Results 61 to 70 of about 79,208 (292)

The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies

open access: yesAdvanced Science, EarlyView.
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang   +5 more
wiley   +1 more source

Association between JAK2V617F Mutation and Mean Platelet Volume among Myeloproliferative Neoplasm Patients

open access: yesJournal of Applied Hematology
BACKGROUND: Myeloproliferative neoplasms (MPNs) are clonal disorders affecting myeloid progenitor cells, with thrombotic events being a major cause of mortality and morbidity. Increased mean platelet volume (MPV) has been linked to higher thrombosis risk.
Mushtaq M. Khazeem, Alaa Fadhil Alwan
doaj   +1 more source

Downregulation of ClC-2 by JAK2 [PDF]

open access: yesCellular Physiology and Biochemistry, 2012
JAK2 (Janus kinase-2) is activated by cell shrinkage and may thus participate in cell volume regulation. Cell volume regulatory ion channels include the small conductance Cl(-) channels ClC-2. The present study thus explored whether JAK2 influences ClC-2 activity.
Hosseinzadeh, Zohreh   +2 more
openaire   +3 more sources

Multi‐Technique Integration Identifies O‐GlcNAc Transferase in Fibroblast‐Like Synoviocytes as a Therapeutic Target for Rheumatoid Arthritis

open access: yesAdvanced Science, EarlyView.
AI‑guided single‑cell transcriptomics identifies OGT as a key regulator enriched in rheumatoid arthritis fibroblast‑like synoviocytes (RA‐FLSs). Inflammatory stimuli activate the OGT–SAP130 axis, which modulates the H3K27ac/H3K27me3 balance and epigenetically silences BTG2, promoting aggressive transformation of RA‑FLSs.
Duoli Xie   +14 more
wiley   +1 more source

NVP-BSK805, an Inhibitor of JAK2 Kinase, Significantly Enhances the Radiosensitivity of Esophageal Squamous Cell Carcinoma in vitro and in vivo

open access: yesDrug Design, Development and Therapy, 2020
Yuhui Hua,1 Weijia Wang,1 Xiaoli Zheng,2 Ling Yang,2 Hongjin Wu,2 Zhaoyang Hu,2 Ying Li,2 Jing Yue,2 Zhenzhen Jiang,2 Xiaoyan Zhang,2 Qiang Hou,2 Shixiu Wu3 1Department of Pharmacy, Hangzhou Cancer Hospital, Hangzhou 310002, People’s Republic of ...
Hua Y   +11 more
doaj  

The JAK2V617F and CALR exon 9 mutations are shared immunogenic neoantigens in hematological malignancy

open access: yesOncoImmunology, 2017
Approximately 90% of patients with the hematological malignancies termed the chronic myeloproliferative neoplasms harbor either the JAK2V617F-mutation or CALR exon 9 mutation.
Morten Orebo Holmström   +2 more
doaj   +1 more source

Random mutagenesis reveals residues of JAK2 critical in evading inhibition by a tyrosine kinase inhibitor. [PDF]

open access: yesPLoS ONE, 2012
The non-receptor tyrosine kinase JAK2 is implicated in a group of myeloproliferative neoplasms including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.
Michael R Marit   +6 more
doaj   +1 more source

Upadacitinib Restrains the Pathogenic Fitness of CD4+ T Cells and Aberrant B Cell Programming in Optic Neuritis

open access: yesAdvanced Science, EarlyView.
Single‐cell profiling and functional perturbation reveal coordinated JAK1‐pSTAT3 downstream programs in optic neuritis, including MCL1‐dependent fitness of pathogenic CD4+ Tem cells and glycolysis‐linked, cholesterol‐sensitive B‐cell responses associated with RORA. Upadacitinib disrupts this reciprocal T‐B‐cell circuit and alleviates neuroinflammation,
Gengchen Jiang   +12 more
wiley   +1 more source

DNA damage stress and inhibition of Jak2-V617F cause its degradation and synergistically induce apoptosis through activation of GSK3β. [PDF]

open access: yesPLoS ONE, 2011
The cytoplasmic tyrosine kinase Jak2 plays a crucial role in cytokine receptor signaling in hematopoietic cells. The activated Jak2-V617F mutant is present in most cases of BCR/ABL-negative myeloproliferative neoplasms and constitutively activates ...
Toshikage Nagao   +4 more
doaj   +1 more source

A Type II JAK2 Inhibitor Is Active in JAK2-Dependent Malignancies [PDF]

open access: yesCancer Discovery, 2015
Abstract CHZ868 inhibits the proliferation of JAK2-mutant and type I JAK inhibitor–persistent cells.
openaire   +1 more source

Home - About - Disclaimer - Privacy