Results 201 to 210 of about 2,672,882 (329)

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

open access: yesMolecular Oncology, EarlyView.
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee   +8 more
wiley   +1 more source

Interferon regulatory factor 4 modulates epigenetic silencing and cancer-critical pathways in melanoma cells. [PDF]

open access: yesMol Oncol
Sobhiafshar U   +10 more
europepmc   +1 more source

Tumor mutational burden as a determinant of metastatic dissemination patterns

open access: yesMolecular Oncology, EarlyView.
This study performed a comprehensive analysis of genomic data to elucidate whether metastasis in certain organs share genetic characteristics regardless of cancer type. No robust mutational patterns were identified across different metastatic locations and cancer types.
Eduardo Candeal   +4 more
wiley   +1 more source

Overcoming mutational complexity in acute myeloid leukemia by inhibition of critical pathways. [PDF]

open access: yesSci Transl Med, 2017
Saito Y   +15 more
europepmc   +1 more source

A brain organoid/ALL coculture model reveals the AP-1 pathway as critically associated with CNS involvement of BCP-ALL

open access: gold
Philip Gebing   +19 more
openalex   +1 more source

Targeting p38α in cancer: challenges, opportunities, and emerging strategies

open access: yesMolecular Oncology, EarlyView.
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley   +1 more source

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