Results 211 to 220 of about 5,108,464 (344)

RELA Ablation Contributes to Progression of Hepatocellular Carcinoma with TP53R249S Mutation and is a Potential Therapeutic Target

open access: yesAdvanced Science, EarlyView.
Genome‐wide CRISPR/Cas9 based screening identified RELA as a key tumor suppressor in TP53R249S‐mutant HCC. Its loss promotes tumorigenesis and metastasis via DVL1‐mediated Wnt/β‐catenin activation, while its agonist betulinic acid suppresses tumor progression.
Zhiping Wu   +17 more
wiley   +1 more source

Flow cytometric analysis of DNA content in human ovarian cancers

open access: green, 1989
Eugenio Erba   +8 more
openalex   +1 more source

Integrative Omics Reveals Glutamine Catabolism‐Driven Apoptotic Suppression in Monocytes upon Mechanical Unloading

open access: yesAdvanced Science, EarlyView.
This research integrated multi‐omics analysis of bone tissue from HLU and control mice revealed that mechanical unloading suppresses intrinsic apoptosis and augments glutamine (Gln) catabolism in osteoclast lineage cells. The findings highlight pivotal roles for SLC1A5‐mediated Gln metabolism and XIAP/Diablo axis‐mediated apoptosis suppression.
Yi Ding   +14 more
wiley   +1 more source

5’‐Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation‐Mediated PAK2 Upregulation to Promote Cadmium‐Induced Breast Cancer Progression by Impairing Autophagic Flux

open access: yesAdvanced Science, EarlyView.
Cadmium, a carcinogenic heavy metal, drives breast cancer progression via metabolic reprogramming and autophagic flux disruption. Multi‐omics revealed cadmium‐induced 5'‐methylthioadenosine depletion activates DOT1L‐mediated H3K79me1 at PAK2 promoter, upregulating PAK2 to block autophagy and driving malignancy. Clinically, 5'‐methylthioadenosine levels
Jingdian Li   +24 more
wiley   +1 more source

Advanced Microfluidics for Single Cell‐Based Cancer Research

open access: yesAdvanced Science, EarlyView.
Cutting‐edge microfluidic platforms are transforming single‐cell cancer research. This review highlights advanced technologies, from droplet microfluidics to tumour‐chips, that enable functional and spatial single‐cell analyses. By integrating biosensing, immune components, and patient‐derived materials, these systems offer new insights into tumour ...
Adriana Carneiro   +10 more
wiley   +1 more source

Author Correction: Tuning microtubule dynamics to enhance cancer therapy by modulating FER-mediated CRMP2 phosphorylation

open access: yesNature Communications, 2022
Yiyan Zheng   +30 more
doaj   +1 more source

Incidence of neuropathy in 395 patients with ovarian cancer treated with or without cisplatin [PDF]

open access: bronze, 1990
R. Gerritsen van der Hoop   +4 more
openalex   +1 more source

Citrullination of AKT2 Catalyzed by PAD1 Facilitates the Maintenance of Stemness Characteristics of Ovarian Cancer Stem‐Like Cells in Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
PAD1 is upregulated within the CD133+ subset or cisplatin‐resistant ovarian cancer cells, which is positively associated with the upregulation of stemness‐related markers and maintenance of stemness in OCSLCs. Mechanistically, PAD1‐catalyzed AKT2 citrullination at R202 facilitates AKT2 phosphorylation, promoting CEBPβ expression and its binding to the ...
Teng Xue   +10 more
wiley   +1 more source

High serum and ascitic soluble interleukin-2 receptor alpha levels in advanced epithelial ovarian cancer [see comments] [PDF]

open access: bronze, 1993
DP Barton   +5 more
openalex   +1 more source

Osteoblast‐CD4+ CTL Crosstalk Mediated by SIRT1/DAAM2 Axis Prevents Age‐Related Bone Loss

open access: yesAdvanced Science, EarlyView.
In the osteoblastic niche, SIRT1 activates and recruits CD4+ CTLs by increasing DAAM2 expression via EZH2 deacetylation and boosting the secretion of key chemokines, such as CCL3, CCL5, and CXCL10. Then, CD4+ CTL directly eliminates senescent osteoblasts in an MHC‐II‐dependent way, thereby slowing down the process of bone ageing and effectively ...
Bin Yang   +20 more
wiley   +1 more source

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