Results 91 to 100 of about 370,667 (257)
PANoptosis in the pathogenesis of myelodysplastic syndromes
Molecular Oncology, EarlyView.PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla +4 more
wiley +1 more source
Frontiers in Cell and Developmental BiologyNeuroblastoma is the most common extracranial solid malignancy in children and accounts for nearly 15% of paediatric cancer-related mortality, underscoring its substantial clinical burden.
Rohan Gupta +8 more
doaj +1 more source
Spatial biology in cancer epigenetics
Molecular Oncology, EarlyView.Spatial epigenomics combines molecular profiling with tissue architecture to reveal how gene regulation is organized within intact tissues. In cancer, these technologies uncover the mechanisms driving tumor heterogeneity and microenvironmental interactions, opening new opportunities for biomarker discovery and precision medicine.
Eva Crespo‐García, Manel Esteller
wiley +1 more source
Aberrant promoter methylation in p53 and ATM genes was not associated with sporadic breast carcinogenesis in Bulgarian patients [PDF]
Journal of BioScience and Biotechnology, 2014 Epigenetic silencing of gene expression has become an intensively studied topic regarding breast cancer during the last years. Previous investigations have shown that hypermethylation in gene promoters is an alternative to mutations cancer-related ...
MARIA E. KRASTEVA +6 more
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Molecular Oncology, EarlyView.This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi +6 more
wiley +1 more source
ADP‐ribosylation: An emerging regulator of the epigenome
Molecular Oncology, EarlyView.ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho +2 more
wiley +1 more source
Molecular Oncology, EarlyView.We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee +3 more
wiley +1 more source
Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk
Molecular Oncology, EarlyView.Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley +1 more source
Molecular Oncology, EarlyView.Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley +1 more source
Genetic alterations in head and neck squamous cell carcinomas
Brazilian Journal of Medical and Biological Research, 1999 The genetic alterations observed in head and neck cancer are mainly due to oncogene activation (gain of function mutations) and tumor suppressor gene inactivation (loss of function mutations), leading to deregulation of cell proliferation and death ...
Nagai M.A.
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