The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform
Raymond T. Chung - One of the best experts on this subject based on the ideXlab platform.
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Management of hepatitis B reactivation in patients receiving Cancer Chemotherapy.
Therapeutic advances in gastroenterology, 2012Co-Authors: Yi-wen Huang, Raymond T. ChungAbstract:Hepatitis B virus (HBV) reactivation is well documented in previously resolved or inactive HBV carriers who receive Cancer Chemotherapy. The consequences of HBV reactivation range from self-limited conditions to fulminant hepatic failure and death. HBV reactivation also leads to premature termination of Chemotherapy or delay in treatment schedules. This review summarizes current knowledge of management of HBV reactivation in patients receiving Cancer Chemotherapy. HBV surface antigen (HBsAg) testing should be performed in patients who require Cancer Chemotherapy. Four meta-analyses support lamivudine prophylaxis for HBV reactivation during Chemotherapy in HBsAg-positive patients. Randomized controlled trials to compare different HBV antiviral agents are needed to define optimal regimens for the prevention and treatment of HBV reactivation in patients receiving Cancer Chemotherapy.
William C. Zamboni - One of the best experts on this subject based on the ideXlab platform.
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Pharmacokinetic Optimisation of Cancer Chemotherapy
Clinical Pharmacokinetics, 1997Co-Authors: Eric Masson, William C. ZamboniAbstract:Cancer Chemotherapy doses are empirical in that the majority are administered at a fixed dose (mg/m^2 or mg/kg). One reason for this is the intrinsic sensitivity of the tumour or host cells to one particular Chemotherapy agent is unknown. Therefore, the likelihood of response or toxicity is unpredictable a priori. This contrasts with antimicrobial Chemotherapy where sensitivity (minimum inhibitory concentration) can be determined for a specific bacterium. The pharmacokinetics of Cancer Chemotherapy agents is also highly variable between patients. In addition, the small therapeutic index of these drugs, combined with the lack of good surrogate markers of toxicity or response, adds to the empiricism of the administration of Cancer Chemotherapy. In the past few years, numerous studies have established good relationships between systemic exposure to Cancer Chemotherapy and both response and toxicity. These relationships have been used to individualise Chemotherapy dose administration a priori and a posteriori. Some examples of drugs which are individualised based on their pharmacokinetics are methotrexate, busulfan and carboplatin. Other examples of antineoplastic agents which may eventually be individualised based on their pharmacokinetics are mercaptopurine, fluorouracil, etoposide and teniposide, topotecan and suramin. New strategies are being investigated to improve the therapeutic index of Cancer Chemotherapy agents such as biomodulation, pharmacogenetics, circadian administration and the modification of drug scheduling. Pharmacokinetic studies have also played a major role in these areas. Thus, despite the empiricism associate with Cancer Chemotherapy administration, some progress has been made and shown to have an impact on outcome. However, more studies are needed to improve Cancer Chemotherapy administra-tion.
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Pharmacokinetic optimisation of Cancer Chemotherapy. Effect on outcomes.
Clinical pharmacokinetics, 1997Co-Authors: Eric Masson, William C. ZamboniAbstract:Cancer Chemotherapy doses are empirical in that the majority are administered at a fixed dose (mg/m2 or mg/kg). One reason for this is the intrinsic sensitivity of the tumour or host cells to one particular Chemotherapy agent is unknown. Therefore, the likelihood of response or toxicity is unpredictable a priori. This contrasts with antimicrobial Chemotherapy where sensitivity (minimum inhibitory concentration) can be determined for a specific bacterium. The pharmacokinetics of Cancer Chemotherapy agents is also highly variable between patients. In addition, the small therapeutic index of these drugs, combined with the lack of good surrogate markers of toxicity or response, adds to the empiricism of the administration of Cancer Chemotherapy.
Yi-wen Huang - One of the best experts on this subject based on the ideXlab platform.
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Management of hepatitis B reactivation in patients receiving Cancer Chemotherapy.
Therapeutic advances in gastroenterology, 2012Co-Authors: Yi-wen Huang, Raymond T. ChungAbstract:Hepatitis B virus (HBV) reactivation is well documented in previously resolved or inactive HBV carriers who receive Cancer Chemotherapy. The consequences of HBV reactivation range from self-limited conditions to fulminant hepatic failure and death. HBV reactivation also leads to premature termination of Chemotherapy or delay in treatment schedules. This review summarizes current knowledge of management of HBV reactivation in patients receiving Cancer Chemotherapy. HBV surface antigen (HBsAg) testing should be performed in patients who require Cancer Chemotherapy. Four meta-analyses support lamivudine prophylaxis for HBV reactivation during Chemotherapy in HBsAg-positive patients. Randomized controlled trials to compare different HBV antiviral agents are needed to define optimal regimens for the prevention and treatment of HBV reactivation in patients receiving Cancer Chemotherapy.
Eric Masson - One of the best experts on this subject based on the ideXlab platform.
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Pharmacokinetic Optimisation of Cancer Chemotherapy
Clinical Pharmacokinetics, 1997Co-Authors: Eric Masson, William C. ZamboniAbstract:Cancer Chemotherapy doses are empirical in that the majority are administered at a fixed dose (mg/m^2 or mg/kg). One reason for this is the intrinsic sensitivity of the tumour or host cells to one particular Chemotherapy agent is unknown. Therefore, the likelihood of response or toxicity is unpredictable a priori. This contrasts with antimicrobial Chemotherapy where sensitivity (minimum inhibitory concentration) can be determined for a specific bacterium. The pharmacokinetics of Cancer Chemotherapy agents is also highly variable between patients. In addition, the small therapeutic index of these drugs, combined with the lack of good surrogate markers of toxicity or response, adds to the empiricism of the administration of Cancer Chemotherapy. In the past few years, numerous studies have established good relationships between systemic exposure to Cancer Chemotherapy and both response and toxicity. These relationships have been used to individualise Chemotherapy dose administration a priori and a posteriori. Some examples of drugs which are individualised based on their pharmacokinetics are methotrexate, busulfan and carboplatin. Other examples of antineoplastic agents which may eventually be individualised based on their pharmacokinetics are mercaptopurine, fluorouracil, etoposide and teniposide, topotecan and suramin. New strategies are being investigated to improve the therapeutic index of Cancer Chemotherapy agents such as biomodulation, pharmacogenetics, circadian administration and the modification of drug scheduling. Pharmacokinetic studies have also played a major role in these areas. Thus, despite the empiricism associate with Cancer Chemotherapy administration, some progress has been made and shown to have an impact on outcome. However, more studies are needed to improve Cancer Chemotherapy administra-tion.
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Pharmacokinetic optimisation of Cancer Chemotherapy. Effect on outcomes.
Clinical pharmacokinetics, 1997Co-Authors: Eric Masson, William C. ZamboniAbstract:Cancer Chemotherapy doses are empirical in that the majority are administered at a fixed dose (mg/m2 or mg/kg). One reason for this is the intrinsic sensitivity of the tumour or host cells to one particular Chemotherapy agent is unknown. Therefore, the likelihood of response or toxicity is unpredictable a priori. This contrasts with antimicrobial Chemotherapy where sensitivity (minimum inhibitory concentration) can be determined for a specific bacterium. The pharmacokinetics of Cancer Chemotherapy agents is also highly variable between patients. In addition, the small therapeutic index of these drugs, combined with the lack of good surrogate markers of toxicity or response, adds to the empiricism of the administration of Cancer Chemotherapy.
Brian J Druker - One of the best experts on this subject based on the ideXlab platform.
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the Cancer Chemotherapy drug etoposide vp 16 induces proinflammatory cytokine production and sickness behavior like symptoms in a mouse model of Cancer Chemotherapy related symptoms
Biological Research For Nursing, 2006Co-Authors: Lisa Wood, Lillian Nail, Nancy A Perrin, Collin R Elsea, April Fischer, Brian J DrukerAbstract:Cancer Chemotherapy-related symptoms such as fatigue, malaise, loss of interest in social activities, difficulty concentrating, and changes in sleep patterns can lead to treatment delays, dose reductions, or termination and have a profound effect on the physical, psychosocial, and economic aspects of quality of life. Clinicians have long suspected that these symptoms are similar to those associated with "sickness behavior," which is triggered by the production of the inflammatory cytokines IL-1beta, TNF-alpha, and IL-6 by macrophages and other cells of the innate immune system in response to immune challenge. The p38 mitogen-activated protein kinase (p38 MAPK) plays a central role in the production of these cytokines and consequently the induction of sickness behavior. Several Cancer Chemotherapy drugs have been shown to activate p38 MAPK, but whether these drugs can also induce the production of inflammatory cytokines to cause sickness behavior is unknown. The aim of this study was to determine whether the Cancer Chemotherapy drug etoposide (VP-16), which is known to activate p38 MAPK, could induce inflammatory cytokine production by murine macrophages and sickness-like behaviors when injected into mice. VP-16 activated p38 MAPK and induced IL-6 production in murine macrophages in a p38 MAPK- dependent manner. VP-16 administration rapidly increased serum levels of IL-6 in healthy mice and induced sickness-like behaviors as evidenced by a decrease in food intake, body weight, hemoglobin level, and voluntary wheel-running activity. These findings support the idea that the induction of IL-1beta, TNF-alpha, and IL-6 by Cancer Chemotherapy drugs underlies the fatigue and associated symptoms experienced by people undergoing Cancer Chemotherapy.
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The Cancer Chemotherapy Drug Etoposide (VP-16) Induces Proinflammatory Cytokine Production and Sickness Behavior–like Symptoms in a Mouse Model of Cancer Chemotherapy–Related Symptoms
Biological research for nursing, 2006Co-Authors: Lisa Wood, Lillian Nail, Collin R Elsea, April Fischer, Nancy Perrin, Brian J DrukerAbstract:Cancer Chemotherapy-related symptoms such as fatigue, malaise, loss of interest in social activities, difficulty concentrating, and changes in sleep patterns can lead to treatment delays, dose reductions, or termination and have a profound effect on the physical, psychosocial, and economic aspects of quality of life. Clinicians have long suspected that these symptoms are similar to those associated with "sickness behavior," which is triggered by the production of the inflammatory cytokines IL-1beta, TNF-alpha, and IL-6 by macrophages and other cells of the innate immune system in response to immune challenge. The p38 mitogen-activated protein kinase (p38 MAPK) plays a central role in the production of these cytokines and consequently the induction of sickness behavior. Several Cancer Chemotherapy drugs have been shown to activate p38 MAPK, but whether these drugs can also induce the production of inflammatory cytokines to cause sickness behavior is unknown. The aim of this study was to determine whether the Cancer Chemotherapy drug etoposide (VP-16), which is known to activate p38 MAPK, could induce inflammatory cytokine production by murine macrophages and sickness-like behaviors when injected into mice. VP-16 activated p38 MAPK and induced IL-6 production in murine macrophages in a p38 MAPK- dependent manner. VP-16 administration rapidly increased serum levels of IL-6 in healthy mice and induced sickness-like behaviors as evidenced by a decrease in food intake, body weight, hemoglobin level, and voluntary wheel-running activity. These findings support the idea that the induction of IL-1beta, TNF-alpha, and IL-6 by Cancer Chemotherapy drugs underlies the fatigue and associated symptoms experienced by people undergoing Cancer Chemotherapy.
