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Cancer etoposide

Lung Cancer Etoposide (VP-16) -plant alkaloid, topoisomerase II inhibitor -bone marrow suppression -nausea and vomiting -mucocutaneous effects (mucositis, stomatitis)—increased at higher doses -chemical phlebitis common -hypotension with rapid administration -hypersensitivity reactions -secondary leukemia... [Pg.172]

II cleaves the two complementary strands of DNA four base pairs apart and the resulting 5 -phosphoryl groups become covalently linked to a pair of tyrosine groups, one in each half of the dimeric topoisomerase II enzyme. Several groups of drugs are known that selectively inhibit topoisomerases in bacteria (quino-lones) or mammalian cells (etoposide, tenoposide). Quinolones are used to treat bacterial infections inhibitors of mammalian topoisomerases are cytostatic drugs used for the treatment of cancer. [Pg.1212]

HASHIMOTO S, XU M, MASUDA Y, AIUCHI T, NAKAJO S, CAO J, MIYAKOSHI M, IDA Y and NAKAYA K (1999) Beta-hydroxyisovalerylshikonin inhibits the cell growth of various cancer cell lines and induces apoptosis in leukemia HL-60 cells through a mechanism different from those of Fas and etoposide , J Biochem (Tokyo), 125 17-23. [Pg.64]

Etoposide (XV) is a semisynthetic gylcoside derivative of podophyllotoxin, which is one of the most extensively used anticancer drugs in the treatment of various types of tumors [64,65]. The anticancer activity of this drug is mainly due to its ability to inhibit an ubiquitous and essential enzyme human DNA topo II [66,67]. Despite its extensive use in the treatment of cancers, it has several limitations, such as poor water solubility, drug resistance, metabolic inactivation, myelosuppression, and toxicity [68]. In order to overcome these... [Pg.63]

Etoposide causes multiple DNA double-strand breaks by inhibiting topoisomerase II. The pharmacokinetics of etoposide are described by a two-compartment model, with an a half-life of 0.5 to 1 hour and a (5 half-life of 3.4 to 8.3 hours. Approximately 30% of the dose is excreted unchanged by the kidney.16 Etoposide has shown activity in the treatment of several types of lymphoma, testicular and lung cancer, retinoblastoma, and carcinoma of unknown primary. The intravenous preparation has limited stability, so final concentrations should be 0.4 mg/mL. Intravenous administration needs to be slow to prevent hypotension. Oral bioavailability is approximately 50%, so oral dosages are approximate two times those of intravenous doses however, relatively low oral daily dosages are used for 1 to 2 weeks. Side effects include mucositis, myelosuppression, alopecia, phlebitis, hypersensitivity reactions, and secondary leukemias. [Pg.1288]

JP is receiving a highly myelosuppressive chemotherapy regimen for the next 3 days for his lymphoma. The chemotherapy orders specify ifosfamide, carboplatin, and etoposide. The goal of this cycle of chemotherapy is to put the cancer into remission so that his lymphoma can be cured with a bone marrow transplant. [Pg.1298]

Risk factors for the development of AML include exposure to environmental toxins, Hispanic ethnicity, and genetics.6 Of greater concern is the increased prevalence of AML as a secondary malignancy, resulting from chemotherapy and radiation treatment for other cancers. Alkylating agents, such as ifosfamide and cyclophosphamide, and topoisomerase inhibitors, such as etoposide, are linked to an increased risk of myelodysplastic syndrome (MDS) and AML.8... [Pg.1399]

Examples of inhibitors of chromatin function derived from flowering plants (Fig. 80) are etoposide (lignan) and alkaloids camptothecin, Vinca alkaloids, and 7 epitaxol. The rhizome of Podophyllum peltatum L. (May apple, Berberidaceae) has been used to remove warts and to relieve the bowels from costiveness since very early times. It contains podophyllo-toxin, a cytotoxic lignan from which etoposide (Vepesid ), which is used to treat lung cancer, lymphomas, and leukemias on account of its ability to inhibit the activity of... [Pg.168]

Inhibition of intestinal P-glycoprotein and effects on etoposide absorption. Cancer Chemother. Pharmacol. 1995,... [Pg.287]

Lorico A, Rappa G, Finch RA, Yang D, Flavell RA, Sartorelli AC. Disruption of the murine MRP (multidrug resistance protein) gene leads to increased sensitivity to etoposide (VP-16) and increased levels of glutathione. Cancer Res 1997 57(23) 5238-5242. [Pg.207]

Chemotherapeutic agents that have significant cancer response when combined with hyperthermia (up to 43°C) include doxorubicin, melphalan, mitomycin C (MMC), mitoxantrone, gemcitabine, etoposide, and especially the platinum-based agents carboplatin and oxaliplatin (Mohamed et al., 2003 Sugarbaker et al., 2005). Agents that do not work well with hyperthermia include irinotecan, paclitaxel, docetaxel, 5-fluorouracil, and floxuridine (Mohamed et al., 2003 Sugarbaker et al., 2005). [Pg.238]

J. D. Allen, S. C. Van Dort, M. Buitelaar, O. van Tellingen, and A. H. Schinkel. Mouse breast cancer resistance protein (Bcrpl/Abcg2) mediates etoposide resistance and transport, but etoposide oral availability is limited primarily by P-glycoprotein. Cancer Res 63 1339-1344 (2003). [Pg.576]

UGTIAI has an important role in the metabolism of irinotecan, etoposide, epiru-bicine, and tipifamib. Irinotecan is a camptothecin derivative used in the treatment of metastatic colon cancer. Irinotecan is a prodrug since it is activated to Ethyl-10-hydroxycamptothecin (SN-38) by carboxyl esterase to exert its antitumor activity mediated by the inhibition of topoisomerase I. SN-38 undergoes UGTIAI-catalyzed glucuronide conjugation to form the inactive SN-38 glucuronide (SN-38G). [Pg.67]

Kluza J, Mazinghien R, Irwin H, Hartley JA, Bailly C. (2006) Relationships between DNA strand breakage and apoptotic progression upon treatment of HL-60 leukemia cells with tafluposide or etoposide. Anti-Cancer Drugs 17 155-164. [Pg.175]

Etoposide is an effective anticancer drug used in the treatment of small-cell lung cancer, testicular cancer and lymphomas. It is a semi-synthetic modification of the natural lignan podophyllotoxin, and contains three acetal linkages. Can you identify them ... [Pg.233]

Etoposide and teniposide are synthetic derivatives of the extract of the American mandragora plant (May Apple). The mechanism of their action has not been completely explained however, they act on the enzyme topoisomerase II, which disturbs the twisting of DNA. In addition, they inhibit DNA and RNA synthesis, as well as transport of nucleotides to cells. Cytotoxic action on normal cells is observed only in very high doses. These drugs exhibit significant activity in lymphomas, leukemia, Kaposi s sarcomas, and in testicular cancer. [Pg.406]

Etoposide is used for germinogenic tumors, ovarian, stomach, and lung cancer, Hodgkin s disease, and non-Hodgkin s lymphoma for both monotherapy and in combination therapy. Synonyms of this drug are vepesid and others. [Pg.407]

Short term treatment with TPA sensitized human 2008 ovarian carcinoma cells to cis-platin. This sensitization disappeared completely by seven hours after treatment, indicating that not inhibition, but activation of PKC sensitizes 2008 cells to the antiproliferative activity of cis-platin (Isonishi et al., 1990). Pretreatment of HeLa cells with TPA or PdBu caused a 9-fold increase in cellular sensitivity to cis-platin and 2.5-fold to melphalan, but had now effect on the antiproliferative activity of bleomycin, adriamycin, vincristine, or mitomycin C. The sensitization of HeLa cells by TPA was associated with a 6-fold stimulation of PKC activation and a concentration- and time-dependent increase in cellular platinum content. (Basu et al. 1990). PKC activity was found to be decreased significantly in cis-platin-resistant human small cell lung H69/CP cancer cells compared to the drug-sensitive variant. A similar reduction in PKC activity was noted in ovarian carcinoma 2008 cells that were resistant to cis-platin. A modest decrease in PKC activity was also observed in etoposide-resistant H69 cells but not in taxol-resistant H69 cells or bleomycin-resistant human head and neck carcinoma A-253 cells (Basu et al., 1996), indicating that reduced PKC activity leads to decreased sensitivity in this system. [Pg.57]

Turrisi AT 3rd, Kim K, Blum R, et al. Twice-daily compared with once-daily thoracic radiotherapy in limited small-cell lung cancer treated concurrently with cisplatin and etoposide. N Engl J Med 1999 340(4) 265-271. [Pg.21]

The earliest combination chemotherapy and radiation trials in nonsmall-cell lung cancer included cisplatin and 5-fluorouracil and concurrent radiation therapy and found survival results comparable to those for sequential chemotherapy and radiation or to daily cisplatin and radiation therapy without surgery (119,121). Phase II studies of stage Ilia and Illb nonsmall-cell lung cancer patients treated with the combination of cisplatin with etoposide and 5 -fluorouracil and either single daily radiation fractionation or twice daily radiation fractionation prior to surgery produced similar clinical results (119,121). Complete surgical resection was accomplished in 70% of the patients, the median survival was 22 mo and the 2-yr survival rate was 45%. [Pg.54]

Hainsworth JD, Gray JR, Stroup SL, Kalman LA, Patten JE, Hopkins LG, Thomas M, Greco FA. Paclitaxel, carboplatin, and extended-schedule etoposide in the treatment of small-cell lung cancer comparison of sequential phase II trials using different dose-intensities. J Clin Oncol 1997 15(12) 3464—3470. [Pg.88]

Bremnes RM, Sundstrom S, Aasebo U, Vilsvik J. Paclitaxel in combination with cisplatin, etoposide and thoracic radiotherapy for limited stage small cell lung cancer (SCLC) a phase II study (abstract 1826). ProAmSoc Clin Oncol 1998 17 475a. [Pg.88]

Perez-Soler R, Glisson BS, Lee JS, et al. Treatment of patients with small-cell lung cancer refractory to etoposide and cisplatin with the topoisomerase I poison topotecan. J Clin Oncol 1996 14(10) 2785-2790. [Pg.103]

CyEP, cyclophosphamide/etoposide/cisplatin EP, etoposide/cisplatin NCI, National Cancer Institute PIM, cisplatin/ifosfarnide/mitomycin VdP, vindesine/ cisplatin preop., preoperatively postop., postoperatively ChT, chemotherapy NS, not significant. [Pg.183]


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See also in sourсe #XX -- [ Pg.582 ]




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