ANTI CANCER DRUGS BY Abenezer Tadesse.pdf

# Introduction to cancer and its types Cancer is a disease defined by a disruption in the regulatory mechanisms controlling cell survival, proliferation, and differentiation [3](#page=3). ### 1.1 Defining cancer and its prevalence * Cancer is characterized by uncontrolled cell growth and differentiation [3](#page=3). * There are over 200 distinct types of cancer [3](#page=3). * The four most prevalent tumor types – breast, lung, colorectal, and prostate – account for more than half of all new cancer diagnoses [3](#page=3). * In females, the lifetime risk of developing breast cancer is 1 in 9 [3](#page=3). * In males, the lifetime risk of developing prostate cancer is 1 in 14 [3](#page=3). ### 1.2 Key terminology: Neoplasm, solid tumors, and liquid tumors * A **neoplasm** is an abnormal mass of tissue that can originate in virtually any part of the body [4](#page=4). * Cancer can manifest as either solid tumors or liquid tumors [4](#page=4). #### 1.2.1 Solid tumors Solid tumors can be further classified into carcinomas and sarcomas: * **Carcinoma**: This type of solid tumor originates from epithelial tissue. Epithelial tissues are the linings of organs and body cavities [4](#page=4). * **Sarcoma**: This type of solid tumor arises from cells found in the supporting tissues of the body, such as bone, cartilage, fat, muscle, and blood vessels [4](#page=4). > **Tip:** The distinction between carcinoma and sarcoma is crucial for diagnosis and treatment planning, as they arise from different cell lineages and often exhibit different behaviors. #### 1.2.2 Liquid tumors Liquid tumors, also known as hematological malignancies, originate from blood-forming tissues. They include: * Leukemia [4](#page=4). * Myeloma [4](#page=4). * Lymphoma [4](#page=4). ### 1.3 Examples of curable cancers Some cancer types are listed as potentially curable [5](#page=5): * Ewing's Sarcoma: A tumor that grows in or around the bones [5](#page=5). * Wilm's Tumor: A rare form of kidney cancer [5](#page=5). * Choriocarcinoma: A cancer that develops in the placenta [5](#page=5). * Burkitt's lymphoma: A type of non-Hodgkin's lymphoma affecting B-cells [5](#page=5). * Hodgkin's Disease: A lymphoma characterized by the presence of Reed-Sternberg cells [5](#page=5). * Non-Hodgkin's Disease: A lymphoma characterized by the absence of Reed-Sternberg cells [5](#page=5). * Seminomas: A type of germ cell tumor originating in the testicle [5](#page=5). --- # Causes and genetic implications of cancer Cancer arises from the accumulation of multiple genetic mutations, stemming from either inherited predispositions or acquired environmental factors. ### 2.1 Origins of cancer All cancers are fundamentally caused by multiple mutations within cells. These mutations can originate from two primary sources: internal factors, specifically inherited mutations, and external or acquired factors. While inherited mutations account for a smaller proportion of cancers, typically around five to ten percent, acquired mutations are far more prevalent, contributing to ninety to ninety-five percent of all cancer cases [6](#page=6). ### 2.2 Environmental and acquired factors A significant majority of cancer-causing mutations are acquired throughout an individual's lifetime due to environmental exposures and lifestyle choices. Key contributors include [6](#page=6): * **Tobacco:** Exposure to tobacco smoke is a major carcinogen [6](#page=6). * **Diet:** Certain dietary patterns can increase cancer risk [6](#page=6). * **Radiation:** Exposure to various forms of radiation, such as UV radiation or ionizing radiation, can damage DNA and lead to mutations [6](#page=6). * **Infectious organisms:** Some viruses and bacteria are known to cause or contribute to cancer development [6](#page=6). * **Alcohol:** Consumption of alcohol is another significant environmental factor linked to increased cancer risk [6](#page=6). ### 2.3 Inherited mutations Inherited mutations are genetic alterations present in germ cells (sperm or egg) and are therefore passed down from parents to offspring. These mutations can increase an individual's susceptibility to developing cancer later in life. While they represent a smaller percentage of overall cancer cases, they can have a profound impact on family cancer syndromes [6](#page=6). ### 2.4 Genes implicated in carcinogenesis The development of cancer involves specific genes that, when mutated, can drive uncontrolled cell growth and proliferation. These genes broadly fall into two categories [7](#page=7): * **Proto-oncogenes:** These genes normally promote cell growth and division. When mutated, they can become oncogenes, leading to excessive cell proliferation [7](#page=7). * **Tumor suppressor genes:** These genes normally inhibit cell division, repair DNA errors, or induce programmed cell death (apoptosis). When mutated or inactivated, they lose their protective function, allowing damaged cells to survive and multiply [7](#page=7). Furthermore, genes involved in DNA repair mechanisms are critical in preventing the accumulation of mutations. For instance, genes belonging to the mismatch repair (MMR) pathway play a crucial role in correcting errors that occur during DNA replication. Defects in MMR genes can lead to a significant increase in the mutation rate and are associated with certain types of hereditary cancers, such as Lynch syndrome [9](#page=9). --- # The cell cycle and its regulation in cancer The cell cycle is a tightly regulated process fundamental to cell division and organismal growth, and its dysregulation is a hallmark of cancer [11](#page=11). ### 3.1 The cell cycle phases The cell cycle is a series of ordered events that lead to cell division. It is typically divided into four main phases: * **G1 (Gap 1) phase:** This is a period of cell growth and synthesis of proteins and organelles necessary for DNA replication [10](#page=10). * **S (Synthesis) phase:** During this phase, DNA replication occurs, resulting in the duplication of the cell's chromosomes. Each chromosome will consist of two identical sister chromatids [10](#page=10). * **G2 (Gap 2) phase:** The cell continues to grow and prepares for mitosis by synthesizing proteins required for cell division [10](#page=10). * **M (Mitosis) phase:** This phase involves nuclear division (mitosis) and cytoplasmic division (cytokinesis), resulting in two daughter cells [10](#page=10). ### 3.2 Cell cycle regulation and checkpoints The cell cycle is meticulously regulated by a system of checkpoints to ensure that each phase is completed accurately and that conditions are favorable for progression. These checkpoints prevent the propagation of errors and damage [11](#page=11). #### 3.2.1 Key molecular players The regulation of the cell cycle hinges on the coordinated action of several key molecular players: * **Cyclins:** These are a group of proteins that accumulate and degrade cyclically during the cell cycle. They act as regulatory subunits [11](#page=11). * **Cyclin-dependent kinases (CDKs):** These are enzymes that, when complexed with cyclins, become active and phosphorylate target proteins, thereby driving cell cycle progression. Different cyclin-CDK complexes are active at specific phases of the cell cycle [11](#page=11). * **Tumor suppressors:** Proteins like p53 play a critical role in cell cycle control by halting the cycle in response to DNA damage and initiating repair mechanisms or apoptosis if damage is irreparable [11](#page=11). #### 3.2.2 Regulatory checkpoints Major checkpoints exist to monitor the integrity and proper execution of cell cycle events: * **G1 checkpoint (Restriction Point):** This checkpoint assesses external conditions (e.g., growth factors) and internal state (e.g., cell size, DNA damage) before committing the cell to DNA replication [10](#page=10). * **G2 checkpoint:** This checkpoint verifies that DNA replication has been completed accurately and that there is no DNA damage before allowing entry into mitosis [10](#page=10). * **Spindle checkpoint (M checkpoint):** This checkpoint ensures that all chromosomes are correctly attached to the mitotic spindle before sister chromatids are separated, preventing aneuploidy [10](#page=10). > **Tip:** The precise regulation by checkpoints ensures that cells only divide when conditions are optimal, preventing genetic instability. ### 3.3 Dysregulation of the cell cycle in cancer Cancer is characterized by uncontrolled cell proliferation, which arises from the accumulation of mutations that disrupt the normal cell cycle regulatory mechanisms. Loss of function in tumor suppressor genes (e.g., p53) or gain of function in oncogenes that promote cell cycle progression can lead to a breakdown in checkpoint control. This allows cells with damaged DNA to divide, leading to genetic instability and tumor formation [11](#page=11). --- # Classification and mechanisms of anticancer drugs This section outlines the various classifications of anticancer drugs based on their chemical structure, mechanism of action, and cell cycle specificity, detailing key drug categories and their therapeutic applications [19](#page=19). ### 4.1 Principles of cancer treatment The primary goals of cancer treatment are curative, aiming for total eradication of cancer cells, or palliative, focused on symptom alleviation. A key objective in chemotherapy is total cell kill, which aims to destroy all malignant cells to prevent relapse and prolong survival. However, chemotherapy faces challenges such as drug resistance, multidrug resistance, toxicity, and the induction of secondary tumors. Adjuvant chemotherapy is administered after surgery or irradiation to eliminate micrometastases, while neoadjuvant chemotherapy is given before surgery or radiotherapy to reduce the size of primary tumors [15](#page=15) [16](#page=16) [18](#page=18). ### 4.2 Classification of anticancer drugs Anticancer drugs can be classified in several ways: * According to chemical structure and source [19](#page=19). * According to biochemical mechanisms of anticancer action [19](#page=19). * According to the cell cycle specificity of the drug [19](#page=19). #### 4.2.1 Classification by cell cycle specificity * **Cell cycle nonspecific agents (CCNSA)**: These drugs act independently of the cell cycle phase. Examples include alkylating agents, platinum compounds, and some antibiotics [20](#page=20). * **Cell cycle specific agents (CCSA)**: These drugs exert their effects during specific phases of the cell cycle [20](#page=20). * **S phase specific drugs**: Antimetabolites [20](#page=20). * **M phase specific drugs**: Vinca alkaloids, taxanes, and podophyllin alkaloids [20](#page=20). * **G2 phase specific drugs**: Bleomycin [20](#page=20). #### 4.2.2 General classification by drug type The general classification of anticancer drugs includes: * Alkylating agents [21](#page=21). * Antimetabolites [21](#page=21). * Antibiotics [21](#page=21). * Alkaloids [21](#page=21). * Hormone antagonists [21](#page=21). * Immunomodulating drugs [21](#page=21). ### 4.3 Alkylating agents Alkylating agents are a class of anticancer drugs characterized by their ability to add alkyl groups to various electronegative groups within cells (#page=22, 23). They inhibit tumor growth by inducing DNA strand breaks and cross-linking nucleotides in DNA, thus directly damaging DNA [22](#page=22) [23](#page=23). #### 4.3.1 Subtypes of alkylating agents Alkylating agents are further categorized into: * **Nitrogen mustards**: Including Cyclophosphamide, Mechlorethamine, Melphalan, Mustine, Ifosfamide, and Chlorambucil [22](#page=22). * **Nitrosoureas**: Such as Carmustine, Lomustine, Semustine, and Streptozocin [22](#page=22). * **Alkyl sulfonates**: Including Busulfan [22](#page=22). * **Ethylenimines**: Such as Thiotepa [22](#page=22). * **Platinum-based alkylating agents**: Including Cisplatin, Carboplatin, and Oxaliplatin [22](#page=22). #### 4.3.2 Mechanisms of resistance to alkylating agents Acquired resistance to alkylating agents can occur through several mechanisms: * Increased capacity to repair DNA lesions [26](#page=26). * Decreased permeability of the cell to the drug [26](#page=26). * Increased production of glutathione [26](#page=26). ### 4.4 Platinum compounds Platinum compounds, such as Cisplatin, have significantly impacted the treatment of germ cell tumors [27](#page=27). #### 4.4.1 Cisplatin * **Pharmacokinetics**: Cisplatin concentrates in the kidney, intestine, and testes. It is highly bound to plasma proteins, poorly penetrates the blood-brain barrier (BBB), and exhibits low myelotoxicity [27](#page=27). * **Indications**: Cisplatin is a first-line intravenous drug for testicular, ovarian, and bladder cancers, and is also used for melanoma and other solid tumors [28](#page=28). * **Adverse effects**: While causing minimal myelosuppression, Cisplatin can induce severe nausea, vomiting, and nephrotoxicity [28](#page=28). ### 4.5 Nitrogen mustards #### 4.5.1 Cyclophosphamide Cyclophosphamide is a prodrug that is metabolized in the liver to aldophosphamide, which is then converted to phosphoramide mustard and acrolein [29](#page=29). * **Indications**: Used in the treatment of Burkitt's lymphoma, neuroblastoma, retinoblastoma, and breast cancer [29](#page=29). * **Adverse effects**: Hemorrhagic cystitis (prevented by Mesna or N-acetylcysteine), alopecia, nausea and vomiting, and hepatic damage [30](#page=30). * **Dosage and administration**: Can be given orally (2-3 mg/kg/day) or intravenously (10-15 mg/kg every 7-10 days). It can be administered via multiple routes including IV, IM, IP, intrapleurally, intraarterially, and directly into the tumor [30](#page=30). ### 4.6 Antimetabolites Antimetabolites are a class of anticancer drugs that interfere with the synthesis or function of essential cellular metabolites. They are S-phase specific [20](#page=20) [31](#page=31). #### 4.6.1 Folic acid antagonists * **Methotrexate (MTX)**: MTX is structurally similar to folic acid and acts by inhibiting dihydrofolate reductase, an enzyme crucial for converting dietary folate to tetrahydrofolate, which is required for thymidine and purine synthesis. Intracellular polyglutamate derivatives of MTX, formed by the enzyme folylpolyglutamate synthase (FPGS), are retained in cancer cells and further enhance enzyme inhibition [32](#page=32) [33](#page=33). * **Pharmacokinetics**: MTX is absorbed orally (50% protein-bound) and is highly polar. It rapidly disappears from the blood but persists longer in tissues than folate, leading to a prolonged inhibitory effect. It is contraindicated in renal impairment [34](#page=34). * **Indications**: Historically significant for its curative potential in choriocarcinoma. It is also effective in treating acute lymphocytic leukemia and meningeal metastases from various tumors [35](#page=35). * **Adverse effects**: Myelosuppression, severe gastrointestinal disturbances, renal toxicity due to crystalluria of its 7-OH metabolite. High-dose therapy may require leucovorin rescue. It is teratogenic and can cause fetal malformations and death [36](#page=36). #### 4.6.2 Purine antagonists * **6-Thiopurines**: This category includes 6-Mercaptopurine (6-MP) and 6-Thioguanine (6-TG) [37](#page=37). * **6-Mercaptopurine (6-MP)**: 6-MP is converted to 6-MP-ribosephosphate, which is incorporated into RNA and DNA, leading to non-functional nucleic acids and subsequently cell cycle arrest and apoptosis. 6-MP is metabolized to an inactive metabolite, 6-thiouric acid, by xanthine oxidase, a process that does not occur with 6-TG [38](#page=38). * **Indications**: Primarily used in the treatment of childhood acute leukemia [38](#page=38). #### 4.6.3 Pyrimidine antagonists Pyrimidine analogues kill cancer cells by interfering with the natural functions of pyrimidine nucleotides (#page=39, 41). Examples include 5-Fluorouracil and Capecitabine [39](#page=39) [41](#page=41). * **Indications**: Used for acute leukemias, GI tract adenocarcinomas (colorectal, pancreatic, esophageal), breast and ovarian cancers, and malignant lymphomas [41](#page=41). ### 4.7 Antitumor antibiotics Antitumor antibiotics are a class of drugs derived from microorganisms, such as anthracyclines, Dactinomycin, Mitomycin, and Bleomycin [42](#page=42). * **Mechanisms of action**: * Intercalation between DNA bases, disrupting DNA helix topology and inhibiting DNA and RNA polymerases [43](#page=43). * Production of free radicals [43](#page=43). * **Indications**: Used for melanoma, carcinomas of the head, neck, and cervix, testicular cancer, and Wilms' tumor [43](#page=43). ### 4.8 Plant alkaloids Plant alkaloids, also known as plant derivatives, are derived from plants and include vincristine, vinblastine, vindesine, and paclitaxel. These are M-phase specific agents [20](#page=20) [44](#page=44). * **Mechanism of action**: Vinca alkaloids prevent microtubule assembly, leading to cell arrest by inhibiting the formation of mitotic filaments essential for nuclear and cell division [44](#page=44). * **Indications**: Vinblastine is used for metastatic testicular tumors, while Vincristine is used for childhood leukemia [44](#page=44). ### 4.9 Hormone antagonists Hormone antagonists are used to treat hormone-dependent cancers by blocking the action of specific hormones or altering hormone production [46](#page=46). #### 4.9.1 Anti-estrogens * **Tamoxifen**: This is the preferred drug for postmenopausal women with or recovering from metastatic breast cancer, especially those with estrogen receptor-positive tumors [46](#page=46). #### 4.9.2 Aromatase inhibitors * **Examples**: Letrozole, Anastrozole, Exemestane, Formestane, and Aminoglutethimide [47](#page=47). * **Mechanism of action**: These orally active drugs inhibit the conversion of testosterone and androstenedione to estrogen through aromatization [47](#page=47). * **Uses**: Employed in postmenopausal women with advanced breast carcinoma and as an adjunct to mastectomy [47](#page=47). * **Adverse effects**: Commonly cause hot flashes [47](#page=47). #### 4.9.3 Anti-androgens * **Examples**: Flutamide, Bicalutamide, and Cyproterone [48](#page=48). * **Uses**: Used to treat prostate tumors [48](#page=48). * **Unwanted effects**: Include gynecomastia, decreased spermatogenesis, and decreased libido [48](#page=48). #### 4.9.4 Ketoconazole Ketoconazole, primarily used for fungal infections, can also be used for prostate cancer [49](#page=49). * **Mechanism of action**: It inhibits testicular and adrenal production of androgens and exhibits direct toxicity to prostate cells [49](#page=49). ### 4.10 Immunomodulating drugs Immunomodulating drugs enhance the body's antitumor immunity and are utilized in treating neoplastic diseases [50](#page=50). * **Types**: Include immunopotentiators such as recombinant interferons and cytokines [50](#page=50). * **Examples**: Interferon-α, Aldeslukin, and Tretinoin [50](#page=50). --- # Adverse effects and management of chemotherapy This section details the challenges associated with anticancer drug therapy, including common adverse effects and strategies for their management. ### 5.1 Adverse effects of anti-cancer drugs Chemotherapy agents often have a low therapeutic index, meaning the dose required for efficacy is close to the dose that causes significant toxicity. Adverse effects can be acute or delayed and affect various organ systems [52](#page=52). #### 5.1.1 Common adverse effects * **Bone marrow (BM) suppression:** This is a frequent and serious side effect, impacting the production of blood cells [52](#page=52). * **Gastrointestinal (GIT) toxicity:** This includes nausea, vomiting, and diarrhea. Vomiting can be particularly severe with potent emetic drugs like Cisplatin, cyclophosphamide, doxorubicin, lomustine, hydroxyurea, tamoxifen, and bleomycin [52](#page=52). * **Hair follicles:** Alopecia (hair loss) is common, though usually transient [52](#page=52). * **Gonads:** Menstrual irregularities, including premature menarche and impaired spermatogenesis, can occur due to effects on reproductive organs [52](#page=52). * **Fetus:** Chemotherapy can cause teratogenicity (birth defects) and mutagenicity (genetic mutations) [52](#page=52). * **Growth and healing:** Depression of growth in children and delayed wound healing are potential adverse effects [53](#page=53). * **Second malignancies:** Alkylating agents, in particular, can increase the risk of developing secondary cancers, such as leukemia, often appearing 10 years after treatment [53](#page=53). * **Metabolic disturbances:** Hyperuricemia, hyperkalemia, hypocalcemia, and hyperphosphatemia can develop [53](#page=53). * **Cardiac and renal toxicity:** Some chemotherapy regimens can lead to cardiac arrhythmias and nephrotoxicity, which can be fatal [53](#page=53). * **Extravasation:** Irritant drugs can cause damage if they leak out of the vein during administration [53](#page=53). #### 5.1.2 Special drug toxicities Specific chemotherapeutic agents are associated with characteristic toxicities: * **Doxorubicin:** Cardiotoxicity (heart damage) [53](#page=53). * **Bleomycin:** Pulmonary fibrosis (lung scarring) [53](#page=53). * **Cyclophosphamide:** Bladder toxicity, which can be irreversible [53](#page=53). * **Cisplatin:** Peripheral neuropathy (nerve damage) [53](#page=53). * **IL2 and interferon:** Can cause symptoms resembling inflammatory disease [53](#page=53). ### 5.2 Minimizing chemotherapy adverse effects Several strategies can be employed to minimize the adverse effects of cancer chemotherapy: * **Local injection:** For specific localized treatments [54](#page=54). * **Bone marrow (BM) transplantation:** To restore suppressed bone marrow function [54](#page=54). * **Diuresis:** Promoting urine excretion to help eliminate certain drugs or metabolites [54](#page=54). * **Folic acid supplementation:** May be used in conjunction with certain chemotherapy agents [54](#page=54). * **Hematopoietic growth factors:** Colony-stimulating factors (CSFs) can be used to increase neutrophil counts in cases of neutropenia. Erythropoietin can be used to stimulate red blood cell production [54](#page=54). * **Blood transfusions:** To manage anemia resulting from BM suppression [54](#page=54). > **Tip:** Understanding the specific toxicities of individual chemotherapeutic agents is crucial for proactive management and patient monitoring [53](#page=53). --- ## Common mistakes to avoid - Review all topics thoroughly before exams - Pay attention to formulas and key definitions - Practice with examples provided in each section - Don't memorize without understanding the underlying concepts

| Term | Definition | |------|------------| | Cancer | A disease characterized by abnormal cell growth and proliferation that can invade and spread to other parts of the body. | | Neoplasm | An abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should. It can be benign or malignant. | | Carcinoma | A malignant tumor originating from epithelial cells, which line the surfaces of the body and internal organs. | | Sarcoma | A malignant tumor that arises from connective tissues, such as bone, cartilage, fat, muscle, or blood vessels. | | Leukemia | A type of cancer that affects the blood and bone marrow, characterized by an abnormal increase of immature white blood cells. | | Lymphoma | A cancer of the lymphatic system, which is part of the body's germ-fighting network. Lymphocytes are a type of white blood cell that fight infection. | | Carcinogenesis | The process by which normal cells are transformed into cancer cells, typically involving genetic mutations and cellular changes. | | Cell Cycle | The series of events that take place in a cell leading to its division and duplication (replication). | | Cyclins | A group of proteins that regulate the cell cycle. They are named for their ability to activate cyclin-dependent kinases (CDKs). | | CDKs (Cyclin-Dependent Kinases) | Enzymes that are critical for the regulation of cell cycle progression. They are dependent on cyclins for their activity. | | Tumor Suppressor Genes | Genes that protect a cell from becoming cancerous. When mutated or inactivated, they can contribute to cancer development. | | p53 | A key tumor suppressor protein that plays a critical role in preventing cancer by regulating cell division, DNA repair, and programmed cell death (apoptosis). | | Cytotoxic | Having a toxic effect on cells, often used to describe drugs that kill cancer cells. | | Curative Treatment | Cancer treatment aimed at completely eliminating cancer from the body and achieving a cure. | | Palliative Treatment | Treatment focused on relieving symptoms and improving the quality of life for patients with advanced or incurable cancer. | | Chemotherapy | The use of drugs to treat cancer. Chemotherapy drugs work by killing cancer cells or slowing their growth. | | Adjuvant Chemotherapy | Chemotherapy given after primary treatment (like surgery or radiation) to kill any remaining cancer cells and reduce the risk of recurrence. | | Neoadjuvant Chemotherapy | Chemotherapy given before primary treatment (like surgery or radiation) to shrink a tumor, making it easier to remove or treat. | | Cell Cycle Nonspecific Agents (CCNSA) | Anticancer drugs that kill cells regardless of their phase in the cell cycle. | | Cell Cycle Specific Agents (CCSA) | Anticancer drugs that are most effective when they target cells in specific phases of the cell cycle. | | Alkylating Agents | A class of anticancer drugs that work by transferring an alkyl group to DNA, which can lead to DNA damage and cell death. | | Platinum Compounds | A type of alkylating agent that contains platinum, such as cisplatin and carboplatin, used in cancer chemotherapy. | | Antimetabolites | Anticancer drugs that interfere with the synthesis or function of essential metabolites, thereby blocking DNA and RNA synthesis and cell division. | | Folic Acid Analogues | A type of antimetabolite that mimics folic acid and interferes with folate metabolism, crucial for DNA synthesis. Methotrexate (MTX) is a prime example. | | Purine Analogues | Anticancer drugs that mimic purine bases, interfering with nucleic acid synthesis and function. 6-Mercaptopurine (6-MP) and 6-Thioguanine (6-TG) are examples. | | Pyrimidine Analogues | Anticancer drugs that mimic pyrimidine bases, disrupting DNA and RNA synthesis. 5-Fluorouracil (5-FU) is a notable example. | | Antitumor Antibiotics | A class of drugs derived from microorganisms that inhibit cancer cell growth by interfering with DNA synthesis or function. Examples include anthracyclines and bleomycin. | | Anthracyclines | A subclass of antitumor antibiotics, like doxorubicin, that work by intercalating into DNA and generating free radicals. | | Alkaloids | A group of naturally occurring chemical compounds derived from plants that have medicinal properties, including some anticancer drugs like Vinca alkaloids. | | Vinca Alkaloids | A class of plant-derived alkaloids (e.g., vincristine, vinblastine) that inhibit cell division by disrupting microtubule formation during mitosis. | | Hormone Antagonists | Drugs that block the action of hormones or inhibit their production, used in hormone-sensitive cancers like breast and prostate cancer. | | Immunomodulating Drugs | Drugs that enhance or suppress the immune system's response, used to boost the body's ability to fight cancer. | | Myelosuppression | A condition where the bone marrow produces fewer blood cells (red blood cells, white blood cells, and platelets) than normal, often a side effect of chemotherapy. | | Nephrotoxicity | Damage to the kidneys caused by exposure to certain drugs or toxins. | | Alopecia | Hair loss, a common side effect of many chemotherapy drugs. | | Teratogenicity | The ability of a substance to cause birth defects. | | Mutagenicity | The ability of a substance to cause genetic mutations. | | Extravasation | The leakage of a intravenously infused, potentially damaging medication into the surrounding tissues. | | Therapeutic Index | The ratio between the toxic dose and the therapeutic dose of a drug, indicating its safety margin. A low therapeutic index means a drug has a narrow safety margin. |