Term
|
Definition
Mechlorethamine
Cyclophosphamide
Ifosfamide
Carmustine
Lomustine
Busulfan
Cisplatin
Carboplatin |
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Term
|
Definition
Methotrexate
Fluorouracil (5-FU)
Capecitabine
6-mercaptopurine
cytarabine |
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Term
|
Definition
Doxorubicin
Epirubicin
Dactinomycin
Bleomycin |
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Term
|
Definition
Vincristine
Vinblastine
Vinorelbine
Paclitaxel
Docetaxel
Etoposide |
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Term
Differentiating agents
- names |
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Definition
Tretinoin
Arsenic trioxide (ATO)
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Term
Hormone/Receptor inhibitors
-names |
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Definition
Aromatase inhibitors
Tamoxifen
Imatinib
Trastubzumab
Cetuximab
Bevacizumab |
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Term
Mechlorethamine
-mechanism
-type of agent
-administration |
|
Definition
Mechanism:
- cause formation of crosslinked DNA (cell cycle nonspecific)
Type:
- Alkylating agent, nitrogen mustard
Administration:
- IV only |
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Term
Cyclophosphamide
-Mechanism
-Type
-Toxicity
-Other |
|
Definition
Mechanism:
- crosslinks DNA, cell cycle nonspecific
Type:
- Alkylating agents, nitrogen mustards
Toxicity:
- cardiotoxicity
- bladder burn
- renal toxicity
Other:
- MESNA used to treat bladder burn side effects
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Term
Ifosfamide
-mechanism
-type
-toxicity
-other |
|
Definition
Mechanism:
- crosslink DNA, cell cycle non-specific
Type:
- alkylating agent, nitrogen mustard
Toxicity:
- Renal toxicity
- CNS (confusion)
- bladder burn
Other:
-IV admin
- Cyt P450 activates drug |
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Term
Carmustine
Lomustine
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
-alkylating agent, nitrosourea
Mechanism:
- inhibit DNA, RNA, and protein synthesis
- lipid soluble so crosses BBB
Clinical use:
- glioblastoma
Toxicity:
- bone marrow depression
- pulmonary fibrosis
Other:
- Carmustine: IV fusion
- Lomustine: taken orally |
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Term
Busulfan
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- alkylating agents, alkyl sulfonates
Mechanism:
- crosslinks DNA, cell cycle nonspecific
Toxicity:
- bone marrow suppression
Other:
- given orally |
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Term
Cisplatin
Carbaplatin
-type
-mechanism
-toxicity
-other |
|
Definition
Type:
- alkylating agent, platinum complex
Mechanism:
- crosslinks w/ GG pairs (bends DNA)
Toxicity:
- peripheral neuropathy
- renal toxicity
Other:
- concentrates in liver, kidney, intestine, and ovaries
- hydration helps renal toxicity
- Carbaplatin is milder and dose dependent in its bone marrow suppression
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Term
Methotrexate
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antimetabolites, cell cycle dependent
Mechanism:
- purine antimetabolite
- folic acid analogue, competitive inhibitor of DHF reductase
- inhibits folate-dependent enzymes of de novo purine and thymidylate synthesis
Toxicity:
- hepatic necrosis
- bone marrow depression
Other:
- used in higher dose for chemo than in RA
- can accumulate if you have renal disease
- leucovorin can rescue from toxicity |
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|
Term
Fluorouracil (5-FU)
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antimetabolite, cell cycle dependent
Mechanism:
- fraudulent nucleotide that inhibits DNA synthesis (T analogue)
Toxicity:
- severe ulceration of GI mucosa
Other:
- leucovorin potentiates action |
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Term
Capecitabine
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antimetabolite, cell cycle dependent
Mechanism:
- prodrug of fluorouracil (thymine analogue)
Toxicity:
- bone marrow suppression
- pain
- sensitivity to touch of the palms and sole
Other:
- severe interaction w/ coumadin derived drugs |
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|
Term
6-mercaptopurine
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antimetabolites, cell cycle dependent
Mechanism:
- inhibits purine (guanine) synthesis
Clinical use:
- leukemia in children
Toxicity:
- bone marrow depression
Other:
- people with TPMT mutation should not receive b/c it can kill |
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Term
Cytarabine
-type
-mechanism
-toxicity
-other |
|
Definition
Type:
- antimetabolites, cell cycle dependent
Mechanism:
- inhibits DNA chain elongation by being a fraudulent nucleotide (cytosine)
Toxicity:
- bone marrow depression
Other:
- S phase specific |
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Term
Doxorubicin
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antibiotics, anthracycline
Mechanism:
- blocks DNA topoisomerase II thus inhibiting resealing of DNA nicks
Toxicity:
- cardiac toxicity (acute and chronic) due to generation of free oxygen radicals |
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Term
Epirubicin
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antibiotic
Mechanism:
- blocks DNA topoisomerase II preventing DNA nick sealing
Toxicity:
- cardiac toxicity
- bone marrow depression
Other:
- drug interacts with cimetidine (H2 antagonist for ulcers) |
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Term
Dactinomycin
-type
-mechanism
-toxicity
-other |
|
Definition
Type:
- antibiotics
Mechanism:
- intercalates b/w GC base pairs;
- inhibits RNA pol
- interferes w/ DNA topo II
Toxicity:
- severe local tissue damage
- necrosis w/ extravasation
- bone marrow depression
Other:
- does not cross BBB |
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Term
Bleomycin
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- antibiotic
Mechanism:
- DNA-[drug]-Fe complex causes DNA fragmentation through formation of free radicals
Toxicity:
- mild bone marrow toxicity
- pulmonary fibrosis in 5-10% of patients |
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Term
Vincristine
Vinblastine
Vinorelbine
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- Plant drugs
Mechanism:
- binds tubulin and inhibits tubulin polymerization
- metaphase arrests and leads to cellular apoptosis
Toxicity:
- neurotoxic (sensory neuropathy)
- bone marrow toxicity
- Neurotoxicity: Vincristine > Vinblastine
- BM toxicity: vinblastine > vincristine
Other:
- vincristine and bleomycin are 2 chemo
- drugs that cause mild bone marrow depression |
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Term
Paclitaxel
Docetaxel
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- plant drug
Mechanism:
- freezes polymerized microtubules leading to metaphase arrest
Toxicity:
- peripheral sensory neuropathy |
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Term
Etoposide
-type
-mechanism
-toxicity |
|
Definition
Type:
- plant drugs
Mechanism:
- causes DNA breaks by blocking DNA topo II
Toxicity:
- bone marrow depression |
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|
Term
Tretinoin (all trans retinoic acid- ATRA)
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- Differentiating agent
Mechanism:
- binds retinoid X receptor RARα dimer to displace repressor of differentiation
Clinical use:
- acute promyelocytic leukemia (APL) - high rate of complete remission
Toxicity:
- retinoic acid syndrome = fever, weight gain, dyspnea, pulmonary infiltrates |
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Term
Arsenic trioxide (ATO)
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- differentiating agent
Mechanism:
- uncouples mitochondrial oxidative phosphorylation
- generates free radicals
- causes differentiation of APL cells and inhibits angiogenesis
Clinical use:
- APL
Toxicity:
- atrial or ventricular arrhythmias |
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Term
Exemestane
Letrozole
Anastrozole
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- aromatase inhibitors, hormone/receptor inhibitors
Mechanism:
- block conversion of androgens to estrogens
Clinical use:
- breast cancer
Toxicity:
- musculoskeletal pain
Other:
- tumor must be estrogen responsive/sensitive
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Term
Tamoxifen
-type
-mechanism
-clinical use
-toxicity
|
|
Definition
Type:
- hormone/receptor inhibitors
Mechanism:
- binds estradiol and is competitive inhibitor of the estrogen receptor
Clinical use:
- estrogen-dependent breast cancer
Toxicity:
- hot flashes
- can reduce serum cholesterol |
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Term
Imatinib
-type
-mechanism
-clinical use
-other |
|
Definition
Type:
- receptor tyrosine kinase inhibitor
Mechanism:
- inhibits BCR-ABL tyrosine kinase and PDGF receptor
Clinical use:
- chronic myelogenous leukemia
- philadelphia chromosome cancers
Other:
- BCR-ABL is detected by FISH |
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Term
Trastubzumab
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
aka Herceptin
Type:
- hormone/receptor inhibitor
- receptor tyrosine kinase inhibitor
Mechanism:
- monoclonal antibody recognizes HER2 and prevents the cellular growth, division, and amplification
Clinical use:
- Breast cancer (25% are HER2+)
Toxicity:
- cardiomyopathy
- CHF |
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Term
Cetuximab
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- monoclonal antibody
- tyrosine kinase inhibitors
Mechanism:
- binds, blocks function of EGFR (HER1)
- inhibits growth and induces apoptosis
Clinical use:
- colorectal cancer
Toxicity:
- rapid onset of airway obstruction and hypotension
- S/e are infusion related |
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Term
Bevacizumab
-type
-mechanism
-clinical use
-toxicity
-other |
|
Definition
Type:
- monoclonal antibody
- tyrosine kinase inhibitor
Mechanism:
- binds VEGF thus inhibiting angiogenesis
Clinical use:
- colorectal cancer
Toxicity:
- hypertension
- GI perforation
- CHF |
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