Results 101 to 110 of about 1,950,176 (266)

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

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, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

Nutrition strategies for obesity management [PDF]

Background Obesity is a chronic disease that necessitates nutritional strategy for effective weight management.  Behavioural modification relating to nutrients intake, food selection and dietary patterns are essential for sustaining long-term ...
Andayani, Diyah Eka, Sunardi, Diana, Linda, Vitia ajeng Nur, Fadilah   +3 more
core   +1 more source

Circulating microRNA signatures of cachexia and cancer in Canis familiaris as a comparative oncology model for human disease

Molecular Oncology, EarlyView.
Circulating microRNAs as biomarkers of cachexia and sex‐specific cancer in senior dogs. In 25 client‐owned dogs, four circulating miRNAs (miR‐15a, miR‐15b, miR‐16, miR‐140) were downregulated in cachexia, with miR‐16 the strongest individual biomarker (AUC = 0.899).
Soon‐Seok Park, Kyongman An, Gyeonghwa Kim, Soo‐Nyun Choi, Hong‐Ki Lee, Keun Hur, Kyu‐Shik Jeong   +6 more
wiley   +1 more source

Targeting transcription factors associated with hemoglobinopathies: Lessons from successful interventions and implications for cancer

Molecular Oncology, EarlyView.
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu, Puspa Das, Xing Zhang, Xiaodong Cheng   +3 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, Chenqian Liu, W. Lee Kraus   +2 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

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

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

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

Molecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico, Veronica La Banca, Silvia D'Amico, Stefano Scalera, Sara Nicolai, Angelo Peschiaroli   +5 more
wiley   +1 more source

Scientific Opinion on the substantiation of health claims related to Saccharomyces cerevisiae var. boulardii CNCM I‐1079 and defence against pathogenic gastro‐intestinal microorganisms (ID 913, further assessment) pursuant to Article 13(1) of Regulation (EC) No 1924/2006

EFSA Journal, 2012
Following a request from the European Commission, the Panel on Dietetic Products, Nutrition and Allergies was asked to provide a scientific opinion on a health claim pursuant to Article 13 of Regulation (EC) No 1924/2006 in the framework of further ...
EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA)
doaj   +1 more source