Results 141 to 150 of about 1,915,617 (250)

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

Molecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad, Silvio Carlo Ermanno Tosatto, Emanuela Leonardi   +2 more
wiley   +1 more source

Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer

Molecular Oncology, EarlyView.
Extracellular vesicle (EV) lipidomic profiling of plasma and ascites from patients with high‐grade serous ovarian cancer and of ovarian cancer cell lines reveals enrichment of triglycerides (TGs), diacylglycerols (DGs), phosphatidylcholine (PCs), sphingomyelins (SMs), reflecting tumor metabolic reprogramming.
Shikha Rani, Dominic Guanzon, Andrew Lai, Katherin Scholz‐Romero, Sarah Reed, Edita Ritmejeryte, Rohan Lourie, Naven Chetty, Kaltin Ferguson, Carlos Salomon   +9 more
wiley   +1 more source

Advances in causal discovery methods for ecological time series. [PDF]

Biol Rev Camb Philos Soc
Suzuki K, Yamamichi M, Osada Y, Ushio M, Nakajima K, Masuya H, Shimizu S.   +6 more
europepmc   +1 more source

A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

Molecular Oncology, EarlyView.
Loss of eIF5A rewires thapsigargin‐mediated endoplasmic reticulum stress responses in multiple myeloma cells by selective translation of mRNA transcripts, consequently dampening thapsigargin‐induced unfolded protein response (UPR) activation and shifting the balance from induction of apoptosis toward cell survival and proliferation.
Demi Both, Ingrid A. M. Derks, Raphaël Vanleyssem, Marine Leclercq, Najla El Hachem, Pierre Close, Eric Eldering, Marco Vincent Haselager   +7 more
wiley   +1 more source

Linear Causal Discovery with Interventional Constraints. [PDF]

Mach Learn
Guo Z, Dong F.
europepmc   +1 more source

Federated Causal Discovery From Interventions [PDF]

Causal discovery serves a pivotal role in mitigating model uncertainty through recovering the underlying causal mechanisms among variables. In many practical domains, such as healthcare, access to the data gathered by individual entities is limited ...
Bauer, Stefan, Scherrer, Nino, Schwab, Patrick, Mehrjou, Arash, Abyaneh, Amin, Schölkopf, Bernhard   +5 more
core  

Extracellular matrix remodeling and immune reprogramming drive residual tumor progression of liver cancer after incomplete microwave ablation

Molecular Oncology, EarlyView.
Incomplete microwave ablation (iMWA) of liver cancer triggers a biphasic progression in residual tumors. At Day 3, the microenvironment is characterized by acute inflammatory responses and extracellular matrix (ECM) remodeling. By Day 14, a profound shift occurs toward oncogenic signal transduction and immunosuppression, marked by macrophage ...
Yu Liu, Yubei He, Nikolaus Berndt, Michael Mülleder, Kathrin Textoris‐Taube, Jing Guo, Matthias Stechele, Justus Ramtke, Shraga Nahum Goldberg, Lynn Jeanette Savic   +9 more
wiley   +1 more source

Causal Discovery in Observational Medical Research: Scoping Review. [PDF]

JMIR Med Inform
Liu Z, Luo T, Ma H, Mo J, Yang X, Huang Z, Li J, Kuang J.   +7 more
europepmc   +1 more source

ALCM: Autonomous LLM-Augmented Causal Discovery Framework [PDF]

To perform effective causal inference in high-dimensional datasets, initiating the process with causal discovery is imperative, wherein a causal graph is generated based on observational data. However, obtaining a complete and accurate causal graph poses
Yang, Zhongqi, Khatibi, Elahe, Azimi, Iman, Rahmani, Amir M., Abbasian, Mahyar   +4 more
core  

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

Molecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim, Aurelie Genoux, Nadiia Zubchuk, Haoyang Zheng, Perla Salameh, Theo Ziegelmeyer, Fabien Dalonneau, Margot Rouchette, Christiane Oddou, Simona Miron, Helene Polveche, Adiilah Mamode Cassim, Carmen Garrido, Eleni Nikolakaki, Didier Auboeuf, Tao Jia, Sophie Zinn‐Justin, Beatrice Eymin   +17 more
wiley   +1 more source