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Aventis pharmaceutical nov 27 2002 docetaxel taxotere for use in combination with prednisone as a treatment for patients with androgen independent hormone refractory ; metastatic prostate cancer aventis pharmaceutical may 19 2004 docetaxel taxotere for use in combination with doxorubicin and cyclophosphamide for the adjuvant treatment of patients with operable nodepositive breast cancer aventis pharmaceutical aug 18 2004 doxorubicin adriamycin pfs for use in combination with cyclophosphamide as a component of adjuvant therapy in patients with evidence of axillary node tumor involvement following resection of primary breast cancer pharmacia may 08 2003 doxorubicin adriamycin, rubex pharmacia & upjohn company aug 07 1974 doxorubicin adriamycin pfs injectionintravenous injection antibiotic, antitumor agent.
Docetaxel is a white to almost-white powder with an empirical formula of C43H53NO14 3H2O, and a molecular weight of 861.9. It is highly lipophilic and practically insoluble in water. TAXOTERE docetaxel ; for Injection Concentrate is a clear yellow to brownish-yellow viscous solution. TAXOTERE is sterile, non-pyrogenic, and is available in single-dose vials containing 20 mg 0.5 mL ; or 80 mg 2.0 mL ; docetaxel anhydrous ; . Each mL contains 40 mg docetaxel anhydrous ; and 1040 mg polysorbate 80. TAXOTERE for Injection Concentrate requires dilution prior to use. A sterile, non-pyrogenic, single-dose diluent is supplied for that purpose. The diluent for TAXOTERE contains 13% ethanol in Water for Injection, and is supplied in 1.5 mL to be used with 20 mg TAXOTERE for Injection Concentrate ; and 6.0 mL to be used with 80 mg TAXOTERE for Injection Concentrate ; vials. CLINICAL PHARMACOLOGY Docetaxel is an antineoplastic agent that acts by disrupting the microtubular network in cells that is essential for mitotic and interphase cellular functions. Docetaxel binds to free tubulin and promotes the assembly of tubulin into stable microtubules while simultaneously inhibiting their disassembly. This leads to the production of microtubule bundles without normal function and to the stabilization of microtubules, which results in the inhibition of mitosis in cells. Docetaxel's binding to microtubules does not alter the number of protofilaments in the bound microtubules, a feature which differs from most spindle poisons currently in clinical use. HUMAN PHARMACOKINETICS The pharmacokinetics of docetaxel have been evaluated in cancer patients after administration of 20-115 mg m2 in phase I studies. The area under the curve AUC ; was dose proportional following doses of 70-115 mg m2 with infusion times of 1 to hours. Docetaxel's pharmacokinetic profile is consistent with a three-compartment pharmacokinetic model, with half-lives for the and phases of 4 min, 36 min, and 11.1 hr, respectively. The initial rapid decline represents distribution to the peripheral compartments and the late terminal ; phase is due, in part, to a relatively slow efflux of docetaxel from the peripheral compartment. Mean values for total body clearance and steady state volume of distribution were 21 L h and 113 L, respectively. Mean total body clearance for Japanese patients dosed at the range of 10-90 mg m2 was similar to that of European American populations dosed at 100 mg m2, suggesting no significant difference in the elimination of docetaxel in the two populations. A study of 14C-docetaxel was conducted in three cancer patients. Docetaxel was eliminated in both the urine and feces following oxidative metabolism of the tert-butyl ester group, but fecal excretion was the main elimination route. Within 7 days, urinary and fecal excretion accounted for approximately 6.
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The calf muscles are involved alone or taxotrre together with other muscle taxoteree taxotere groups in 69 % and taaxotere 31 % of cases, respectively.
Blockers not recommended as initial therapy If used may consider additional antihypertensive agent ; . Monitor for Hypokalemia: seldom if using low dose thiazide K + sparing diuretics rarely needed ; Hypokalemiaseldom if using low dose thiazide K + sparing diuretics rarely needed ; If Scr 150 umol l, use a loop diuretic rather than thiazide if needed to reduce edema. If CrCl 30ml minthiazide diuretic less effective ; CALM, COOPERATE May consider ACEI + ARB combination Low dose thiazides have evidence for CV outcome benefits in diabetes & minimal effect on glucose. ALLHAT included 15, 000 patients2, 13 with diabetes, the largest antihypertensive trial ever in this population. Vasospastic anginalong acting CCB avoid -blocker ; . AVOID short-acting nifedipine. If using CCB, only LA-DHP if also HF.
106 cells ml in M199 supplemented with 1% serum. HUVECs 105 ; were seeded into 8.0- m-pore transwell inserts Costar ; precoated with 10 g ml fibronectin. Inserts containing HUVECs were placed into a 24-well plate Costar ; containing M199 supplemented with 1% serum and incubated for 1 h at 37C. HUVEC migration was stimulated by addition of the chemotactic factors, TP 100 ng ml ; or VEGF 10 ng ml ; , the lower well of the Boyden chamber. The effect of Taxotere or Taxol on endothelial migration was observed by inclusion of either agent in the lower chamber. After 5 h, HUVECs were fluorescently stained with 10 M cell tracker green Molecular Probes, Eugene, OR ; , and the upper surface of the insert was swabbed to remove nonmigrated cells. Inserts were washed three times with PBS, fixed in 3.7% formaldehyde, and mounted on microscope slides. HUVEC migration was quantitated by counting the number of cells in three random fields 100 total magnification ; per insert. Data are expressed as cells field mean SE ; as a percentage of TP- or VEGFstimulated migration in the absence of Taxotere or Taxol. Assay of in Vitro Tubule Formation. The spontaneous formation of capillary-like structures by RFPECs on a basement membrane matrix preparation, Matrigel Becton Dickinson, Bedford, MA ; , was used to assess angiogenic potential. Twelve-well plates Costar ; were coated with Matrigel 10 mg ml ; according to the manufacturer's instructions. RFPECs 1.5 105 cells well ; were seeded on Matrigel-coated plates and incubated at 37C for 60 min. The indicated concentrations of Taxotere or Taxol were added, and the cultures were incubated at 37C for 24 h. In vitro endothelial tubule formation was observed and photographed after 24 h as described above. The degree of tubule formation was determined by counting the number of tubes contained in two random fields from each well. Data are expressed as a percentage of the number of tubes in untreated control wells mean SE ; . Endothelial Cell Proliferation Assay. RFPECs and HUVECs were seeded into gelatin-coated 24-well plates Costar ; at 2 104 cells well and allowed to attach for 24 h. Cells were washed twice with PBS, and RFPECs were treated with media containing 10 12, 10 or 10 8 Taxotere. HUVECs were treated with media containing 10 14, 10 or 10 8 Taxotere. Control RFPEC or HUVEC cultures received media alone. Cells were harvested with trypsin EDTA every 24 h for 3 days, and cell number was determined in a dual threshold cell counter Coulter Electronics ; . Data are expressed as cells well mean SD ; . Immunofluorescence Staining of Endothelial Microtubules. HUVECs or RFPECs were seeded on fibronectincoated glass coverslips in 12-well plates Costar ; and grown to confluence. HUVECs were treated for 20 h with media containing Taxotere at 10 14, 10 or 10 8 RFPECs were treated with media containing Taxotere at 10 12, 10 or 10 8 Control HUVEC and RFPEC cultures received media alone. After 20 h, cells were washed twice with PBS and rendered permeable by treatment with 0.5% Triton X-100 in PEM buffer [100 mM PIPES, 2 mM EGTA, and 2 mM MgCl2 pH 6.8 ; ] for 4 min. Cells were washed twice with PEM buffer, fixed in 3% formaldehyde in PEM buffer, washed four times with PEM buffer, and blocked with 5% BSA in PBS and tazorac.
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5. Senderowicz, A. M., Headlee, D., Stinson, S., Lush, R. M., Figg, W. D., Pluda, J., and Sausville, E. A. Phase I trial of a novel cyclic-dependent kinase inhibitor flavopiridol in patients with refractory neoplasms. J. Clin. Oncol., 16: 2986 2999, Kaur, G., Stetler-Stevenson, M., Sebers, S., Worland, P., Sedlacek, H., Myers, C., Czech, J., Naik, R., and Sausville, E. Growth inhibition with reversible cell cycle arrest of carcinoma cells by flavone L86-8275. J. Natl. Cancer Inst. Bethesda ; , 84: 1736 1740, Losiewicz, M. D., Carlson, B. A., Kaur, G., Sausville, E. A., and Worland, P. J. Potent inhibition of cdc2 kinase activity by the flavonoid L86-8275. Biochem. Biophys. Res. Commun., 201: 589 595, Carlson, B. A., Dubay, M. M., Sausville, E. A., Brizuela, L., and Worland, P. J. Flavopiridol induces G1 arrest with inhibition of cyclin-dependent kinase CDK2 and CDK4 in human breast carcinoma cells. Cancer Res., 56: 29732978, 1996. Schwartz, G. K., Farsi, K., Maslak, P., Kelsen, D. P., and Spriggs, D. Potentiation of apoptosis by flavopiridol in mitomycin-C-treated gastric and breast cancer cells. Clin. Cancer Res., 3: 14671472, 1997. Motwani, M., Delohery, T. M., and Schwartz, G. K. Sequential dependent enhancement of caspase activation and apoptosis by flavopiridol on paclitaxel-treated human gastric and breast cancer cells. Clin. Cancer Res., 5: 1876 1883, Motwani, M., Jung, C. P., Gonen, M., Sirotnak, F., and Schwartz, G. K. Augmentation of apoptosis and tumor regressions by flavopiridol in the presence of CPT-11 in HCT-116 colon cancer monolayers and xenografts. Clin. Cancer Res., 7: 4209 4219, Bible, K. C., and Kaufmann, S. H. Cytotoxic synergy between flavopiridol NSC 649890, L86-8275 ; and various antineoplastic agents: the importance of sequence of administration. Cancer Res., 57: 33753380, 1997. Schiff, P. B., Fant, J., and Horwitz, S. B. Promotion of microtubule assembly in vitro by Taxol. Nature Lond. ; , 277: 665 667, Shen, S., Huang, Jee, S., and Kuo, M. Taxol-induced p34cdc2 kinase activation and apoptosis inhibited by in human breast MCF-7 carcinoma cells. Cell Growth Differ., 9: 2329, 1998. Riou, J. F., Naudin, A., and Lavelle, F. Effects of Taxotere on murine and human tumor cell lines. Biochem. Biophys. Res. Commun., 187: 164 170, Haldar, S., Basu, A., and Croce, C. M. Bcl2 is the guardian of microtubule integrity. Cancer Res., 57: 229 233, Sirotnak, F. M., DeGraw, J. I., Colwell, W. T., and Piper, J. R. A new analogue of 10-deazaaminopterin with markedly enhanced curative effects against human tumor xenografts in mice. Cancer Chemother. Pharmacol., 42: 313318, 1998. Panvichian, R., Orth, K., Day, M., Day, K. C., Pilat, M. J., and Pienta, K. J. Docetaxel-associated multimininucleation is permitted by the inhibition of caspase activation: a potential early step in drug resistance. Cancer Res., 58: 4667 4672, Murray, A. W., Solomon, M. J., and Kirchner, M. W. The role of cyclin synthesis and degradation in the control of maturation promoting factor activity. Nature Lond. ; , 339: 280 286, Lorca, T. C., Labbe, J. C., Devault, A., Fesquet, D., Capony, J. P., Cavadore, J. C., Le Bouffant, F., and Doree, M. Dephosphorylation of cdc-2 on Thr161 is required for cdc-2 kinase inactivation and normal anaphase. EMBO J., 11: 23812390, 1992. Poon, R. Y. C., Chau, M. S., Yamashita, K., and Hunter, T. The role of Cdc2 feedback loop control in the DNA damage checkpoint in mammalian cells. Cancer Res., 57: 5168 5178, Weinberg, R. A. The retinoblastoma protein and cell cycle control. Cell, 81: 323330, 1995.
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CHD in 10 years ; will require concomitant application of drug therapy and TLC from the onset of treatment. For patients at the highest risk for coronary events, the LDL-C threshold for initiation of therapy is 130 mg dL after a 3-month trial of TLC ; . Drug therapy is optional for patients with LDL-C between 100 mg and 129 mg dL, and prescribers are encouraged to use professional clinical judgment in determining the most appropriate approach to risk reduction in these patients. Data from the recent Heart Protection Study have led many experts to recommend early initiation of statins in patients with CHD and CHD risk equivalents, even when the baseline LDL-C is 130 mg dL. For patients with moderate risk without CHD or CHD risk equivalents, but with 2 major risk factors and a 10-year risk of 10% to 20%, the treatment threshold is 130 mg dL. For patients at moderate risk, with a 10-year risk 10%, the LDL-C threshold is 160 mg dL. For patients without CHD and with 0 to 1 major risk factor, drug treatment should be considered if LDL-C cholesterol is 190 mg dL after 3 months of TLC, with a goal of 160 mg dL. In all cases of drug therapy, TLC should continue to be maintained and reinforced. Current Lipid-Modifying Drugs There are currently 3 classes of lipid-modifying drugs recommended by ATP III for the reduction of LDL-C: bile acid sequestrants; nicotinic acids; and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins. A fourth class, the fibric acid derivatives fibrates ; , are not recommended because they have minimal direct effect on lowering LDL-C. However, ATP III does recommend fibrates for patients with very high triglycerides to reduce the risk of acute pancreatitis and for patients with certain other types of dyslipidemia, and fibrates are, therefore, discussed below. Statins, currently the most widely used lipid-modifying agent, decrease LDL-C by 18% to 55% in a dose-dependent manner. These agents exert their effect by inhibiting cholesterol synthesis and promoting LDL-C uptake from the circulation via activation of liver LDL-C receptors. Currently, there are 5 statins on the market. These products are primarily differentiated by the degree of LDL-C lowering elicited by each dose. Several large clinical outcome trials have demonstrated unequivocally that statin use reduces the incidence of CHD events, including myocardial infarction, coronary death, stroke, and total mortality.2-5 These agents are also highly cost effective, especially in high-risk patients. ATP III recommends statins as first-line agents when LDL-lowering drugs are indicated to achieve LDL treatment goals. Bile acid sequestrants are another commonly used agent that can be used as monotherapy or as add-on therapy to statins. Monotherapy with sequestrants can lead to attainment of treatment goal when moderate reductions in LDL-C are required. However, when more aggressive LDL-C reduction is required, sequestrants must be used in combination with statins. Although generally safe, adherence to a therapeutic regimen and telithromycin.
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Rubber catheter that has two side holes facilitate oral intubation fig. 1 ; . Because pliable, narrow-gauge catheter, it seems and a slightly curved tip to it is extremely soft and to be tolerated by patients.
| Taxotere doseWhat is TAXOTERE? TAXOTERE is a concentrate and solvent to be made up into a solution for infusion drip into a vein ; . It contains the active substance docetaxel. What is TAXOTERE used for? TAXOTERE is an anticancer medicine. It is used in: breast cancer. It can be used on its own after other treatments have failed. It can also be used with other anticancer medicines doxorubicin, cyclophosphamide, trastuzumab or capecitabine ; in patients who have not yet received any treatment for their cancer or after other treatments have failed, depending on the type and stage of the breast cancer being treated. non-small cell lung cancer. It can be used on its own after other treatments have failed. It can also be used with cisplatin another anticancer medicine ; in patients who have not yet received any treatment for their cancer. prostate cancer, when the cancer does not respond to hormonal treatment. It is used with prednisone or prednisolone anti-inflammatory medicines ; . gastric adenocarcinoma a type of stomach cancer ; in patients who have not yet received any treatment for their cancer. It is used with cisplatin and 5-fluorouracil other anticancer medicines ; . head and neck cancer in patients whose cancer is advanced. It is used with cisplatin and 5-fluorouracil. See the Summary of Product Characteristics, also part of the EPAR, for full details. The medicine can only be obtained with a prescription. How is TAXOTERE used? TAXOTERE should be used in specialised chemotherapy wards and it should only be given under the supervision of a doctor who is qualified in the use of anticancer chemotherapy. TAXOTERE is only used when the neutrophil count a type of white blood cell ; is at least 1, 500 cells mm3. Treatment with dexamethasone an anti-inflammatory medicine ; should be given to the patient on the day before treatment for prostate cancer or the day before and the two days after treatment for other types of cancer. TAXOTERE is given as a one-hour infusion every three weeks. The dose, length of treatment, and its use with other medicines depend on the type of cancer being treated. For more information, see the Summary of Product Characteristics and temodar.
III patients, 42% developed regional wall motion abnormalities 7 of the 8 of which were nferoapical ; and 32% developed global abnormalities. All patients with exercise-induced regional wall motion abnormalities had an abnormal ejection fraction response as did all but one of the patients who developed a global abnor mality. In the presence of valvular heart disease, exercise-induced regional wall motion abnormalities are not reliable indicators of coronary artery disease.
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Besides skin cancer, prostate cancer is the most common type of cancer diagnosed in men. The American Cancer Society estimates that in 2007, there will be nearly 219, 000 new cases of prostate cancer diagnosed in American men. Most patients are initially treated with surgery, radiation, or hormone suppression therapy. Eventually, almost all prostate cancers will become resistant to hormone therapy hormonerefractory ; if treated long enough. Until recently, treatment of HRPC with chemotherapy improved symptoms but did not increase survival. In 2004, however, Taxotere docetaxel ; became the first medication approved for the treatment of advanced HRPC that showed a survival benefit. Today, Taxotere in combination with prednisone is still the treatment of choice in these patients. Satraplatin, in combination with prednisone, has been shown to prolong progression-free survival the length of time between a patient starting treatment in a clinical trial until tumor growth or death ; in patients with HRPC who have failed Taxotere or other chemotherapies. The median time to progression in the phase III registration trial was 11.1 weeks in the satraplatin group, versus 9.7 weeks in the placebo group. The overall survival data for this study are expected by the end of the year. GPC Biotech and Spectrum Pharmaceuticals completed the submission of an NDA for satraplatin on February 15, 2007. The FDA granted a priority review status to the NDA and a response is expected by August 15, 2007. Satraplatin is currently available to eligible patients through an expanded access program and tenex.
| Anderson cancer center, houston, texas - page 1 of 4 - abstract: docetaxel taxotere ; -based regimens can be included among the most effective treatment options for the management of patients with advanced, androgen-independent prostate cancer.
Palliative surgery, often considered noncurative, is done to alleviate symptoms of tumors or complications that can arise from tumors or medical or surgical treatment. The goal of palliative care, and by definition palliative surgery, is to improve quality of life for the patient. The first surgical entity to officially recognize palliative surgery was the American College of Surgeons in its Statement and teniposide.
Were 0.88 0.10, 0.91 and 0.98 0.11. The vari ability of these ratios was lower than the variability of the measurement of the distribution volumes themselves: 7.9 6.3%, 7.8 and 5.4 61% for the frontal, cingulate and temporal to occipital ratios, respectively. However, because of the large variation in variability, this improvement did not reach statistical significance p 0.09 ; . The intraclass correlation coefficients of the regional ratios were lower than of VT', with p values of 0.66, 0.65 and 0.74 for the frontal, cingulate, and temporal to occipital ratios, respectively.
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JR. Bianchetti C, Morselli PL. pharmacodynamic effects of betaxolol and tenofovir.
Dosage taxotere should be administered strictly intravenously and taxotere
Aging- and photoaging-dependent changes of enzymic and nonenzymic antioxidants in the epidermis and dermis of human skin in vivo and tequin.
Neither the sparrows from which the viruses were isolated, nor the taxotere ducks that were experimentally taotere infected with these viruses, taxotere showed any symptoms.
Fig. 2 A, clonogenic survival of clone 6C Dc or cells with or without chemodrugs. 6C Dc or cells were cultured in 60-mm culture dishes 1, 000 cells per dish ; and exposed to COL-3 10 mol L ; or Taxotere 30 mol L; TXTR ; for 24 hours. Data represent mean SE from three assays. * , P 0.05, t test, 6C Dc versus 6 Dc. B, determination of apoptotic activity in 6C Dc Dc. Apoptotic activities in 6C Dc cells 1 104 cells per well; 48-well plates ; treated with COL-3 10 mol L ; or Taxotere 30 nmol L ; for 24 hours were assayed. Data shown are mean SE n 3 ; 0.05, t test, 6C Dc versus 6C Dc for each treatment. * , P 0.05, t test, 6C Dc versus 6C Dc for each treatment and terfenadine.
Case Example: Combined Psychotherapy and Medication Treatment as a Prelude to Psychoanalysis. Dr. R, a 33-year-old mathematician newly appointed to a university faculty, was referred to a medical analyst by a social worker he had consulted for treatment of a lifelong depression. He had been treated with a number of antidepressant medication regimens prescribed by internists and general psychiatrists over the previous 10 years, with widely varying success. He felt subject to uncontrollable changes in his mood that sometimes left him literally unable to function. Medications that seemed to work for a few months could suddenly have no effect, and he descended into a deep depression from which it took months to emerge. His superior intelligence and capacity for bursts of sustained effort had made it possible for him to finish his doctorate, and he had been married to a devoted and loving wife for 6 years. They were reluctant to have children because of his precarious emotional states. He had never engaged in intensive psychotherapy but had seen a number of social workers for brief supportive therapy. Dr. R was the youngest of five children born to parents who accumulated considerable wealth through the father's ruthless business acumen. As a child Dr. R had been the object of much sadistic emotional and physical abuse not only at his father's hands, but also by his older brothers who were unsupervised by their alcoholic mother. He does not remember sexual improprieties, but is troubled by a recurrent dream of being penetrated from behind by an older man who means to trick him and ridicule him. Among his siblings only Dr. R was able to leave the family emotionally to a substantial extent. He had essentially ended contact with his father and had only brief, painful contacts with mother who was usually inebriated and always highly self-absorbed. Family visits left him in a depressed, overwhelmed state. Over the course of several years of weekly and twice-weekly sessions, Dr R developed a strong alliance with his analyst who helped him begin tolerating more awareness of the impact of his childhood and the relevance of childhood patterns to current relationships. At one point the analyst raised discussion of converting the treatment to analysis, but Dr. R declined. The analyst felt Dr. R might be instinctively protecting himself from the awareness of negative transference, which he couldn't afford. He needed to maintain a positive transference to the good maternal figure he had found in the analyst but also began bringing in dreams and attempting to make connections between childhood events and reactions in his current life. After several more mood cycles that seemed unresponsive to the effects of psychotropic medications, Dr. R and the analyst came to understand his bursts of high energy as the equivalent of a manic phase of manic-depressive illness, a condition likely affecting other family members. With the addition of valproate and olanzapine to an SSRI and a stimulant, Dr. R had a brief period of stability that was interrupted by the development of an inability to finish a paper that threatened his chances for promotion. This inhibition was clearly related to earlier conflicts about success and competition. At this point Dr. R understood fully the limits of medication treatment and the risk of losing his job due to unresolved psychological conflicts; he asked about entering psychoanalysis. It was agreed that the long history of supportive treatment with the prescribing analyst would make it difficult to switch to an analytic format. He and tazorac.
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Tients: An analysis of National Cancer Institute of Canada Clinical Trials Group and Intergroup BR.10. J Clin Oncol 2006; 24: 366s. Sandler A, Gray R, Perry MC et al. Paclitaxel carboplatin alone or with bevacizumab for non-small cell lung cancer. N Engl J Med 2006; 355: 2542 Fossella F, Pereira JR, von Pawel J et al. Randomized, multinational, phase III study of docetaxel plus platinum combinations versus vinorelbine plus cisplatin for advanced non-small-cell lung cancer: the TAX 326 study group. J Clin Oncol 2003; 21: 3016 Kubota K, Watanabe K, Kunitoh H et al. Phase III randomized trial of docetaxel plus cisplatin versus vindesine plus cisplatin in patients with stage IV non-small-cell lung cancer: The Japanese Taxotere Lung Cancer Study Group. J Clin Oncol 2004; 22: 254 Schiller JH, Harrington D, Belani CP et al. Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer. N Engl J Med 2002; 346: 9298. Kato H, Ichinose Y, Ohta M et al. A randomized trial of adjuvant chemotherapy with uracil-tegafur for adenocarcinoma of the lung. N Engl J Med 2004; 350: 17131721. Hamada C, Ohta M, Wada H, et al: Survival benefit of oral UFT for adju and teriparatide.
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