Findings from prior systematic reviews suggest that exercise results in meaningful improvements in many clinically relevant physiologic and quality of life (QOL) outcomes during and following cancer treatment. However, the majority of exercise-cancer studies have focused upon the benefits of aerobic exercise (AE) and knowledge of the efficacy of resistance exercise (RE) alone as a supportive care intervention for cancer patients and survivors remains limited. Consequently, the purpose of this review was to provide the first systematic evaluation of the effects of RE alone upon clinically relevant physiologic and QOL outcomes during and following cancer treatment. Literature searches were conducted to identify studies examining RE interventions in cancer patients and survivors. Data were extracted on physiologic (fitness, physical function, and body composition) and QOL (fatigue, psychological well-being, and cancer-specific and global QOL outcomes. Cohen's d effect sizes were calculated for each outcome. A total of 15 studies (6 in samples undergoing active cancer treatment and 9 in samples having completed cancer treatment) involving 1,077 participants met the inclusion criteria. Findings revealed that, on average, RE resulted in large effect-size improvements in muscular strength (d = 0.86), moderate effect-size improvements in physical function (d = 0.66), and small effect-size improvements in body composition (d = 0.28) and QOL (d = 0.25) outcomes. The effect sizes observed following RE are comparable in magnitude to the effects of exercise interventions reported in prior comprehensive reviews of the exercise-cancer literature which primarily focused upon AE. Additionally, the methodologic quality of the studies was generally strong. Taken collectively, results of this systematic review suggest that RE is a promising supportive care intervention that results in meaningful improvements in clinically relevant physiologic and QOL outcomes during and following cancer treatment.
Download full-text PDF |
Source |
---|
Clin Cancer Res
January 2025
United States Food and Drug Administration, Silver Spring, Maryland, United States.
On April 23, 2024, FDA granted accelerated approval to tovorafenib, a type II RAF kinase inhibitor, for the treatment of patients 6 months of age and older with relapsed or refractory pediatric low-grade glioma (pLGG) harboring a BRAF fusion or rearrangement, or BRAF V600 mutation. Efficacy was evaluated in FIREFLY-1 (NCT04775485), a single-arm, open-label, multicenter trial that enrolled patients 6 months to 25 years of age with relapsed or refractory pLGG with an activating BRAF alteration who had received prior systemic therapy. The major efficacy outcome measure was radiologic overall response rate (ORR), defined as the proportion of patients with complete response, partial response, or minor response as determined by blinded independent central review using Response Assessment in Pediatric Neuro-Oncology (RAPNO) criteria.
View Article and Find Full Text PDFClin Cancer Res
January 2025
University of Lyon System, Lyon, France.
The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent HER3 activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET-inhibitor tumor responses.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Laboratory of Translational Oncology and Translational Cancer Therapeutics, Warren Alpert Medical School of Brown University, Providence, United States of America.
Radiotherapy can be limited by pneumonitis which is impacted by innate immunity, including pathways regulated by TRAIL death receptor DR5. We investigated whether DR5 agonists could rescue mice from toxic effects of radiation and found two different agonists, parenteral PEGylated trimeric-TRAIL (TLY012) and oral TRAIL-Inducing Compound (TIC10/ONC201) could reduce pneumonitis, alveolar-wall thickness, and oxygen desaturation. Lung protection extended to late effects of radiation including less fibrosis at 22-weeks in TLY012-rescued survivors versus un-rescued surviving irradiated-mice.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Laboratory Medicine, Division of Translational Cancer Researc, Lund University Cancer Centre, Lund University, Lund, Sweden.
The biology centered around the TGF-beta type I receptor Activin Receptor-Like Kinase (ALK)1 (encoded by ACVRL1) has been almost exclusively based on its reported endothelial expression pattern since its first functional characterization more than two decades ago. Here, in efforts to better define the therapeutic context in which to use ALK1 inhibitors, we uncover a population of tumor-associated macrophages (TAMs) that, by virtue of their unanticipated Acvrl1 expression, are effector targets for adjuvant anti-angiogenic immunotherapy in mouse models of metastatic breast cancer. The combinatorial benefit depended on ALK1-mediated modulation of the differentiation potential of bone marrow-derived granulocyte-macrophage progenitors, the release of CD14+ monocytes into circulation, and their eventual extravasation.
View Article and Find Full Text PDFJ Am Chem Soc
January 2025
Department of Chemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, United States.
Lysine demethylases (KDMs) catalyze the oxidative removal of the methyl group from histones using earth-abundant iron and the metabolite 2-oxoglutarate (2OG). KDMs have emerged as master regulators of eukaryotic gene expression and are novel drug targets; small-molecule inhibitors of KDMs are in the clinical pipeline for the treatment of human cancer. Yet, mechanistic insights into the functional heterogeneity of human KDMs are limited, necessitating the development of chemical probes for precision targeting.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!