Drugs

, Volume 51, Issue 6, pp 1075–1092 | Cite as

Docetaxel

A Review of its Pharmacodynamic and Pharmacokinetic Properties and Therapeutic Efficacy in the Management of Metastatic Breast Cancer
  • Bret Fulton
  • Caroline M. Spencer
Drug Evaluation

Abstract

Summary

Docetaxel is a member of the taxoid class of antineoplastic agents. Its mechanism of action is primarily related to its ability to enhance microtubule assembly and to stabilise microtubules by preventing their depolymerisation, thus disrupting normal cell division. Docetaxel has significant cytotoxic activity against human breast cancer cell lines and freshly explanted human breast cancer cells in vitro. It has also shown activity in mice against mammary tumours and human mammary tumour xenografts.

Docetaxel has been investigated in the treatment of patients with advanced and/or metastatic breast cancer in European and North American phase II trials using an initial dose of 100 mg/m infused over 1 hour every 3 weeks. As first-line treatment, monotherapy with docetaxel was associated with complete and partial response rates of 5 to 16% and 49 to 53%, respectively, with an overall (complete plus partial) response rate of 54 to 68%. The median overall survival time of patients in one study was ≥71 weeks. Docetaxel monotherapy has shown impressive activity as second-line therapy in patients with metastatic breast cancer who had relapsed while receiving adjuvant therapy or who had progressive disease following previous treatment, with overall response rates of 53 and 58% reported in 2 studies.

A number of issues need to be addressed before the ultimate place of docetaxel in the management of metastatic breast cancer is fully established. The efficacy of docetaxel compared with standard agents and in combination regimens and its effect on quality-of-life aspects require further evaluation. Nevertheless, docetaxel is a promising new agent which has produced impressive clinical results and should be considered an alternative second-line treatment of patients with metastatic breast cancer.

Pharmacodynamic Properties

The cytotoxic activity of docetaxel is believed to primarily result from its ability to enhance microtubule assembly and to stabilise microtubules, preventing their depolymerisation and thus preventing normal cell division. This mechanism is supported by in vitro studies which demonstrate that docetaxel reduces the lag time for the initiation of polymerisation, decreases the minimum concentration of tubulin required for microtubule assembly and induces polymerisation in the near absence of the microtubule assembly cofactor guanosine 5-triphosphate.

In vitro studies in human breast cancer cell lines or in freshly explanted human breast cancer cells show docetaxel has significant cytotoxic activity, which in most instances is greater than that reported for paclitaxel in fresh cell isolates. Docetaxel had in vivo activity against 3 of 4 murine mammary tumours studied and, at the highest tolerated dose, produced complete regression in 100% (30/30) of nude mice with human mammary tumour xenografts. Docetaxel dernonstrated schedule-dependent in vitro synergism against human breast cancer cell lines when combined with edatrexate. Synergism has also been observed in mice with mammary adenocarcinoma receiving docetaxel plus cyclophosphamide.

Acquired resistance to docetaxel occurs via two identified mechanisms; one is associated with the expression of the multidrug resistance phenotype, whereas the other is associated with alterations in tubulin. Cross-resistance between docetaxel and other antitumour agents has been reported in many, but not all, cell lines which express the multidrug resistance phenotype, which suggests that cross-resistance does not automatically occur in cells expressing this gene.

Pharmacokinetic Properties

At doses ≥70 mg/m2, the pharmacokinetic profile of docetaxel fitted a 3-compartment model. The maximum plasma concentration (Cmax) and the area under the plasma concentration-time curve (AUC) were proportional to dose. In 2 studies, Cmax values were 2.41 and 3.67 mg/L and AUC values were 5.93 and 4.59 mg/L · h after doses of 100 mg/m2 administered over 1 hour. The drug is 93 to 94% protein bound.

Docetaxel is primarily metabolised by cytochrome P450 (CYP) enzymes, and 4 largely inactive major metabolites have been identified. The predominant route of elimination is metabolism then faecal excretion via the biliary tract. A population pharmacokinetics study in 547 patients who received docetaxel in phase II trials estimated total body clearance and elimination half-life to be, respectively, 21 L/h · m2 and 11.2 hours. Clearance appears to be reduced in patients with moderate hepatic dysfunction.

The in vitro metabolism of docetaxel is reduced by drugs which are substrates of the CYP3A4 isozyme (erythromycin, ketoconazole, nifedipine, troleandomycin, testosterone, orphenadrine and midazolam). Some in vitro inhibition of docetaxel metabolism was also produced by vinorelbine, vinblastine and doxorubicin; however, other drugs including cisplatin, fluorouracil, cyclophosphamide and etoposide had little effect on the in vitro metabolism of docetaxel. When docetaxel was administered prior to cisplatin as part of sequential therapy, the white blood cell DNA-adduct levels of cisplatin were significantly lower than when cisplatin was administered first.

Therapeutic Efficacy in Metastatic Breast Cancer

In dose-finding studies in patients with various solid tumours, the maximum tolerated dose of docetaxel was 80 to 115 mg/m2 per course of therapy. Based on these results, a dose of 100 mg/m2 infused once every 3 weeks was considered to be optimal for phase II trials in Europe and North America. In Japan, a lower dosage (60 mg/m2/3 weeks) was used.

Four trials have evaluated docetaxel 100 mg/m2 every 3 weeks as first-line therapy in 137 evaluable patients with advanced and/or metastatic breast cancer. Complete response was reported in 5 to 16% of patients and partial response in 49 to 53%. The overall response rate (complete plus partial response) ranged from 54 to 68%. One study reported no difference in response rates between patients who had received prior adjuvant chemotherapy and those who had not. In this study, the median duration of response was ≥44 weeks and the median overall survival time was ≥71, weeks. In 2 studies which used a dosage of 75 mg/m2 every 3 weeks, the overall response rates were 40 and 52%.

Docetaxel 100 mg/m2 /3 weeks has also been evaluated as second-line therapy in patients with histologically and/or cytologically verified advanced and/or metastatic breast cancer who had relapsed while receiving adjuvant therapy or who had progressive disease following previous treatment. In 2 studies which evaluated a total of 69 patients with anthracycline- or anthracenedione-resistant breast cancer, 3 patients experienced a complete response, and the partial response rates were 49 and 53%.

In Japanese trials evaluating docetaxel 60 mg/m every 3 to 4 weeks, complete and partial response rates ranged, respectively, from 4 to 7% and 37 to 50% in 186 patients, most of whom had received prior chemotherapy.

Tolerability

Neutropenia is the primary dose-limiting adverse effect of docetaxel after short term infusion, occurring in >90% of patients receiving docetaxel 100 mg/m2. However, neutropenia is generally rapidly reversible, with only 14.8% of patients requiring hospitalisation and/or treatment with antibiotics. Fluid retention, usually characterised by peripheral oedema, is related to the cumulative dose of docetaxel. However, premedication with corticosteroids delays the onset of this adverse event. Hypersensitivity reactions occur in 31.3% of patients, are usually observed within minutes of administration of docetaxel, and are reversible upon discontinuing the infusion. Premedication decreases the severity of hypersensitivity reactions and discontinuation of therapy is required only rarely. Various types of cutaneous events including mucositis, desquamation and nail changes have been reported in a large proportion of patients (up to 70%). Other reported adverse events include peripheral neuropathy, alopecia, asthenia, nausea and diarrhoea.

Dosage and Administration

The recommended initial intravenous dose of docetaxel is 100 mg/m2 infused over 1 hour every 3 weeks. Pretreatment with corticosteroids is recommended to reduce the incidence of docetaxel-related fluid retention and the severity of hypersensitivity reactions. Dosage reductions are recommended in patients with severe drug-related toxicity and in those with hepatic dysfunction.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Gelmon K. The taxoids: paclitaxel and docetaxel. Lancet 1994 Nov 5; 344: 1267–72PubMedCrossRefGoogle Scholar
  2. 2.
    Kaye SB. Taxoids. Eur J Cancer A 1995; 31A (5): 824–6PubMedCrossRefGoogle Scholar
  3. 3.
    Bissery M-C, Nohynek G, Sanderink G-J, et al. Docetaxel (Taxotere®): a review of preclinical and clinical experience. Part I: preclinical experience. Anticancer Drugs 1995 Jun; 6: 339–68Google Scholar
  4. 4.
    Spencer CM, Faulds D. Paclitaxel: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the treatment of cancer. Drugs 1994 Nov; 48 (5): 794–847PubMedCrossRefGoogle Scholar
  5. 5.
    Ringle I, Horwitz SB. Studies with RP56976 (taxotere): a semisynthetic analogue of taxol. J Natl Cancer Inst 1991 Feb 20; 83: 288–91CrossRefGoogle Scholar
  6. 6.
    Diaz JF, Andreu JM. Assembly of purified GDP-tubulin into microtubules induced by Taxol and Taxotere: reversibility, ligand stoichiometry, and competition. Biochemistry 1993 Mar 23; 32: 2747–55PubMedCrossRefGoogle Scholar
  7. 7.
    Kumar N. Taxol-induced polymerization of purified tubulin. J Biol Chem 1981; 256: 10435–41PubMedGoogle Scholar
  8. 8.
    Andreu JM, Díaz JF, Gil R, et al. Solution structure of Taxotereinduced microtubules to 3-nm resolution. The change in protofilament number is linked to the binding of the taxol side chain. J Biol Chem 1994 Dec 16; 269: 31785–92Google Scholar
  9. 9.
    Fromes Y, Gounon P, Bissery MC, et al. Differential effects of Taxol and Taxotere (RP56976, NSC628503) on Tau and MAP2 containing microtubules [abstract no. 3055]. Proceedings of the American Association Cancer Research 1992; 33: 511Google Scholar
  10. 10.
    Hennequin C, Giocanti N, Favaudon V. S-phase specificity of cell killing by docetaxel (Taxotere) in synchronised HeLa cells. Br J Cancer 1995 Jun; 71: 1194–8PubMedCrossRefGoogle Scholar
  11. 11.
    Vogel M, Hilsenbeck SG, Depenbrock H, et al. Preclinical activity of taxotere (RP 56976, NSC 628503) against freshly explanted clonogenic human tumour cells: comparison with taxol and conventional antineoplastic agents. Eur J Cancer A 1993; 29A (14): 2009–14PubMedCrossRefGoogle Scholar
  12. 12.
    Hanauske A-R, Degen D, Hilsenbeck S-G, et al. Effects of Taxotere and taxol on in vitro colony formation of freshly explanted human tumor cells. Anticancer Drugs 1992 Apr; 3: 121–4PubMedCrossRefGoogle Scholar
  13. 13.
    Hill BT, Whelan RDH, Shellard SA, et al. Differential cytotoxic effects of docetaxel in a range of mammalian tumor cell lines and certain drug resistant sublines in vitro. Invest New Drugs 1994; 12 (3): 169–82PubMedCrossRefGoogle Scholar
  14. 14.
    Riou J-F, Naudin A, Lavelle F. Effects of taxotere on murine and human tumor cell lines. Biochem Biophys Res Commun 1992 Aug 31; 187: 164–70PubMedCrossRefGoogle Scholar
  15. 15.
    Untch M, Untch A, Sevin B-U, et al. Comparison of paclitaxel and docetaxel (Taxotere) in gynecologic and breast cancer cell lines with the ATP-cell viability assay. Anticancer Drugs 1994 Feb; 5: 24–30PubMedCrossRefGoogle Scholar
  16. 16.
    Braakhuis BJM, Hill BT, Dietel M, et al. In vitro antiproliferative activity of docetaxel (Taxotere®), paclitaxel (Taxol) and cisplatin against human tumour and normal bone marrow cells [abstract no. 149-0348]. Anticancer Res 1994 Jan–Feb; 14: 205–8Google Scholar
  17. 17.
    Zoli W, Flamigni A, Frassineti GL, et al. In vitro activity of taxol and taxotere in comparison with doxorubicin and cisplatin on primary cell cultures of human breast cancers. Breast Cancer Res Treat 1995 Apr; 34: 63–9PubMedCrossRefGoogle Scholar
  18. 18.
    Kelland LR, Abel G. Comparative in vitro cytotoxicity of taxol and Taxotere against cisplatin-sensitive and -resistant human ovarian carcinoma cell lines. Cancer Chemother Pharmacol 1992 Sep; 30: 444–50PubMedCrossRefGoogle Scholar
  19. 19.
    Bissery MC, Vrignaud P, Bayssas M, et al. Docetaxel (RP 56976, Taxotere®) efficacy as a single agent or in combination against mammary tumors in mice [abstract no. 1946]. Proceedings of the American Association Cancer Research 1994 Mar; 35: 327Google Scholar
  20. 20.
    Bissery M-C, Guénard D, Guéritte-Voegelein F, et al. Experimental antitumor activity of Taxotere (RP 56976, NSC 628503), a taxol analogue. Cancer Res 1991 Sep 15; 51: 4845–52PubMedGoogle Scholar
  21. 21.
    Dykes DJ, Bissery MC, Harrison Jr. SD, et al. Response of human tumor xenografts in athymic nude mice to docetaxel (RP 56976, Taxotere®). Invest New Drugs 1995; 13: 1–11Google Scholar
  22. 22.
    Lavelle F, Bissery MC, Riou JF, et al. Preclinical evaluation of docetaxel (Taxotere). Semin Oncol 1995 Apr; 22 Suppl. 4: 3–16Google Scholar
  23. 23.
    Riou JF, Petitgenet O, Aynie I, et al. Establishment and characterization of docetaxel (Taxotere®) resistant human breast carcinoma (Calc18/TXT) and murine leukemic (P388/TXT) cell lines. Proceedings of the American Association Cancer Research 1994; 35: 399Google Scholar
  24. 24.
    Chou T-C, Otter GM, Sirotnak FM. Schedule-dependent synergism of taxol or taxotere with edatrexate against human breast cancer cells in vitro. Cancer Chemother Pharmacol 1996; 37: 222–8PubMedCrossRefGoogle Scholar
  25. 25.
    Bissery MC, Vrignaud P, Bayssas M, et al. Taxotere® synergistic combination with cyclophosphamide, etoposide and 5-fluorouracil in mouse tumor models. Proceedings of the American Association Cancer Research 1993; 34: 299Google Scholar
  26. 26.
    Manthey CL, Qureshi N, Stutz PL, et al. Lipopolysaccharide antagonists block Taxol-induced signaling in murine macrophages. J Exp Med 1993 Aug 1; 178: 695–702PubMedCrossRefGoogle Scholar
  27. 27.
    Burkhart CA, Berman JW, Swindell CS, et al. Relationship between the structure of taxol and other taxanes on induction of tumor necrosis factor-α gene expression and cytotoxicity. Cancer Res 1994 Nov 15; 54: 5779–82PubMedGoogle Scholar
  28. 28.
    Choy H, Rodriguez F, Wilcox B, et al. Radiation sensitizing effects of Taxotere® (RP 56976) [abstract no. 2991]. Proceedings of the American Association Cancer Research 1992; 33: 500Google Scholar
  29. 29.
    Aapro MS, Zulian G, Alberto P, et al. Phase I and pharmacokinetic study of RP 56976 in a new ethanol-free formulation of taxotere [abstract no. 208]. Ann Oncol 1992; 3 Suppl. 5: 53Google Scholar
  30. 30.
    Burris H, Irvin R, Kuhn J, et al. Phase I clinical trial of taxotere administered as either a 2-hour or 6-hour intravenous infusion. J Clin Oncol 1993 May; 11: 950–8PubMedGoogle Scholar
  31. 31.
    Extra J-M, Rousseau F, Bruno R, et al. Phase I and pharmacokinetic study of taxotere (RP 56976; NSC 628503) given as a short intravenous infusion. Cancer Res 1993 Mar 1; 53: 1037–42PubMedGoogle Scholar
  32. 32.
    Rhône-Poulenc Rorer. Docetaxel product monograph. 2nd edition, 1996.Google Scholar
  33. 33.
    Launay-Iliadis MC, Bruno R, Cosson V, et al. Population pharmacokinetics of docetaxel during phase I studies using nonlinear mixed-effect modeling and nonparametric maximum-likelihood estimation. Cancer Chemother Pharmacol 1995; 37: 47–54PubMedCrossRefGoogle Scholar
  34. 34.
    Marre F, De Sousa G, Placidi M, et al. Élucidation des voies de biotransformation hépatique du Taxotère au moyen de modèles in vitro d’origine humaine [abstract]. Bull Cancer 1993; 80 (6): 527Google Scholar
  35. 35.
    Commerçon A, Bourzat J-D, Bézard J-D, et al. Partial synthesis of major human metabolites of docetaxel. Tetrahedron 1994; 50 (34): 10289–98CrossRefGoogle Scholar
  36. 36.
    Bruno R, Sanderink GJ. Pharmacokinetics and metabolism of Taxotere™ (docetaxel). Cancer Surv 1993; 17: 305–13PubMedGoogle Scholar
  37. 37.
    de Valeriola D, Brassinne C, Gaillard C, et al. Study of excretion balance, metabolism and protein binding of C14radiolabelled Taxotere (TXT) (RP56976, NSC628503) in cancer patients [abstract no. 2221]. Proceedings of the American Association Cancer Research 1993 March; 34: 373Google Scholar
  38. 38.
    Royer I, Monsarrat B, Sonnier M, et al. Metabolism of docetaxel by human cytochromes P450: interactions with paclitaxel and other antineoplastic drugs. Cancer Res 1996; 56: 58–65PubMedGoogle Scholar
  39. 39.
    Schellens JHM, Ma J, Bruno R, et al. Pharmacokinetics of cisplatin and Taxotere® (docetaxel) and WBC DNA-adduct formation of cisplatin in the sequence Taxotere®/cisplatin and cisplatin/Taxotere® in a phase I/II study in solid tumor patients [abstract]. Proc Am Soc Clin Oncol 1994 Mar; 13: 132Google Scholar
  40. 40.
    Bissett D, Setanoians A, Cassidy J, et al. Phase I and pharmacokinetic study of taxotere (RP 56976) administered as a 24-hour infusion. Cancer Res 1993 Feb 1; 53: 523–7PubMedGoogle Scholar
  41. 41.
    Pazdur R, Newman RA, Newman BM, et al. Phase I trial of Taxotere: five-day schedule. J Natl Cancer Inst 1992 Dec 2; 84: 1781–8PubMedCrossRefGoogle Scholar
  42. 42.
    Tomiak E, Piccart MJ, Kerger J, et al. Phase I study of docetaxel administered as a 1-hour intravenous infusion on a weekly basis. J Clin Oncol 1994 Jul; 12: 1458–67PubMedGoogle Scholar
  43. 43.
    Taguchi T, Furue H, Niitani H, et al. Phase I clinical trial of RP56976 (docetaxel) a new anticancer drug [in Japanese]. Gan to Kagaku Ryoho 1994 Sep; 21: 1997–2005PubMedGoogle Scholar
  44. 44.
    Miller AB, Hoogstraten B, Staquet M, et al. Reporting results of cancer treatment. Cancer 1981 Jan; 47: 207–14PubMedCrossRefGoogle Scholar
  45. 45.
    Chevallier B, Fumoleau P, Kerbrat P, et al. Docetaxel is a major cytotoxic drug for the treatment of advanced breast cancer: a phase II trial of the Clinical Screening Cooperative Group of the European Organization for Research and Treatment of Cancer. J Clin Oncol 1995 Feb; 13: 314–22PubMedGoogle Scholar
  46. 46.
    Dieras V, Chavallier B, Kerbrat P, et.al. A mulicentre phase II study of docetaxel 75 mg/m2 as first-line chemotherapy for patients with advanced breast cancer: report of the Clinical Screening Group of the EORTC. Br J Cancer. In press.Google Scholar
  47. 47.
    Fumoleau P, Chevallier B, Kerbrat P, et al. A multicentre phase II study of the efficacy and safety of docetaxel as first-line treatment of advanced breast cancer: Report of the Clinical Screening Group of the EORTC. Ann Oncol In pressGoogle Scholar
  48. 48.
    Hudis CA, Seidman AD, Crown JPA, et al. Phase II and pharmacologic study of docetaxel as initial chemotherapy for metastatic breast cancer. J Clin Oncol 1996 Jan; 14 (1): 58–65PubMedGoogle Scholar
  49. 49.
    Trudeau ME, Eisenhauer EA, Higgins BP, et al. Docetaxel in patients with metastatic breast cancer: a phase II study of the National Cancer Institute of Canada-Clinical Trials Group. J Clin Oncol 1996 Feb; 14 (2): 422–8PubMedGoogle Scholar
  50. 50.
    Dieras V, Fumoleau P, Chevallier B, et al. Second EORTC-Clinical Screening Group (CSG) phase II trial of Taxotere® (docetaxel) as first line chemotherapy in advanced breast cancer (ABC) [abstract]. Proc Am Soc Clin Oncol 1994 Mar; 13: 78Google Scholar
  51. 51.
    Ravdin PM, Burris III HA, Cook G, et al. Phase II trial of docetaxel in advanced anthracycline-resistant or anthracenedione-resistant breast cancer. J Clin Oncol 1995 Dec; 13 (12): 2879–85PubMedGoogle Scholar
  52. 52.
    ten Bokkel Huinink WW, Prove AM, Piccart M, et al. A phase II trial with docetaxel (Taxotere®) in second line treatment with chemotherapy for advanced breast cancer: a study of the EORTC Early Clinical Trials Group. Ann Oncol 1994 Jul; 5: 527–32PubMedGoogle Scholar
  53. 53.
    Valero V, Holmes FA, Walters RS, et al. Phase II trial of docetaxel: a new, highly effective antineoplastic agent in the management of patients with anthracyclin-resistant metastatic breast cancer. J Clin Oncol 1995 Dec; 13 (12): 2886–94PubMedGoogle Scholar
  54. 54.
    Bellet R, Riva A, Ravdin P, et al. Docetaxel (Taxotere): a new active agent in antracycline resistant metastatic breast cancer. Rhône-Poulenc Rorer (data on file).Google Scholar
  55. 55.
    Adachi I, Watanabe T, Takashima S, et al. A late phase II study of RP56976 (docetaxel) in patients with advanced or recurrent breast cancer. Br J Cancer 1996; 73: 210–6PubMedCrossRefGoogle Scholar
  56. 56.
    Taguchi T. An early phase II clinical study of RP56976 (docetaxel) in patients with cancer of the gastrointestinal tract [in Japanese]. Gan to Kagaku Ryoho 1994 Oct; 21: 2431–7PubMedGoogle Scholar
  57. 57.
    Taguchi T, Mori S, Abe R, et al. Late phase II clinical study of RP56976 (docetaxel) in patients with advanced/recurrent breast cancer [in Japanese]. Gan to Kagaku Ryoho 1994 Nov; 21: 2625–32PubMedGoogle Scholar
  58. 58.
    Mouridsen HT. Systemic therapy of advanced breast cancer Drugs; 1992 (44): SupplGoogle Scholar
  59. 59.
    Gruia G, Misset JL, Giachetti S, et al. A phase I–II study of Taxotere (TXTR) in combination with Adriamycin (AD) as first line chemotherapy (CT) in patients with metastatic breast cancer [abstract no. 258]. Proc Am Soc Clin Oncol 1995; 14: 140Google Scholar
  60. 60.
    Zalcberg J, Bishop JF, Webster LK, et al. A phase I trial of the combination Taxotere (docetaxel) and cisplatin in patients with advanced non-small cell lung cancer (NSCLC) [abstract no. P773]. Ann Oncol 1994; 5 Suppl. 8: 154Google Scholar
  61. 61.
    Cole JT, Gralla RJ, Marques CB, et al. Phase I-II study of cisplatin + docetaxel (Taxotere) in non-small cell lung cancer (NSCLC) [abstract no. 1087]. Proc Am Soc Clin Oncol 1995; 14: 357Google Scholar
  62. 62.
    Verweij J, Planting AST, van der Burg MEL, et al. A phase I study of docetaxel (Taxotere) and cisplatin in patients with solid tumors [abstract no. 386]. Proc Am Soc Clin Oncol 1994 Mar; 13: 148Google Scholar
  63. 63.
    Burris III HA, Fields S, Peacock N. Docetaxel (Taxotere) in combination: a step forward. Semin Oncol 1995 Dec; 95(22) Suppl. 6: 35–40Google Scholar
  64. 64.
    Cortes JE, Pazdur R. Docetaxel. J Clin Oncol 1995 Oct; 13: 2643–55PubMedGoogle Scholar
  65. 65.
    Fumoleau P, Chevallier B, Dieras V, et al. Safety evaluation of two doses of Taxotere® (docetaxel) without routine premedication as first line in advanced breast cancer (ABC)-EORTC Clinical Screening Group (CSG) report [abstract]. Proc Am Soc Clin Oncol 1994 Mar; 13: 109Google Scholar
  66. 66.
    Van Oosterom AT, Schriivers D. Docetaxel (Taxotere®), a review of preclinical and clinical experience. Part II: clinical experience. Anticancer Drugs 1995 Jun; 6: 356–68Google Scholar
  67. 67.
    Jaffrézou J-P, Laurent G. Docetaxel (Taxotere): current status and clinical prospects. Expert Opin Invest Drug 1995 Dec; 4 (12): 1185–95CrossRefGoogle Scholar
  68. 68.
    Tomiak E, Kerger J, Lips S, et al. Unexpected pleural changes observed in patients treated with Taxotere (RP 56976): a new drug toxicity? [abstract]. Ann Oncol 1992 Nov; 3 Suppl. 5: 48Google Scholar
  69. 69.
    Piccart MJ, Klijn J, Paridaens R, et al. Steroids do reduce the severity and delay the onset of docetaxel (DXT) induced fluid retention: final results of a randomized trial of the EORTC investigational drug branch for breast cancer (IDBBC) [abstract]. Eur J Cancer 1995 Nov; 31A Suppl. 5: S75CrossRefGoogle Scholar
  70. 70.
    Oulid-Aïssa D, Béhar A, Spielmann M, et al. Management of fluid retention syndrome in patients treated with Taxotere® (docetaxel): effect of premedication [abstract]. Proc Am Soc Clin Oncol 1994 Mar; 13: 465Google Scholar
  71. 71.
    Balmaceda C, Forsyth P, Seidman AD, et al. Peripheral neuropathy in patients receiving taxotere chemotherapy [abstract]. Ann Neurol 1993 Aug; 34: 313Google Scholar
  72. 72.
    New PZ, Barohn R. Neurotoxicity of Taxotere [abstract]. Neurology 1993 Apr; 43 Suppl. 2: A191Google Scholar
  73. 73.
    Van den Bent MJ, Hilkens PHE, Verwey J, et al. Docetaxel induces a mild dose-dependent sensory neuropathy [abstract]. Neurology 1995 Apr; 45 Suppl. 4: 322Google Scholar
  74. 74.
    Hilkens PHE, Verweij J, Stoter G, et al. Peripheral neurotoxicity induced by docetaxel. Neurology 1996 Jan; 46: 104–8PubMedCrossRefGoogle Scholar
  75. 75.
    Cavaletti G, Tredici G. Platinum compounds and taxoids: is combination neurotoxicity a possibility?. Cancer J 1995 Mar–Apr; 8: 46–7Google Scholar
  76. 76.
    Wanders J, Schrijvers D, Bruntsch U, et al. The EORTC-ECTG experience with acute hypersensitivity reactions in Taxotere studies [abstract]. Proc Am Soc Clin Oncol 1993 Mar; 12: 73Google Scholar
  77. 77.
    Eisenhauer EA, Lu F, Muldal A, et al. Predictors and treatment of docetaxel (D) toxic effects [abstract]. Ann Oncol 1994; 5 Suppl. 5: 202Google Scholar
  78. 78.
    Wanders J, Van Oosterom A, Gore M, et al. Taxotere toxicity — protective effects of premedication [abstract no. S206]. Eur J Cancer 1993; 29A Suppl. 6: 1148Google Scholar
  79. 79.
    Zimmerman GC, Keeling JH, Burris HA, et al. Acute cutaneous reactions to docetaxel, a new chemotherapeutic agent. Arch Dermatol 1995 Feb; 131: 202–6PubMedCrossRefGoogle Scholar
  80. 80.
    Battafarano DF, Zimmerman GC, Older SA, et al. Docetaxel (Taxotere) associated scleroderma-like changes of the lower extremities: a report of three cases. Cancer 1995 Jul 1; 76: 110–5PubMedCrossRefGoogle Scholar
  81. 81.
    Harris JR, Lippman ME, Veronesi U, et al. Breast cancer (first of three parts). N Engl J Med 1992 July 30; 327 (5): 319–28PubMedCrossRefGoogle Scholar
  82. 82.
    McPherson K, Steel CM, Dixon JM. Breast cancer-epidemiology, risk factors, and genetics. BMJ 1994 Oct 15; 309: 1003–6PubMedCrossRefGoogle Scholar
  83. 83.
    Early Breast Cancer Trialist’s Collaborative Group. Sytemic treatment of early breast cancer by hormonal, cytotoxic, or immune therapy: 133 randomised trials involving 31 000 recurrances and 24 000 deaths among 75 000 women. Lancet 1992; 339: 1–15,71-85Google Scholar
  84. 84.
    Sledge Jr GW, Antman KM. Progress in chemotherapy for metastatic breast cancer. Semin Oncol 1992 June; 19 (3): 317–32PubMedGoogle Scholar
  85. 85.
    Rubens RD. Improving treatment for advanced breast cancer. Cancer Surv 1993; 18: 199–208PubMedGoogle Scholar
  86. 86.
    Hutton J, Brown R, Borowitz M, et al. A new decision model for cost-utility comparisons of chemotherapy in recurrent metastatic breast cancer. PharmacoEconomics. In pressGoogle Scholar

Copyright information

© Adis International Limited 1996

Authors and Affiliations

  • Bret Fulton
    • 1
  • Caroline M. Spencer
    • 1
  1. 1.Adis International LimitedMairangi Bay, Auckland 10New Zealand

Personalised recommendations