Pharmacokinetic study of paclitaxel in malignant ascites from advanced gastric cancer patients

Kobayashi, Mariko; Sakamoto, Junichi; Namikawa, Tsutomu; Okamoto, Ken; Okabayashi, Takehiro; Ichikawa, Kengo; Araki, Keijiro

doi:10.3748/wjg.v12.i9.1412

Cited by 61 publications

(48 citation statements)

References 19 publications

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“…The other patient, given 80 mg/m 2 of PTX, had serum PTX levels measured 168 h after PTX administration. In these two patient's, the plasma levels of PTX remained within the effective range for 60 and 72 h respectively [20]. These results together with those cited above [7,9,10], suggest that sequential chemotherapy using PTX and S-1 is promising for the prevention of peritoneal dissemination of T3/T4 advanced gastric cancer following R0 resection.…”

Section: Discussionsupporting

confidence: 72%

A feasibility study of sequential paclitaxel and S-1 (PTX/S-1) chemotherapy as postoperative adjuvant chemotherapy for advanced gastric cancer

et al. 2006

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Section: Discussionsupporting

confidence: 72%

A feasibility study of sequential paclitaxel and S-1 (PTX/S-1) chemotherapy as postoperative adjuvant chemotherapy for advanced gastric cancer

et al. 2006

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“…The minimally effective plasma paclitaxel concentration in patients is reported to be 100 nM (Sekine et al, 1996;Malingre et al, 2001;Mross et al, 2006;Kobayashi et al, 2006). Both 100 and 7 nM paclitaxel concentrations were analyzed but only immunofluorescence data from cells treated with 100 nM paclitaxel were shown.…”

Section: Discussionmentioning

confidence: 99%

Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Taylor

McNeely

Miller

et al. 2008

Toxicology and Applied Pharmacology

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Arsenite, a known mitotic disruptor, causes cell cycle arrest and cell death at anaphase. The mechanism causing mitotic arrest is highly disputed. We compared arsenite to the spindle poisons nocodazole and paclitaxel. Immunofluorescence analysis of α-tubulin in interphase cells demonstrated that, while nocodazole and paclitaxel disrupt microtubule polymerization through destabilization and hyperpolymerization, respectively, microtubules in arsenite-treated cells remain comparable to untreated cells even at supra-therapeutic concentrations. Immunofluorescence analysis of α-tubulin in mitotic cells showed spindle formation in arsenite-and paclitaxel-treated cells but not in nocodazole-treated cells. Spindle formation in arsenite-treated cells appeared irregular and multi-polar. γ-tubulin staining showed that cells treated with nocodazole and therapeutic concentrations of paclitaxel contained two centrosomes. In contrast, most arsenite-treated mitotic cells contained more than two centrosomes, similar to centrosome abnormalities induced by heat shock. Of the three drugs tested, only arsenite treatment increased expression of the inducible isoform of heat shock protein 70 (HSP70i). HSP70 and HSP90 proteins are intimately involved in centrosome regulation and mitotic spindle formation. HSP90 inhibitor 17-DMAG sensitized cells to arsenite treatment and increased arsenite-induced centrosome abnormalities. Combined treatment of 17-DMAG and arsenite resulted in a supra-additive effect on viability, mitotic arrest, and centrosome abnormalities. Thus, arsenite-induced abnormal centrosome amplification and subsequent mitotic arrest is independent of effects on tubulin polymerization and may be due to specific stresses that are protected against by HSP90 and HSP70.

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“…In case studies, complete disappearance of gastric ascites was reported to have been brought n, number of patients; C, cisplatin; U, UFT; F, 5-FU; L, folinic acid (LV); P, paclitaxel; S, S-1; 5′DFUR, doxifl uridine; RR, response rate; NR, not reported about by treatment with weekly [66] and biweekly [67] paclitaxel plus either S-1 or doxifl uridine [68]. Two pharmacokinetic studies demonstrated that the paclitaxel concentration in ascites remained within the optimal effective level for 72 h after intravenous administration [69,70]. In two clinical trials, the effi cacy of second-line paclitaxel or paclitaxel-containing regimens against gastric ascites was examined in patients whose disease had been refractory to fl uorinated pyrimidine therapy.…”

Section: Paclitaxel Chemotherapy For Peritoneal Dissemination and Ascmentioning

confidence: 99%

Paclitaxel chemotherapy for the treatment of gastric cancer

2009

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cause of cancer mortality. Although the incidence of gastric cancer has been declining in most developed countries, esophago-gastric junctional tumor and tumor in the cardia has, conversely, been increasing [2] and these tumors still remain one of the biggest problems worldwide.The prognosis of patients with advanced (i.e., unresectable or metastatic) gastric cancer is very poor. The median survival time for such patients is 6 to 9 months [3]. For many years, various chemotherapeutic agents have been used in attempts to improve survival, progression free-survival, response rate, and quality of life in patients with advanced gastric cancer as well as to improve disease-free survival in patients in whom curative resection of the cancers has been performed. 5-Fluorouracil (5-FU) and cisplatin-based regimens have long been considered reference treatments. Commonly used regimens have included epirubicin, cisplatin, and continuous infusion of 5-FU; 5 days' infusion of 5-FU plus cisplatin every 4 weeks; a weekly infusion regimen of 5-FU/leucovorin (LV) over 24 h plus cisplatin every 2 weeks; and 5-FU bolus plus 22-h infusion of 5-FU on days 1 and 2, in combination with cisplatin every 2 weeks. The results with these regimens, together with other study results, suggested that combination regimens including fl uorinated pyrimidines, cisplatin, doxorubicin, epirubicin, and methotrexate, had better response rates than single agents. Although gastric cancer is a relatively chemosensitive disease, with response rates of 30% to 40%, these treatments have shown a modest but unsatisfactory increase in overall survival [4]. In this regard, chemotherapy in the advanced gastric cancer setting is limited by a low complete response rate, response durations that are shortlived, and considerable toxicities.Nevertheless, recently, the development of new chemotherapeutic and molecular targeting agents has opened the door to various clinical trials to fi nd novel therapeutic strategies to improve the outcome of Abstract A comprehensive review of phase I and phase II clinical trials of paclitaxel and paclitaxel-containing chemotherapy regimens for advanced gastric cancer was performed. Response rates, median progression-free survivals, and median overall survivals were examined, together with the treatment regimens and the numbers of patients registered in each trial. Although paclitaxel monotherapy produced considerable improvement in tumor response and prognosis, combination doublet or triplet chemotherapy with fl uoropyrimidines and/ or platinum compounds showed better results than the paclitaxel monotherapy. With regard to the schedule of paclitaxel administration, weekly injection seemed to show less toxicity and better results than administration every 3 weeks. Adjuvant therapies, chemoradiation therapies, and paclitaxel treatment for gastric ascites were also investigated and are discussed.

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Pharmacokinetic study of paclitaxel in malignant ascites from advanced gastric cancer patients

Abstract: The concentration of paclitaxel in ascites is maintained within the optimal level for the treatment of cancer cells for up to 72 h after intravenous administration. Paclitaxel is a promising drug for the treatment of malignant ascites of gastric cancer.

Cited by 61 publications

References 19 publications

A feasibility study of sequential paclitaxel and S-1 (PTX/S-1) chemotherapy as postoperative adjuvant chemotherapy for advanced gastric cancer

A feasibility study of sequential paclitaxel and S-1 (PTX/S-1) chemotherapy as postoperative adjuvant chemotherapy for advanced gastric cancer

Arsenite-induced mitotic death involves stress response and is independent of tubulin polymerization

Paclitaxel chemotherapy for the treatment of gastric cancer

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