This document discusses cancer and chemotherapy. It provides an overview of cancer physiology, causes, stages of development and treatments. It describes different classes of chemotherapeutic agents including alkylating agents, antimetabolites, anthracyclines and bleomycin. For each drug class and individual drugs, it discusses mechanisms of action, clinical applications, pharmacokinetics, resistance mechanisms and common adverse effects.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
The document discusses various classes of anticancer drugs including cytotoxic drugs derived from natural sources like plants and microbes. It focuses on the mechanisms of action and classification of antitumor antibiotic drugs derived from Streptomyces bacteria. Specifically, it describes the structures, mechanisms involving DNA intercalation and inhibition of topoisomerases, and clinical uses of important anthracycline antibiotics like doxorubicin, daunorubicin and actinomycin antibiotics like dactinomycin and mitomycin C.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document summarizes various types of anti-cancer drugs and their mechanisms of action. It discusses how chemotherapy drugs like alkylating agents and antimetabolites target rapidly dividing cancer cells by damaging DNA or interfering with DNA synthesis. Newer targeted therapies include monoclonal antibodies that target specific proteins in cancer cells or hormone therapies that block estrogen production in breast cancer. The document also outlines how different drug classes like plant alkaloids, antibiotics, and topoisomerase inhibitors damage DNA or disrupt cell division to kill cancer cells.
This document discusses chemotherapy for cancer treatment. It describes the main types of anticancer drugs as cytotoxic, targeted, and hormonal drugs. Cytotoxic drugs are further broken down into categories like alkylating agents, platinum coordination compounds, antimetabolites, and microtubule damaging agents. The document also covers general principles of chemotherapy like using combination therapy to achieve total tumour cell kill and targeting actively dividing cancer cells. Adverse effects of cytotoxic drugs are explained, like bone marrow depression and immunosuppression. The goal of cancer therapy is outlined as cure, prolonging remission, or palliation depending on the cancer type and stage.
Recent advances in cancer treatment include new drug carrier systems and nanotechnology to more precisely target cancer cells. New drug carrier systems such as polymer drug conjugates, cyclodextrins, and self-emulsifying drug delivery formulations aim to enhance drug delivery to tumors while avoiding healthy tissues to reduce side effects. Nanotechnology uses carbon nanotubes and nanoparticles to transport drugs across biological barriers and directly into cancer cells. Additionally, newer cancer vaccines using antigens, dendritic cells, and DNA aim to stimulate the immune system to recognize and destroy cancerous cells.
Chemotherapy uses anti-cancer drugs to destroy cancer cells. It can be curative for some cancers like leukemias, Wilms tumor, and Hodgkin's lymphoma. The drugs work by interfering with cell division through different mechanisms and can be cell cycle specific or non-specific. Alkylating agents are a common class of chemotherapy drugs that work by transferring alkyl groups to DNA, causing cross-linkages and strand breaks to damage DNA and inhibit cell proliferation. Combination chemotherapy and intermittent dosing regimens are often used to improve outcomes.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
The document discusses various classes of anticancer drugs including cytotoxic drugs derived from natural sources like plants and microbes. It focuses on the mechanisms of action and classification of antitumor antibiotic drugs derived from Streptomyces bacteria. Specifically, it describes the structures, mechanisms involving DNA intercalation and inhibition of topoisomerases, and clinical uses of important anthracycline antibiotics like doxorubicin, daunorubicin and actinomycin antibiotics like dactinomycin and mitomycin C.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document summarizes various types of anti-cancer drugs and their mechanisms of action. It discusses how chemotherapy drugs like alkylating agents and antimetabolites target rapidly dividing cancer cells by damaging DNA or interfering with DNA synthesis. Newer targeted therapies include monoclonal antibodies that target specific proteins in cancer cells or hormone therapies that block estrogen production in breast cancer. The document also outlines how different drug classes like plant alkaloids, antibiotics, and topoisomerase inhibitors damage DNA or disrupt cell division to kill cancer cells.
This document discusses chemotherapy for cancer treatment. It describes the main types of anticancer drugs as cytotoxic, targeted, and hormonal drugs. Cytotoxic drugs are further broken down into categories like alkylating agents, platinum coordination compounds, antimetabolites, and microtubule damaging agents. The document also covers general principles of chemotherapy like using combination therapy to achieve total tumour cell kill and targeting actively dividing cancer cells. Adverse effects of cytotoxic drugs are explained, like bone marrow depression and immunosuppression. The goal of cancer therapy is outlined as cure, prolonging remission, or palliation depending on the cancer type and stage.
Recent advances in cancer treatment include new drug carrier systems and nanotechnology to more precisely target cancer cells. New drug carrier systems such as polymer drug conjugates, cyclodextrins, and self-emulsifying drug delivery formulations aim to enhance drug delivery to tumors while avoiding healthy tissues to reduce side effects. Nanotechnology uses carbon nanotubes and nanoparticles to transport drugs across biological barriers and directly into cancer cells. Additionally, newer cancer vaccines using antigens, dendritic cells, and DNA aim to stimulate the immune system to recognize and destroy cancerous cells.
Chemotherapy uses anti-cancer drugs to destroy cancer cells. It can be curative for some cancers like leukemias, Wilms tumor, and Hodgkin's lymphoma. The drugs work by interfering with cell division through different mechanisms and can be cell cycle specific or non-specific. Alkylating agents are a common class of chemotherapy drugs that work by transferring alkyl groups to DNA, causing cross-linkages and strand breaks to damage DNA and inhibit cell proliferation. Combination chemotherapy and intermittent dosing regimens are often used to improve outcomes.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
QSAR attempts to correlate biological activity to measurable physicochemical properties through mathematical equations. It relates parameters like lipophilicity (log P), electronic effects (Hammett constants), and steric effects to biological response. Various QSAR methods exist, including Hansch analysis which uses these substituent constants in its equations. More advanced techniques like CoMFA analyze fields around aligned molecules to model activity landscapes and identify favorable regions for activity. QSAR provides a framework for drug design and predicting activities of untested compounds.
Antineoplastic agents can be classified as cytotoxic drugs, hormones, or miscellaneous agents. Cytotoxic drugs include alkylating agents, antimetabolites, plant derivatives, and antibiotics. They work by directly damaging DNA or interfering with cell division and metabolism. Combination therapy is more effective than single agents to increase response rates and decrease resistance development.
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
This document discusses cancer chemotherapy. It begins by providing background on the origins of chemotherapy, noting that its modern era began in 1948 with the introduction of nitrogen mustard. It then covers various classifications of chemotherapeutic drugs including their mechanisms of action and side effects. Specific drugs discussed include alkylating agents like cyclophosphamide and cisplatin, antimetabolites like methotrexate and purine analogues, and hormonal drugs. The objectives and cell cycle effects of chemotherapy are also summarized.
The document discusses natural products taxanes and podophyllotoxins that have led to new anti-cancer drugs. It describes how over 60% of anti-cancer drugs originate from natural products. Taxanes such as paclitaxel and docetaxel stabilize microtubules, preventing cell division and causing cancer cell death. Podophyllotoxins like etoposide and teniposide inhibit topoisomerase and DNA synthesis in cancer cells. Both classes are effective against various cancer types with side effects like low blood counts and hair loss that require careful treatment. Natural products continue providing leads for developing new anti-cancer pharmaceuticals.
The document discusses various types of anticancer agents, including their classification and mechanisms of action. It focuses on alkylating agents, specifically nitrogen mustards. Nitrogen mustards were some of the first chemicals used to treat cancer and work by alkylating DNA at the N7 position of guanine. This prevents replication and can activate apoptosis. Examples discussed include mechlorethamine, chlorambucil, melphalan, and cyclophosphamide. Cyclophosphamide must be activated in the body to form an aziridinium ion that alkylates DNA. The document also briefly mentions mitomycin C, an antibiotic used in cancer treatment.
cancer chemotherapy
Introduction,Types of cancer,Aetiology of cancer,Pathogenesis of cancer,Diagnosis of cancer,Treatment of cancer,Novel drugs for cancer,Future prospects
1) Recent advances in cancer chemotherapy include the development of newer alkylating agents, platinum compounds, antimetabolites, mitotic spindle inhibitors, and topoisomerase inhibitors with improved efficacy and reduced toxicity profiles.
2) Many newer agents aim to overcome resistance to existing drugs by bypassing drug efflux pumps or having activity in cisplatin/taxane resistant settings.
3) Several new drugs have received FDA approval in the last decade for cancers like breast cancer, lung cancer, and leukemia, offering additional treatment options.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
Plasmodium parasites cause malaria in humans. The document discusses various antimalarial agents, including:
1. Chloroquine, a 4-aminoquinoline that inhibits heme polymerization in parasites and is effective against several Plasmodium species but resistance has developed.
2. Mefloquine, a quinoline-methanol with strong blood-stage activity against multidrug resistant P. falciparum.
3. Quinine, a cinchona alkaloid that remains effective against some resistant strains and has moderate activity against hepatic and transmission stages.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
Combinatorial chemistry is a technique used to rapidly produce large libraries of potential drug molecules. It allows scientists to create and evaluate thousands of similar compounds in parallel. The key advantages are that it is faster and more economical than traditional drug discovery methods. Some challenges include ensuring diversity in the compound libraries and identifying the active components within mixture samples. Solid phase synthesis and parallel/mixed synthesis are common techniques used in combinatorial chemistry approaches.
This document summarizes recent advances in cancer treatment. It begins with an introduction discussing the prevalence of cancer worldwide and the integration of nanotechnology with medicine to provide new tumor therapy opportunities. It then discusses circulating tumor cells that can be identified in blood, chemodynamic therapy that uses CDT agents to inhibit immunity and cause cell death, and various oligonucleotide therapeutics including CpG oligonucleotides, miRNAs, aptamers, and DNAzymes. It also discusses combination immunotherapy using multiple therapeutic agents, and photoimmunotherapy which combines photodynamic therapy with immunotherapy. The document concludes by stating the goal is to cure cancer patients or prolong their lives while maintaining a good quality of life.
Cancer is caused by uncontrolled cell growth and can spread through the body. Risk factors include tobacco, sunlight, viruses, and family history. Diagnosis involves biopsy and imaging tests while treatment aims to cure, palliate, or induce remission through surgery, radiation, chemotherapy, and targeted therapy. Chemotherapy drugs work by various mechanisms including alkylating DNA, blocking DNA synthesis, and affecting microtubule function. Major classes include alkylating agents, antimetabolites, antitumor antibiotics, plant alkaloids, and miscellaneous cytotoxic drugs. Combination regimens and consideration of each drug's cell cycle specificity can improve outcomes.
Combinatorial chemistry allows for the rapid synthesis of large libraries of compounds. It works by synthesizing many structures in parallel rather than one at a time. There are two main approaches: solid phase synthesis which attaches compounds to resin beads to isolate products, and solution phase which synthesizes in solvent. The libraries can be screened to identify active compounds more efficiently than traditional methods. This technique has increased the success of drug discovery by allowing testing of more structures at once.
THIS PRESENTATION ABOUT ANTIMALARIAL DRUGS DETAILING THE COMPLETE INFORMATION ABOUT THE DRUGS USED WITH ITS MECHANISM OF ACTION, STRUCTURAL ACTIVITY AND DOSES.
1. Solid cancer tumors generally have a low growth fraction and thus respond poorly to chemotherapy, often requiring surgery for removal. Disseminated cancers generally have a high growth fraction and often respond well to chemotherapy.
2. There are several classes of chemotherapeutic agents that work through different mechanisms such as alkylating DNA, inhibiting synthesis of DNA/RNA precursors, or inhibiting microtubule polymerization. Combination chemotherapy is often used to increase effectiveness.
3. Dosage must be modified based on toxicity monitoring like myelosuppression as measured by absolute neutrophil count and platelet count to minimize risks of side effects. Preventative measures and dose modifications can manage toxicities from chemotherapy.
This document discusses cancer and chemotherapy. It defines cancer as uncontrolled cell growth and describes its characteristics. Cancer treatment may involve surgery, radiation, chemotherapy, or combinations. Chemotherapy uses chemical agents to kill cancer cells and can be used as adjuvant therapy after other treatments or as neo-adjuvant therapy before the main treatment. The document then describes the cell cycle, principles of chemotherapy including drug mechanisms and scheduling, problems like resistance and toxicities, and examples of different classes of chemotherapeutic agents including alkylating agents, antimetabolites, microtubule inhibitors, antibiotics, hormonal agents, and monoclonal antibodies.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
QSAR attempts to correlate biological activity to measurable physicochemical properties through mathematical equations. It relates parameters like lipophilicity (log P), electronic effects (Hammett constants), and steric effects to biological response. Various QSAR methods exist, including Hansch analysis which uses these substituent constants in its equations. More advanced techniques like CoMFA analyze fields around aligned molecules to model activity landscapes and identify favorable regions for activity. QSAR provides a framework for drug design and predicting activities of untested compounds.
Antineoplastic agents can be classified as cytotoxic drugs, hormones, or miscellaneous agents. Cytotoxic drugs include alkylating agents, antimetabolites, plant derivatives, and antibiotics. They work by directly damaging DNA or interfering with cell division and metabolism. Combination therapy is more effective than single agents to increase response rates and decrease resistance development.
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
This document discusses cancer chemotherapy. It begins by providing background on the origins of chemotherapy, noting that its modern era began in 1948 with the introduction of nitrogen mustard. It then covers various classifications of chemotherapeutic drugs including their mechanisms of action and side effects. Specific drugs discussed include alkylating agents like cyclophosphamide and cisplatin, antimetabolites like methotrexate and purine analogues, and hormonal drugs. The objectives and cell cycle effects of chemotherapy are also summarized.
The document discusses natural products taxanes and podophyllotoxins that have led to new anti-cancer drugs. It describes how over 60% of anti-cancer drugs originate from natural products. Taxanes such as paclitaxel and docetaxel stabilize microtubules, preventing cell division and causing cancer cell death. Podophyllotoxins like etoposide and teniposide inhibit topoisomerase and DNA synthesis in cancer cells. Both classes are effective against various cancer types with side effects like low blood counts and hair loss that require careful treatment. Natural products continue providing leads for developing new anti-cancer pharmaceuticals.
The document discusses various types of anticancer agents, including their classification and mechanisms of action. It focuses on alkylating agents, specifically nitrogen mustards. Nitrogen mustards were some of the first chemicals used to treat cancer and work by alkylating DNA at the N7 position of guanine. This prevents replication and can activate apoptosis. Examples discussed include mechlorethamine, chlorambucil, melphalan, and cyclophosphamide. Cyclophosphamide must be activated in the body to form an aziridinium ion that alkylates DNA. The document also briefly mentions mitomycin C, an antibiotic used in cancer treatment.
cancer chemotherapy
Introduction,Types of cancer,Aetiology of cancer,Pathogenesis of cancer,Diagnosis of cancer,Treatment of cancer,Novel drugs for cancer,Future prospects
1) Recent advances in cancer chemotherapy include the development of newer alkylating agents, platinum compounds, antimetabolites, mitotic spindle inhibitors, and topoisomerase inhibitors with improved efficacy and reduced toxicity profiles.
2) Many newer agents aim to overcome resistance to existing drugs by bypassing drug efflux pumps or having activity in cisplatin/taxane resistant settings.
3) Several new drugs have received FDA approval in the last decade for cancers like breast cancer, lung cancer, and leukemia, offering additional treatment options.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
Plasmodium parasites cause malaria in humans. The document discusses various antimalarial agents, including:
1. Chloroquine, a 4-aminoquinoline that inhibits heme polymerization in parasites and is effective against several Plasmodium species but resistance has developed.
2. Mefloquine, a quinoline-methanol with strong blood-stage activity against multidrug resistant P. falciparum.
3. Quinine, a cinchona alkaloid that remains effective against some resistant strains and has moderate activity against hepatic and transmission stages.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
Combinatorial chemistry is a technique used to rapidly produce large libraries of potential drug molecules. It allows scientists to create and evaluate thousands of similar compounds in parallel. The key advantages are that it is faster and more economical than traditional drug discovery methods. Some challenges include ensuring diversity in the compound libraries and identifying the active components within mixture samples. Solid phase synthesis and parallel/mixed synthesis are common techniques used in combinatorial chemistry approaches.
This document summarizes recent advances in cancer treatment. It begins with an introduction discussing the prevalence of cancer worldwide and the integration of nanotechnology with medicine to provide new tumor therapy opportunities. It then discusses circulating tumor cells that can be identified in blood, chemodynamic therapy that uses CDT agents to inhibit immunity and cause cell death, and various oligonucleotide therapeutics including CpG oligonucleotides, miRNAs, aptamers, and DNAzymes. It also discusses combination immunotherapy using multiple therapeutic agents, and photoimmunotherapy which combines photodynamic therapy with immunotherapy. The document concludes by stating the goal is to cure cancer patients or prolong their lives while maintaining a good quality of life.
Cancer is caused by uncontrolled cell growth and can spread through the body. Risk factors include tobacco, sunlight, viruses, and family history. Diagnosis involves biopsy and imaging tests while treatment aims to cure, palliate, or induce remission through surgery, radiation, chemotherapy, and targeted therapy. Chemotherapy drugs work by various mechanisms including alkylating DNA, blocking DNA synthesis, and affecting microtubule function. Major classes include alkylating agents, antimetabolites, antitumor antibiotics, plant alkaloids, and miscellaneous cytotoxic drugs. Combination regimens and consideration of each drug's cell cycle specificity can improve outcomes.
Combinatorial chemistry allows for the rapid synthesis of large libraries of compounds. It works by synthesizing many structures in parallel rather than one at a time. There are two main approaches: solid phase synthesis which attaches compounds to resin beads to isolate products, and solution phase which synthesizes in solvent. The libraries can be screened to identify active compounds more efficiently than traditional methods. This technique has increased the success of drug discovery by allowing testing of more structures at once.
THIS PRESENTATION ABOUT ANTIMALARIAL DRUGS DETAILING THE COMPLETE INFORMATION ABOUT THE DRUGS USED WITH ITS MECHANISM OF ACTION, STRUCTURAL ACTIVITY AND DOSES.
1. Solid cancer tumors generally have a low growth fraction and thus respond poorly to chemotherapy, often requiring surgery for removal. Disseminated cancers generally have a high growth fraction and often respond well to chemotherapy.
2. There are several classes of chemotherapeutic agents that work through different mechanisms such as alkylating DNA, inhibiting synthesis of DNA/RNA precursors, or inhibiting microtubule polymerization. Combination chemotherapy is often used to increase effectiveness.
3. Dosage must be modified based on toxicity monitoring like myelosuppression as measured by absolute neutrophil count and platelet count to minimize risks of side effects. Preventative measures and dose modifications can manage toxicities from chemotherapy.
This document discusses cancer and chemotherapy. It defines cancer as uncontrolled cell growth and describes its characteristics. Cancer treatment may involve surgery, radiation, chemotherapy, or combinations. Chemotherapy uses chemical agents to kill cancer cells and can be used as adjuvant therapy after other treatments or as neo-adjuvant therapy before the main treatment. The document then describes the cell cycle, principles of chemotherapy including drug mechanisms and scheduling, problems like resistance and toxicities, and examples of different classes of chemotherapeutic agents including alkylating agents, antimetabolites, microtubule inhibitors, antibiotics, hormonal agents, and monoclonal antibodies.
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.
3. Natural products used in the cancer treatment.pptxHarshikaPatel6
This document summarizes several natural chemotherapeutic agents. It discusses antibiotics such as anthracyclines which act by intercalating DNA and generating oxygen radicals. Specific antibiotics mentioned include doxorubicin, daunorubicin and epirubicin. It also covers topoisomerase inhibitors like etoposide and camptothecin analogs, microtubule inhibitors including vinca alkaloids and taxanes, as well as bleomycin and L-asparaginase. For each class or drug, the document provides mechanisms of action, clinical uses, pharmacokinetics and adverse effects.
PHARMACOTHERAPY OF ANTICANCER DRUGS-1.pptxAmos15720
This document discusses various groups of anticancer drugs used in pharmacotherapy. It describes several classes of drugs including antibiotics like doxorubicin and bleomycin that work by damaging DNA. Other drug classes discussed are alkylating agents like cyclophosphamide that modify DNA, antimetabolites like methotrexate and gemcitabine that interfere with DNA synthesis, taxanes and vinca alkaloids that affect microtubule function during cell division, and hormonal therapies like tamoxifen and aromatase inhibitors. For each drug, a brief overview of mechanism of action, administration route, and common side effects is provided.
Cancer Epidemiology. description of incidence and mortality of cancerabduljaji1
Cancer is defined as uncontrolled abnormal cell growth that can spread to other parts of the body. It affects people worldwide and is one of the leading causes of death. The incidence of cancer is increasing as communicable diseases decline. Some common types of cancer include lung, breast, prostate, colorectal cancers. Risk factors include chemicals, tobacco, alcohol, genetics, viruses, radiation exposure and more. Cancer develops due to genetic changes in oncogenes and tumor suppressor genes. Management involves a multidisciplinary team using treatments like surgery, radiotherapy, chemotherapy, targeted therapy and controlling side effects.
This document discusses antineoplastic agents, which are used to treat cancer. It begins by explaining how normal cell growth becomes dysregulated, leading to neoplasms or tumors. Tumors can be benign or malignant. The goals of cancer treatment are curative, palliative, or adjuvant therapy. The main treatment modalities are surgery, radiotherapy, chemotherapy, endocrine therapy, immunotherapy, and biological therapy. The document then focuses on the mechanisms and classes of chemotherapeutic agents, including alkylating agents, antimetabolites, antibiotics, alkaloids, hormones, and other drugs. It provides details on specific examples like cyclophosphamide, methotrexate, and 6-mercaptopurine.
This document discusses chemotherapy and its use in treating cancer. It begins by defining chemotherapy as using chemical agents that are selectively toxic to cancer cells. The objectives of chemotherapy are to maximize cancer cell death, cure the patient if possible, control tumor growth if a cure is not possible, and extend lifespan and quality of life. It then describes how chemotherapy works by targeting cells that are actively dividing, explains the cell cycle and how different drugs work at specific phases, and classifies common chemotherapy drugs like alkylating agents and antimetabolites. Side effects of chemotherapy like bone marrow suppression and nausea are also summarized.
Chemotherapy and rdiotherapy by heena mehtamehtaheena
This document discusses chemotherapy and its use in treating cancer. It begins by defining chemotherapy as using chemical agents that are selectively toxic to cancer cells. The objectives of chemotherapy are to maximize cancer cell death, cure the patient if possible, control tumor growth if a cure is not possible, and extend lifespan and quality of life. It then explains how chemotherapy works by targeting cells that are actively dividing, specifically during the S and M phases of the cell cycle. The document classifies chemotherapy drugs and discusses their mechanisms of action and side effects, focusing on alkylating agents and anti-metabolites.
This document summarizes cancer chemotherapy and the various classes of chemotherapeutic drugs. It describes the mechanisms of action, indications, and side effects of alkylating agents, antimetabolites, plant alkaloids, antibiotics, and other classes of drugs. The principles of cancer chemotherapy are to arrest tumor progression by causing cytotoxicity or apoptosis in cancer cells, often targeting DNA or metabolic pathways essential for cell replication. Drugs are generally used in combination to achieve maximal cell killing while remaining within a tolerable toxicity range.
The document discusses principles of cancer chemotherapy and summarizes various classes of chemotherapeutic agents. It describes how chemotherapy can be used at different stages of treatment and highlights common toxicities. It also reviews mechanisms of action and examples of classical anticancer agents like alkylating agents, antimetabolites, natural products and hormone therapies. Novel targeted agents are discussed such as tyrosine kinase inhibitors, PARP inhibitors, angiogenesis inhibitors, HSP90 inhibitors and others.
1. Chemotherapeutic agents can be classified according to their chemical structure, mechanism of action, or cell cycle specificity. Common classes include alkylating agents, antimetabolites, antitumor antibiotics, and mitotic spindle agents.
2. The mechanisms of action of these drug classes vary but include alkylating DNA, inhibiting nucleic acid synthesis, interfering with transcription and RNA synthesis, and influencing protein synthesis and function. Many agents act during specific phases of the cell cycle.
3. Examples of specific chemotherapeutic drugs discussed include cyclophosphamide, cisplatin, methotrexate, 5-fluorouracil, vincristine, paclitaxel, doxorubicin,
Cancer chemotherapy- General IntroductionpptxAbarna Ravi
General introduction..References from pharmacology text books
1. KD TRIPATHY-ESSENTIALS OF MEDICAL PHARMACOLOGY
2.LIPPINCOTT'S ILLUSTRATED REVIEWS -PHARMACOLOGY
Chemotherapy is the main treatment for disseminated cancers. It involves using multiple drugs in cycles to target rapidly dividing cancer cells. Common drugs include alkylating agents, antimetabolites, microtubule inhibitors, and monoclonal antibodies. Combination chemotherapy aims to maximize responses while avoiding overlapping toxicities. Doses are based on body surface area and adjusted for individual factors. Treatment intervals allow time for normal tissues to recover between cycles. Toxicities include myelosuppression, nausea/vomiting, and alopecia. Response is evaluated based on tumor shrinkage or progression.
This document discusses anticancer drugs, also known as chemotherapy drugs. It describes the main classes of anticancer drugs, including alkylating agents, antimetabolites, cytotoxic antibiotics, hormones, and enzymes. Alkylating agents work by alkylating DNA and inhibiting its replication. Common alkylating agents include cyclophosphamide and cisplatin. Antimetabolites are structurally similar to essential metabolites and interfere with DNA synthesis, examples include methotrexate and fluorouracil. Cytotoxic antibiotics like doxorubicin act directly on DNA. The document also covers the mechanisms of action, clinical uses, and side effects of several important chemotherapy drugs.
Chemotherapy uses cytotoxic drugs to treat cancer by interfering with cancer cell replication and metabolism. There are several classes of chemotherapy drugs including alkylating agents, antimetabolites, antitumor antibiotics, mitotic inhibitors, hormones and antagonists, and miscellaneous agents. Chemotherapy can be used adjuvantly after surgery or neoadjuvantly before surgery or radiation to destroy micrometastases or reduce tumor size. Common side effects include nausea, vomiting, bone marrow depression, alopecia, and organ toxicity.
Future research on leukemia treatment is focusing on targeted therapies, immunotherapy, and modifications to chemotherapy regimens. Targeted therapies include drugs that inhibit proteins crucial for leukemia cell growth like FLT3, IDH1/2, BCL-2, and hedgehog pathway proteins. Immunotherapies harness the immune system through antibodies and CAR T-cells targeting leukemia cell markers. Researchers are also testing new chemotherapy combinations and regimens inspired by pediatric protocols. The goal is to improve outcomes by developing more effective and less toxic treatments.
Proteins are composed of amino acids linked together through peptide bonds. Peptides are short chains of amino acids, while proteins can be made of long chains of amino acids folded into shapes. Proteins can be classified based on their size and shape as globular or fibrous proteins, or based on their functions such as structural, regulatory, catalytic, transport, genetic, storage and defense proteins. Some peptides act as toxins or have important roles as hormones, antibiotics, or in oxidation reduction systems.
The document discusses the four levels of protein structure: primary, secondary, tertiary, and quaternary. The primary structure is the linear sequence of amino acids in the peptide chain. The secondary structure involves hydrogen bonding that causes the chain to fold into structures like alpha helices or beta sheets. Tertiary structure describes further folding and interactions that result in the protein's three-dimensional shape. Quaternary structure refers to multiple peptide chains linked together in a protein.
Lipoproteins are spherical complexes formed by lipids and proteins that transport insoluble lipids through the blood. There are four main classes of lipoproteins: chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). Chylomicrons and VLDL are involved in transporting triglycerides, LDL transports cholesterol, and HDL transports excess cholesterol from tissues back to the liver.
This document provides information about lipids and fatty acids. It begins with an outline of chapter topics on the chemistry and classification of lipids. It then defines lipids and lists their main functions in the body. Lipids are classified as simple, complex, or derived, and as saponifiable or non-saponifiable. Key reactions for lipids include hydrolysis. Fatty acids are classified based on saturation and chain length. Essential fatty acids, which must be obtained through diet, are discussed. Neutral fats are described as triacylglycerols composed of glycerol and fatty acids.
This document discusses lipids and fatty acids. It defines lipids and lists their main functions. Lipids are classified as simple, complex, or derived, and as saponifiable or non-saponifiable. Fatty acids are described, including their chemistry, classification as saturated or unsaturated, nomenclature, and examples of biologically important fatty acids. Essential fatty acids are discussed along with their importance.
This document summarizes the digestion, absorption, and transport of dietary lipids in the human body. Dietary lipids undergo limited digestion in the mouth and stomach by lipases before entering the intestine, where pancreatic enzymes emulsify and break down triglycerides, phospholipids, and cholesterol esters into absorbable components. These components are absorbed via micelle transport into intestinal cells and repackaged into chylomicrons that enter the bloodstream. Chylomicrons deliver lipids to tissues and lose triglycerides due to lipoprotein lipase activity before remnants are removed from circulation by the liver.
This document provides information about lipids and fatty acids. It begins by defining lipids and listing their main functions in the body. It then classifies lipids as simple, complex, or derived, and as saponifiable or non-saponifiable. The document further describes the chemistry and classification of fatty acids, including saturated, unsaturated, monounsaturated, and polyunsaturated fatty acids. It also discusses the nomenclature and isomerism of fatty acids. The key reactions of triacylglycerols are described.
Hormones are chemical messengers that are secreted into the blood by endocrine glands and have profound effects on metabolic processes and cellular communication. They can be classified based on their chemical composition, location of receptors, or solubility. The major classes of hormones include steroids such as sex and adrenal hormones, peptides/proteins such as insulin and growth hormone, and amines such as epinephrine. Steroid hormones are derived from cholesterol and include estrogens, androgens, progesterone, corticosteroids, and aldosterone. Peptide hormones include insulin, glucagon, and somatostatin which are secreted by the pancreas, as well as hormones from the pituitary, parathyroid,
This document discusses enzymes and their properties. It begins by defining enzymes as globular proteins that act as biological catalysts to facilitate chemical reactions in living organisms. It then describes general enzyme characteristics such as their catalytic power, specificity, and ability to have their activity regulated. The document discusses how enzymes are named using systematic and common nomenclature systems. It also covers enzyme classification, cofactors/coenzymes, mechanisms of action, factors that influence activity, and kinetic models like Michaelis-Menten. Overall, the document provides a comprehensive overview of the key concepts regarding enzymes.
1. The urea cycle is a series of enzymatic reactions that occurs primarily in the liver to convert toxic ammonia produced from amino acid catabolism into urea for excretion.
2. The cycle involves five principal reactions: carbamoyl phosphate synthesis, citrulline synthesis, argininosuccinate synthesis, argininosuccinate cleavage, and arginine cleavage into ornithine and urea.
3. The urea cycle serves two major biological roles - detoxification of ammonia into urea and biosynthesis of the amino acid arginine from ornithine in tissues like liver, kidney, and intestine.
1) Fatty acids undergo beta-oxidation in the mitochondria to break them down into acetyl-CoA units, releasing energy.
2) Beta-oxidation involves a four-step cycle that removes two-carbon acetyl-CoA units from the fatty acid.
3) The complete breakdown of a fatty acid like stearic acid yields 9 acetyl-CoA molecules which enter the citric acid cycle, producing a total of 146 ATP molecules through electron transport chain reactions.
Glycogen metabolism involves the breakdown of glycogen to glucose-6-phosphate through glycogenolysis. Glycogenolysis occurs in three steps: 1) glycogen phosphorylase cleaves glucose from glycogen, 2) transferase and alpha-1,6-glucosidase remodel glycogen to allow further degradation, and 3) phosphoglucomutase converts glucose-1-phosphate to glucose-6-phosphate. In liver, glucose-6-phosphatase converts glucose-6-phosphate to glucose for blood glucose regulation. In muscle, glucose-6-phosphate enters glycolysis for rapid energy production.
This document discusses glycogen metabolism. It notes that glycogen is a readily available form of glucose storage found primarily in the liver and muscles. Glycogen synthesis, or glycogenesis, occurs in the fed state in these tissues and involves three steps - isomerization of glucose-6-phosphate to glucose-1-phosphate, activation of glucose-1-phosphate to UDP-glucose, and linkage of UDP-glucose to a glycogen chain catalyzed by glycogen synthase. Glycogen branching is accomplished by the enzyme amylo-(1,4-1,6)-trans-glycosylase which transfers glycogen segments to form branches. The synthesis and breakdown of glycogen in the liver and muscles
Gluconeogenesis is the metabolic pathway by which glucose is synthesized from non-carbohydrate materials to maintain blood glucose levels during periods without food intake. It takes place primarily in the liver and involves bypasses of three irreversible steps in glycolysis. Precursors like lactate, glycerol, and certain amino acids are converted to pyruvate and then glucose. The pathway requires energy in the form of 6 ATP molecules to synthesize one glucose molecule from two pyruvate. Gluconeogenesis is important for supplying glucose to tissues like the brain and helps maintain normal blood sugar through processes like the Cori cycle.
The citric acid cycle is the principal process for generating reduced coenzymes NADH and FADH2, which are necessary for ATP synthesis. It takes place in the mitochondrial matrix and involves eight steps catalyzed by different enzymes. Acetyl-CoA enters the cycle and is oxidized, producing carbon dioxide and the reduced coenzymes that fuel ATP production. Regulation occurs at three steps to precisely adjust the cycle's rate according to cellular energy needs. Overall, 12 ATP molecules are generated for each acetyl-CoA molecule that completes the citric acid cycle.
This document provides an overview of cholesterol biosynthesis, which occurs in most cells but primarily in the liver and intestine. There are 5 stages: 1) acetyl-CoA is converted to mevalonate, 2) mevalonate is converted to activated isoprene units, 3) six isoprene units condense to form squalene, 4) squalene is cyclized to lanosterol, and 5) lanosterol is converted to cholesterol over 20 steps. HMG-CoA reductase, which converts HMG-CoA to mevalonate, is the rate-limiting step and is regulated by feedback from cholesterol and bile acids as well as hormones like insulin, glucagon
This document provides information on carbohydrates and monosaccharides. It defines carbohydrates and explains their four main functions in living organisms. It then classifies carbohydrates into monosaccharides, disaccharides, oligosaccharides, and polysaccharides. The document focuses on monosaccharides, describing their structures, classifications, stereochemistry including D and L isomers, anomers, mutarotation, and important naturally occurring monosaccharides like glucose, fructose, and ribose. It also outlines important reactions of monosaccharides such as oxidation, reduction, glycoside formation, and phosphate ester formation.
This document provides an overview of carbohydrate biochemistry. It defines carbohydrates as polyhydroxy aldehydes or ketones and classifies them based on molecular size into monosaccharides, disaccharides, oligosaccharides, and polysaccharides. Monosaccharides are further classified as aldoses or ketoses depending on whether they have an aldehyde or ketone functional group. The document discusses carbohydrate stereochemistry, including D and L isomers, enantiomers, and diastereomers. It also covers optical activity and how carbohydrate enantiomers can rotate plane-polarized light. Epimers are described as diastereomers that differ at only one chiral carbon.
This document summarizes the processes of transcription and translation. It explains that during transcription, RNA polymerase makes an mRNA copy of a gene from DNA. The mRNA then moves to the ribosomes in the rough ER for translation. During translation, ribosomes and tRNA molecules work together to translate the mRNA into a polypeptide chain according to the mRNA's codon sequence. The process continues until a stop codon is reached, and the polypeptide chain is released. Mutations can occur during these processes, potentially resulting in non-functional or disease-causing proteins. Examples of different mutation types and their effects are provided.
Nucleic acids are macromolecules made of nucleotides that contain three components: a 5-carbon sugar, phosphate group, and nitrogenous base. DNA and RNA are the two main types of nucleic acids. DNA contains the sugar deoxyribose and has a double helix structure, while RNA contains the sugar ribose and is single-stranded. Both are composed of nucleotides joined by phosphodiester bonds and function to carry genetic information for protein synthesis. Their primary differences are that DNA contains the base thymine while RNA contains uracil, and RNA is found in the cytoplasm while DNA remains in the nucleus.
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
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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 ..
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তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
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How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
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This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
2. Objectives
• Cancer physiology
• Causes of cancer
• Stage of development of cancer
• Treatment of cancer
• Alkylating agents
• Anti-metabolites
• Anti-cancer antibiotics
• Microtubules inhibitors
• Steroidal drugs
3. What is Cancer?
• Cancer is loss in the normal control mechanisms
that govern
Cell survival
Proliferation and
Differentiation
4. Cancer
• Cancer – a large group of diseases characterized by the
uncontrolled growth and spread of abnormal cells
Leukemia -Cancer of blood forming tissues
Lymphomas-Cancer of the lymph nodes
Sarcomas -Cancerous (malignant) tumors of the
connective tissues
( connective tissue include, fat, blood vessels, nerves,
bones, muscles, deep skin tissues, and cartilage)
8. Causes of Cancer
• The incidence, geographic distribution, and behavior
of specific types of cancer are related to multiple
factors, including sex, age, race, genetic
predisposition, and exposure to environmental
carcinogens.
• Of these environmental factors are more important.
• Several viruses have been implicated in the etiology of
various human cancers.
9. Carcinogens
Ionising radiation
• X Rays
• UV light
• Gamma Rays etc.
Chemicals
• Tar from cigarettes (Lung Cancer)
• Herbicides/pesticides
Virus infection
• papilloma virus can be responsible for cervical cancer.
Bacterial Infections
• Helicobacter pylori causes ulcers which are a major factor
in the development of stomach cancer
10. • tumor suppressor genes(p53)
A tumor suppressor gene, or antioncogene, is a gene that
protects a cell from one step on the path to cancer. When
this gene mutates to cause a loss or reduction in its
function, the cell can progress to cancer
• Oncogenes:
An oncogene is a gene that has the potential to cause
cancer. In tumor cells, they are often mutated or expressed
at high levels.
14. Cell-cycle specificity of
drugs
• Chemotherapeutic agents that are effective only against
replicating cells ”that is, those cells that
are cycling and are said to be cell-cycle specific.
• Other agents are said to be cell-cycle nonspecific. The
nonspecific drugs, although having generally more
toxicity in cycling cells, are also useful against tumors
that have a low percentage of replicating cells.
16. Drug Resistance
• Some tumor types, eg, malignant melanoma, renal cell
cancer, and brain cancer, exhibit primary resistance, ie,
absence of response on the first exposure to currently
available agents.
17. Common adverse effects:
• Most agents have a narrow therapeutic index.
• Severe vomiting, bone marrow suppression,
and alopecia occur.
• Some specific toxicities are cardiotoxicity with
doxorubicin and pulmonary fibrosis with
bleomycin.
18. Alkylating Agents
• Alkylating agents are Busulfan, Carmustine,
Ifosfamide, Chlorambucil, Cyclophosphamide.
• Mechanism of action:
• Alkylating agents exert their cytotoxic effects via transfer
of their alkyl groups to various cellular constituents.
• Alkylations of DNA within the nucleus probably represent
the major interactions that lead to cell death.
• These drugs react chemically with sulfhydryl, amino,
hydroxyl, carboxyl, and phosphate groups of other
cellular nucleophiles as well.
19. Alkylating agents
• They are used in combination with other agents to treat a
wide variety of lymphatic and solid cancers.
• Resistance:
The mechanism of acquired resistance to
alkylating agents may involve increased capability to repair
DNA lesions and decreased transport of the alkylating drug
into the cell
20. Cyclophosphamide
• Widely used
• Oral bioavailability
• It is inactive in its parent form, and must be activated to
cytotoxic forms by liver microsomal enzymes.
• Mechanism involve Formation of DNA cross-links,
resulting in inhibition of DNA synthesis and function.
• Clinical applications include Breast cancer, ovarian
cancer, non-Hodgkin's lymphoma, soft tissue sarcoma,
neuroblastoma, rhabdomyosarcoma.
21.
22. ADRs
• Acute toxicities are nausea and vomiting.
• Delayed toxicities include Moderate depression of
peripheral blood count; excessive doses produce severe
bone marrow depression with leukopenia,
thrombocytopenia, and bleeding
• Alopecia and hemorrhagic cystitis occasionally occur
with cyclophosphamide.
23. Mechlorethamine
• Developed as a vesicant (nitrogen mustard) during
World War I.
• Mechanism of action:
• Mechlorethamine is transported into the cell, where the
drug forms a reactive intermediate that alkylates the N7
nitrogen of a guanine residue in one or both strands of a
DNA molecule.
• This alkylation leads to cross-linkages between guanine
residues in the DNA chains and/or depurination, thus
facilitating DNA strand breakage.
24.
25. Pharmacokinetics
• Mechlorethamine is very unstable, and solutions must be
made up just prior to administration.
• Mechlorethamine is also a powerful vesicant (blistering
agent) and is only administered IV.
• Its clinical applications include Hodgkin's and non-
Hodgkin's lymphoma.
• Toxicity is same as that of Cyclophosphamide.
26. Nitrosoureas
• Carmustine and lomustine are closely related
nitrosoureas.
• The nitrosoureas are highly lipid-soluble and are able to
cross the blood-brain barrier, making them effective in
the treatment of brain tumors.
• Streptozocin is also a nitrosourease.
27. • In spite of the similarities in their structures, Carmustine
is administered IV, whereas Lomustine is given orally.
• Lipophil Drugs
• Clinical applications include Brain cancer, Hodgkin's and
non-Hodgkin's lymphoma.
28. ADRs
• Delayed hematopoietic depression
• Aplastic marrow may develop on prolonged use
• Renal toxicity
• Pulmonary fibrosis
29. Dacarbazine
• Undergo biotransformation to an active metabolite,
methyltriazenoimidazole carboxamide (MTIC).
• MTIC will form methylcarbonium ions that can attack the
nucleophilic groups in the DNA molecule.
• Used in the treatment of melanoma.
• Adverse effects are nausea and vomiting.
Myelosuppression (thrombocytopenia and neutropenia).
• Hepatotoxicity on long term use.
30. Temozolomide
• Approved for use against treatment-resistant Gliomas
and anaplastic Astrocytomas.
• Undergo biotransformation to an active metabolite,
MTIC.
• Temozolomide also has the property of inhibiting the
repair enzyme, O6-guanine-DNA-alkyltransferase.
• A property that distinguishes temozolomide from
dacarbazine is the former's ability to cross the blood-
brain barrier.
31. • Temozolomide is taken orally and has excellent oral
bioavailability.
• The parent drug and metabolites are excreted in the
urine.
• Temozolomide is taken for five consecutive days and
repeated every 28 days.
• Toxicity is same as that of Dacarbazine.
32. Platinum Analogs
• Drugs include cisplatin, carboplatin, and oxaliplatin.
• Cisplatin was the first member of this class
• Oxaliplatin a new member of this class of drugs, is a
closely related analog of carboplatin.
• Cisplatin has found wide application in the treatment of
solid tumors, such as metastatic testicular carcinoma in
combination with vinblastine
• And with bleomycin, ovarian carcinoma
• in combination with cyclophosphamide, or alone for
bladder carcinoma.
33. • The mechanism of action for this class of drugs is similar
to that of the alkylating agents.
• Cytotoxicity can occur at any stage of the cell cycle, but
cells are most vulnerable to the actions of these drugs in
the G1 and S phases.
34. • These agents are administered IV in saline solution.
They can also be given intraperitoneally for ovarian
cancer and intra-arterially to perfuse other organs.
• Plasma protein binding is 90%.
• The renal route is the main avenue for excretion.
35. ADRs
• Severe, persistent vomiting
• Dose-related nephrotoxicity. This can be ameliorated by
aggressive hydration and diuresis.
• Hypomagnesemia and hypocalcemia
• Ototoxicity
• Bone marrow suppression
• Neurotoxicity and hypersensitivity reactions
• Unlike cisplatin, carboplatin causes only mild nausea
and vomiting, and it is not nephro-, neuro-, or ototoxic.
Its dose-limiting toxicity is myelosuppression.
36. Antimetabolites
• Antimetabolites are structurally related to normal
compounds that exist within the cell.
• They generally interfere with the availability of normal
purine or pyrimidine nucleotide precursors, either by
inhibiting their synthesis or by competing with them in
DNA or RNA synthesis.
• Their maximal cytotoxic effects are in S-phase (and,
therefore, cell-cycle specific.
37. Methotrexate
• Folic acid analog
• Binds with high affinity to the active
catalytic site of dihydrofolate reductase
(DHFR), interfering with the synthesis of
tetrahydrofolate (THF).
38.
39. Therapeutic uses:
• MTX, usually in combination with other drugs, is effective
against
Acute lymphocytic Leukemia
Choriocarcinoma
Burkitt's lymphoma in children
Breast cancer
Head and neck carcinomas
Other uses include in rheumatoid arthritis, psoriasis and
in Crohn’s disease.
40. • Burkitt lymphoma is a form of non-Hodgkin's lymphoma
in which cancer starts in immune cells called B-cells
41. Pharmacokinetics
• MTX is variably absorbed at low doses from the GI tract,
but it can also be administered by intramuscular,
intravenous (IV), and intrathecal routes.
• Do not cross Blood brain barrier.
• MTX is metabolized to polyglutamate derivatives. This
property is important, because the polyglutamates, which
also inhibit DHFR, remain within the cell even in the
absence of extracellular drug.
44. 6-Mercaptopurine
• Thiol analog of hypoxanthine
• Mechanism of action:
Nucleotide formation
Inhibition of purine synthesis
Incorporation into nucleic acids
45. 6-Mercaptopurine
(Mechanism of Action)
Nucleotide formation:
• To exert its antileukemic effect, 6-MP must penetrate target
cells and be converted to the nucleotide analog, 6-MP-ribose
phosphate (better known as 6-thioinosinic acid or TIMP)
• The addition of the ribose phosphate is catalyzed by the
salvage pathway enzyme, hypoxanthine– guanine
phosphoribosyltransferase (HGPRT).
Inhibition of purine synthesis:
• A number of metabolic processes involving purine
biosynthesis and interconversions are affected by the
nucleotide analog, TIMP. Similar to nucleotide
monophosphates, TIMP can inhibit the first step of purine ring
biosynthesis .
46. Incorporation into nucleic acids:
• TIMP is converted to thio-guanine monophosphate,
which after phosphorylation to di- and triphosphates can
be incorporated into RNA.
• The deoxyribonucleotide analogs that are also formed
are incorporated into DNA.
• This results in nonfunctional RNA and DNA.
47. Resistance
• 1) an inability to biotransform 6-MP to the corresponding
nucleotide because of decreased levels of HGPRT (for
example, in Lesch-Nyhan syndrome, in which patients
lack this enzyme).
• 2) increased metabolism of the drug to thiouric acid
49. 5-Fluorouracil
• Pyrimidine analog
• Has a stable fluorine atom in place of a hydrogen atom
at position 5 of the uracil ring.
• 5-FU is employed primarily in the treatment of slowly
growing solid tumors (for example, colorectal, breast,
ovarian, pancreatic, and gastric carcinomas).
• 5-FU is also effective for the treatment of superficial
basal cell carcinomas.
50.
51. Pharmacokinetics
• Resistance is encountered when the cells have lost their
ability to convert 5-FU into its active form (5-FdUMP) or
when they have altered or increased thymidylate
synthase levels.
• 5-FU is given IV or, in the case of skin cancer, topically.
• The dose of 5-FU must be adjusted in the case of
impaired hepatic function.
52. ADRs
• Nausea, vomiting, Diarrhea, and Alopecia, Severe
ulceration of the oral and GI mucosa
• Bone marrow depression (with bolus injection),
• Anorexia
• dermopathy
53. Fludarabine
• 5'-phosphate of 2-fluoroadenine arabinoside ,a purine
nucleotide analog.
• Treatment of chronic lymphocytic leukemia
• Effective against hairy-cell leukemia and non-Hodgkin's
lymphoma.
54. Anti tumor antibiotics
• Exert cytotoxic action primarily to their interactions with
DNA, leading to disruption of DNA function.
• In addition inhibit topoisomerases (I and II) and
produce free radicals also play a major role in their
cytotoxic effect.
• High affinity binding to DNA.
• Binding to cellular membranes to alter fluidity and
ion transport.
• Derived from “Streptomyces” a soil microbe.
55. Anthracyclines
• Administered by IV route.
• Metabolized extensively by the liver.
• Hydroxylated metabolite is an active specie.
• 50% of the drug eliminated from the feces via billiary
excretion.
• Drugs include in this group are Doxorubicin,
Daunorubicin, Idarubicin, Mitoxantrone.
56. Doxorubicin
• Clinical uses include breast, endometrium, ovary,
testicle, thyroid, bladder, soft tissues sarcomas, and in
neuroblastomas.
• It has clinical efficacy in hematological malignancies.
• Generally used in combination with other anticancer
drugs such as fluoruracil, cyclophosphamide and
cisplation.
57. Doxorubicin (cont.)
• Mechanism of Action:
• The anthracyclines have three major activities that may
vary with the type of cell.
• Intercalation in the DNA
• Binding to cell membranes
• Generation of oxygen radicals
• Administered IV
58. ADRs
• Irreversible, dose-dependent cardiotoxicity
• Irradiation of the thorax increases the risk of
cardiotoxicity.
• liposomal-encapsulated doxorubicin.. Less cardiotoxic
• Transient bone marrow suppression
• GI tract disturbances.
• Increased skin pigmentation is also seen.
• Alopecia is usually severe.
59. Daunorubicin
• First agent in this class to be Isolated.
• Used in acute myeloid leukemia.
• Less used today
60. Mitoxantrone
• It binds to DNA to produce strand breakage and inhibit
both DNA and RNA synthesis.
• Currently used in the treatment of advanced, hormone
refractory prostate cancer and low grade non Hodgkin's
lymphoma.
• Also indicated for breast cancer.
• Myelosuppression with leukopenia is the dose limiting
toxicity.
• Less cardiotoxic than Doxorubicin.
61. Bleomycin
• Small peptide that contain DNA binding region and an
iron binding domain at opposite ends.
• Bind to DNA Single and double chain strand
breakage following free radical formation.
• Cell cycle specific and affects G2 phase.
• Indicated for Hodgkin and non Hodgkin lymphoma.
• For Squammous cell cancer of skin, cervix and vulva.
63. ADRs
• Pulmonary toxicity… chief complaint
• Alopecia
• Hyperpigmentation of the hands
• High incidence of fever and chills and a low incidence of
serious anaphylactoid reactions.
64. Microtubule Inhibitors
• Mitotic spindle is essential for the equal partitioning of
DNA into the two daughter cells that are formed when a
eukaryotic cell divides.
• Several plant-derived substances used as anticancer
drugs disrupt this process by affecting the equilibrium
between the polymerized and depolymerized forms of
the microtubules, thereby causing cytotoxicity.
• Microtubule inhibitors are;
1. Vincristine
2. Vinblastine
65. • Vincristine and vinblastine are both cell-cycle specific
and phase specific (M phase)
• Blocks the ability of tubulin to polymerize to form
microtubules.
• Intravenous injection
• Excreted into bile and feces
66.
67. Vincristine and
vinblastine
• Derived from plant, Vinca rosea.
• Vinca alkaloids
• MOPP regimen for Hodgkin's lymphoma.
• VBL is administered with bleomycin and cisplatin
for the treatment of metastatic testicular
carcinoma.
68.
69. ADRs
• Phlebitis
• Nausea, vomiting, diarrhea, and alopecia.
• Vinblastine is a more potent myelosuppressant than
Vincristine.
• Peripheral neuropathy (paresthesias, loss of reflexes,
and ataxia) is associated with Vincristine.
70. Paclitaxel and docetaxel
• Docetaxel which is the more potent of the two drugs.
• Paclitaxel has shown good activity against advanced
ovarian cancer and metastatic breast cancer.
• Both drugs are active in the G2/M phase of the cell cycle.
72. ADRs
• Dose-limiting toxicity of paclitaxel and docetaxel is
neutropenia.
• Treatment with granulocyte colony stimulating
• factor (Filgrastim) can help to reverse neutropenia.
• Peripheral neuropathy
• Bradycardia is sometimes observed with paclitaxel.
• Serious hypersensitivity reactions
74. Prednisone
• Synthetic corticosteroid with less
mineralocorticoid activity.
• Used in Lymphomas associated with Cushing
syndrome.
• Prednisone is primarily employed to induce
remission in patients with acute lymphocytic
leukemia and in the treatment of both Hodgkin's
and non-Hodgkin's lymphomas.
77. Tamoxifen
• Estrogen antagonist
• First-line therapy in the treatment of estrogen
receptor positive breast cancer Estrogen
competes with tamoxifen.
• Therefore, in premenopausal women, the drug is
used with a gonadotropin-releasing hormone
(GnRH) analog such as leuprolide, which lowers
estrogen levels.
• Cell cycle nonspecific agent.
78. ADRs
• Hot flashes, nausea, vomiting, skin rash, vaginal
bleeding, and discharge (due to some slight
estrogenic activity of the drug and some of its
metabolites).
• Hypercalcemia
• Cause endometrial cancer.
79. Aromatase inhibitors
• Aromatase reaction is responsible for the extra-
adrenal synthesis of estrogen from
androstenedione.
• Peripheral aromatization is an important source
of estrogen in postmenopausal women.
80. Aminoglutethimide
• Approved for metastatic breast cancer in
postmenopausal women.
• Aminoglutethimide was shown to inhibit both the
adrenal synthesis of pregnenolone (a precursor
of estrogen) from cholesterol as well as the
extra-adrenal synthesis.
81. Anastrozole and letrozole:
• Approved for breast cancer.
• More potent
• More selective
• They are devoid of the androgenic side effects that occur
with the steroidal aromatase inhibitors.
• Do not predispose to endometrial cancer.
• They do not need to be supplemented with
hydrocortisone.
82. • second-line therapy after Tamoxifen for
hormone-dependent breast cancer in the United
States.
• Have become first-line drugs in other countries
for the treatment of breast cancer in
postmenopausal women.
• Orally active
83. Progestins
• Megestrol acetate was formerly the progestin used most
widely in treating metastatic hormone responsive.
• Breast and endometrial neoplasms.
• It is orally effective.
84. Leuprolide and goserelin
• The synthetic non peptides, Leuprolide and Goserelin
are analogs of GnRH.
• GnRH agonists, bind to GnRH receptor in the pituitary,
which leads to its desensitization and, consequently,
inhibition of release of FSH and LH.
• Androgen and Estrogen syntheses are reduced
85. • Leuprolide used in Prostatic cancer.
• These drugs have some benefit in premenopausal
women with advanced breast cancer and have largely
replaced estrogens in therapy for prostate cancer.
• Leuprolide is available
• 1) as a sustained-release preparation
• 2) subcutaneous
• 3) as a depot intramuscular injection to treat
metastatic carcinoma of the prostate.
• Goserelin acetate is implanted intramuscularly.
86. Estrogens
• Estrogens, such as ethinyl estradiol or diethylstilbestrol,
had been used in the treatment of prostatic cancer.
• However, they have been largely replaced by the GnRH
analogs because of fewer adverse effects.
• ARDs include thromboemboli, myocardial infarction,
strokes, and hypercalcemia.
• Men who are taking estrogens may experience
Gynecomastia and impotence.
87. Flutamide, nilutamide,
and bicalutamide
• Used in the treatment of prostate cancer.
• These drugs compete with the natural hormone for
binding to the androgen receptor and prevent its
translocation into the nucleus.
• Antiandrogens are taken orally.
• Side effects include gynecomastia and GI distress and,
in the case of flutamide, liver failure could occur.
• Nilutamide can cause visual problems.
88. Monoclonal Antibodies
• Directed at specific targets and often have fewer adverse
effects.
• Produced by Recombinant DNA technology.
• These includes;
1. Trastuzumab,
2. rituximab,
3. bevacizumab, and
4. cetuximab.
89.
90. Trastuzumab
• In patients with metastatic breast cancer, overexpression
of transmembrane human epidermal growth factor
receptor protein 2 (HER2) is seen in 25 to 30 percent of
patients.
• This drug targets the extracellular domain of the HER2
growth receptor that has intrinsic tyrosine kinase activity.
• Used in breast cancer
• S phase specific
91. • Mechanism of action:
Down-regulation of HER2-receptor expression,
an induction of antibody-dependent cytotoxicity,
or a decrease in angiogenesis due to an effect on
vascular endothelial growth factor.
• Administered IV
94. Irinotecan and topotecan
• Semisynthetic derivatives of an earlier, more toxic drug,
Camptothecin.
• Topotecan is employed in metastatic ovarian cancer.
• S-phase specific
• Inhibit topoisomerase I
• Infused IV
95.
96. ADRs
• Bone marrow suppression particularly
neutropenia.
• Thrombocytopenia and anemia.
• Diarrhea may be severe.
97. Etoposide and Teniposide
• Semisynthetic derivatives of the plant alkaloid,
podophyllotoxin.
• Block cells in the late S to G2 phase of the cell cycle.
• Major target is topoisomerase II.
• Major clinical use in the treatment of oat-cell carcinoma
of the lung and in combination with Bleomycin and
Cisplatin for testicular carcinoma.
• Used in acute lymphocytic leukemia.
100. Interferons
• Interferons (IFNs) are a group of signaling proteins made
and released by host cells in response to the presence
of several pathogens, such as;
1. viruses,
2. bacteria,
3. parasites, and
4. tumor cells.
101. Interferons
• IFNs also have various other functions
• they activate immune cells, such as natural killer cells
and macrophages
• Certain symptoms of infections, such as fever, muscle
pain and "flu-like symptoms", are also caused by the
production of IFNs and other cytokines.
• Administration of interferons has been shown
experimentally to inhibit tumor growth in animals
102. Interferons
• Classified as alpha, beta and gamma.
• Alpha is primarily leukocytic.
• Interferon alpha 2a approved for the management of;
1. hairy-cell leukemia,
2. chronic myeloid leukemia, and
3. acquired immunodeficiency syndrome (AIDS) related
Kaposi sarcoma.