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MYC activation is a known hallmark of cancer as it governs the gene targets involved in various facets of cancer progression. Of interest, MYC governs oncometabolism through the interactions with its partners and cofactors, as well as cancer immunity via its gene targets. Recent investigations have taken interest in characterizing these interactions through multi-Omic approaches, to better understand the vastness of the MYC network. Of the several gene targets of MYC involved in either oncometabolism or oncoimmunology, few of them overlap in function. Prominent interactions have been observed with MYC and HIF-1α, in promoting glucose and glutamine metabolism and activation of antigen presentation on regulatory T cells, and its subsequent metabolic reprogramming. This review explores existing knowledge of the role of MYC in oncometabolism and oncoimmunology. It also unravels how MYC governs transcription and influences cellular metabolism to facilitate the induction of pro- or anti-tumoral immunity. Moreover, considering the significant roles MYC holds in cancer development, the present study discusses effective direct or indirect therapeutic strategies to combat MYC-driven cancer progression.
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http://dx.doi.org/10.3389/fimmu.2024.1324045 | DOI Listing |
Reprod Biol
September 2025
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China; Engineering Research Center of Biopreservation and Artificial Organs, Ministry of Education, No 218 Jixi Road, Hefei Anhui230022, China; Key Laboratory of Population Health Across
Current research indicates that polyethylene terephthalate microplastics (PET-MPs) may significantly impair male reproductive function. This study aimed to investigate the potential molecular mechanisms underlying this impairment. Potential gene targets of PET-MPs were predicted via the SwissTargetPrediction database.
View Article and Find Full Text PDFMutat Res Rev Mutat Res
September 2025
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:
To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions.
View Article and Find Full Text PDFEur J Gastroenterol Hepatol
September 2025
Department of Gastroenterology, First Affiliated Hospital of Shantou University Medical College, Shantou.
Background: Crohn's disease (CD) and rheumatoid arthritis (RA) are autoimmune diseases. CD is known to be closely associated with RA. However, the mechanisms underlying these relationships remain unclear.
View Article and Find Full Text PDFNeurol Neuroimmunol Neuroinflamm
November 2025
Department of Neurology, UC Davis Medical Center, Sacramento, CA.
Objectives: Complement factor I (CFI) deficiency is a rare condition that can present with fulminant relapsing CNS autoinflammation. In this report, we highlight the utility of genetic testing in unexplained CNS autoinflammation.
Methods: This case report describes a young adult with partial CFI deficiency, presenting with acute hemorrhagic leukoencephalitis and longitudinally extensive transverse myelitis.
JCO Precis Oncol
September 2025
Division of Hematology and Oncology, University of California Los Angeles, Los Angeles, CA.
Purpose: mutations are classically seen in non-small cell lung cancers (NSCLCs), and EGFR-directed inhibitors have changed the therapeutic landscape in patients with -mutated NSCLC. The real-world prevalence of -mutated ovarian cancers has not been previously described. We aim to determine the prevalence of pathogenic or likely pathogenic mutations in ovarian cancer and describe a case of -mutated metastatic ovarian cancer with a durable response to osimertinib, an EGFR-directed targeted therapy.
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