Metabolic reprogramming occurs to meet cancer cells’ high energy demand. Its function is essential to the survival of malignancies. Comparing cancer cells to non-malignant cells has revealed that cancer cells have altered metabolism. Several pathways, particularly mTOR, Akt, PI3K, and HIF-1 (hypoxia-inducible factor-1) modulate the metabolism of cancer. Among other aspects of cancer biology, gene expression in metabolism, survival, invasion, proliferation, and angiogenesis of cells are controlled by HIF-1, a vital controller of cellular responsiveness to hypoxia. This article examines various cancer cell metabolisms, metabolic alterations that can take place in cancer cells, metabolic pathways, and molecular aspects of metabolic alteration in cancer cells placing special attention on the consequences of hypoxia-inducible factor and summarising some of their novel targets in the treatment of cancer including leukemia. A brief description of HIF-1α’s role and target in a few common types of hematological malignancies (leukemia) is also elucidated in the present article.

Background Inflammation plays a very important role in the pathogenesis of a wide range of diseases, such as atherosclerosis myocardial infarction, sepsis, rheumatoid arthritis, and cancer. This study aimed to investigate the association of IL-8 in T-cell acute lymphoblastic leukemia (T-ALL) patients. Methodology IL-8 levels were estimated in 52 individuals. Of the study population, 26 were T-ALL patients (all phases of leukemia were included in the study) and 26 were disease-free healthy volunteers. In this study, we employed flow cytometry, enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction test, and western blot analysis. Results IL-8 was significantly higher in all T-ALL patients than in healthy volunteers. IL-8 levels showed a significant positive correlation in T-ALL patients at the genomic and proteomic levels. Conclusions Higher serum IL-8 levels were associated with the advanced disease stage of the clinicopathological parameters. Our results indicate that monitoring IL-8 has a role in modulating disease sensing in T-ALL and may represent a target for innovative diagnostic and therapeutic strategies.

Glioblastoma (GB) remains a major challenge owing to its extremely aggressive nature and resistance to conventional therapies. This review focuses on the intricate roles of progenitor cells, microglia, and non-coding RNAs (ncRNAs) in orchestrating GB pathogenesis and therapy resistance. Glioma stem cells (GSCs), derived from progenitor cells, are important drivers of tumor initiation and recurrence and exhibit remarkable plasticity and resistance to treatment. Microglia, the immune cells of the brain, are hijacked by GB cells to create an immunosuppressive microenvironment that supports tumor growth and resistance to therapy. Non-coding RNAs, including microRNAs and long noncoding RNAs, regulate multiple resistance mechanisms by modulating gene expression and influencing the interactions between progenitor cells and microglia. This review highlights new insights into these interconnected signaling pathways and explores potential therapeutic strategies targeting these molecular players to overcome treatment resistance and improve outcomes in patients with GB.