The dysregulation of non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), leads to the development and advancement of multiple myeloma (MM). miRNAs, in particular, are paramount in post-transcriptional gene regulation, promoting mRNA degradation and translational inhibition. As a result, miRNAs can serve as oncogenes or tumor suppressors depending on the target genes. In MM, miRNA disruption could result in abnormal gene expression responsible for cell growth, apoptosis, and other biological processes pertinent to cancer development. The dysregulated miRNAs inhibit the activity of tumor suppressor genes, contributing to disease progression. Nonetheless, several miRNAs are downregulated in MM and have been identified as gene regulators implicated in extracellular matrix remodeling and cell adhesion. miRNA depletion potentially facilitates the tumor advancement and resistance of therapeutic drugs. Additionally, lncRNAs are key regulators of numerous cellular processes, such as gene expression, chromatin remodeling, protein trafficking, and recently linked MM development. The lncRNAs are uniquely expressed and influence gene expression that supports MM growth, in addition to facilitating cellular proliferation and viability via multiple molecular pathways. miRNA and lncRNA alterations potentially result in anomalous gene expression and interfere with the regular functioning of MM. Thus, this review aims to highlight the dysregulation of these ncRNAs, which engender novel therapeutic modalities for the treatment of MM.

Multiple myeloma (MM) is an exceptionally complicated and heterogeneous disease that is caused by the abnormal proliferation of malignant monoclonal plasma cells initiated in the bone marrow. In disease progression, a multistep process including differentiation, proliferation, and invasion is involved. Despite great improvement in treatment outcomes in recent years due to the substantial discovery of novel therapeutic drugs, MM is still regarded as an incurable disease. Patients with MM are afflicted by confronting remission periods accompanied by relapse or progression outcomes, which inevitably progress to the refractory stage. In this regard, MM may need new medications or modifications in therapeutic strategies to overcome resistance. A variety of genetic abnormalities (e.g., point mutations, translocations, and deletions) and epigenetic changes (e.g., DNA methylation, histone modification, and non-coding RNA) contribute to the pathogenesis and development of MM. Here, we review the significant roles of epigenetic mechanisms in the development and progression of MM. We also highlight epigenetic pathways as potential novel treatment avenues for MM, including their interplay, use of epigenetic inhibitors, and major involvement in immuno-oncology.

Burkitt lymphoma (BL) is a form of B-cell malignancy that progresses aggressively and is most often seen in children. While Epstein–Barr virus (EBV) is a double-stranded DNA virus that has been linked to a variety of cancers, it can transform B lymphocytes into immortalized cells, as shown in BL. Therefore, the estimated prevalence of EBV in a population may assist in the prediction of whether this population has a high risk of increased BL cases. This systematic review and meta-analysis aimed to estimate the prevalence of Epstein–Barr virus in patients with Burkitt lymphoma. Using the appropriate keywords, four electronic databases were searched. The quality of the included studies was assessed using the Joanna Briggs Institute’s critical appraisal tool. The results were reported as percentages with a 95% confidence interval using a random-effects model (CI). PROSPERO was used to register the protocol (CRD42022372293), and 135 studies were included. The prevalence of Epstein–Barr virus in patients with Burkitt lymphoma was 57.5% (95% CI: 51.5 to 63.4, n = 4837). The sensitivity analyses demonstrated consistent results, and 65.2% of studies were of high quality. Egger’s test revealed that there was a significant publication bias. EBV was found in a significantly high proportion of BL patients (more than 50% of BL patients). This study recommends EBV testing as an alternative for predictions and the assessment of the clinical disease status of BL.

Background: Multiple myeloma (MM) is a hematological malignancy characterized by the exponential growth of malignant plasma cells. Individuals diagnosed with MM exhibit a deficiency in vitamin D and may suffer fatigue, a loss of muscular strength, persistent musculoskeletal aches, and pain. The objective of this systematic review and meta-analysis is to determine the prevalence of vitamin D insufficiency and deficiency in individuals diagnosed with MM. Methods: We searched five electronic databases using relevant keywords. The quality of the included studies was evaluated using the critical appraisal tool developed by the Joanna Briggs Institute. We employed a random-effects model and presented the findings in the form of percentages accompanied by 95% confidence intervals (CI). This protocol has been officially registered in PROSPERO under the registration number CRD42021248710. Results: The meta-analysis comprised a total of eighteen studies and found that, among patients with MM, the occurrence of serum vitamin D deficiency and insufficiency was 39.4% (95% CI: 25.8 to 52.9, n = 3746) and 34.1% (95% CI: 20.9 to 47.2, n = 3559), respectively. The findings indicate that a greater proportion of newly diagnosed patients exhibited vitamin D deficiency and insufficiency, with rates of 43.0% and 41.6%, respectively, compared to those receiving treatment (rates of 41.6% and 32.3%, respectively). The findings of the sensitivity analyses were consistent, and most of the studies (72.2%) were deemed to be of high quality. The results of Egger’s test indicated the absence of publication bias. Conclusions: Patients diagnosed with MM have been found to exhibit significantly elevated levels of both vitamin D deficiency and insufficiency. Therefore, it is recommended to consider vitamin D testing as an additional parameter in the current criteria for the clinical evaluation of MM.

The practice of complementary and alternative medicine has significantly gained acceptance worldwide, such as Al-Hijama, also known as cupping therapy. Despite the growing popularity of therapeutic cupping among athletes, little is known about the impact of cupping therapy on sports fields. The current study was designed to explore the effect of wet cupping therapy on the haematological and inflammatory parameters in Jordanian national team players. The procedure was carried out at a specialized centre for cupping in Amman on the morning of the 19th Rajab. The data were obtained from 14 healthy male participants aged between 21 and 22 years. The haematological and inflammatory parameters were assessed by comparing venous blood components before and after four weeks of wet cupping. Complete blood count (CBC) analysis of venous blood samples four weeks after wet cupping showed a significant increase in the values of total white blood cells (WBCs), neutrophils, lymphocytes, red blood cells (RBCs), haematocrit, and haemoglobin as compared with venous blood samples before cupping. Blood film examination of venous blood samples post-cupping revealed normocytic normochromic RBCs; WBCs and platelets were unremarkable. Analysis of inflammatory markers post cupping showed a significant decrease in the monocyte/lymphocyte ratio (MLR) and platelet/lymphocyte ratio (PLR) but no differences in neutrophil/lymphocyte ratio (NLR). The findings of this study suggest that wet cupping has an indispensable influence on haematological and immunological parameters in athletes, where it reinforces cellular immunity, generates younger blood cells, and reduces inflammation markers. It is probable, therefore, that cupping improves sports performance and achievement. The evidence from this research adds to a growing body of literature on cupping therapy in sports.

Cancer remains a major global health challenge, marked by profound heterogeneity and adaptability that frequently limit the success of conventional and targeted therapies. Among the diverse cellular populations within tumors, cancer stem cells (CSCs) have emerged as key drivers of initiation, progression, metastasis, and therapeutic resistance. Sharing core features with normal stem cells, including self-renewal and multipotency, CSCs sustain tumor growth and contribute to intratumoral heterogeneity. Importantly, the traditional hierarchical model has been revised with the recognition of CSC plasticity—the dynamic ability of cells to transition between CSC and non-CSC states or among distinct CSC subsets. This phenotypic flexibility, governed by intrinsic genetic and epigenetic mechanisms and strongly influenced by extrinsic cues from the tumor microenvironment (TME), underpins therapeutic resistance, immune evasion, and disease recurrence. The TME represents a complex, dynamic ecosystem composed of stromal cells, immune populations, extracellular matrix components, and soluble factors. Far from a passive scaffold, the TME actively engages in reciprocal crosstalk with CSCs, sustaining stemness, modulating plasticity, and shaping tumor progression. This bidirectional interplay reinforces CSC survival, fuels metastatic potential, and contributes to therapeutic failure. A comprehensive understanding of CSC plasticity and CSC–TME interactions is therefore essential for the design of durable therapeutic strategies. This review synthesizes current knowledge of the molecular and cellular mechanisms driving CSC plasticity and their microenvironmental regulation. It further evaluates emerging approaches—including small molecules, epigenetic modulators, and TME-normalizing therapies—that target these processes, and discusses challenges and future directions for translating these strategies into precision oncology.