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Relevant bibliographies by topics / Antineoplastic Dexamethasone Dexamethasone Antineoplastic agents

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Academic literature on the topic 'Antineoplastic Dexamethasone Dexamethasone Antineoplastic agents'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Antineoplastic Dexamethasone Dexamethasone Antineoplastic agents"

1

Erin, K. Morrison, J. Aubrey Waddell, and A. Solimando Dominic. "Cyclophosphamide, Bortezomib and Dexamethasone (CyBorD) Regimen for Multiple Myeloma." Hospital Pharmacy 46, no. 11 (2011): 839–47. http://dx.doi.org/10.1310/hpj4611-839.

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The complexity of cancer chemotherapy requires pharmacists be familiar with the complicated regimens and highly toxic agents used. This column reviews various issues related to preparation, dispensing, and administration of antineoplastic therapy, and the agents, both commercially available and investigational, used to treat malignant diseases.

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Punke, Alexandra P., J. Aubrey Waddell, and Dominic A. Solimando. "Lenalidomide, Bortezomib, and Dexamethasone (RVD) Regimen for Multiple Myeloma." Hospital Pharmacy 52, no. 1 (2017): 27–32. http://dx.doi.org/10.1310/hpj5201-27.

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The complexity of cancer chemotherapy requires pharmacists be familiar with the complicated regimens and highly toxic agents used. This column reviews various issues related to preparation, dispensing, and administration of antineoplastic therapy, and the agents, both commercially available and investigational, used to treat malignant diseases.

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3

Gattis, Wendy A., and D. Byron May. "Possible Interaction Involving Phenytoin, Dexamethasone, and Antineoplastic Agents: A Case Report and Review." Annals of Pharmacotherapy 30, no. 5 (1996): 520–26. http://dx.doi.org/10.1177/106002809603000516.

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OBJECTIVE: TO describe a patient with subtherapeutic phenytoin concentrations and to review the literature regarding a possible interaction between phenytoin and chemotherapeutic agents as well as dexamethasone. CASE SUMMARY: A 29-year-old white man with brain metastases secondary to malignant melanoma consistently had suboptimal phenytoin concentrations while receiving chemotherapy consisting of cisplatin, carmustine, dacarbazine, and tamoxifen. In addition, this patient received dexamethasone, which may have influenced his phenytoin concentrations. DATA SOURCES AND STUDY SELECTION: Case repo

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4

Hesketh, Paul J., Mark G. Kris, Ethan Basch, et al. "Antiemetics: American Society of Clinical Oncology Clinical Practice Guideline Update." Journal of Clinical Oncology 35, no. 28 (2017): 3240–61. http://dx.doi.org/10.1200/jco.2017.74.4789.

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Purpose To update the ASCO guideline for antiemetics in oncology. Methods ASCO convened an Expert Panel and conducted a systematic review of the medical literature for the period of November 2009 to June 2016. Results Forty-one publications were included in this systematic review. A phase III randomized controlled trial demonstrated that adding olanzapine to antiemetic prophylaxis reduces the likelihood of nausea among adult patients who are treated with high emetic risk antineoplastic agents. Randomized controlled trials also support an expanded role for neurokinin 1 receptor antagonists in p

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Narang, Vishal S., Charles Fraga, Narendra Kumar, et al. "Dexamethasone increases expression and activity of multidrug resistance transporters at the rat blood-brain barrier." American Journal of Physiology-Cell Physiology 295, no. 2 (2008): C440—C450. http://dx.doi.org/10.1152/ajpcell.00491.2007.

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Brain edema is an important factor leading to morbidity and mortality associated with primary brain tumors. Dexamethasone, a synthetic glucocorticoid, is routinely prescribed with antineoplastic agents to alleviate pain associated with chemotherapy and reduce intracranial pressure. We investigated whether dexamethasone treatment increased the expression and activity of multidrug resistance (MDR) transporters at the blood-brain barrier. Treatment of primary rat brain microvascular endothelial cells with submicromolar concentrations of dexamethasone induced significantly higher levels of drug ef

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6

Gandhi, Anita K., Jian Kang, Lori Capone, et al. "Antiproliferative Effects of Lenalidomide in Combination with Chemotherapeutic Agents in Lymphoma Cell Lines." Blood 112, no. 11 (2008): 4990. http://dx.doi.org/10.1182/blood.v112.11.4990.4990.

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Abstract Introduction: Lenalidomide (Revlimid®) is approved for the treatment of patients with myelodysplastic syndromes with a del(5q), and in combination with dexamethasone for previously treated multiple myeloma. It is currently being evaluated in lymphomas, as monotherapy or combination therapy. This study aims to identify beneficial combinations of lenalidomide with established or potential chemotherapeutic agents for lymphoma therapy. Methods: Lenalidomide-sensitive lymphoma cell lines were selected for in vitro tumor cell proliferation studies. These included mantle cell lymphoma (MCL)

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7

Bisping, Guido, Doris Wenning, Martin H. Kropff, et al. "Enhanced Anti-Myeloma Activity by Combination of Receptor Tyrosine Kinase (RTK) Inhibition, Proteasome Inhibition, and Dexamethasone: Therapeutic Implications for t(4;14) and t(14;16) Multiple Myeloma (MM) Subgroups." Blood 106, no. 11 (2005): 112. http://dx.doi.org/10.1182/blood.v106.11.112.112.

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Abstract Novel antineoplastic agents have opened perspectives to more selective treatment of multiple myeloma (MM). Targets include FGFR3 or c-maf and VEGFR1 expressed in MM subgroups carrying t(4;14)(p16.4;q32) or t(14;16)(q32;q23), respectively. The t(4;14) MM subgroup, overexpressing FGFR3, has been recently demonstrated to be sensitive to induction of apoptosis by receptor tyrosine kinase (RTK) inhibitors [Bisping, Blood102, 661, 2003; Podar, Blood103, 3474, 2004; Trudel, Blood105, 2941, 2005]. The present study aimed at investigating mechanisms of enhanced anti-myeloma effects of BIBF 100

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Hamasaki, Makoto, Teru Hideshima, Kenji Ishitsuka, et al. "SDX-101 Is Cytotoxic and Overcomes Drug Resistance in Multiple Myeloma." Blood 104, no. 11 (2004): 3466. http://dx.doi.org/10.1182/blood.v104.11.3466.3466.

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Abstract SDX-101 is an oral antineoplastic agent, has been evaluated in a phase I/II study in B-cell malignancies. It induces cytotoxicity at least in part, by significantly inhibiting expression of Mcl-1, an anti-apoptotic Bcl-2 family protein which is highly expressed in CLL cells. Here, we examined the cytotoxicity of SDX-101 against multiple myeloma (MM) cell lines. SDX-101 significantly inhibited growth in MM.1S, U266, RPMI8226 MM cell lines using MTT assays in a time- and dose-dependent fashion, with IC50s of 0.6mM, 1.0mM, and 0.4mM, respectively. In contrast, SDX-101 did not induce cyto

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9

Carroll, Michael P., Olin Feuerbacher, Andrew M. Yeager та Terry H. Landowski. "Bortezomib Induces Rapid Upregulation of Topoisomerase IIα and Demonstrates Schedule-Dependent Synergistic Cytotoxicity with Anthracyclines and Etoposide in Acute Myeloid Leukemia and Myeloma Cell Lines." Blood 106, № 11 (2005): 2478. http://dx.doi.org/10.1182/blood.v106.11.2478.2478.

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Abstract The proteasome inhibitor bortezomib (BZ) has significant antineoplastic activity in multiple myeloma, lymphoma and acute leukemia. Recently, it has been shown that BZ can potentiate the activity of other antitumor agents in vitro. Topoisomerase IIα (topo IIα) is known to be regulated by proteasomal degradation, suggesting that proteasomal inhibition might increase intracellular topo IIα levels and thereby enhance sensitivity to topo IIα-targeted agents, including etoposide, daunorubicin and mitoxantrone. Incubation with sublethal concentrations of BZ led to rapid upregulation of topo

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10

Gribben, John G., Nathan Fowler, and Franck Morschhauser. "Mechanisms of Action of Lenalidomide in B-Cell Non-Hodgkin Lymphoma." Journal of Clinical Oncology 33, no. 25 (2015): 2803–11. http://dx.doi.org/10.1200/jco.2014.59.5363.

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Lenalidomide is an orally active immunomodulatory drug that has direct antineoplastic activity and indirect effects mediated through multiple types of immune cells found in the tumor microenvironment, including B, T, natural killer (NK), and dendritic cells. Recently, the E3 ubiquitin ligase cereblon was identified as a molecular target that may underlie the effects of lenalidomide on tumor cells, as well as on cells in the tumor microenvironment. Decreases in cereblon attenuate these effects and also confer resistance to lenalidomide. Tumoricidal effects of lenalidomide are associated with re

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Dissertations / Theses on the topic "Antineoplastic Dexamethasone Dexamethasone Antineoplastic agents"

1

Laane, Edward. "Cell death mechanisms of anti-cancer agents and treatment response in acute leukemia /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-854-1/.

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Lundström, Staffan. "Corticosteroids in advanced cancer : epidemiology, symptom relief and patient experiences /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-131-9/.

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