The circadian clock, a fundamental cellular mechanism, regulates the rhythmic expression of numerous genes and biological processes across various organs. Disruptions in this system, driven by genetic or environmental factors, have been reported to be involved in cancer progression. This review explores the role of the circadian clock in cancer hallmarks and its impact on cellular homeostasis within haematological malignancies. Drawing on findings from in vitro, in vivo, and clinical trials, this review highlights the potential of clock genes as diagnostic and prognostic biomarkers, and as therapeutic targets for optimising treatment timing. It discusses how circadian rhythms can enhance treatment efficacy through both pharmacological and non-pharmacological interventions, outlining strategies for optimising dosing schedules and implementing personalised chronobiological interventions, with a particular focus on haematological malignancies, including cutaneous lymphoma. Ongoing research holds promise for advancing personalised therapeutic approaches and ultimately improving cancer care standards.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11617894 | PMC |
| http://dx.doi.org/10.1016/j.ebiom.2024.105451 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Impact of Recent Translational and Therapeutic Developments on Clinical Course of BCR::ABL1-Positive and -Negative Myeloproliferative Neoplasms.
Hematol Oncol
January 2025
University of California Irvine, Irvine, California, USA.
Despite the study of BCR::ABL1-positive and -negative myeloproliferative neoplasms (MPNs) providing seminal insights into cancer biology, tumor evolution and precision oncology over the past half century, significant challenges remain. MPNs are clonal hematopoietic stem cell-derived neoplasms with heterogenous clinical phenotypes and a clonal architecture which impacts the often-complex underlying genetics and microenvironment. The major driving molecular abnormalities have been well characterized, but debate on their role as disease-initiating molecular lesions continues.
View Article and Find Full Text PDFThe important role of the histone acetyltransferases p300/CBP in cancer and the promising anticancer effects of p300/CBP inhibitors.
Cell Biol Toxicol
January 2025
Department of Ultrasound, Shengjing Hospital of China Medical University, 110004, Shenyang, Liaoning, China.
Histone acetyltransferases p300 (E1A-associated protein p300) and CBP (CREB binding protein), collectively known as p300/CBP due to shared sequence and functional synergy, catalyze histone H3K27 acetylation and consequently induce gene transcription. p300/CBP over-expression or over-activity activates the transcription of oncogenes, leading to cancer cell growth, resistance to apoptosis, tumor initiation and development. The discovery of small molecule inhibitors targeting p300/CBP histone acetyltransferase activity, bromodomains, dual inhibitors of p300/CBP and BRD4 bromodomains, as well as proteolysis-targeted-chimaera p300/CBP protein degraders, marks significant progress in cancer therapeutics.
View Article and Find Full Text PDFIn vitro ILC differentiation from human HSCs.
Methods Cell Biol
January 2025
Innate Lymphoid Cells Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
The Innate Lymphoid Cells (ILCs) are a family of innate immune cells composed by the Natural Killer (NK) cells and the helper ILCs (hILCs) (ILC1, ILC2, ILC3), both developing from a common ILC precursor (ILCP) derived from hematopoietic stem cells (HSCs). A correct ILC reconstitution is crucial, particularly in patients receiving HSC transplantation (HSCT), the only therapeutic option for many adult and pediatric high-risk hematological malignancies. Indeed, mainly thanks to their cytotoxic activity, NK cells have a strong Graft-versus-Leukemia (GvL) effect.
View Article and Find Full Text PDFExploring treatment-driven subclonal evolution of prognostic triple biomarkers: Dual gene fusions and chimeric RNA variants in novel subtypes of acute myeloid leukemia patients with KMT2A rearrangement.
Drug Resist Updat
January 2025
Loma Linda University Cancer Center, Loma Linda, CA 92354, United States; Department of Basic Sciences, Loma Linda University, Loma Linda, CA 92354, United States. Electronic address:
Chromosomal rearrangements (CR) initiate leukemogenesis in approximately 50 % of acute myeloid leukemia (AML) patients; however, limited targeted therapies exist due to a lack of accurate molecular and genetic biomarkers of refractory mechanisms during treatment. Here, we investigated the pathological landscape of treatment resistance and relapse in 16 CR-AML patients by monitoring cytogenetic, RNAseq, and genome-wide changes among newly diagnosed, refractory, and relapsed AML. First, in FISH-diagnosed KMT2A (MLL gene, 11q23)/AFDN (AF6, 6q27)-rearrangement, RNA-sequencing identified an unknown CCDC32 (15q15.
View Article and Find Full Text PDFAdvances of signal transducer and activator of transcription 3 inhibitors in acute myeloid leukemia (Review).
Oncol Lett
March 2025
Department of Hematology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
Signal transducer and activator of transcription 3 (STAT3), a crucial transcription factor, exerts a notable influence by hyperactivating or acquiring functional mutations in the occurrence and progression of cancers. Hyperactive STAT3 is also implicated in a range of hematopoietic malignancies, especially acute myeloid leukemia (AML). The function of STAT3 is associated with the phosphorylated parallel dimer structure, enabling them to stimulate the transcription of specific genes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!