Results 151 to 160 of about 63,224 (282)

Histone deacetylase inhibitors as venetoclax‐sensitising partners in acute myeloid leukaemia: Mechanisms, pharmacology and translational perspectives

open access: yesBritish Journal of Pharmacology, EarlyView.
Abstract Venetoclax combined with hypomethylating agents has improved treatment for older or unfit patients with acute myeloid leukaemia (AML), but resistance and relapse remain common. This review analyses the rationale for combining venetoclax with inhibitors of histone deacetylase (HDAC).
Jaebok Lee, Marc Diederich
wiley   +1 more source

A Three‐Dimensional Culture–Drug Sensitivity Test Predicts MDM2 Inhibitor–Sensitivity in SMARCB1/INI1‐Deficient Tumors

open access: yesCancer Science, EarlyView.
This study aimed to determine whether personalized selection of effective drugs for SMARCB1/INI1‐deficient tumors is feasible using in vitro drug sensitivity profiling. Drug sensitivity was assessed using a short‐term collagen gel–embedded three‐dimensional drug sensitivity test (3D‐DST) in tumors derived from SMARCB1/INI1‐deficient tumor cell line ...
Hiroaki Goto   +12 more
wiley   +1 more source

Pleiotropic Roles of FBXO11 in Tumorigenesis: Implications for Targeted Therapy

open access: yesCancer Science, EarlyView.
This complex comprises of scaffold CUL1, SKP1, RBX1 and FBXO11 receptor. The substrate is phosphorylated by specific kinase enzyme and recognized by the substrate recognition domain. FBXO11 targets numerous substrates for ubiquitination and degradation, FBXO11 substrates mainly include Snail, ZEB1, p53, BCL6, CDT2, CIITA, Cdc25a, hnRNPA2B1, SAMD1 and ...
Yuqi Zhang   +6 more
wiley   +1 more source

Ploidy‐Dependent Response to Anticancer Drugs of Human Embryonic Stem Cells

open access: yesCell Proliferation, EarlyView.
Using isogenic hESCs, differing only in their ploidy level, we show the effect of ploidy on the resistance to anticancer drugs. We demonstrate that polyploidy, by itself, confers sensitivity to chemotherapies, leading to higher apoptosis and delayed proliferation, while the loss of p53 reverses the phenotype, demonstrating higher resistance.
Guy Haim‐Abadi, Nissim Benvenisty
wiley   +1 more source

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