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101 Cards in this Set
- Front
- Back
What are the 4 basic tissue types from which tumors arise?
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1. Epithelial tissue
2. Connective tissue 3. Lymphoid tissue 4. Nerve tissue |
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Malignancy on surface epithelium
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carcinoma
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Malignancy on glandular tissue
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adenocarcinoma
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Malignancy on fibrous tissue
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fibrosarcoma
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Malignancy on bone
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osteosarcoma
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Malignancy on smooth muscle
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leiomyosarcoma
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Malignancy on striated muscle
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rhabdomyosarcoma
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Malignancy on fat
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liposarcoma
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Malignancy on bone marrow elements
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leukemias
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Malignancy on lymphoid tissue
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Hodgkin's and non-Hodgkin's lymphoma
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Malignancy on plasma cell
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multiple myeloma
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Malignancy on glial tissue
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glioblastoma multiforme, astrocytoma
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Malignancy on nerve sheath
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neurofibrosarcoma
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Malignancy on melanocytes
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malignant melanoma
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Malignancy on gonadal tissue
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teratocarcinoma
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Tissue of origin of carcinoma
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surface epithelium
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Tissue of origin of adenocarcinoma
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glandular tissue
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Tissue of origin of fibrosarcoma
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fibrous tissue
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Tissue of origin of osteosarcoma
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bone
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Tissue of origin of leiomyosarcoma
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smooth muscle
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Tissue of origin of rhabdomyosarcoma
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striated muscle
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Tissue of origin of liposarcoma
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fat
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Tissue of origin of leukemias
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bone marrow elements
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Tissue of origin of Hodgkin's and non-Hodgkin's lymphoma
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lymphoid tissue
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Tissue of origin of multiple myeloma
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plasma cell
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Tissue of origin of glioblastoma multiforme, astrocytoma
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glial tissue
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Tissue of origin of neurofibrosarcoma
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nerve sheath
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Tissue of origin of malignant melanoma
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melanocytes
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Tissue of origin of teratocarcinoma
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gonadal tissue
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Benign tumor characterisitics
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noncancerous, localized, seldom metastasize, once removed they rarely recur
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Malignant tumor characteristics
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invade and destroy surrounding tissue, genetically unstable, atypical of their tissue of origin, metastasize frequently, recurrences are common after removal
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What are the 7 warning signs of cancer?
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1. Change in bowel or bladder habits
2. A sore that does not heal 3. Unusual bleeding or discharge 4. Thickening or lump in breast or elsewhere 5. Indigestion or difficulty in swallowing 6. Obvious change in wart or mole 7. Nagging cough or hoarseness |
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What are the principles of tumor growth?
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In early stages tumor growth is exponential. It takes a constant amount of time to double its size. This is called the growth fraction. When the growth fraction is high the tumor is most sensitive to chemotherapy.
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List out the cell cycle
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1. Mitosis - cell division occurs
2. G0 - dormant phase 3. G1 - first gap phase, prepares for DNA synthesis 4. S - DNA synthesis, can be used to determine aggressiveness of tumors 5. G2 - second gap phase, prepares for mitosis and produces RNA |
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Are the cell cycle specific agents schedule or dose dependent?
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schedule dependent
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Are the cell cycle nonspecific agents schedule or dose dependent?
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dose dependent
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What drugs work in the G1 phase of the cell cycle?
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aspariginase
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What drugs work in the S phase of the cell cycle?
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Antimetabolites
-methotrexate -cytarabine, fluorouracil, gemcitabine, capecitabine -mercaptopurine, fludarabine |
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What drugs work in the G2 phase of the cell cycle?
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-bleomycin
-etoposide |
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What drugs work in the M phase of the cell cycle?
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-vincristine, vinblastine, vinorelbine
-paclitaxel, docetaxel |
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Malignancy on plasma cell
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multiple myeloma
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Malignancy on glial tissue
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glioblastoma multiforme, astrocytoma
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Malignancy on nerve sheath
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neurofibrosarcoma
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Malignancy on melanocytes
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malignant melanoma
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Malignancy on gonadal tissue
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teratocarcinoma
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Tissue of origin of carcinoma
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surface epithelium
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Tissue of origin of adenocarcinoma
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glandular tissue
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Tissue of origin of fibrosarcoma
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fibrous tissue
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Tissue of origin of osteosarcoma
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bone
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Tissue of origin of leiomyosarcoma
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smooth muscle
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What are the cell-cycle phase-nonspecific agents?
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-alkylating agents
-anthracycline antibiotics -dacarbazine -cisplatin -nitrogen mustards |
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What are the stages of carcinogenesis?
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1. Initiation - exposure of normal cells to carcinogenic substance; irreversible cellular mutations occur
2. Promotion - growth of mutated cell population, reversible process 3. Progression - spread to distant sites |
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What are the two major classes of genes involved in carcinogenesis?
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oncogenes and tumor suppressor genes
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What are oncogenes and how do they become carcinogens?
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They develop from normal genes called protooncogenes. Protooncogenes are present in all cells and help regulate normal cellular function. Genetic alterations of protooncogenes via point mutations, chromosomal rearrangement, or gene amplification activates them into oncogenes. This can be caused by carcinogens, radiation, chemicals, viruses, or genetics.
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What are tumor suppressor genes and how do they become carcinogens?
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They regulate and inhibit inappropriate cellular growth and proliferation. They promote programmed cell death. Tumors may lack or have a defect in this gene.
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Which viruses are linked to cancers?
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Herpesviruses (simplex 1 and 2, cytomegalovirus, Epstein-Barr virus, roseolovirus)
Hepatitis B and C HTLV (T cell lymphoma) HIV |
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What types of cancer can HSV1 and HSV2 lead to?
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Kaposi's sarcoma
Carcinoma of lip and cervix |
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What types of cancer can HHV5 (cytomegalovirus) lead to?
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Kaposi's sarcoma
Prostatic cancer |
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What types of cancer can HHV4 (Epstein-Barr virus) lead to?
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Burkitt's lymphoma
PTLD lymphoma Nasopharyngeal carcinoma |
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What types of cancer can HHV6 (roseolovirus) lead to?
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lymphoproliferative disorders
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What types of cancer can hepatitis B lead to?
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hepatocellular disorder
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What types of cancer can hepatitis C lead to?
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hepatocellular carcinoma
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What types of cancer can HTLV lead to?
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T cell lymphoma
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What types of cancer can HIV lead to?
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Kaposi's and lymphomas
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What is the MOA of direct-acting carcinogens?
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electrophile, organic compound, genotoxic; interacts with DNA
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What is the MOA of procarcinogens?
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Requires conversion ghrough metabolic activation by host or in vitro to type 1
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What is the MOA of a hormone carcinogen?
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Mainly alters the endocrine system balance and differentiation; often acts as promoter; usually not genotoxic
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What is an example of a hormone carcinogen?
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estradiol
diethylstilbestrol |
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What is the MOA of an immunosuppressor carcinogen?
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Mainly stimulates "virally induced", transplanted, or metastatic neoplasms; usually not genotoxic
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What is the MOA of a cocarcinogen?
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Not genotoxic or carcinogenic, but enhances effect of type 1 or type 2 agent when given at the same time; may modify conversion of type 2 to type 1
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What is the MOA of a cytotoxin?
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Not genotoxic or carcinogenic; above specific dosages kills cells, increases regeneration and cell cycling
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What is the MOA of a promoter?
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Not genotoxic or carcinogenic, but enhances effect of type 1 or type 2 agent when given subsequently
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What is an example of a promoter?
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phorbol esters, phenol, bile acids, sodium saccharin
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What are the genotoxic carcinogens?
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-direct acting agents
-procarcinogens |
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What are the epigenetic carcinogens?
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-hormones
-immunosuppressor -cocarcinogen -cytotoxin -promoter |
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What is responsible for 1/3 of all US cancer deaths?
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smoking
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What are the most common sites of secondary tumors?
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breast, prostate, or colon
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What are the common sites of metastatic disease?
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liver, brain, bone, lung, spleen, adrenal glands
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How big must tumors get before they are detectable?
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greater than 10^9 cells
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What is the Fractional Cell Kill Hypothesis?
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a given concentration of drug for a given time period kills a constant fraction of the cell population
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When using the Fractional Cell Kill Hypothesis, what is the frequency limited by?
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the dose limiting toxicity (bone marrow suppression or GI toxicity)
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How can resistance to cancer drugs develop?
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1. alteration in membrane transport
2. depleted activating enzymes 3. changes in target enzymes 4. new alternative pathways 5. altered binding of drugs to macromolecules 6. multi-drug resistance |
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Describe multi-drug resistance and how it can be inhibited.
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Many tumors develop resistance to a number of unrelated naturally occurring chemotherapy agents. The mechanism of the resistance is the presence of an intercellular pump, p-glycoprotein. The pump can be inhibited by a number of agents such as verapamil.
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What are some ways to overcome drug resistance?
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1. Change method of drug administration (dose, schedule, route)
2. Change the drug preparation 3. Use combination products and combined modalities |
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What is rationale behind combination chemotherapy?
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-some cells may be resistant to a single agent
-prevent the development of resistance -by using different agents one can increase efficacy without increasing toxicity |
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What should you look for when selecting agents to be in a combination chemo regimen?
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Drugs that are active against tumor, have different mechanisms, lack cross resistance, and have different toxicities.
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How to space out a chemo regimen.
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-Start with cell cycle nonspecific agents to reduce tumor bulk and recurit cells into cycle
-follow with cycle specific agents -use non-myelosuppressive durgs during "off" period to suppress tumor growth |
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Dose modification of methotrexate in renal failure or decreased creatinine clearance.
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decrease dose in proportion to decrease in creatinine clearance (normal is 60)
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Dose modification of cis-Platinum (cisplatin) in renal failure.
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decrease dose in proportion to creatinine clearance
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Dose modification of cyclophosphamide in renal failure (creatinine clearance below 25)
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50% decrease
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Dose modification of bleomycin in renal failure (creatinine clearance below 25)
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50-75% decrease
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Dose modification of streptozotocin in renal failure (creatinine clearance below 25)
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50-75% decrease
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Dose modification of carboplatin in renal failure
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decrease in proportion to creatinine clearance
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Dose modification of hydroxyurea, VP-16, and deoxycoformycin in renal failure
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decrease in proportion to creatinine clearance
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Dose modification of mAMSA, doxorubicin, daunorubinin, vincristine, and vinblastine in hepatic dysfunction
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1. for bilirubin greater than 1.5mg/100ml, reduce initial dose by 50%
2. for bilirubin greater than 3.0mg/100ml, reduce initial dose by 75% |
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What is the therapy and probable cure rate of diffuse histiocytic lymphoma?
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Therapy is combination chemotherapy
Cure rate is greater than 50% |
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What is the therapy and probable cure rate for Hodgkin's disease?
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Therapy is combination chemotherapy
Cure rate is greater than 50% |
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What is the therapy and probable cure rate for Testicular carcinoma?
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Therapy is combination chemotherapy plus surgery
Cure rate is greater than 75% |
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What is the therapy and probable cure rate for Gestational choriocarcinoma?
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Therapy is methotrexate plus actinomycin D
Cure rate is 90% |
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What is the therapy and probable cure rate for Ovarian carcinoma?
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Therapy is combination chemotherapy
Cure rate is 10-20% |
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What is the therapy and probable cure rate for AML?
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Therapy is combination chemotherapy
Cure rate is 20% |