Results 81 to 90 of about 991,638 (260)
Scarred by a death receptor [PDF]
The Journal of Cell Biology, 2007 ![Graphic][1] The fibrin (red) that blocks nerve healing is degraded when p75NTR isn't around (right) to dampen tPA levels. Even when it's not killing, a death receptor still finds ways to inflict damage. On page [1119][2], Sachs et al.
openaire +1 more source
Molecular Oncology, EarlyView.Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen +9 more
wiley +1 more source
Molecular Oncology, EarlyView.Circulating tumor cells (CTCs) and plasma cell‐free DNA (cfDNA) were analyzed to detect ESR1 mutations and methylation in patients with advanced breast cancer. CTC‐derived DNA showed higher sensitivity for mutation detection and revealed complementary genetic and epigenetic alterations, highlighting the added value of CTC analysis for understanding ...
Dimitra Stergiopoulou +12 more
wiley +1 more source
Role Of S-Nitrosylation In The Extrinsic Apoptotic Signalling Pathway In Cancer
Redox Biology, 2015 One of the key features of tumour cells is the acquisition of resistance to apoptosis. Thus, determining therapeutic strategies that circumvent apoptotic resistance and result in tumor regression is a challenge.
Stéphanie Plenchette
doaj +1 more source
Molecular Oncology, EarlyView.Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata +10 more
wiley +1 more source
The prevalence of TNFα-induced necrosis over apoptosis is determined by TAK1-RIP1 interplay.
PLoS ONE, 2011 Death receptor-induced programmed necrosis is regarded as a secondary death mechanism dominating only in cells that cannot properly induce caspase-dependent apoptosis.
Seda Çöl Arslan, Claus Scheidereit
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Molecular Oncology, EarlyView.Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Hepatocyte growth factor enhances death receptor-induced apoptosis by up-regulating DR5
BMC Cancer, 2008 Background Hepatocyte growth factor (HGF) and its receptor c-MET are commonly expressed in malignant gliomas and embryonic neuroectodermal tumors including medulloblastoma and appear to play an important role in the growth and dissemination of these ...
Goodwin C Rory +4 more
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Molecular Oncology, EarlyView.Both cg12821679MAPRE3 methylation and MAPRE3 expression are significantly associated with overall survival (OS) of non‐small cell lung cancer. Meanwhile, MAPRE3 expression significantly modified the effect of smoking cessation on OS. Smoking cessation benefits OS merely for patients with high MAPRE3 expression.
Chao Chen +14 more
wiley +1 more source