Results 61 to 70 of about 79,208 (292)
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
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]
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
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
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
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]
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
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]
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]
Abstract CHZ868 inhibits the proliferation of JAK2-mutant and type I JAK inhibitor–persistent cells.
openaire +1 more source

