Intraperitoneal Chemotherapy for Unresectable Peritoneal Surface Malignancies
Niels A.D. GuchelaarBo Jan NoordmanStijn L.W. KoolenBianca MostertEva V. E. MadsenJacobus W. A. BurgerAlexandra R. M. Brandt‐KerkhofGeert-Jan CreemersIgnace H. J. T. de HinghMisha LuyerSander BinsEsther van MeertenSjoerd M. LagardeCornelis VerhoefBas P. L. WijnhovenRon H.J. Mathijssen
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Abstract:
Malignancies of the peritoneal cavity are associated with a dismal prognosis. Systemic chemotherapy is the gold standard for patients with unresectable peritoneal disease, but its intraperitoneal effect is hampered by the peritoneal-plasma barrier. Intraperitoneal chemotherapy, which is administered repeatedly into the peritoneal cavity through a peritoneal implanted port, could provide a novel treatment modality for this patient population. This review provides a systematic overview of intraperitoneal used drugs, the performed clinical studies so far, and the complications of the peritoneal implemental ports. Several anticancer drugs have been studied for intraperitoneal application, with the taxanes paclitaxel and docetaxel as the most commonly used drug. Repeated intraperitoneal chemotherapy, mostly in combination with systemic chemotherapy, has shown promising results in Phase I and Phase II studies for several tumor types, such as gastric cancer, ovarian cancer, colorectal cancer, and pancreatic cancer. Two Phase III studies for intraperitoneal chemotherapy in gastric cancer have been performed so far, but the results regarding the superiority over standard systemic chemotherapy alone, are contradictory. Pressurized intraperitoneal administration, known as PIPAC, is an alternative way of administering intraperitoneal chemotherapy, and the first prospective studies have shown a tolerable safety profile. Although intraperitoneal chemotherapy might be a standard treatment option for patients with unresectable peritoneal disease, more Phase II and Phase III studies focusing on tolerability profiles, survival rates, and quality of life are warranted in order to establish optimal treatment schedules and to establish a potential role for intraperitoneal chemotherapy in the approach to unresectable peritoneal disease.Keywords:
Peritoneal cavity
Tolerability
Peritoneal cavity
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OBJECTIVE: To review the mechanism involved in paclitaxel-induced hypersensitivity reactions and to evaluate the potential use of docetaxel after acute hypersensitivity reactions (HSRs) to paclitaxel. DATA SOURCES: Literature identified through a MEDLINE search (1966–September 2000) and through secondary sources. DATA SYNTHESIS: HSRs to paclitaxel can be life-threatening. The exact etiology involved in paclitaxel-induced HSRs has not been fully elucidated; the reactions may be due to the Cremophor EL vehicle or to paclitaxel itself. Options for treatment following HSRs are limited. A rechallenge attempt can be made, but is not always successful. Docetaxel, a semisynthetic taxane, may have a role in therapy for patients unable to tolerate paclitaxel therapy. This review examines the etiology of paclitaxel-induced HSRs and the potential role of docetaxel following these acute reactions. CONCLUSIONS: Docetaxel may be a viable alternative for patients who experience HSRs to paclitaxel.
Taxane
Hypersensitivity reaction
Etiology
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The taxoid drugs, docetaxel (Taxotere) and paclitaxel (Taxol), represent a new class of antitumour agents which act by promoting the assembly and inhibiting the disassembly of microtubules. Docetaxel has been shown to be more potent than paclitaxel with regard to the formation and stabilization of microtubules in vitro. Docetaxel also has a higher cell uptake than paclitaxel and a longer intracellular retention time. Docetaxel is a more potent antitumour agent than paclitaxel in most model systems. The observation that the cytotoxic concentration for docetaxel is lower than that for paclitaxel in cultures of human haematopoietic cells supports the clinical observation that dose-limiting neutropenia is seen at a lower dose of docetaxel than paclitaxel. The concentration of docetaxel required to kill tumour cells in vitro is well within the plasma concentrations recorded in clinical studies, and docetaxel has shown extensive clinical activity against a variety of solid tumours. Most drugs are used in combination regimens in the clinic and combinations of docetaxel with other agents are under active investigation. The agents to be combined with docetaxel include those which showed synergism with docetaxel in vitro and can be delivered at optimal doses without additive toxicity.
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e13567 Background: Paclitaxel and docetaxel share major parts of their structures and mechanism of action, but differ in several aspects. Both paclitaxel and docetaxel act at microtubule causing tubulin polymer generation but exhibit pharmacodynamic differences. These pharmacological differences may account for the differences observed between taxanes in their clinical activity and toxicity. Methods: Review of articles providing details of taxane pharmacology was conducted to evaluate pharmacological basis. Results: Greater uptake and slower efflux of docetaxel from tumor cells leads to longer retention time; whereas equal uptake and efflux of paclitaxel shorter retention time for paclitaxel. Hence, apoptotic and mitotic responses of paclitaxel is complete within 4 days implying that more frequent (weekly) administration of paclitaxel will be superior. High affinity to β-tubulin with docetaxel (1.9) than with paclitaxel (1.0) allows higher inhibition of tumor growth. Secondly, drug concentration causing maximum polymerization is 0.2 µM and 0.4 µM for docetaxel and paclitaxel, respectively; indicating that docetaxel is twice as potent as paclitaxel in causing microtubule polymerization. Docetaxel arrests cells in the radiosensitive G2/M phase of the cell cycle making it a potent radiosensetizer than paclitaxel. Mechanisms consistent with allosteric modulation of the reductases increase doxorubicinol formation at clinically relevant concentrations of paclitaxel when it is administered with doxorubicin. Enhanced formation of doxorubicinol aglycone, a metabolite potentially involved in the reversible phase of cardiotoxicity causes higher cardiotoxicty when doxorubicin is administered with paclitaxel than with docetaxel. Non linear pharmacokinetics and hypersensitivity with paclitaxel and fluid retention with docetaxel is attributed to excepient of the drug rather than drug itself. Conclusions: Influx and efflux mechanism support superior weekly administration of Paclitaxel. Pharmacological differences between taxanes justify the incomplete resistance seen between taxanes. The incomplete cross resistance is specifically related to docetaxelactivity in paclitaxel resistant cases.
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Cabazitaxel
Cardiotoxicity
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The in vitro effects of paclitaxel (Tx) and docetaxel (Taxotere, Txt) are compared in this study using the adenosine triphosphate cell viability assay (ATP-CVA) in 14 cancer cell lines. Eleven cell lines were sensitive and three were partially sensitive to paclitaxel. Nine cell lines were sensitive, three were partially sensitive and two were resistant to docetaxel. Mean IC50s were 3.7–660 ng/ml paclitaxel and 5.4–540 ng/ml docetaxel. In five sensitive cancer cell lines docetaxel was more active than paclitaxel, and in six sensitive cell lines paclitaxel was more active than docetaxel on a concentration basis. Two cell lines were sensitive to paclitaxel and resistant to docetaxel. In one cell line the two compounds had similar activities. In the ATP-CVA, paclitaxel and docetaxel are very active and are partially non-cross-resistant.
Viability assay
Gynecologic cancer
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Successful treatment with nab-paclitaxel after hypersensitivity reaction to paclitaxel and docetaxel
•First case report of successfully treating severe paclitaxel and docetaxel hypersensitivity reaction with nab-paclitaxel•We demonstrated that nab-paclitaxel is a safe taxane chemotherapy treatment option for patients who could not tolerate paclitaxel or docetaxel.
Hypersensitivity reaction
Nab-paclitaxel
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The taxanes paclitaxel and docetaxel represent a novel class of antineoplastic agents. A major problem of both drugs is their low aqueous solubility and the design of suitable formulations has been a difficult step in the process of therapeutic development. The formulations currently used are mixtures of Cremophor EL:ethanol for paclitaxel (Taxol) and Tween 80:ethanol for docetaxel (Taxotere), but many new approaches have been tested or are under investigation. Paclitaxel and docetaxel have a similar mechanism of action, which is based on promotion of tubulin assembly and inhibition of microtubule disassembly. Pharmacokinetic studies revealed a marked non-linearity of paclitaxel in mice, which appeared to result exclusively from Cremophor EL, the major component present in the pharmaceutical formulation. An almost linear pharmacokinetic behavior was observed in the case of docetaxel. The reported plasma protein binding of both compounds ranged from 76 to 97% in different animal species. Paclitaxel and docetaxel widely distribute into most tissues of mice and rats, including tumor tissue, but only low concentrations were detected in the central nervous system. Despite the great similarity in the chemical structures of paclitaxel and docetaxel, their metabolic profile is very distinct. Furthermore, whereas paclitaxel metabolism is largely species dependent, docetaxel metabolism is similar across species in both isolated hepatic microsomal fractions and in vivo models. For both taxanes, hepatobiliary excretion is the major pathway of elimination and a major fraction of the dose is excreted in feces as parent drug or hydroxylated metabolites.
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Objective To provide the basis for the clinical application of paclitaxel and docetaxel,compare their differences on pharmacological profiles and patterns of clinical activity. Methods The literature of taxanes was analyzed. Results The two taxanes differed in structures,pharmacokinetic charateristics,drug interactions,toxicity and administrations. Conclusion The rational use of the two taxanes should be based on their differences.
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Taxane
Mechanism of Action
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