Results 101 to 110 of about 564,677 (319)
FEBS Open Bio, EarlyView.The A3 adenosine receptors (A3ARs) are overexpressed in prostate cancer. AR 292 and AR 357, as A3AR antagonists, are capable of blocking proliferation, modulating the expression of drug transporter genes involved in chemoresistance, ferroptosis, and the hypoxia response, and inducing cell death.
Maria Beatrice Morelli +15 more
wiley +1 more source
Model of pathogenesis of psoriasis. Part 2. Local processes [PDF]
arXiv, 2012 Analytical research of results of experimental and theoretical studies on pathogenesis of psoriatic disease is carried out. The new model of pathogenesis - skin reaction to systemic psoriatic process SPP is formulated. ... Psoriatic inflammation is regarded as a reaction of the skin immune system to activity of Mo-R and DC-R involved in derma from ...
arxiv
Proceedings of the National Academy of Sciences of the United States of America, 1996 The conventional approach to cytotoxic T-lymphocyte (CTL) induction uses maximal antigen concentration with the intent of eliciting more CTL. However, the efficacy of this approach has not been systematically explored with regard to the quality of the ...
M. Alexander-Miller +2 more
semanticscholar +1 more source
The role of circular RNAs in regulating cytokine signaling in cancer
FEBS Open Bio, EarlyView.Cytokines present in the tumor microenvironment fuel cancer development. Aberrant expression of circRNAs contributes to cancer progression. Cytokines are involved in regulating circRNA biogenesis. Furthermore, aberrantly expressed circRNAs regulate the expression of ligands, receptors, and downstream effectors involved in cytokine signaling to promote ...
Vandana Joshi +4 more
wiley +1 more source
Proceedings of the National Academy of Sciences of the United States of America, 1982 Alloreactive human T lymphocytes were cloned in soft agar or by limiting dilution and subsequently propagated with interleukin 2 and alloantigen for 8 months or more. By indirect immunofluorescence every clone was reactive with anti-Ia antibodies as well
S. Meuer, S. Schlossman, E. Reinherz
semanticscholar +1 more source
Understanding and Overcoming Immunotherapy Resistance in Skin Cancer: Mechanisms and Strategies
Aging and Cancer, EarlyView.This narrative review explores the mechanisms driving immunotherapy resistance in skin cancer, including tumor microenvironment factors, genetic mutations, and immune evasion strategies. It highlights potential strategies to overcome resistance, offering insights for improving therapeutic outcomes and guiding future research in personalized ...
Shreya Singh Beniwal +8 more
wiley +1 more source
LYMPHOCYTE SUBPOPULATION PROFILE IN YOUNG MEN WITH METABOLIC SYNDROME
Медицинская иммунология, 2016 Metabolic syndrome is a chronic subclinical inflammation. Published data on the immune state in metabolic syndrome are inconsistent, and, moreover, the gender features of metabolic syndrome are not described in details.
V. A. Sumerkina +4 more
doaj +1 more source
Rapamycin improves Graves’ orbitopathy by suppressing CD4+ cytotoxic T lymphocytes
JCI Insight, 2023 CD4+ cytotoxic T lymphocytes (CTLs) were recently implicated in immune-mediated inflammation and fibrosis progression of Graves’ orbitopathy (GO). However, little is known about therapeutic targeting of CD4+ CTLs.
Meng Zhang +13 more
doaj +1 more source
Whole‐Blood RNA Sequencing Profiling of Patients With Rheumatoid Arthritis Treated With Tofacitinib
ACR Open Rheumatology, EarlyView.Objective Patients with rheumatoid arthritis (RA) often fail to respond to therapies, including JAK inhibitors (JAKi), and treatment allocation is made via a trial‐and‐error strategy. A comprehensive analysis of responses to JAKi, including tofacitinib, by RNA sequencing (RNAseq) would allow the discovery of transcriptomic markers with a two‐fold ...
Chiara Bellocchi +11 more
wiley +1 more source
Effects of space structure and combination therapies on phenotypic heterogeneity and drug resistance in solid tumors [PDF]
arXiv, 2013 Histopathological evidence supports the idea that the emergence of phenotypic heterogeneity and resistance to cytotoxic drugs can be considered as a process of adaptation, or evolution, in tumor cell populations. In this framework, can we explain intra-tumor heterogeneity in terms of cell adaptation to local conditions?
arxiv