Next-generation sequencing (NGS) has emerged as a pivotal technology in the field of oncology, transforming the approach to cancer diagnosis and treatment. This paper provides a comprehensive overview of the integration of NGS into clinical settings, emphasizing its significant contributions to precision medicine. NGS enables detailed genomic profiling of tumors, identifying genetic alterations that drive cancer progression and facilitating personalized treatment plans targeting specific mutations, thereby improving patient outcomes. This capability facilitates the development of personalized treatment plans targeting specific mutations, leading to improved patient outcomes and the potential for better prognosis. The application of NGS extends beyond identifying actionable mutations; it is instrumental in detecting hereditary cancer syndromes, thus aiding in early diagnosis and preventive strategies. Furthermore, NGS plays a crucial role in monitoring minimal residual disease, offering a sensitive method to detect cancer recurrence at an early stage. Its use in guiding immunotherapy by identifying biomarkers that predict response to treatment is also highlighted. Ethical issues related to genetic testing, such as concerns around patient consent and data privacy, are also important considerations that need to be addressed for the broader implementation of NGS. These include the complexities of data interpretation, the need for robust bioinformatics support, cost considerations, and ethical issues related to genetic testing. Addressing these challenges is essential for the widespread adoption of NGS. Looking forward, advancements such as single-cell sequencing and liquid biopsies promise to further enhance the precision of cancer diagnostics and treatment. This review emphasizes the transformative impact of NGS in oncology and advocates for its incorporation into routine clinical practice to promote molecularly driven cancer care.

Lymphoid cells play a critical role in the immune system, which includes three subgroups of T, B, and NK cells. Recognition of the complexity of the human genetics transcriptome in lymphopoiesis has revolutionized our understanding of the regulatory potential of RNA in normal lymphopoiesis and lymphoid malignancies. Long non-coding RNAs (lncRNAs) are a class of RNA molecules greater than 200 nucleotides in length. LncRNAs have recently attracted much attention due to their critical roles in various biological processes, including gene regulation, chromatin organization, and cell cycle control. LncRNAs can also be used for cell differentiation and cell fate, as their expression patterns are often specific to particular cell types or developmental stages. Additionally, lncRNAs have been implicated in lymphoid differentiation, such as regulating T-cell and B-cell development, and their expression has been linked to immune-associated diseases such as leukemia and lymphoma. In addition, lncRNAs have been investigated as potential biomarkers for diagnosis, prognosis, and therapeutic response to disease management. In this review, we provide an overview of the current knowledge about the regulatory role of lncRNAs in physiopathology processes during normal lymphopoiesis and lymphoid leukemia.

Objective: Fetuin-A serves a dual function; its high levels are associated with metabolic syndrome, type 2 diabetes, obesity, insulin resistance, and nonalcoholic fatty liver disease, and on the other hand, it serves as a potent inhibitor of ectopic vascular calcification. Due to the opposing findings, the aim of the current study was to investigate serum fetuin-A levels in men with coronary artery disease (CAD). Methods: In the case-control study, anthropometric and biochemical parameters were determined in 83 men (43 CAD patients and 40 control subjects). At last, the serum fetuin-A levels were measured using the fetuin-A human enzyme-linked immunosorbent assay (ELISA) kit. Results: A significant difference was detected among the two groups for triglyceride and cholesterol levels (P=0.003 and P=0.002, respectively). The mean fetuin-A levels were determined 230.57 ± 63.76 and 286.35 ± 64.07 μg/ml for the control group and the CAD patients, respectively (P<0.001). Fetuin- A was significantly correlated to the severity of CAD (r 0.393, P<0.001) and associated with the risk of CAD in subjects (OR [CI] = 1. 144 [1.060-1. 235]; p = 0.001). A cut-off value of 237.4 μg/ml had good sensitivity (76.7%) and specificity (65.0%) for differentiating between two groups [area under curve (AUC) = 0.732 (CI=0.621-0.842); p < 0.001]. Conclusion: Our results indicated that fetuin-A levels were positively correlated to the severity of CAD. The findings suggest that there is a possible link between pathogenic mechanisms of atherosclerosis and fetuin-A; however, more investigations are needed in this regard.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor superfamily, triggering apoptosis in malignant cell without affecting healthy cells. However, varied types of the cancerous cells (e.g., leukemia) show resistance to TRAIL-induced apoptosis (TIA). Herein, we evaluated the effect of quercetin (QUE) in combination with TRAIL to defeat the resistance of the human acute myeloid leukemia KG-1 cell lines against TIA. Briefly, we treated the KG-1 cells with TRAIL (50 and 250 ng/ml) and QUE (100 μM) alone and in combination together. Then, the expression levels of the pro-apoptotic proteins, including caspase 3, 8, and 9 along with the anti-apoptotic proteins such as survivin and Mcl-1 expressions levels were evaluated by real-time PCR in KG-1 cells 12, 14 and 48 hours upon exposure with TRAIL and QUE (100 μM). Based on results, the combination of TRAIL and QUE augmented the expression levels of the caspase 3, 8, and 9 compared with the cells treated with TRAIL and QUE alone. Conversely, expression rates of the survivin and Mcl-1 were strongly diminished in cells treated with TRAIL plus QUE in comparison to KG-1 cells that treated with TRAIL and QUE alone. Considering finding, QUE can not only improve caspase 3, 8, and 9 when used plus TRAIL, it also made a positive effect on their activation due to the inhibitory impacts on anti-apoptotic protein Mcl-1 and survivin expressions in KG-1 cells, possibly leading to the desired therapeutic outcome in leukemic cells.