Results 81 to 90 of about 115,636 (264)
Molecular Oncology, EarlyView.CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak +10 more
wiley +1 more source
The inhibitors – a challenge for the management of patients with hereditary haemophilia A
Romanian Journal of Internal Medicine, 2018 Introduction. Our research strategy was aimed at evaluating the possible implication of the type of factor VIII product administered as substitution treatment to haemophilia A patients in the occurrence of inhibitors and their consequences on the ...
Mihăilă Romeo-Gabriel
doaj +1 more source
Molecular Oncology, EarlyView.Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen +9 more
wiley +1 more source
Molecular Oncology, EarlyView.Both cg12821679MAPRE3 methylation and MAPRE3 expression are significantly associated with overall survival (OS) of non‐small cell lung cancer. Meanwhile, MAPRE3 expression significantly modified the effect of smoking cessation on OS. Smoking cessation benefits OS merely for patients with high MAPRE3 expression.
Chao Chen +14 more
wiley +1 more source
Molecular Oncology, EarlyView.Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens +6 more
wiley +1 more source
Molecular Oncology, EarlyView.We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
Molecular Oncology, EarlyView.MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Molecular Oncology, EarlyView.The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source
Molecular Oncology, EarlyView.The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +1 more source
Molecular Oncology, EarlyView.BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi +11 more
wiley +1 more source