Chemotherapy Flashcards
Describe classes of anti-cancer therapeutics.
- Chemotherapy
Chemotherapy refers to the use of cytotoxic drugs that target rapidly dividing cells, a hallmark of cancer. These drugs are usually non-selective and affect both cancerous and some normal, fast-growing cells (like those in the bone marrow, digestive tract, and hair follicles).
Alkylating Agents: These drugs interfere with the DNA by adding alkyl groups, causing DNA damage that prevents cell division and triggers cell death.
Examples: Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil
Mechanism: They bind to DNA, forming cross-links that prevent the strands from separating, blocking DNA replication.
Antimetabolites: These are structural analogs of natural metabolites and interfere with DNA and RNA synthesis, leading to cell death.
Examples: Methotrexate, 5-Fluorouracil (5-FU), Gemcitabine, Cytarabine
Mechanism: Inhibit key enzymes in nucleotide biosynthesis, impairing DNA replication.
Plant Alkaloids: These drugs are derived from plants and interfere with the processes of cell division, particularly during mitosis.
Examples: Vincristine, Vinblastine (Vinca alkaloids); Paclitaxel, Docetaxel (Taxanes)
Mechanism: Taxanes stabilize microtubules, preventing them from depolymerizing during mitosis, while vinca alkaloids disrupt the formation of the mitotic spindle.
Topoisomerase Inhibitors: These drugs interfere with the enzymes that manage DNA structure during replication.
Examples: Doxorubicin, Etoposide, Irinotecan, Topotecan
Mechanism: Inhibit topoisomerase enzymes (Type I and II), causing DNA breaks that the cell cannot repair, leading to apoptosis.
Platinum-based Agents: These are a group of chemotherapy drugs that form cross-links in DNA, leading to cell cycle arrest and apoptosis.
Examples: Cisplatin, Carboplatin, Oxaliplatin
Mechanism: Bind to DNA, causing cross-links that prevent DNA replication and trigger cell death.
2. Targeted Therapy
Targeted therapies are drugs designed to target specific molecules involved in cancer cell growth, survival, and spread. These therapies are more specific than chemotherapy, as they target molecular alterations in cancer cells, often leading to fewer side effects.
Tyrosine Kinase Inhibitors (TKIs): These drugs target enzymes (tyrosine kinases) involved in cancer cell signaling pathways that regulate cell growth and survival.
Examples: Imatinib (Gleevec), Erlotinib, Gefitinib, Dasatinib
Mechanism: Inhibit specific receptor tyrosine kinases (e.g., BCR-ABL in CML, EGFR in lung cancer) involved in cell signaling.
Monoclonal Antibodies: These are laboratory-made molecules that can mimic the immune system’s ability to fight off harmful pathogens. They can target specific proteins on cancer cells or their blood supply.
Examples: Trastuzumab (Herceptin), Rituximab, Bevacizumab (Avastin), Cetuximab
Mechanism: Bind to cancer cell surface antigens (e.g., HER2 in breast cancer), blocking tumor growth or marking the cells for immune attack.
Proteasome Inhibitors: These drugs target the proteasome, a structure responsible for degrading unneeded or damaged proteins, which is often upregulated in cancer cells.
Examples: Bortezomib, Carfilzomib
Mechanism: Inhibit the proteasome, leading to the accumulation of damaged proteins and inducing cancer cell death.
Angiogenesis Inhibitors: These drugs prevent the formation of new blood vessels (angiogenesis), which tumors need to grow beyond a certain size.
Examples: Bevacizumab (Avastin), Axitinib, Sunitinib
Mechanism: Block VEGF (vascular endothelial growth factor) or its receptor, reducing the tumor’s blood supply.
PARP Inhibitors: These drugs target PARP enzymes, which help repair damaged DNA. Inhibition leads to DNA damage accumulation and cell death, especially in tumors with DNA repair deficiencies.
Examples: Olaparib, Rucaparib
Mechanism: Inhibit PARP (poly ADP ribose polymerase), leading to the accumulation of DNA breaks in cancer cells with defects in other repair pathways (e.g., BRCA mutations).
3. Immunotherapy
Immunotherapy enhances or modifies the body’s immune system to better recognize and attack cancer cells. It includes therapies that either stimulate the immune system directly or block immune checkpoints that prevent immune cells from attacking cancer cells.
Checkpoint Inhibitors: These drugs block immune checkpoints, which are molecules that normally prevent the immune system from attacking normal cells. By inhibiting these checkpoints, the immune system is better able to target cancer cells.
Examples: Pembrolizumab (Keytruda), Nivolumab (Opdivo), Ipilimumab (Yervoy)
Mechanism: Block checkpoint proteins like PD-1/PD-L1 or CTLA-4, allowing T-cells to attack cancer cells.
CAR T-cell Therapy (Chimeric Antigen Receptor T-cell Therapy): This involves modifying a patient’s T-cells to express a receptor that targets cancer cells, and then reinfusing these modified cells into the patient.
Examples: Kymriah, Yescarta
Mechanism: T-cells are genetically engineered to express receptors that specifically recognize cancer antigens, such as CD19 on B-cell malignancies.
Monoclonal Antibodies in Immunotherapy: Some monoclonal antibodies can directly stimulate the immune system or flag cancer cells for destruction.
Examples: Rituximab, Trastuzumab (Herceptin)
Mechanism: Bind to tumor-specific antigens and recruit immune cells to destroy cancer cells.
Cytokine Therapy: These therapies involve the use of cytokines (proteins that help cells communicate) to enhance the immune response.
Examples: Interleukin-2 (IL-2), Interferons
Mechanism: Boost immune system activity, particularly T-cells and NK (natural killer) cells.
4. Hormonal Therapy
Hormonal therapies are used to treat cancers that are driven by hormones, such as breast cancer and prostate cancer, by either reducing the levels of hormones or blocking their action.
Anti-estrogens: These drugs block the effects of estrogen, which can promote the growth of estrogen receptor-positive breast cancer.
Examples: Tamoxifen, Fulvestrant
Mechanism: Block estrogen receptors or reduce estrogen levels, inhibiting cancer cell growth.
Aromatase Inhibitors: These drugs reduce the production of estrogen in post-menopausal women, which can fuel estrogen receptor-positive breast cancer.
Examples: Letrozole, Anastrozole, Exemestane
Mechanism: Inhibit the enzyme aromatase, which converts androgens to estrogens.
Androgen Deprivation Therapy (ADT): Used primarily in prostate cancer to block the production or action of testosterone, which can fuel prostate cancer growth.
Examples: Leuprolide, Bicalutamide, Flutamide
Mechanism: Lower levels of testosterone or block its receptors on prostate cancer cells.
5. Radiation Therapy
Radiation therapy uses high-energy particles (e.g., X-rays) or rays to kill or damage cancer cells. It is particularly effective for localized cancers and can be used to shrink tumors before surgery or alleviate symptoms in advanced cancers.
External Beam Radiation: Radiation is directed from outside the body to the tumor site.
Brachytherapy (Internal Radiation): Radioactive material is placed inside or near the tumor.
Systemic Radiation: Radioactive substances are injected into the bloodstream to target cancer cells.
6. Other Emerging Therapies
Gene Therapy: Involves modifying the genes inside cancer cells to correct abnormalities or introduce new genetic material to make cancer cells more susceptible to other treatments.
Oncolytic Virus Therapy: Uses genetically modified viruses that selectively infect and kill cancer cells.
Cancer Vaccines: These are designed to stimulate the immune system to recognize and attack cancer cells. Examples include Bacillus Calmette–Guérin (BCG) for bladder cancer and HPV vaccines for cervical cancer.
