Purpose Of Review: Cancer treatment-related cardiotoxicity (CTRC) represents a significant cause of morbidity and mortality worldwide. The purpose of our review is to summarize the epidemiology, natural history, and pathophysiology of cardiotoxicity-related to cancer treatment. We also summarize appropriate screening, surveillance, and management of CTRC. While cardiotoxicity is characteristically associated with anthracyclines, HER2-B antagonists, and radiation therapy (XRT), there is growing recognition of toxicity with immune checkpoint inhibitors (ICI), tyrosine kinase inhibitors, and proteasome inhibitors.
Recent Findings: Patients at risk for cardiotoxicity should be screened based on available guidelines, generally with serial echocardiograms. The role of medical heart failure (HF) therapies is controversial in patients with asymptomatic left ventricular dysfunction but may be considered in some instances. Once symptomatic HF has developed, treatment should be in accordance with ACC/AHA guidelines. The goal in caring for patients receiving cancer treatment is to optimize cardiac function and prevent interruptions in potentially lifesaving cancer treatment.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7860625 | PMC |
http://dx.doi.org/10.1007/s11897-020-00453-3 | DOI Listing |
Alzheimers Dement
December 2024
B.S.A. College of Engineering and Technology, Mathura, Uttar Pradesh, India.
Background: Cognitive dysfunction emerges as a manifestation of reduced estrogen levels following ovariectomy in an individual. However, the conventional use of estrogen replacement therapy could increase the risk of breast cancer and thromboembolism. Icariin is a natural compound that has been reported to be a neuroprotective agent against dementia.
View Article and Find Full Text PDFNanoscale
January 2025
Cancer Institute of The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao 266061, China.
Correction for 'Camptothecin-based prodrug nanomedicines for cancer therapy' by Renshuai Zhang , , 2023, , 17658-17697, https://doi.org/10.1039/D3NR04147F.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The TT & WF Chao Center for BRAIN and Houston Methodist Neal Cancer Center, Houston Methodist Hospital, Houston, TX, USA.
Background: Global epidemiological studies involving over nine million participants have shown a 35% lower incidence of Alzheimer's Disease (AD) in older cancer survivors compared to those without a history of cancer. This inverse relationship, consistent across recent studies with methodological controls, suggests that cancer itself, rather than cancer treatments, may offer protective factors against AD. This insight opens avenues for novel therapeutic strategies targeting early AD by harnessing cancer-associated protective factors.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is the most common cause of age-related dementia, and the presence of amyloid-β (Aβ) plaques and tau-containing neurofibrillary tangles is associated with the neurodegeneration and cognitive impairment in this incurable disease. Growing evidence shows that epigenetic dysregulation through histone deacetylases (HDACs) plays a critical role in synaptic dysfunction and memory loss in AD, and HDACs have been highlighted as a novel class of anti-Alzheimer targets. Moreover, restoring Wnt/β-catenin signaling, which is greatly suppressed in AD brains, is a promising therapeutic strategy for AD.
View Article and Find Full Text PDFBackground: Understanding the fundamental differences between the human and pre-human brain is a prerequisite for designing meaningful models and therapies for AD. Expressed CHRFAM7A, a human restricted gene with carrier frequency of 75% in the human population predicts profound translational significance.
Method: The physiological role of CHRFAM7A in human brain is explored using multiomics approach on 600 post mortem human brain tissue samples (ROSMAP).
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!