Results 131 to 140 of about 171,145,466 (283)

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

open access: yesMolecular 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   +9 more
wiley   +1 more source

On the Design of LAS Spreading Codes

open access: yes, 2002
A family of Large Area Synchronised (LAS) codes is studied, which exhibits a so-called Interference Free Window (IFW), where both the Inter Symbol Interference (ISI) and the Multiple User Interference (MAI) are suppressed, provided that the relative time
Choi, B.J., Hanzo, L
core   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

open access: yesMolecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault   +12 more
wiley   +1 more source

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

open access: yesMolecular 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   +9 more
wiley   +1 more source

Concatenated Space Time Block Codes and TCM, Turbo TCM Convolutional as well as Turbo Codes

open access: yes, 2000
Space-time block codes provide substantial diversity advantages for multiple transmit antenna systems at a low decoding complexity. In this paper, we concatenate space-time codes with Convolutional Codes (CC), Turbo Convolutional codes (TC), Turbo BCH ...
Pliquett, J.   +4 more
core   +1 more source

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso   +5 more
wiley   +1 more source

[Project Summary: Mapping Area of Hard Bottom and Other Important Bottom Types: Outer Continental Shelf and Upper Continental Slope]

open access: yes, 2005
Summary describing the work completed at Louisiana State University for 'Mapping Area of Hard Bottom and Other Important Bottom Types: Outer Continental Shelf and Upper Continental Slope.' It includes background information on the project funding and ...
Louisiana State University
core  

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

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