Last One Flashcards
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Hormonal Therapy
Anti-oestrogens, progestogens, and testosterone: promote growth of hormone-sensitive cancers like breast and prostate cancers.
Hormone Synthesis Inhibitors
Aromatase inhibitors (block androgen conversion to estrogen): Anastrozol, Letrozole, Exemestane.
Hormone Synthesis Inhibitors
GnRH analogs: Leuprolide, Goserelin; Androgen synthesis inhibitor: Abiraterone.
Hormone Receptor Antagonists
Selective estrogen receptor modulators (SERMs): Tamoxifen.
Hormone Receptor Antagonists
Androgen receptor antagonists: Flutamide, Bicalutamide.
Hormone Receptor Antagonists
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant.
Glucocorticoids
Induce apoptosis of lymphocytes; used for lymphoma and lymphocytic leukemias.
Targeted Therapy
Interacts with specific molecules like proteins to inhibit tumor growth and progression (e.g., monoclonal antibodies, small molecule inhibitors).
Growth Factor Signaling
Growth factors bind receptors, activating tyrosine kinase, leading to cell proliferation, invasion, and metastasis.
Growth Factor Signaling
Inhibition options: tyrosine kinase domain inhibitors or blocking GF binding with antibodies (e.g., Bevacizumab, Cetuximab, Trastuzumab).
Tyrosine Kinase Inhibitors
Gefitinib, Erlotinib (EGFR tyrosine kinase inhibitors for non-small cell lung cancer).
Tyrosine Kinase Inhibitors
Sorafenib, Sunitinib (multiple RTKs, including VEGF-R2, VEGF-R3 inhibitors for renal cell cancer).
Monoclonal Antibodies
Bevacizumab (VEGF); Cetuximab, Panitumumab (EGFR); Trastuzumab (HER-2).
Drug Combination
Combining drugs with different mechanisms increases effectiveness and prevents resistance.
Drug Combination
Principles: avoid similar toxicities; use drugs with significant activity against the tumor and optimal doses.
Drug Resistance
Primary: no response initially. Acquired: develops after initial success due to DNA repair, altered targets, or drug efflux.
Side Effects
Bone marrow suppression (anemia, leukopenia, thrombocytopenia); mucositis, alopecia, nausea/vomiting.
Side Effects
Organ toxicity: hepatotoxicity (methotrexate, 6-mercaptopurine), nephrotoxicity (cisplatin), cardiovascular (anthracyclines).
Side Effects
Specific toxicities: pulmonary toxicity (bleomycin), neuropathy (taxanes, vinca alkaloids), coagulopathy (L-asparaginase).
Chemotherapy Administration
Routes: IV, IM, SC, Oral, Topical, Regional (e.g., intrathecal, intracavitary, intra-arterial).
When to Start Therapy
Neoadjuvant: pre-surgery to shrink tumor. Adjuvant: post-surgery to target residual disease.
Folinic Acid
Also called Leucovorin; rescues normal cells after high-dose methotrexate, enhances 5-FU cytotoxicity.
Other Targeted Therapies
CDK4/6 inhibitors: Palbociclib, Ribociclib, Abemaciclib. Block cell cycle, reduce tumor proliferation (metastatic breast cancer).
Other Targeted Therapies
PARP inhibitors: Olaparib (blocks DNA repair for ovarian cancer).
Immune Checkpoint Inhibitors
Block CTLA-4 (e.g., Ipilimumab), PD-1 (e.g., Nivolumab, Pembrolizumab), or PD-L1 (e.g., Atezolizumab).
Immune Checkpoint Inhibitors
Mechanism: Enhance T-cell activity by blocking inhibitory signals (CTLA-4, PD-1, PD-L1).
Immune Checkpoint Inhibitors
Used for melanoma, urothelial carcinoma, non-small cell lung cancer, and others.
Chemotherapy Administration
Intrathecal route: methotrexate, cytarabine. Intracavitary route: bladder, peritoneal cavity.
Chemotherapy Administration
Intra-arterial route: hepatic artery infusion for hepatic tumors.
Side Effects: Extravasation Injury
Vesicant drugs (e.g., anthracyclines, vinca alkaloids) cause tissue damage when leaking into subcutaneous tissue.
Drug Resistance: Causes
Mechanisms include decreased drug uptake, increased efflux, drug target alteration, and drug inactivation.
Immune Checkpoints
CTLA-4 interacts with B7 ligands (APCs); PD-1 interacts with PD-L1 (tumor cells). Blocking restores T-cell activity.
