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Cancer 5-fluorouracil

Advantage is taken of the properties of antimctabolitcs in chemotherapy. In cancer chemotherapy, several antimetabolites are used. These include methotrexate, 6-mercaptopunne, 6-thioguanine, 5-fluorouracil, and cystine arabinoside. In the chemotherapy of metastatic breast cancer, 5-fluorouracil and methotrexate, in combination with cyclophosphamide, have been used. Antimetabolites, sometimes along with corticosteroids, are used in the therapy of various autoimmune diseases, such as thrombocytenic purpura, thyroiditis, Goodpasture s syndrome, among others. [Pg.135]

Apart from its topical use in curing skin cancers, 5-fluorouracil (usually as the ribotide, 5FUdR) is given intravenously to increase the postoperative survival rate in cancer of the colon and rectum (Li and Ross, 1976) and in adenocarcinoma of the breast or colon, and in metastases of the liver (once thought to be inevitably fatal). However, it has yet to be shown that systemic use of this drug can prolong the survival rate beyond 5 years. [Pg.111]

Other routes of administration can be employed in certain situations. Methotrexate and cytarabine are given intrathecally or intraventricularly to prevent relapses in the meninges in acute lymphocytic leukemia and to treat carcinomatous meningitis. Thiotepa and bleomycin have been administered by intravesical instillation to treat early bladder cancers. Fluorouracil can be applied topically for certain skin cancers. [Pg.634]

Fluorouracil (5-FU) is a fluoropyrimi-dine analogue that was developed more than 50 years ago and continues to be widely used in the treatment of cancer. Fluorouracil often forms the backbone of combination chemotherapy regimens and is used in the management of colorectal cancer and cancers of the breast and respiratory and digestive tracts. In colorectal cancer, higher response rates and better tolerability are seen from infusions than bolus regimens and with the addition of leucovorin (folinic acid) [70 ]. Fluorouracil is also used topically to treat basal cell carcinoma. [Pg.737]

C4H4N2O2. Colourless crystalline powder, turning brown at 280 C and melting at 338 C (decomp.). Uracil is a constituent of ribose nucleic acid. Used as a diuretic and derivatives have pharmaceutical importance. 5-Fluorouracil is used in cancer treatment. [Pg.412]

Fluorouracil is one component of a mixture of three drugs used in breast cancer chemotherapy What is its stmcture" ... [Pg.1189]

Fluorinated Heterocyclic Compounds. HeterocycHc compounds containing the CF group are prepared by methods similar to those used in the fluorination of aHphatic compounds. The direct action of fluorine on uracil yields the cancer chemotherapy agent, 5-fluorouracil [51-21-8] as one special example of a selective fluorination on a commercial scale (25). [Pg.269]

Fluoropyrknidine derivatives are of tremendous importance in cancer chemotherapy, eg, 5-fluorouracil [51-21-8] (5-FU). The original 5-fluorouracil process featured a multistep low yield route based on ethyl fluoroacetate (451). Direct fluorination (fluorine) of uracil [66-22-8] gives high yields of 5-FU (452—455). This process has now been commercialized. [Pg.339]

Interest contmues in prodrugs of 5-fluorouracil (5-FU) Doxifluridine (8) was recently mtroduced and appears to be more potent and less toxic than 5 FU [10 Flutamide (9) and nilutamide (/O) are both available for the treatment of prostatic cancer [//, 12]... [Pg.1120]

Therapeutic Function Cancer chemotherapy Chemical Name 5-fluoro-2,4(1 H,3H)-pyrimidinedione Common Name 5-fluorouracil Structural Formula h... [Pg.676]

Capecitabine is used for the treatment of colorectal and breast cancers. It is contraindicated in patients with known hypersensitivity to capecitabine or any of its components or to 5-fluorouracil and in patients with known dihydropyrimidine dehydrogenase (DPD) deficiency. The use of capecitabine is restricted in patients with severe renal impairment. The drag can induce diarrhea, sometimes severe. Other side effects include anemia, hand-foot syndrome, hyperbilirubinemia, nausea, stomatitis, pyrexia, edema, constipation, dyspnea, neutropenia, back pain, and headache. Cardiotoxicity has been observed with capecitabine. A clinically important drag interaction between capecitabine and warfarin has been demonstrated. Care should be exercised when the drag is co-administered with CYP2X9 substrates. [Pg.150]

In vitro nifedipine inhibits proliferation of colon cancer cells with a DNA mismatch repair defect that are resistant to 5-fluorouracil. Whether this also... [Pg.299]

Note that application in the particular indications is usually restricted either to patients expressing the target (e.g. trastuzumab, cetuximab, lapatinib, imatinib) and/or after failure of prior therapies (e.g. cetuximab, erlotinib, lapatinib, sutinib, dasatinib). Furthermore, for cancer treatment most tyrosine kinase inhibitors are applied in combination with conventional chemotherapeutic drugs, such as fluorouracil, taxanes, platin-based regimens, anthracylines and irinotecan or radiotherapy. [Pg.1255]

Hurwitz H, Fehrenbacher L, Novotny W et al (2004) Bevacizumab plus irinotecan, fluorouracil, and leucovor-in for metastatic colorectal cancer. N Engl J Med 350 2335-2342... [Pg.1272]

Cytotoxic drugs that have been used alone and in combination as adjuvant therapy in breast cancer include doxorubicin, epirubicin, cyclophosphamide, methotrexate, fluorouracil,... [Pg.1310]

Adjuvant therapy consisting of 5-fluorouracil-based chemotherapy in combination with radiation therapy should be offered to patients with stage II or III cancer of the rectum. [Pg.1341]

Fluorouracil-based chemotherapy is the standard of care for the adjuvant treatment of colorectal cancer either as a single agent or, more commonly, in combination with other agents. 5-Fluorouracil (5-FU) alone results in a small improvement in survival that can vary based on the method of 5-FU administration. Studies suggest that protracted or continuous intravenous (IV) 5-FU infusion treatment schedules are more effective than bolus therapy.20... [Pg.1346]

Goldberg RM, Sargent DJ, Morton RF, et al. A randomized, controlled trial of fluorouracil plus leucovorin, irinotecan, and oxaliplatin combinations in patients with previously untreated metastatic colorectal cancer. J Clin Oncol 2004 22 23-30. [Pg.1355]

Since many essential nutrients (e.g., monosaccharides, amino acids, and vitamins) are water-soluble, they have low oil/water partition coefficients, which would suggest poor absorption from the GIT. However, to ensure adequate uptake of these materials from food, the intestine has developed specialized absorption mechanisms that depend on membrane participation and require the compound to have a specific chemical structure. Since these processes are discussed in Chapter 4, we will not dwell on them here. This carrier transport mechanism is illustrated in Fig. 9C. Absorption by a specialized carrier mechanism (from the rat intestine) has been shown to exist for several agents used in cancer chemotherapy (5-fluorouracil and 5-bromouracil) [37,38], which may be considered false nutrients in that their chemical structures are very similar to essential nutrients for which the intestine has a specialized transport mechanism. It would be instructive to examine some studies concerned with riboflavin and ascorbic acid absorption in humans, as these illustrate how one may treat urine data to explore the mechanism of absorption. If a compound is... [Pg.48]

Saltz LB, Cox JV, Blanke C et al. Irino-tecan plus fluorouracil and leucovorin for metastatic colorectal cancer. Irinotecan Study Group. N Engl J Med 2000 343 905-914. [Pg.304]

Diasio RB, Johnson MR. The role of pharmacogenetics and pharmacoge-nomics in cancer chemotherapy with 5-fluorouracil. Pharmacology 2000 61 199-203. [Pg.305]

Harris BE, Carpenter JT, Diasio RB. Severe 5-fluorouracil toxicity secondary to dihydropyrimidine dehydrogenase deficiency. A potentially more common phar-macogenetic syndrome. Cancer 1991 68 499-501. [Pg.305]

Lu Z, Zhang R, Diasio RB. Dihydropyrimidine dehydrogenase activity in human peripheral blood mononuclear cells and liver population characteristics, newly identified deficient patients, and clinical implication in 5-fluorouracil chemotherapy. Cancer Res 1993 53 5433-5438. [Pg.305]

Milano G, Etienne MC, Pierrefite V et al. Dihydropyrimidine dehydrogenase deficiency and fluorouracil-related toxicity. Br J Cancer 1999 79 627-630. [Pg.305]

Johnson MR, Hageboutros A, Wang K et al. life-threatening toxicity in a dihydropyrimidine dehydrogenase-deficient patient after treatment with topical 5-fluorouracil. Clin Cancer Res 1999 5 2006-2011. [Pg.305]

Identification of novel mutations in the dihydropyrimidine dehydrogenase gene in a Japanese patient with 5-fluorouracil toxicity. Clin Cancer Res 1998 4 2999-3004. [Pg.305]


See other pages where Cancer 5-fluorouracil is mentioned: [Pg.237]    [Pg.151]    [Pg.40]    [Pg.2397]    [Pg.2399]    [Pg.2402]    [Pg.280]    [Pg.581]    [Pg.132]    [Pg.84]    [Pg.243]    [Pg.1283]    [Pg.1319]    [Pg.1319]    [Pg.1337]    [Pg.1341]    [Pg.1348]    [Pg.1392]    [Pg.557]    [Pg.283]    [Pg.289]    [Pg.300]    [Pg.304]    [Pg.305]   
See also in sourсe #XX -- [ Pg.235 , Pg.236 , Pg.237 , Pg.238 , Pg.239 , Pg.240 , Pg.241 , Pg.242 , Pg.243 , Pg.244 , Pg.245 , Pg.246 , Pg.247 , Pg.248 , Pg.249 , Pg.250 ]

See also in sourсe #XX -- [ Pg.55 , Pg.111 ]




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5-fluorouracil

5-fluorouracil breast cancer

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5-fluorouracil ovarian cancer

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Fluorouracil in breast cancer

Fluorouracil in colorectal cancer

Pancreatic cancer 5-fluorouracil

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