Results 1 to 10 of about 955 (158)

Targeting Oxidative Stress With Auranofin or Prima-1Met to Circumvent p53 or Bax/Bak Deficiency in Myeloma Cells [PDF]

open access: yesFrontiers in Oncology, 2019
Prima-1Met (APR-246) was previously shown to be dependent on glutathione inhibition and on ROS induction in cancer cells with mutated or deleted TP53.
Benoit Tessoulin   +15 more
doaj   +10 more sources

Molecular Mechanisms of Synergistic Effect of PRIMA‐1met and Oxaliplatin in Colorectal Cancer With Different p53 Status [PDF]

open access: yesCancer Medicine
Background The toxicity and drug resistance associated with oxaliplatin (L‐OHP) limit its long‐term use for colorectal cancer (CRC) patients. p53 mutation is a common genetic trait of CRC.
Xiao‐lan Li   +7 more
doaj   +3 more sources

PRIMA-1Met suppresses colorectal cancer independent of p53 by targeting MEK. [PDF]

open access: yesOncotarget, 2016
This work was supported by Grant No. 81201779 (Hua Xiong) from the National Natural Science Youth Foundation; Grant No. 81502118 (Yanmei Zou) from the National Natural Science Youth Foundation; Grant No.
Lu T   +15 more
europepmc   +8 more sources

PRIMA-1MET-induced neuroblastoma cell death is modulated by p53 and mycn through glutathione level [PDF]

open access: yesJournal of Experimental & Clinical Cancer Research, 2019
Background Neuroblastoma is the most common extracranial solid tumor in children. This cancer has a low frequency of TP53 mutations and its downstream pathway is usually intact.
Vid Mlakar   +7 more
doaj   +5 more sources

Synergistic effects of PRIMA-1Met (APR-246) and 5-azacitidine in TP53-mutated myelodysplastic syndromes and acute myeloid leukemia [PDF]

open access: yesHaematologica, 2020
Myelodysplastic syndromes and acute myeloid leukemia with TP53 mutations are characterized by frequent relapses, poor or short responses, and poor survival with the currently available therapies including chemotherapy and 5-azacitidine (AZA).
Nabih Maslah   +16 more
doaj   +5 more sources

PRIMA-1MET Inhibits Growth of Mouse Tumors Carrying Mutant p53 [PDF]

open access: yesCellular Oncology, 2008
Reactivation of the tumor suppressor activity to mutant p53 should trigger massive apoptosis and eliminate tumors. The low molecular weight compounds PRIMA-1 and the structural analog PRIMA-1MET reactivate human mutant p53 in vitro and suppress growth of
Nicole Zache   +3 more
doaj   +4 more sources

PRIMA-1Met induces apoptosis in Waldenström's Macroglobulinemia cells independent of p53 [PDF]

open access: yesCancer Biology and Therapy, 2015
PRIMA-1Met has shown promising preclinical activity in various cancer types. However, its effect on Waldenström's Macroglobulinemia (WM) cells as well as its exact mechanism of action is still elusive. In this study, we evaluated the anti- tumor activity of PRIMA-1Met alone and in combination with dexamethasone or bortezomib in WM cell lines and ...
Hong Chang
exaly   +5 more sources

A thiol‐bound drug reservoir enhances APR‐246‐induced mutant p53 tumor cell death [PDF]

open access: yesEMBO Molecular Medicine, 2020
The tumor suppressor gene TP53 is the most frequently mutated gene in cancer. The compound APR‐246 (PRIMA‐1Met/Eprenetapopt) is converted to methylene quinuclidinone (MQ) that targets mutant p53 protein and perturbs cellular antioxidant balance.
Sophia Ceder   +15 more
doaj   +2 more sources

PRIMA-1MET induces apoptosis through accumulation of intracellular reactive oxygen species irrespective of p53 status and chemo-sensitivity in epithelial ovarian cancer cells. [PDF]

open access: yesOncol Rep, 2016
名古屋大学Nagoya University博士(医学)doctoral ...
Yoshikawa N   +10 more
europepmc   +3 more sources

Pan-cancer landscape of disulfidptosis across human tumors [PDF]

open access: yesHeliyon
Objective: Disulfidptosis is a newly discovered disulfide stress-induced cell death form. Clinical significance and biological mechanisms of disulfidptosis in human cancers need to be further elucidated.
Kun Fang   +4 more
doaj   +2 more sources

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