Results 31 to 40 of about 56,569 (202)

TERT Mutation Is Accompanied by Neutrophil Infiltration and Contributes to Poor Survival in Isocitrate Dehydrogenase Wild-Type Glioma

open access: yesFrontiers in Cell and Developmental Biology, 2021
Mutation of the telomerase reverse transcriptase (TERT) promoter has been demonstrated as an unfavorable prognostic marker in patients with isocitrate dehydrogenase wild-type (IDHwt) glioma.
Mengqi Gao   +12 more
doaj   +1 more source

Differential structural remodelling of heparan sulfate by chemokines: the role of chemokine oligomerization [PDF]

open access: yesOpen Biology, 2017
Chemokines control the migration of cells in normal physiological processes and in the context of disease such as inflammation, autoimmunity and cancer.
Douglas P. Dyer   +5 more
doaj   +1 more source

Chemokines [PDF]

open access: yes, 2014
Chemokines are a family of structurally related cytokines with four cysteines at their well-conserved positions. Most chemokines are secreted proteins with a molecular weight about 10.
30182067   +3 more
core   +1 more source

Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential

open access: yesFEBS Letters, EarlyView.
Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta   +3 more
wiley   +1 more source

Ccl2 and Ccl3 Mediate Neutrophil Recruitment via Induction of Protein Synthesis and Generation of Lipid Mediators [PDF]

open access: yes, 2009
Objective: Although the chemokines monocyte chemoattractant protein-1 (Ccl2/JE/MCP-1) and macrophage inflammatory protein-1α (Ccl3/MIP-1α) have recently been implicated in neutrophil migration, the underlying mechanisms remain largely unclear.
Alexander Georg Khandoga   +15 more
core   +1 more source

An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes

open access: yesFEBS Letters, EarlyView.
GPR35 generates two functionally distinct isoforms with previously unresolved roles. GPR35‐short mediates immune‐cell chemotaxis, while GPR35‐long is enriched in colorectal cancer epithelium, where it supports increased metabolism, proliferation, and tumor‐associated transcriptional programs.
Jørgen D. Rønneberg   +14 more
wiley   +1 more source

The role of CXC chemokines in the transition of chronic inflammation to esophageal and gastric cancer

open access: yes, 2012
<p>Chronic inflammation may increase the risk to develop cancer, for instance esophagitis or gastritis may lead to development of esophageal or gastric cancer, respectively.
S. Struyf   +7 more
core   +1 more source

Engineering peptides into antibodies—opportunities and strategies for therapeutic innovation

open access: yesFEBS Letters, EarlyView.
Peptides and antibodies occupy complementary therapeutic niches. Peptides recognize difficult targets in a compact format, while antibodies add specificity, long half‐life, and effector functions. This review examines strategies that merge both modalities—peptide grafting into loops, terminal and Fc fusions, and bioconjugation—highlighting how ...
Jinling Wang   +2 more
wiley   +1 more source

SPATA2 and CYLD inhibit T cell infiltration into colorectal cancer via regulation of IFN-γ/STAT1 axis

open access: yesFrontiers in Oncology, 2022
IntroductionColorectal cancer (CRC) is largely refractory to currently available immunotherapies such as blockade of programmed cell death protein-1 (PD-1).ResultsIn this study, we identified SPATA2 and its protein partner CYLD as novel regulators of CXC-
Tze Guan Tan   +8 more
doaj   +1 more source

Epigenetic reprogramming of lineage switching in cancer

open access: yesFEBS Letters, EarlyView.
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı   +4 more
wiley   +1 more source

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