Damage-associated molecular patterns (DAMPs) are released in response to cell death and stress, and are potent triggers of sterile inflammation. Recent evidence suggests that DAMPs may also have a key role in the development of cancer, as well as in the host response to cytotoxic anti-tumor therapy. As such, DAMPs may exert protective functions by alerting the immune system to the presence of dying tumor cells, thereby triggering immunogenic tumor cell death. On the other hand, cell death and release of DAMPs may also trigger chronic inflammation and, thereby promote the development or progression of tumors. Here, we will review the contribution of candidate DAMPs and their receptors, and discuss the evidence for DAMPs as tumor-promoting and anti-tumor effectors, as well as unsolved questions such as DAMP release from non-tumor cells as well as the existence of tumor-specific DAMPs.
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http://dx.doi.org/10.1038/onc.2016.104 | DOI Listing |
Clin Lung Cancer
December 2024
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD.
Objective: To determine the association between concurrent statin use with immune checkpoint inhibitors (ICIs) and lung cancer-specific and overall mortality in patients with nonsmall cell lung cancer (NSCLC).
Materials And Methods: SEER-Medicare was used to conduct a retrospective study of Medicare beneficiaries ≥65 years of age diagnosed with NSCLC between 2007 and 2017 treated with an ICI. Patients were followed from date of first ICI claim until death, 1 month from last ICI claim, or 12/31/2018, whichever came first.
Exp Cell Res
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Ohio-45267, United States of America; School of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur-613401, Tamil Nadu, India. Electronic address:
Multiple forms of cell death contribute significantly to cardiovascular pathologies, negatively impacting cardiac remodeling and leading to heart failure. While myocardial cell death has been associated with PM induced cardiotoxicity, the temporal dynamics of various cell death forms, such as apoptosis, ferroptosis, necroptosis, and pyroptosis, in relation to inflammatory processes, remain underexplored. This study examines the time-dependent onset and progression of these cell death pathways in the myocardium and their correlation with inflammation in a Wistar rat model.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
School of Biological and Food Engineering, Guangxi Science & Technology Normal University, Laibin, Guangxi 546199, China. Electronic address:
Targeting DNA repair mechanisms, particularly PARP-1 inhibition, has emerged as a promising strategy for developing anticancer therapies. we designed and synthesized two 2-thiazolecarboxaldehyde thiosemicarbazone palladium(II) complexes (C1 and C2), and evaluated their anti-cancer activities. These Pd(II) complexes exhibited potent PARP-1 enzyme inhibition and demonstrated considerable antiproliferative activity against various cancer cell lines.
View Article and Find Full Text PDFMutat Res Rev Mutat Res
January 2025
Radiation Epidemiology Branch, National Cancer Institute, MD 20892-9778, USA; Faculty of Health, Science and Technology, Oxford Brookes University, Headington Campus, OX3 0BP, UK.
Biological effects of ionizing radiation vary with radiation quality, which is often expressed as the amount of energy deposited per unit length, i.e., linear energy transfer (LET).
View Article and Find Full Text PDFComp Biochem Physiol C Toxicol Pharmacol
January 2025
Graduate School of Science and Engineering, Iwate University, 4-3-5, Ueda, Morioka-city 020-8551, Japan.
As temperatures rise due to increasingly severe global warming, the effect of high temperatures on wildlife, including green sea turtles, is one of the issues that must be addressed to ensure the conservation of biodiversity. In the current study, we found that green sea turtle cell death due to apoptosis occurred at 37 °C, which suppressed cell proliferation. We also found that high temperature-induced heat stress led to the accumulation of DNA damage in green sea turtle cells.
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