Results 191 to 200 of about 1,301,037 (308)

3D-super-enhancers are condensate-associated cis-regulatory communities. [PDF]

open access: yesNucleic Acids Res
Lv J   +13 more
europepmc   +1 more source

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular 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

Insights into a long life without cancer: The case of the bowhead whale

open access: yesMolecular Oncology, EarlyView.
Long‐lived, large‐bodied organisms have evolved powerful anticancer mechanisms that preserve cellular and tissue integrity across extended lifespans. A recent study by Firsanov et al. shows that greater genome stability is a key factor underlying the remarkable longevity and cancer resistance of one such species, the bowhead whale.
Inés Paniagua, Johanna A. Joyce
wiley   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

Checkpoint blockade and the stem‐like T cell trade‐off

open access: yesMolecular Oncology, EarlyView.
Stem‐like T cells are key to the success of programmed cell death protein 1 (PD1) blockade, as they sustain long‐term anti‐tumor response by continuously generating effector CD8+ T cells. However, how these cells are maintained in cancer is not fully understood. Hor et al.
Julie M. Mazet, Johanna A. Joyce
wiley   +1 more source

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