T cells represent the major contributors to antitumor-specific immunity among the tumor-infiltrating lymphocytes. However, tumors acquire ways to evade immunosurveillance and anti-tumor responses are too weak to eradicate the disease. T cells are often functionally impaired as a result of interaction with, or signals from, transformed cells and the tumor microenvironment, including stromal cells. Among these, nutrients use and consumption is critically important for the control of differentiation and effector mechanisms of T cells. Moreover, Treg cells-skewing conditions often coexist within the cancer milieu, which sustains the notion of immune privileged tumors. Additionally, cancer cells contend with tumor infiltrating lymphocytes for nutrients and can outcompete the immune response. PD1- and CTLA-based immunotherapies partially remodel cell metabolism leading the way to clinical approaches of metabolic reprogramming for therapeutic purposes. Here we shortly discuss T cell fates during anti-tumor immune responses and how signals within tumor microenvironment influence T cell metabolism, altering functions and longevity of the cell.
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http://dx.doi.org/10.1016/j.canlet.2017.10.014 | DOI Listing |
Cell Death Differ
December 2024
Georgetown University Medical Center, Lombardi Comprehensive Cancer Center, Washington, D.C., USA.
Germline inactivating mutations of the SLC25A1 gene contribute to various human disorders, including Velocardiofacial (VCFS), DiGeorge (DGS) syndromes and combined D/L-2-hydroxyglutaric aciduria (D/L-2HGA), a severe systemic disease characterized by the accumulation of 2-hydroxyglutaric acid (2HG). The mechanisms by which SLC25A1 loss leads to these syndromes remain largely unclear. Here, we describe a mouse model of SLC25A1 deficiency that mimics human VCFS/DGS and D/L-2HGA.
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December 2024
Department of Pharmaceutical Chemistry, Dr. D. Y. Patil Institute of Pharmaceutical Sciences and Research, Pimpri, Pune, India.
The emergence of self-propelling magnetic nanobots represents a significant advancement in the field of drug delivery. These magneto-nanobots offer precise control over drug targeting and possess the capability to navigate deep into tumor tissues, thereby addressing multiple challenges associated with conventional cancer therapies. Here, Fe-GSH-Protein-Dox, a novel self-propelling magnetic nanobot conjugated with a biocompatible protein surface and loaded with doxorubicin for the treatment of triple-negative breast cancer (TNBC), is reported.
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December 2024
Department of Biological Sciences, Université de Montréal, Montréal, QC, Canada.
Mitochondrial epigenetics, particularly mtDNA methylation, is a flourishing field of research. MtDNA methylation appears to play multiple roles, including regulating mitochondrial transcription, cell metabolism and mitochondrial inheritance. In animals, bivalves with doubly uniparental inheritance (DUI) of mitochondria are the exception to the rule of maternal mitochondrial inheritance since DUI also involve a paternal mtDNA transmitted from the father to sons.
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December 2024
Department of Genetic Engineering and Biotechnology, University of Rajshahi, Rajshahi, 6205, Bangladesh.
This study investigated the potential genotoxic and carcinogenic effects of N-nitrosodimethylamine (NDMA), a hazardous compound found in ranitidine formulations that are used to treat excessive stomach acid. The study first examined the effects of NDMA-contaminated ranitidine formulation on Allium cepa root growth and mitotic activity. The results demonstrated dose-dependent decreases in both root growth and mitotic index indicating genotoxicity and cell division disruption.
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December 2024
Interventional Oncology, Johnson & Johnson Enterprise Innovation, Inc, 10th Floor 255 Main St, 02142, Cambridge, Boston, MA, USA.
The introduction of anti-PD-1/PD-L1 therapies revolutionized treatment for advanced non-small cell lung cancer (NSCLC), yet response rates remain modest, underscoring the need for predictive biomarkers. While a T cell inflamed gene expression profile (GEP) has predicted anti-PD-1 response in various cancers, it failed in a large NSCLC cohort from the Stand Up To Cancer-Mark (SU2C-MARK) Foundation. Re-analysis revealed that while the T cell inflamed GEP alone was not predictive, its performance improved significantly when combined with gene signatures of myeloid cell markers.
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