Anti-Cancer Rx – Flashcards
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Recall: Cell Cycle
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• G1 Phase: Preparation for DNA synthesis. Synthesis of substrates (ribo and deoxyribo nucleotides) and enzymes necessary for DNA formation. • S Phase: DNA replication • G2 Phase: Proof reading of synthesized DNA & correction of any mismatch, protein synthesis for cell division. • M Phase: Separation of chromatids and division of cell into 2 daughter cell. • G0 Phase: Differentiation of cell into mature cell
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Anticancer Rx can cause killing of rapidly dividing normal cells. Name some of these cells and their clinical consequences
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Bone marrow: neutropenia, thrombocytopenia GI mucosa: mucositis & blsitsers Hair follicles: alopecia Gonads: infertility Most anticancer drugs are carcinogenic (DNA damage).
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Major toxicity of some Rx:
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*Cyclophosphamide & Ifofamide*: Hemorrhagic cystitis *Bleomycin*: Pulmonary fibrosis *Cisplatin*: Nephrotoxicity & Deafness *Doxorubicin & Daunorubicin*: Dilated cardiomyopathy *Vincristine*: Peripheral neuropathy *Etoposide, Methotrexate & Vinblastine*: Bonemarrow suppression *L-Asparaginase*: Pancreatitis and bleeding
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What can be used to prevent some of the common drug-induced damages?
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Hemorrhagic cystitis by cyclophosphamide & ifosfamide: *MESNA* Cisplatin-induced nephrotoxicity: *Good hydration and amifostine* Doxorubicin & daunorubicin induced dilated cardiomyopathy: *Dexrazoxane* Bonemarrow suppression by various drugs: *Filgrastim (GM-CSF)* Methotrexate induced bonemarrow suppression: *Leucovorin (Tetrahydrofolic acid)*
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What is the ABVD regimen and what does it Tx?
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Adriamycin (Doxorubicin) Bleomycin Vincristine Dacarbazine Tx: *Hodgkin's Lymphoma*
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ABVD - toxicity profile
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Adriamycin/Doxorubicin - cardiotoxicity Vincristine - neurotoxicity (peripheral neuropathy) Bleomycin - pulmonary fibrosis Dacarbazine - bone marrow toxicity
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What is the BEP regimen and what does it Tx?
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Bleomycin Etoposide Platinum (Cisplatin) Tx: *Testicular Cancer*
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What is the BEP regimen toxicity profile?
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Bleomycin - PF Etoposide - BM toxicity Cisplatin - Ototoxicity, Nephrotoxicity
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Define: Adjuvant chemotherapy
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Chemotherapy in addition to surgery or radiotherapy
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Define: Neo-adjuvant chemotherapy
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Chemotherapy given before surgery to decrease the size of the tumor
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Define: Induction chemotherapy
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Chemo given to obtain complete remission from tumor, usually blood cancers.
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Define: Maintenance chemotherapy
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Chemo given to maintain remission from the cancer
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What are the classifications of Anti-Cancer Rx?
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Antimetabolites, Antitumor Antibiotics, Epipodophyllotoxins, Vinca Alkaloids, Taxanes, Camptothecins Alkylating Agents: - Nitrogen mustards - Alkyl sulfonates (Busulfan) - Nitrosoureas - Triazenes (Dacarbazine) - Methylhydrazines (procarbazine) - Platinum Complexes Hormonal Agents - Glucocorticoids - Estrogens - Estrogen Inhibitors - Progestins - Androgens - Anrogen Inhibitors - Androgen Receptor Blockers (Flutamide) Signal Transduction Inhibitors Miscellaneous
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Alkylating Agents - MOA
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- Alkylation at *N7 position of guanine *in DNA - Miscoding through *abnormal base pairing with thymine* or in depurination by *excision of guanine* residues, leading to *strand breakage* - Cross-linking of DNA and ring cleavage may occur
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Alkylating Agents - basic properties
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*Cell cycle nonspecific* agents Mutagenic, carcinogenic Cyclophosphamide - most common
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Name the nitrogen mustards
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Cyclophosphamide Ifosfamide Mechlorethamine Melphalan Chlorambucil
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Cyclophosphamide - MOA
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Needs to be* activated by hepatic enzymes* ? *acrolein* (toxic)
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Cyclophosphamide - use
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Neoplastic Disease, in combo: - Adrenal cortex cancer - Bladder cancer - Bone cancer - Cervical cancer - Endometrial cancer - Lung cancer - Non-hodgkins lymphoma
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Cyclophosphamide - AE
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• Bone marrow suppression • Immunosuppression • Hemorrhagic cystitis • Nausea and vomiting • Alopecia • Gonadal failure: amenorrhea ; sterility • SIADH
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Why is MESNA used with cyclophosphamide?
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To prevent irritation of the bladder by acrolein ? hemorrhagic cystitis Also recommended to maintain urine output ; 3L/day
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Ifosfamide - details
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MOA ; AE similar to cyclophosphamide *More potent* than cyclo. More potential to cause *hemorrhagic cystitis* *Prior admin of MESNA is a must for each dose*
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Mechlorethamine - use, AE
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Tx: Nonhodgkin's Lymphoma Highly *vesicant*
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Mephalan - use
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Tx: Multiple myeloma
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Chlorambucil - use
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Tx: CLL
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What is the name of the alkylsulfonate?
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Busulfan
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Busulfan - use, AE
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Chronic myelogenous leukemia (CML) AE: adrenal insufficiency, *pulmonary fibrosis*, skin pigmentation
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Name the Nitrosoureas
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Carmustine (BCNU) Lomustine (CCNU) Semustine
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Carmustine Lomustine Semustine - MOA
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Chloroethyl moiety of nitrosoureas ? alkylates nucleic acids & proteins ? single-strand breaks & inter-strand cross-linkage of DNA *Cross BBB*
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Carmustine Lomustine - use, AE
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Highly lipophilic ? BBB *Used as adjuncts in Tx of brain tumors* AE: GI distress, delayed myelosuppression, CNS dysfunction
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Name the triazene
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Dacarbazine (DTIC)
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Dacarbazine - details
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• Synthetic drug; requires *activation by liver microsomal system* • Tx: *Hodgkin's disease, soft tissue sarcoma and melanoma* • AE: Myelosuppression, nausea ; vomiting
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Name the methylhydrazine
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Procarbazine
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Procarbazine - details
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Combo Tx: Hodgkin's Disease Teratogenic, mutagenic, *leukemogenic* AE: n/v, myelosuppresion, hemolytic anemia, pulmonary effects, peripheral sensory neuropathy, disulfiram-like reaction
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Name the platinum compounds
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Cisplatin Carboplatin Oxaliplatin
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Cisplatin Carboplatin Oxaliplatin - basic properties
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Cell cycle *nonspecific* agents Minimal bone marrow suppression
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Cisplatin Carboplatin Oxaliplatin - MOA, use
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*Alkylates N7 position of guanine in DNA* Tx: Wide range of solid tumors like germ cell tumors, ovarian cancer, non small cell lung cancer, etc.
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Cisplatin Carboplatin Oxaliplatin - AE
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- *Severe nausea and vomiting* due to intense stimulation of CTZ (Chemoreceptor Trigger Zone) - *Neurotoxicity*- peripheral neuropathy and deafness (cochlear nerve damage) - *Nephrotoxicity*- leads to electrolyte imbalance
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How to combat Cisplatin-induced nephrotoxicity?
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• Osmotic diuresis with *mannitol* • Forced chloride diuresis with 0.1% NaCl •* Amifostine* -cytoprotective agent which gives Thiol (-SH) compound on activation inactivates free radicals generated by cisplatin
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What drug is commonly co-admin with cisplatin to reduce AE?
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*Amifostine* It ? frequency of cisplatin-induced nephrotoxicity, ototoxicity, neurotoxicity, and myelosuppression. FDA-approved to ? cumulative renal toxicity in pts receiving repeated doses of cisplatin for advanced ovarian cancer and non-small- cell lung cancer
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Compare contrast cisplatin with other platinum compounds
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Carboplatin & oxaliplatin: • Has more acceptable toxicity profile than cisplatin- less nephrotoxic, less neurotoxic & less emetogenic. • More myelosuppression than cisplatin.
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Antimetabolites - basic properties
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• Structurally similar to natural substances like vitamins, nucleosides, nucleotides or amino acids. • Block important biosynthetic pathway by *competing with natural substances*. • Are incorporated, instead of natural substances. • Cell cycle specific drugs, acting mostly on *S phase*
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Name the antimetabolites:
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Folate antagonist: Methotrexate Purine antagonists: 6-Mercaptopurine, 6-Thioguanine Pyrimidine antagonists: 5-Fluorouracil, Capecitabine, Cytarabine, Gemcitabine
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Methotrexate - MOA
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Inhibits the enzyme *dihydrofolate reductase*, which converts dihydrofolic acid to tetrahydrofolic acid
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Methotrexate - uses
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• Choriocarcinoma • Acute Lymphoblastic Leukemia (ALL) • Burkitt's lymphoma • Osteosarcoma • Breast cancer
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Methotrexate - AE
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Common: BM suppression, immune-suppression, mucositis, alopecia Renal damage: due to crystal deposits in kidney tubules (good hydration prevents this) Pulmonary toxicity: esp in kids Hepatic fibrosis: LT Tx
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What is the Leucovorin rescue? Why is it given?
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*Leucovorin or Folinic acid* • Used in cases of OD or in high-dose methotrexate protocols. • Leucovorin provides cells a source of reduced folate, thereby overcoming blockade by methotrexate.
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6-Mercaptopurine (6-MP) - MOA
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*Purine Antagonists* 6-MP ? 6 thioinosinic acid (TIMP) ? inhibits de novo purine synthesis TIMP ? blocks formation AMP, GMP
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6-Mercaptopurine (6-MP) - coadmin with allopurinol?
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6-MP metabolized to thiouric acid by xanthine oxidase Allopurinol (xanthine oxidase inhibitor) is used to reduce uric acid synthesis *Dose of 6-MP must be reduced if co-admin with allopurinol*
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6-Mercaptopurine (6-MP) - use, AE
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Acute Lymphocytic Leukemia (ALL) AE: BM suppression, hepatotoxicity, n/v
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6- Thioguanine- details
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MOA:* inhibits DNA ; RNA synthesis by ? intracellular [GMP]* Use: Tx acute lymphoid leukemia (ALL). *No drug interaction with allopurinol* AE: BM suppression, Hepatotoxicity, n/v
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5-Flurouracil Capecitabine Cytarabine Gemcitabine
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*Pyramidine antagonists*
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5-Flurouracil (5-FU) - MOA
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5-FU ? deoxyribonucleotide ? *inhibits thymidylate synthase* ? thymidine deficiency ? inhibits DNA synthesis 5-FU also incorporated into RNA
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Coadmin of 5-FU with leucorvorin - what happens
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Supplementing leucovorin (folinic acid) along with 5-FU leads to incorporation of more 5-FU metabolite into RNA- generation of more nonfunctional RNA. *Addition of leucovorin increases the cytotoxic effects of 5-FU*
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5-FU - Use, AE
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Systemic use: Adenocarcinomas Topical use: Skin cancer AE: - Myelosuppression - Mucositis - *Hand-foot syndrome* (skin exfoliation on palm, feet) - Alopecia
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Capecitabine - details
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*Oral prodrug of 5-FU* • Converted into 5-FU by *thymine phosphorylase* inside the tumor cells. • Use: *metastatic breast cancer ; colorectal cancer* • Adverse effects: similar to 5-FU
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Gemcitabine - MOA
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*Pyrimidine analog* Incorporated into DNA, inhibits chain elongation - Competes with cytidine
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Gemcitabine - AE, use
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Use: *Pancreatic cancer*, non-small cell lung cancer, ovarian cancer AE: myelosuppression, alopecia, flu-like Sx, ? liver enzymes
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Cytarabine (ara-C) - details
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• MOA: *S phase*-specific antimetabolite. • Biotransformed to active forms: Ara-CTP *competitively inhibits the enzyme DNA polymerase*. • Use: AML for induction ; CML in blast crisis • Adverse effects: Myelosuppression (common) ; ataxia
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Vincristine Vinblastine Vinrelbine - class
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Vinca Alkaloids, natural products
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Vincristine Vinblastine Vinrelbine - origin, MOA
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Derived from plant vinca rosea MOA: Bind to ?-tubulin and *prevents formation of microtubules* "Mitotic spindle poisons" *Cells arrested
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Vincristine - use, AE
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Use: Hodgkin's lymphoma AE: *Neuropathy* (myelosuppression is minimal, considered a *bone marrow-sparing drug*)
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Vinblastine - use, AE
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Use: Testicular cancers AE: myelosuppression
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Vinrelbine - Use, AE
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Use: Non-small cell lung cancer AE: Granulocytopenia
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Paclitaxel Docetaxel - class
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Taxanes Derivative of Western Yew
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Paclitaxel Docetaxel - MOA
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Enhances tubulin polymerization and *stabilizes microtubules in polymerized state* Cell is *Arrested in metaphase (M phase)*
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Paclitaxel Docetaxel - Use
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Use: Ovarian, breast cancer
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Paclitaxel - AE
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Severe allergic reaction attribute to cremophor vehicle, neutropenia, alopecia
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Docetaxel - AE
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Skin toxicity and fluid retention leading to pleural and peritoneal effusions
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Etoposide Tenoposide - class
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Epipodophyllotoxins
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Etoposide Tenoposide - MOA
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*Topoisomerase II inhibition*, prevents re-ligation of DNA strand breaks Acts at *late S and early G2* phases of cell cycle
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Etoposide Tenoposide - Use, AE
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Use: Germ cell tumor, AML, lung cancer AE: myelosuppression Association between etoposide use and leukemia (in survivors)
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Topotecan Irinotecan - class
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Camptothecins
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Topotecan Irinotecan - MOA
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Topoisomerase I inhibition
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Topotecan - Use, AE
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Metastatic ovarian cancer (cisplatin-resistant) AE: Neutropenia, thrombocytopenia, anemia
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Irinotecan - use, AE
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Colon and rectal cancer AE: severe diarrhea, myelosuppression (caution in patients with *Gilbert's syndrome*)
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What are the antitumor antibiotics?
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Bleomycin Anthracyclines - Doxorubicin - Daunorubicin Dactinomycin
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Bleomycin - basic properties
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Cell cycle specific agent: *G? Phase* PK: eliminated by kidney Inactivated by cellular metabolism via enzyme: *bleomycin hydrolase*
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Bleomycin - MOA
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Induces free radical-mediated DNA strand breaks Reduced iron mediates the reduction of molecular oxygen into damaging free radicals
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Bleomycin - Use, toxicity
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Use: Hodgkin's lymphoma, testicular cancer, kaposi sarcoma Toxicity: seen in tissues low in enzyme bleomycin hydrolase: - *Pneumonitis followed by pulmonary fibrosis* - Skin reaction - Raynauld's phenomenon - Retroperitoneal fibrosis No significant effect on BM (*Bone marrow sparing drug*)
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Doxorubicin Daunorubicin - class
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*Anthracyclines * Derived from streptomyces fungi
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Doxorubicin Daunorubicin - MOA
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Inhibition of *topoisomerase II* ? DNA breaks Formation of highly reactive oxygen free radical species which damages DNA, cell membrane, proteins, etc Alters membrane fluidity, and ion transport
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Doxorubicin Daunorubicin - use, AE
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Broad anti-tumor activity: Breast cancer, AML, lymphomas, sarcomas, etc AE: *Cardiotoxicity*, myelosuppression, n/v, alopecia, mucositis, erythema at sites of prior radiation "Radiation recall reaction", highly vesicant
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Doxorubicin Daunorubicin - Cardiotoxicity Tx
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Free radical damage Heart vulnerable because limited capacity to neutralize free radicals *Dexrazoxane* - iron chelating agent, ? free radical damage
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What is Dexrazoxane?
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Iron chelating agent, ? free radical damage
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Dactinomycin - details
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Cell cycle *nonspecific* agent MOA: binds to DNA *noncovalently* Use: *Wilm's tumor, sarcomas* AE: - Highly vesicant (extravasation ? tissue necrosis) - Erythema at sites of prior radiation (Radiation recall reaction)
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Dexamethasone Hydrocortisone Prednisone Prednisolone - class
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Glucocorticoids used to Tx Cancer
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Dexamethasone Hydrocortisone Prednisone Prednisolone - MOA
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Bind to intra-cytoplasmic receptor ? steroid-receptor complex binds to nuclear receptor ? modulates protein expression
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Dexamethasone Hydrocortisone Prednisone Prednisolone - AE
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Immunosuppression ?? infections, mood swings, osteoporosis, hyperglycemia, poor wound healing
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Dexamethasone Hydrocortisone Prednisone Prednisolone - Use in Cancer Tx
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• Acute Lymphocytic Leukemia, Hodgkins lymphoma, non-hodgkins lymphoma, multiple myeloma, etc. • Palliative care to improve feeling of well being. • Used in spinal cord compression due to metastasis to relieve edema. • Management of autoimmune anemia and thrombocytopenia.
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Diethylstilbestrol Ethinylestradiol - class
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Estrogens
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Diethylstilbestrol Ethinylestradiol - MOA
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Bind to intra-cytoplasmic receptor ? steroid-receptor complex binds to nuclear receptor ? modulates protein expression
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Diethylstilbestrol Ethinylestradiol - AE
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? risk thromboembolism, migraine, cholestasis, mood changes - Gynecomastia and impotence in men
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Diethylstilbestrol Ethinylestradiol - Use in Cancer, contraindications
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*Prostate cancer* Contraindicated in pts with breast & endometrial cancers
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Tamoxifen Raloxifene - class
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*Selective Estrogen Receptor Modulator* Exhibit agonistic action in some tissue and antagonistic action in others
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Tamoxifen Raloxifene - AE
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Hot flushes, thrombosis Fluid retention *Risk of endometrial cancer* with LT use
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Tamoxifen - E modulation
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Antagonist @ breast Agonist @ endometrium, bone
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Raloxifene - E modulation
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Antagonist @ breast, endometrium Agonist @ bone
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Tamoxifen - Use
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*Primary therapy for metastatic breast cancer* in both men & postmenopausal women Decreases incidence of breast cancer in women who are at high risk for developing the disease
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Aromatase
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After menopause, E produced by peripheral conversion of androstenedione ? estriol by aromatase in adipose tissue
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Types of Aromatase inhibitors
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Competitive or reversible: - Steroidal: Aminogluthethimide - Non-steroidal: anastrozole, letrozole Steroidal irreversible inhibitors: - Exemestane, Formestane
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Aminogluthethimide - MOA
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• Inhibitor of adrenal steroid synthesis at the first step, conversion of cholesterol to pregnenolone • Inhibits the extra-adrenal synthesis of estrone and estradiol. • Inhibits the enzyme aromatase that converts androstenedione to estrone.
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Aminogluthethimide - Use, AE
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*ER+ metastatic breast cancer* AE: - Adrenal insufficiency - Dizziness - Lethargy - Visual blurring - Rash
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Anastrozole Letrozole - use, AE
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*Selective non-steroidal inhibitor of aromatase enzyme* Use: Tx advanced ER+ breast cancer that is *resistant to tamoxifen* AE: Hot flushes & headache
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Exemestane Formestane - use, AE
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*Steroidal irreversible inhibitors* Use: Advanced ER+ cancer AE: Mood changes, acne and hair growth.
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Hydroxyprogesterone Megestrole - class
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Progestins used in Cancer Tx
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Hydroxyprogesterone Megestrole - use, AE
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Use: endometrial cancer; palliative care (? appetite in terminally ill cancer patients) AE: Weight gain, Depression, Edema, acne, ?HDL
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Fluoxymesterone Testosterone - class, use
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Androgens used in Cancer Tx Use: palliative care to improve feeling of well being and appetite
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Leuprolide Goserelin - class
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Antiandrogens: Gonadotropin-releasing analogues
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Leuprolide Goserelin - MOA
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Continuous dose (not pulsatile) will produce reversible medical castration ? ? release of LH & FSH Initial flare-up of androgen dependent cancer may occur
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Leuprolide Goserelin - Use, AE
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Prostate cancer, sometimes for uterine fibroids AE: ? bone mass, hot flushes, initial tumor flare up, impotence
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Flutamine - class, MOA, use
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Androgen Receptor Blocker Antagonizes androgenic effects Approved for *prostate cancer* Tx Given with GnRH agonists to prevent initial tumor flare-up
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Flutamine - AE
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Gynecomastia, GI distress
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Hydroxyurea - MOA
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Urea analog *Inhibits ribonucleotide reducase* ? ? deoxynucleoside triphosphate pools ? inhibiting DNA synthesis *S phase specific agent*
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Hydroxyurea - use
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Tx: Melanoma, chronic myelogenous leukemia (CML), sickle cell disease to ?HbF
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Hydroxyurea - AE
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Leukopenia (reversible upon discontinuation of drug) Mild GI toxicity Mild dermatologic changes with prolonged therapy
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L-Asparaginase - MOA
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Enzyme isolated from bacteria Causes catabolic depletion of serum asparagine ? aspartic acid & ammonia ? ?blood glutamine levels ? inhibits protein synthesis *Neoplastic cells require external source of asparagine*
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L-Asparaginase - Use, AE
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*Childhood acute leukemia* Hypersensitivity rxns (shock), hemorrhage, hyperglycemia, headache, pancreatitis
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Arsenic trioxide - Use
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Tx: Acute pro-myelocytic leukemia In PML/RAR-? positive AML, arsenic trioxide causes differentiation of leukemic cells
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Arsenic trioxide - AE
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headache, cardiac arrhythmias, fluid retention, increases risk of skin cancers
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Interferon - MOA
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Produced by recombinant DNA technology MOA not clearly understood INF-? stimulates NK cells ? expression of HLA molecules on tumor cells
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Interferon - Use
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INF-2?: CML, hairy cell leukemia, kaposi sarcoma INF-2?: Melanoma, follicular lymphoma, AIDS related Kaposi sarcoma
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Interferon - AE
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Fever, myalgia, headache, loss of appetite, depression
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How do signal transduction inhibitors work to Tx cancer?
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• Specifically act on tumor cells hence usually* lack non specific toxicities like bone marrow suppression, alopecia, mucositis, etc.* • Over-expression of one particular pathway in tumor is targeted.
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Imatinib - MOA
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Inhibits tumor *tyrosine kinase* activity
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Imatinib - Use
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Tx* BCR-ABL+ CML*, ALL, & GIST
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Imatinib - AE
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Fluid retention, edema, hepatotoxicity, thrombocytopenia
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Gefitinib - MOA
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Inhibits *epidermal growth factor receptor* signal transduction
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Gefitinib - Use, AE
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Tx: non-small cell lung cancer AE: Acne-like skin lesions, nausea, diarrhea
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Cetuximab - MOA, use, AE
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Inhibits EGFR signaling Colorectal cancer, head and neck cancer AE: Infusion reaction, skin rash, fatigue
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Trastuzumab - MOA, use, AE
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Epidermal growth factor receptor protein 2 Breast cancer AE: CHF, infusion reaction
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Bortezomib - MOA, Use, AE
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Inhibits *proteosome* which has chymotrypsin-like activity MM, mantle cell lymphoma AE: Thrombocytopenia, neuropathy
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Sunitinib - MOA, use, AE
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Multiple receptor kinase inhibition, like VEGF-1, 2, 3; PDGFR Renal cell cancer, GIST AE: skin rash, bleeding
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Erlotinib Lapatinib - MOA, use, AE
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EGFR tyrosine kinase inhibitor Non-small cell lung cancer, pancreatic cancer AE: skin rash, interstitial lung disease
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Sorsfenib - MOA, use, AE
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Multiple receptor kinase inhibition like VEGF-2, 3; PDGFR Renal cell cancer, hepatocellular cancer AE: skin rash, fatigue
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Which anticancer drugs are bone marrow sparing? Which cause minimal BM suppression?
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Vincristine Bleomycin Signal transduction inhibitors (Bortezomib, Cetuximab, Erlotinib, Gefitinib, Imatinib, Lapatinib, Sorafenib, Sunitinib, Trastuzumab) Minimal bone marrow suppression: Platinum compounds (cisplatin, carboplatin, oxaliplatin)
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Which anticancer drug causes "hand-foot syndrome"?
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5-Flurouracil (5-FU) Skin exfoliation on palms, feet
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Which anticancer drugs cause Radiation Recall reaction, and what is that?
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Erythema at sites of prior radiation Caused by: anthracyclines (doxorubicin, daunorubicin) & Dactinomycin
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Which anticancer drugs are highly vesicant?
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Mechlorethamine Anthracyclines (doxorubicin, Daunorubicin) Dactinomycin
