Anticancer Flashcards
what is BUSULFAN (which is a non cell specific ALKYLATING agent used in CML therapy) main AE?
Profound MYELOSUPPRESSION
(additionally: Pulmonary fibrosis, skin pigmentation & seizures)
first line anticancer treatment for TESTICULAR CANCER
-what phase of the cell cycle does this cell cycle specific drug effect?
BLEOMYCIN
G2 exclusiviely
what is one of DOCETAXEL’s (taxane MT inhibitor) main AE’s?
Fluid retention:
Pre-treatment with Dexamethasone is required to prevent fluid retention.
- Inhibits Angiogenesis.
- Inhibits VEGFR-1, VEGFR-2, and PDGFR.
name that drug
SUNITINIB
What the main difference btw the AE profile of Vincristine vs Vinblastine
Vincristine’s main AE is associated with NEUROTOXICITY (Peripheral neuropathy) with almost NO BM suppression
vs
VinBLASTINE’s main AE is BM suppression…and its a potent vesicant:(
which Inhibitors of the EGFR tyrosine kinase fits the following description:
• Colorectal cancer (efficacy is restricted to tumors expressing wild-type KRAS).
CETUXIMAB
What is trastuzimab’s main AE?
CARDIOTOXICITY
vats the difference between Cell cycle-specific drugs & Cell cycle-NON-specific drugs:
• Cell cycle-specific drugs:
Antineoplastic drugs that exert their action only on cells traversing the cell cycle.
Cell cycle-nonspecific drugs:
Can kill tumor cells whether they are cycling or resting in the G0 compartment. (Although cycling cells are more sensitive).
Whats the difference between the route of Elimination of Irinotecan and Topotecan (these are Camptothecins) and both inhibir Topo 1
- Irinotecan and its metabolites are mainly eliminated in bile and feces, and dose reduction is required in case of liver dysfunction.
- For Topotecan: The main route of elimination is renal excretion and dosage must be adjusted in patients with renal impairment.
do the following anticancer drugs have strong, moderate or mild MYELOSUPPRESSIVE EFFECTS
Cytarabine
Alkylating agents
Doxorubicin
Daunorubicin
Vinblastine
STRONG
What are the 2 Nitrosoureas (Carmustine & Lomustine) used to treat mainly and why is this so. Lastly, which one is IV admin and which one is ORAL admin.
They are used to treat BRAIN TUMORS (primary or mets, including glioblastoma multiforme) bc they are EXTREMELY LIPOPHILIC AND CAN CROSS THE BBB
the -MUSTINES!
Carmustine (IV) & LOmustine (ORAL)
• Some drugs have specific adverse effects:
• Doxorubicin causes…
• Cyclophosphamide & ifosphamide cause…
• Bleomycin causes…
cardiotoxicity.
pulmonary fibrosis.
hemorrhagic cystitis.
• Doxorubicin causes cardiotoxicity
D*_oxo CAUSES _*Dilated Cardiomyopathy
- Cyclophosphamide & ifosphamide cause hemorrhagic cystitis.
- Bleomycin causes pulmonary fibrosis.
Erythema and desquamation of the skin observed at sites of prior radiation therapy “radiation recall reaction” is associated with what group of Antitumor antibiotics?
The Anthracyclines!
DOXOrubicin
DAUNOrubicin
(both non cell cycle specific)
Which of the 4 Pyrimidine analogues are limited exclusively to hematologic malignancies, including acute myelogenous leukemia and non-Hodgkin’s lymphoma.
• Not active against solid tumors.
CYTARABINE (ARA-C) A deoxycytidine analogue
Cisplatin and Carboplatin are both Platinum compounts. How do their AE profiles differ?
Cisplatin-maninly NEPHROTOXICITY
Carboplatin mainly BM SUPPRESION
[both dose limiting]
How can Cisplatin’s main AE of NEPHROTOXICITY be helped?
Name 3 things that can be given
1. Pre-treatment hydration
- Diuretics
- Amifostine is a thiophosphate cytoprotective agent indicated to reduce the cumulative renal toxicity associated with repeated administration of cisplatin.
is the following an example of primary or acquired resistance?
• No response to the drug on the first exposure.
PRIMARY RESISTANCE
name that drug
- Stimulates natural killer cells to kill the transformed cells.
- Increases the expression of HLA molecules on tumor cells.
Clinical applications:
Kaposi sarcoma
Hairy cell leukemia
Renal cell carcinoma
Antiviral activity against HPV(condyloma acuminata),HBV and HCV.
Adverse effects:
• Flu like symptoms.
INTERFERON-a
DOC for Non-small cell lung cancer.
GETFITINIB
Inhibitors of the EGFR tyrosine kinase
Name that alkylation agent!
CNS depression (acute toxicity).
Leukopenia and thrombocytopenia.
Potent immunosuppressive agent.
Disulfiram-like reaction.
One metabolite is a weak monoamine oxidase (MAO) inhibitor
Carcinogenic potential is higher than that of most other alkylating agents (increased risk of secondary cancers in the form of acute leukemia).
PROCARBAZINE
• Treatment-induced neoplasms are especially a problem after therapy with what group of anticancer drugs
alkylating agents.
Amongst the Microtubule inhibitors (list them), VINCA ALKALOIDS (2) VS TAXANES (2)
what the main differentce in their MOA as it relates to their effect on the Mitotic spindle
VINCA ALKALOIDS: Vincristine, Vinblastine
TAXANES: Paclitaxel, Docetaxel
• Vinca alkaloids bindto β-tubulin. This disrupts assembly of microtubules. (VINCA ALKALOIDS BIND B TUBULIN AND INHIBIT ITS POLYMERIZATION INTO MICROTUBULES–> PREVENTS FORMATION OF MITOTIC SPINDLE–> M PHASE ARREST)
Taxanes promote microtubule polymerization and inhibit depolymerization (HYPERSTABILIZE POLYMERIZED MICROTUBULES IN THE M PHASE SO THE MITOTIC SPINDLE CANNOT BREAK DOWN–> ANANPHASE CANNOT OCCUR.
• Stabilization of the microtubules in a polymerized state arrests cells in mitosis and eventually leads to the activation of apoptosis.
What is CISPLATINs MAIN AE?
NEPHROTOXICITY (dose-limiting)–> leading to electrolyte disturbances (hypoMG2+, hypo Ca2+, etc)
The following drugs block DNA synthsis
Mix and match the drug with the action it has on DNA
Alkalating agents (cisplatin, busulfan, cyclophosphamide, Nitrosoureas (Carmustine, Lomustine)
Antitumor Antibiotics (Doxorubicin, Daunorubicin)
Etoposide & Teniposide
Antitumor Antibiotics (Bleomycin)
Irinotecan & Topotecan
Cross LInks DNA
are DNA intercalators
Inhibit topo II
Induces Breaks in DNA
Inhibits topi I
*Cross LInks DNA = Alkalating agents (eg: cisplatin)
*are DNA intercalators = Antitumor Antibiotics (Doxorubicin, Daunorubicin)
*Inhibit topo II = Etoposide & Teniposide
*Induces Breaks in DNA = Antitumor Antibiotics (Bleomycin)
*Inhibits topi I = Irinotecan & Topotecan
does Raloxifene use lead to endometrial Hyperplasia? What is its effect on Osteoporosis and is it used in the treatment OR prevention of breast cancer?
- NO it does NOT cause endometiral Hyperplasia
- It is used to prevent and manage Osteoporosis due to its anabolic effects on bone
- it PREVENTS doen NOT treat Breast cancer
the Hypersensitivity AE of WHICH drug is reduced by premedication with dexamethasone, diphenhydramine and an H2 blocker
PACLITAXEL (taxane)-MT inhibitor
What are L Asparaginases main 2 AE
- Hemorrhage
- Pancreatitis
Mesna
Leucovorin
Dexrazoxane
rescues bone marrow from methotrexate.
reduces anthracycline-induced cardiotoxicity.
reduces anthracycline-induced cardiotoxicity.
mix&match.
Leucovorin rescues bone marrow from methotrexate.
Mesna reduces hemorrhagic cystitis caused by cyclophosphamide and ifosfamide.
Dexrazoxane reduces anthracycline-induced cardiotoxicity.
- ________ is N5-formyl-THF.
- its an Antidote to drugs that decrease levels of folic acid, such as methotrexate, to rescue the bone marrow.
- It provides the normal tissues with the reduced folate, thus circumventing the inhibition of DHFR.
Leucovorin
Filgrastim reverses________caused by many anticancer agents.
Amifostine is a cytoprotective agent that reduces renal toxicity caused by….
neutropenia
cisplatin
Name that drug:
Its an antimetablite
DOC for Colorectal Cancer
One of its classic AE is “Hand/foot” Syndrome
what happens when you give Leucovorin with it?
what enzyme is it catabolized by?
5FU (pyrimidine analogue) & Capecitabine (both Uracil analogues-Pyrimidine Analogues)
If you give Leucovorin with it, its enhances the cytotoxic effects (which is favorable for an anticancer drug)
• Is mainly catabolized by the enzyme
Dihydropyrimidine dehydrogenase (DPD).
Amifostine is combined with what alkylating agent in order to reduce its AE which include OTOTOXICITY, NEPHROTOXICITY, NEUROTOXICITY
Oxaliplatin could be combined with what drug (in same class as the one alluded to above)
CISPLATIN + AMIFOSTINE (free radical scavenger)
CARBOPLATIN + OXALIPLATIN
If a patient has Tamoxifen resistant breast cancer whats and alternative?
FULVESTRANT a SERD (downregulator)
• Pure estrogen receptor antagonist with no agonist activity.
- Increases ER degradation.
- Reduces the number of ER molecules in cells.
do the following anticancer drugs have strong, moderate or mild MYELOSUPPRESSIVE EFFECTS
Carboplatin
Methotrexate
5-FU
MODERATE
list the drugs that are potent Vesicants (3 specific ones)
Vinblastine (vinca alkaloid in the broad class of MIcrotubule inhibitors)
Alkalating agens
MECHLORETHAMINE (a Nitrogen mustard in the broad clas of Alkalating agents)
DACARBAZINE (DTIC) (the only Triazine in the broad clas of Alkalating agents)
List cytotoxic drugs that, unlike most cytotoxic durgs, simply cause Mild-mod BM suppression
Dacarbazine-(Triazine)-Alkylating agent-its too busy being a potent Vesicant!
CIsplatin (Platinum Analogue)-Alkylating agent -its too busy causing Nephrotoxicity–> leading to electrolyte disturbances and OTOtoxicity
Vincristine (MT inhibitor)-its too busy causing AE like Peripheral Neuropathy bc of its Neurotoxic effects
Bleomycin (Antitumor Ab)-its too busy causing AE in tissues with decreased hydrolase activity like Lung and Skin.
TRASTUZUMAB AE = ?
Cardiotoxicity.
TRASTUZUMAB is Humanized Monoclonal antibody against ErbB2 (HER2).
do the following anticancer drugs have strong, moderate or mild MYELOSUPPRESSIVE EFFECTS
Bleomycin
Vincristine
Asparaginase
MILD
PROTEASOME inhibitors
BORTEZOMIB
- Proteasome Inhibitor.
- Induces growth inhibition and apoptosis of tumor cells.
Clinical applications:
- Multiple myeloma.
- Mantle cell lymphoma.
• First-line treatment of metastatic colorectal cancer.
this med is activated by a three-steps enzymatic conversion to 5-FU.
The first two steps occur in the liver .
The last step occurs in the tumor and it is catalyzed by the enzyme Thymidine phosphorylase.
CAPECITABINE
