the cell surface. For example, EGF binds to epidermal growth
factor receptor (EGFR).
35. • A cancer growth blocker is a targeted drug that blocks the growth
factors that trigger cancer cells to divide and grow. Scientists are
looking at different ways of doing this such as:
• lowering levels of the growth factor in the body
• blocking the growth factor receptor on the cancer cell
• blocking the signals inside the cell that start up when the growth factor
triggers the receptor
• Most of these treatments work by blocking the signalling processes
that cancer cells use to divide.
• Cancer cells are often very sensitive to growth factors. So if we can
block them, we can stop some types of cancer from growing and
dividing. Scientists are developing different inhibitors for the different
types of growth factors.
Cancer Growth Blockers
36. Types of cancer growth blockers
Tyrosine kinase inhibitors
Tyrosine kinase inhibitors (TKIs) block chemical messengers (enzymes)
called tyrosine kinases. Tyrosine kinases help to send growth signals in
cells, so blocking them stops the cell growing and dividing.
Cancer growth blockers can block one type of tyrosine kinase or more
than one type. TKIs that block more than one type of tyrosine kinase are
called multi TKIs.
Examples of TKIs include:
•axitinib (Inlyta)
•dasatinib (Sprycel)
•erlotinib (Tarceva)
•imatinib (Glivec)
•nilotinib (Tasigna)
•pazopanib (Votrient)
•sunitinib (Sutent)
37. • Tyrosine Kinases are chemical messengers (enzymes) used by cells to
control how they grow and divide. They act like an ‘on-off’
switch. When the growth factor attaches to the outside of the cell it
switches the tyrosine kinase ‘on’. This signals the cell to divide.
Cancer Growth Blockers
39. Types of cancer growth blockers
• Proteasome inhibitors
• Proteasomes are tiny, barrel shaped structures found in all
cells. They help break down proteins the cell doesn't need
into smaller parts. The cell can then use them to make new
proteins that it does need.
• Drug treatments that block proteasomes from working are
called proteasome inhibitors. They cause a build up of
unwanted proteins in the cell, which makes the cancer cells
die.
• Doctors use proteasome inhibitors to treat myeloma.
Examples include:
• bortezomib (Velcade)
• carfilzomib (Kyprolis)
• ixazomib (Ninlaro)
40. Types of cancer growth blockers
• mTOR inhibitors
• mTOR(Mammalian target of rapamycin) is a type of protein called a
kinase protein. It can make cells produce chemicals (such as cyclins) that
trigger cell growth. It may also make cells produce proteins that trigger
the development of new blood vessels. Cancers need new blood vessels
in order to grow.
• In some types of cancer mTOR is switched on, which makes the cancer
cells grow and produce new blood vessels. mTOR blockers (inhibitors)
can stop the growth of some types of cancer.
• mTOR inhibitors include:
• temsirolimus (Torisel)
• everolimus (Afinitor)
41. Types of cancer growth blockers
• PI3K inhibitors
• PI3Ks are a group of closely related kinase proteins. Their full name
is phospho inositide 3 kinases.
• They do a number of different things in cells. For example, they act like
switches in the cell turning on other proteins such as mTOR
• Switching on PI3Ks might make cells grow and multiply, or trigger the
development of blood vessels, or help cells to move around.
• In some cancers PI3K is permanently switched on, which means that the
cancer cells grow uncontrollably. Researchers have been developing new
treatments that inhibit PI3K.
• For example, idelalisib (Zydelig) is now available as a treatment for some
people with chronic lymphocytic leukaemia (CLL).
42. Types of cancer growth blockers
• Histone deacetylase inhibitors
• Histone deacetylase inhibitors are also called HDAC inhibitors or HDIs.
• They block the action of a group of enzymes that remove chemicals
called acetyl groups from particular proteins. This can stop the cancer
cell from using some genes that would help it to grow and divide.
This might kill the cancer cell completely.
• HDACs are a newer type of cancer growth blocker. Panobinostat is an
example of an HDAC. It is a treatment for myeloma. Researchers are
looking at some other HDACs including:
• vorinostat
• romidepsin
43. Types of cancer growth blockers
• Hedgehog pathway blockers
• Hedgehog pathway blockers are drugs that target a group of proteins
known as the hedgehog pathway. In the developing embryo, these
proteins send signals that help cells to grow in the right place and in the
right way.
• The hedgehog pathway can also control the growth of blood vessels and
nerves. In adults, hedgehog pathway proteins are not usually active. But
in some people, changes in a gene switch them on. Hedgehog pathway
blockers are designed to switch off the proteins and stop the growth of
the cancer.
• Vismodegib (Erivedge) is an example of a hedgehog pathway blocker. It is
used in some situations to treat people with basal cell skin cancer that
has spread.
44. Types of cancer growth blockers
• BRAF and MEK inhibitors
• BRAF inhibitors directly block a protein called BRAF. BRAF is a chemical messenger (enzyme)
that controls how cells grow and send signals.
• Some cancers have a change (mutation) in the BRAF gene. This genetic change makes the
cancer cells produce too much BRAF protein, which can make cancer cells grow. BRAF
inhibitors block the BRAF proteins and can stop cancer cells growing.
• BRAF inhibitors are a treatment for advanced melanoma. Examples include:
• vemurafenib (Zelboraf)
• dabrafenib (Tafinlar)
• encorafenib (Braftovi)
• The BRAF protein can affect other proteins, such as MEK, which makes cancer cells divide and
grow in an uncontrolled way. MEK inhibitors are another type of targeted cancer drug. They
work by blocking the MEK protein, which slows down the growth of cancer cells. Two MEK
inhibitors for melanoma are:
• trametinib (Mekinist)
• binimetinib (Mektovi)
• You usually have a BRAF inhibitor with a MEK inhibitor. This is because having the combination
of both drugs can work better.
45. Drugs that block cancer blood vessel growth
(anti angiogenics)
• Angiogenesis means the growth of new blood vessels. So anti
angiogenic drugs are treatments that stop tumours from growing
their own blood vessels. If the drug is able to stop a cancer from
growing blood vessels, it might slow the growth of the cancer or
sometimes shrink it.
• Some cancer cells make a protein called vascular endothelial growth
factor (VEGF). The VEGF protein attaches to receptors on cells that
line the walls of blood vessels within the tumour. The cells are called
endothelial cells. This triggers the blood vessels to grow so the
cancer can then grow.
46. Types of anti angiogenesis treatment
• Drugs that block blood vessel growth factor
• Some drugs block vascular endothelial growth factor (VEGF) from
attaching to the receptors on the cells that line the blood vessels.
This stops the blood vessels from growing.
• An example of a drug that blocks VEGF is bevacizumab (Avastin).
Bevacizumab is also a monoclonal antibody. It is a treatment for
several different types of cancer. Other examples include:
• aflibercept
• ramucirumab
47. Types of anti angiogenesis treatment
• Drugs that block signalling within the cell
• Some drugs stop the VEGF receptors from sending growth signals
into the blood vessel cells. These treatments are also called cancer
growth blockers or tyrosine kinase inhibitors (TKIs).
• Examples of TKIs that block signals inside blood vessels cells include:
• sunitinib
• sorafenib
• axitinib
• regorafenib
• cabozantinib
48. Types of anti angiogenesis treatment
• Drugs that affect signals between cells
• Some drugs act on the chemicals that cells use to signal to each other
to grow. This can block the formation of blood vessels.
• Drugs that works in this way include thalidomide and lenalidomide
(Revlimid). They are used to treat some people with multiple
myeloma.
49. PARP inhibitors
• PARP is a protein (enzyme) found in our cells, it stands for poly-ADP
ribose polymerase. It helps damaged cells to repair themselves.
• As a cancer treatment, PARP inhibitors stop the PARP from doing its
repair work in cancer cells and the cell dies.
• Researchers first looked at these drugs in cancers that already had
problems repairing cell damage. They focused on cancers with a
change (or fault) in genes called BRCA.
• Normally, BRCA1 and BRCA2 genes play a part in cell repair in the
body. Cells are less likely to repair themselves if there is a fault in one
or both of these genes. People who have faulty BRCA genes have an
increased risk of certain cancers including:
• breast cancer
• ovarian cancer
• prostate cancer
• Cancer cells with BRCA gene faults already have a poor repair system.
So blocking PARP with a PARP inhibitor drug means that the cells are
not able to repair themselves and they die.
50. PARP inhibitors
• PARP inhibitors are a treatment for the following types of cancer:
• ovarian cancer
• fallopian tube cancer
• peritoneal cancer
• Researchers think that they might work in cancers that have
weaknesses in the cell similar to the BRCA gene fault. There are trials
to find whether they are useful in other types of cancer including:
• lung cancer
• pancreatic cancer
• head and neck cancer
• a type of brain tumour called glioblastoma multiforme
• prostate cancer
• cancer of the stomach and foodpipe (oesophagus)
• womb and cervical cancer
• kidney and bladder cancer
51. Types of PARP inhibitors
•There are different types of PARP inhibitors
including:
• olaparib (Lynparza)
• rucaparib (Rubraca)
• niraparib (Zejula)
•These PARP inhibitors are for some women with
one of the following types of cancer:
• ovarian cancer
• fallopian tube cancer
• peritoneal cancer
52. Small Molecules
Many are tyrosine-kinase inhibitors.
• Imatinib (Gleevec, also known as STI–571) is approved for chronic myelogenous
leukemia, gastrointestinal stromal tumor and some other types of cancer. Early clinical
trials indicate that imatinib may be effective in treatment of dermatofibrosarcoma
protuberans.
• Gefitinib (Iressa, also known as ZD1839), targets the epidermal growth factor receptor
(EGFR) tyrosine kinase and is approved in the U.S. for non small cell lung cancer.
• Erlotinib (marketed as Tarceva). Erlotinib inhibits epidermal growth factor receptor,
and works through a similar mechanism as gefitinib. Erlotinib has been shown to
increase survival in metastatic non small cell lung cancer when used as second line
therapy. Because of this finding, erlotinib has replaced gefitinib in this setting.
• Sorafenib (Nexavar), Sunitinib (Sutent), Dasatinib (Sprycel), Lapatinib (Tykerb),
Nilotinib (Tasigna)
• Bortezomib (Velcade) is an apoptosis-inducing proteasome inhibitor drug that causes
cancer cells to undergo cell death by interfering with proteins. It is approved in the
U.S. to treat multiple myeloma that has not responded to other treatments.
54. • The selective estrogen receptor modulator tamoxifen has been described as
the foundation of targeted therapy.
• Janus kinase inhibitors, e.g. FDA approved tofacitinib
• ALK inhibitors, e.g. crizotinib
• Bcl-2 inhibitors (e.g. FDA approved venetoclax, obatoclax in clinical trials,
navitoclax, and gossypol.
• PARP inhibitors (e.g. FDA approved olaparib, rucaparib, niraparib and
talazoparib)
• PI3K inhibitors (e.g. perifosine in a phase III trial)
• Apatinib is a selective VEGF Receptor 2 inhibitor which has shown encouraging
anti-tumor activity in a broad range of malignancies in clinical trials.
• Apatinib is currently in clinical development for metastatic gastric carcinoma,
metastatic breast cancer and advanced hepatocellular carcinoma.
• Zoptarelin doxorubicin (AN-152), doxorubicin linked to [D-Lys(6)]- LHRH, Phase
II results for ovarian cancer.
Small Molecules
55. • Braf inhibitors (vemurafenib, dabrafenib, LGX818) used to treat metastatic melanoma
that harbors BRAF V600E mutation
• MEK inhibitors (trametinib, MEK162) are used in experiments, often in combination
with BRAF inhibitors to treat melanoma
• CDK inhibitors, e.g. PD-0332991, LEE011 in clinical trials
• Hsp90 inhibitors, some in clinical trials
• Hedgehog pathway inhibitors (e.g. FDA approved vismodegib and sonidegib).
• salinomycin has demonstrated potency in killing cancer stem cells in both laboratory-
created and naturally occurring breast tumors in mice.
• VAL-083 (dianhydrogalactitol), a “first-in-class” DNA-targeting agent with a unique bi-
functional DNA cross-linking mechanism. NCI-sponsored clinical trials have
demonstrated clinical activity against a number of different cancers including
glioblastoma, ovarian cancer, and lung cancer. VAL-083 is currently undergoing Phase 2
and Phase 3 clinical trials as a potential treatment for glioblastoma (GBM) and ovarian
cancer. As of July 2017, four different trials of VAL-083 are registered.
Small Molecules
56. Serine/threonine kinase inhibitors (small molecules)
• Vintafolide is a small molecule drug conjugate consisting of a small
molecule targeting the folate receptor. It is currently in clinical trials
for platinum-resistant ovarian cancer (PROCEED trial) and a Phase 2b
study (TARGET trial) in non-small-cell lung carcinoma (NSCLC).
Small molecule drug conjugates
• Temsirolimus (Torisel)
• Everolimus (Afinitor)
• Vemurafenib (Zelboraf)
• Trametinib (Mekinist)
• Dabrafenib (Tafinlar)
57. Monoclonal antibodies
Examples of licensed monoclonal antibodies include:
• Pembrolizumab (Keytruda) binds to PD-1 proteins found on T cells.
Pembrolizumab blocks PD-1 and help the immune system kill cancer cells. It is
used to treat melanoma, Hodgkin's lymphoma, non-small cell lung carcinoma and
several other types of cancer.
• Rituximab targets CD20 found on B cells. It is used in non Hodgkin lymphoma
• Trastuzumab targets the Her2/neu (also known as ErbB2) receptor expressed in
some types of breast cancer
• Alemtuzumab
• Cetuximab target the epidermal growth factor receptor (EGFR). It is approved for
use in the treatment of metastatic colorectal cancer and squamous cell carcinoma
of the head and neck.
• Panitumumab also targets the EGFR. It is approved for the use in the treatment of
metastatic colorectal cancer.
• Bevacizumab targets circulating VEGF ligand. It is approved for use in the
treatment of colon cancer, breast cancer, non-small cell lung cancer, and is
investigational in the treatment of sarcoma. Its use for the treatment of brain
tumors has been recommended.
• Ipilimumab (Yervoy)
• Many antibody-drug conjugates (ADCs) are being developed and also ADEPT
(antibody-directed enzyme prodrug therapy).