Ras–GAP SH3 domain binding protein (G3BP) is a modulator of USP10, a novel human ubiquitin specific protease

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Utilizing Tissue Microarrays for Medium-Throughput Validation of Antibodies Against Immune Markers

https://openworks.mdanderson.org/sumexp21/1201/thumbnail.jp

Convergent evolutionary trajectories uncover metastatic drivers in renal cancer

View full abstracthttps://openworks.mdanderson.org/leading-edge/1060/thumbnail.jp

Lineage-coupled clonal capture identifies clonal evolution mechanisms and vulnerabilities of BRAF

Targeted cancer therapies have revolutionized treatment but their efficacies are limited by the development of resistance driven by clonal evolution within tumors. We developed CAPTURE , a single-cell barcoding approach to comprehensively trace clonal dynamics and capture live lineage-coupled resistant cells for in-depth multi-omics analysis and functional exploration. We demonstrate that heterogeneous clones, either preexisting or emerging from drug-tolerant persister cells, dominated resistance to vemurafenib in BRA

Ether phospholipids metabolism is a latent vulnerability for pancreatic cancer resistance

View full abstracthttps://openworks.mdanderson.org/leading-edge/1062/thumbnail.jp

Targeting Medium-Chain Acyl-CoA Dehydrogenase for Glioblastoma

View full abstracthttps://openworks.mdanderson.org/leading-edge/1041/thumbnail.jp

DPY30 loss leads to DNA re-replication and immunoediting in pancreatic ductal adenocarcinoma

View full abstracthttps://openworks.mdanderson.org/leading-edge/1036/thumbnail.jp

Pectenotoxin-2 from Marine Sponges: A Potential Anti-Cancer Agent—A Review

Pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, has been reported to display significant cytotoxicity to human cancer cells where it inhibits mitotic separation and cytokinesis through the depolymerization of actin filaments. In the late stage of endoreduplication, the effects of PTX-2 on different cancer cells involves: (i) down-regulation of anti-apoptotic Bcl-2 members and IAP family proteins; (ii) up-regulation of pro-apoptotic Bax protein and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-receptor 1/receptor 2 (DR4/DR5); and (iii) mitochondrial dysfunction. In addition, PTX-2 induces apoptotic effects through suppression of the nuclear factor κB (NF-κB) signaling pathway in several cancer cells. Analysis of cell cycle regulatory proteins showed that PTX-2 increases phosphorylation of Cdc25c and decreases protein levels of Cdc2 and cyclin B1. Cyclin-dependent kinase (Cdk) inhibitor p21 and Cdk2, which are associated with the induction of endoreduplication, were upregulated. Furthermore, it was found that PTX-2 suppressed telomerase activity through the transcriptional and post-translational suppression of hTERT. The purpose of this review was to provide an update regarding the anti-cancer mechanism of PTX-2, with a special focus on its effects on different cellular signaling cascades