Temozolomide
Mostrando 1-12 de 19 artigos, teses e dissertações.
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1. Complexation and enhancement of temozolomide solubility with cyclodextrins
ABSTRACT Temozolomide is a poorly soluble anti-cancer drug used in the treatment of some brain cancers. Following literature reports about the enhancement of solubility and stability for these kinds of drugs upon complexation with cyclodextrins, we aimed to form an inclusion complex between temozolomide and the different types of cyclodextrins (CDs) to enhan
Braz. J. Pharm. Sci.. Publicado em: 26/07/2018
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2. Temozolomide in aggressive pituitary adenomas and carcinomas
Temozolomide is an alkylating agent used in the treatment of gliomas and, more recently, aggressive pituitary adenomas and carcinomas. Temozolomide methylates DNA and, thereby, has antitumor effects. O6-methylguanine-DNA methyltransferase, a DNA repair enzyme, removes the alkylating adducts that are induced by temozolomide, thereby counteracting its effects.
Clinics. Publicado em: 2012
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3. Antiproliferative effects of Tubi-bee propolis in glioblastoma cell lines
Propolis is a resin formed by a complex chemical composition of substances that bees collect from plants. Since ancient times, propolis has been used in folk medicine, due to its biological properties, that include antimicrobial, anti-inflammatory, antitumoral and immunomodulatory activities. Glioblastoma is the most common human brain tumor. Despite the imp
Genetics and Molecular Biology. Publicado em: 2011
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4. Assessment of cellular responses mediated by temozolomide combined with metoxiamina, an inhibitor of DNA repair, in glioblastoma cell lines. / Avaliação da resposta celular mediada pelo quimioterápico temozolomida associada ao inibidor do reparo do DNA metoxiamina em linhagens de glioblastoma.
Gliomas represent more than 70% of primary brain tumors. Even following an aggressive therapies, the mean survival rate of patients with these tumors is less than one year after diagnosis. Chemotherapy based on alkyklating agents, such as temozolomide (TMZ) has been reported to increase the survival rate. N7-metyl-G and N3-metyl-A adducts comprise more than
Publicado em: 2009
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5. Mecanismos de indução de apoptose pela presença de danos ao DNA: um estudo sobre o papel de p53 na resistência de células de glioma a agentes quimioterápicos. / Mechanisms of apoptosis induction by DNA damage: a study on the role of p53 to the resistance that glioma cells present to chemotherapeutical agents.
Induction of DNA lesions leads to several different endpoints in mammalian cells, such as replication blockage, activation of DNA repair pathways, mutagenesis and induction of apoptosis. Although apoptosis induction might be involved in deleterious conditions, it can also bring benefit, as for instance to avoid the uncontrolled propagation of a mutated cell.
Publicado em: 2008
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6. A phase II trial of lomeguatrib and temozolomide in metastatic colorectal cancer
Nature Publishing Group.
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7. Extent of MGMT promoter methylation correlates with outcome in glioblastomas given temozolomide and radiotherapy
Nature Publishing Group.
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8. Talampanel With Standard Radiation and Temozolomide in Patients With Newly Diagnosed Glioblastoma: A Multicenter Phase II Trial
American Society of Clinical Oncology.
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9. Randomized Phase II Trial of Chemoradiotherapy Followed by Either Dose-Dense or Metronomic Temozolomide for Newly Diagnosed Glioblastoma
American Society of Clinical Oncology.
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10. Two phase II trials of temozolomide with interferon-α2b (pegylated and non-pegylated) in patients with recurrent glioblastoma multiforme
Nature Publishing Group.
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11. Dexamethasone protected human glioblastoma U87MG cells from temozolomide induced apoptosis by maintaining Bax:Bcl-2 ratio and preventing proteolytic activities
BioMed Central.
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12. Msh2 status modulates both apoptosis and mutation frequency in the murine small intestine
Deficiency in genes involved in DNA mismatch repair increases susceptibility to cancer, particularly of the colorectal epithelium. Using Msh2 null mice, we demonstrate that this genetic defect renders normal intestinal epithelial cells susceptible to mutation in vivo at the Dlb-1 locus. Compared with wild-type mice, Msh2-deficient animals had higher basal le
The National Academy of Sciences.