Antineoplastic Drugs Part 1: Cancer Overview and Cell-Cycle–Specific Drugs

Vocabulary flashcards covering key terms, drug classes, mechanisms, indications, and adverse effects from the lecture on cancer overview and cell-cycle–specific antineoplastic drugs.

Cellular transformation

Process in which normal cells undergo uncontrolled, rapid growth, invasion, and possible metastasis.

Cancer

Malignant disease marked by loss of growth control and lack of positive physiologic function in cells.

Primary lesion

The original site of a malignant tumor.

Metastasis

Spread of cancer cells from the primary lesion to distant, secondary sites via blood or lymph.

Neoplasm

A “new tissue” mass; synonymous with tumor (benign or malignant).

Tumor – Benign

Non-cancerous neoplasm that does not invade or metastasize.

Tumor – Malignant

Cancerous neoplasm capable of invasion and metastasis.

Carcinoma

Cancer that originates from epithelial tissue.

Sarcoma

Cancer arising from connective or supportive tissues such as bone or muscle.

Lymphoma / Leukemia

Hematologic malignancies originating in lymphoid tissue or bone marrow; often called circulating tumors.

Paraneoplastic syndrome

Collection of symptoms (e.g., cachexia, fever, weight loss) not directly caused by tumor spread but associated with malignancy.

Cachexia

Wasting syndrome of weight loss and weakness commonly seen in cancer patients.

G0 phase

Resting phase of the cell cycle where the cell is not dividing.

G1 phase

First gap phase; cellular components (excluding DNA) are synthesized.

S phase

Synthesis phase; DNA replication occurs.

G2 phase

Second gap phase; cell prepares for mitosis.

M phase

Mitosis phase; actual cell division and reproduction.

Antineoplastic drug

Medication used to treat cancer; also called anticancer drug, cytotoxic chemotherapy, or simply chemotherapy.

Cell-cycle–specific (CCS) drug

Antineoplastic agent cytotoxic only during a particular cell-cycle phase.

Cell-cycle–nonspecific (CCNS) drug

Agent cytotoxic in any phase of the cell cycle.

Antimetabolite

CCS drug class that interferes with metabolic pathways during the S phase (e.g., methotrexate, 5-FU).

Mitotic inhibitor

CCS agents (e.g., vinca alkaloids, taxanes) that block mitosis, usually in late S, G2, or M phase.

Alkaloid topoisomerase II inhibitor

Drug subclass (e.g., etoposide) that interferes with topoisomerase II, hindering DNA unwinding.

Topoisomerase I inhibitor

Camptothecin-derived CCS drugs (topotecan, irinotecan) that prevent DNA relegation during S phase.

Antineoplastic enzyme

Drug class produced by recombinant DNA technology (e.g., asparaginase) that deprives leukemic cells of asparagine.

Narrow therapeutic index

Small margin between therapeutic and toxic drug levels common to many antineoplastics.

Dose-limiting adverse effect

Toxicity severe enough to prevent dose escalation (e.g., myelosuppression).

Myelosuppression

Bone marrow suppression leading to decreased blood cell counts.

Nadir

Lowest point of a patient’s blood cell counts after chemotherapy.

Extravasation

Leakage of IV chemotherapy into surrounding tissue causing local damage; requires prompt antidote measures.

Targeted drug therapy

Treatment aimed at specific molecular targets on cancer cells with less harm to normal cells.

Tumor lysis syndrome

Metabolic emergency with hyperuricemia, hyperphosphatemia, hyperkalemia, and hypocalcemia after rapid tumor cell destruction.

Leucovorin rescue

Administration of folinic acid to reduce bone marrow toxicity from high-dose methotrexate.

Folic acid antagonist

Antimetabolite (e.g., methotrexate) that blocks folate use, inhibiting DNA synthesis.

Purine antagonist

Antimetabolite subclass (e.g., 6-MP) that disrupts purine nucleotide pathways.

Pyrimidine antagonist

Antimetabolite subclass (e.g., 5-FU, cytarabine) that blocks pyrimidine metabolism.

Vinca alkaloid

Periwinkle-derived mitotic inhibitors (vincristine, vinblastine); fatal if given intrathecally.

Taxane

Mitotic inhibitors (paclitaxel, docetaxel) that promote microtubule stabilization, halting mitosis.

Vincristine

Vinca alkaloid notable for pronounced neurotoxicity but minimal bone marrow suppression.

Topotecan

Topoisomerase I inhibitor used for ovarian, colorectal, and small cell lung cancers; causes BMS and GI effects.

Irinotecan

Topoisomerase I inhibitor associated with severe hematologic toxicity and cholinergic diarrhea.

Asparaginase

Enzyme that depletes asparagine in leukemic cells; used in acute lymphocytic leukemia.

Pegaspargase

Pegylated form of asparaginase with prolonged half-life.

Erwinia asparaginase

Non-E. coli–derived asparaginase reserved for patients allergic to standard asparaginase.

Cholinergic diarrhea

Severe, early-onset diarrhea caused by irinotecan due to cholinesterase inhibition.

Stomatitis

Inflammation and ulceration of oral mucosa from chemotherapy.

Alopecia

Loss of hair resulting from destruction of hair follicle cells during chemotherapy.

Neutropenia

Low neutrophil count increasing infection risk after chemotherapy.

Thrombocytopenia

Low platelet count leading to bleeding risk.

Emetic potential

Capacity of a drug to induce nausea and vomiting.

Palmar-plantar dysesthesia

Hand-foot syndrome; painful redness and swelling of palms and soles, seen with certain antimetabolites.

Stevens-Johnson syndrome

Severe, life-threatening skin reaction that can occur with some antineoplastic drugs.

Toxic epidermal necrolysis

Most severe form of drug-induced skin necrosis, potentially fatal.