Ewing sarcoma (ES) is an uncommon cancer that arises in mesenchymal tissues and represents the second most widespread malignant bone neoplasm after osteosarcoma in children. Amplifications in genomic, proteomic, and metabolism are characteristics of sarcoma, and targeting altered cancer cell molecular processes has been proposed as the latest promising strategy to fight cancer. Recent technological advancements have elucidated some of the underlying oncogenic characteristics of Ewing sarcoma. Offering new insights into the physiological basis for this phenomenon, our current review examines the dynamics of ES signaling as it related to both ES and the microenvironment by integrating genomic and proteomic analyses. An extensive survey of the literature was performed to compile the findings. We have also highlighted recent and ongoing studies integrating metabolomics and genomics aimed at better understanding the complex interactions as to how ES adapts to changing biochemical changes within the tumor microenvironment.

Purpose: T-cell lymphomas, refer to a diverse set of lymphomas that originate from T-cells, a type of white blood cell, with limited treatment options. This investigation aimed to assess the efficacy and mechanism of a novel fluorinated nucleoside analogue (FNA), 2′-deoxy-2′-β-fluoro-4′-azidocytidine (FNC), against T-cell lymphoma using Dalton’s lymphoma (DL)-bearing mice as a model. Methods: Balb/c mice transplanted with the DL tumor model received FNC treatment to study therapeutic efficacy against T-cell lymphoma. Behavioral monitoring, physiological measurements, and various analyses were conducted to evaluate treatment effects for mechanistic investigations. Results: The results of study indicated that FNC prevented DL-altered behavior parameters, weight gain and alteration in organ structure, hematological parameters, and liver enzyme levels. Moreover, FNC treatment restored organ structures, attenuated angiogenesis, reduced DL cell viability and proliferation through apoptosis. The mechanism investigation revealed FNC diminished MMP levels, induced apoptosis through ROS induction, and activated mitochondrial-mediated pathways leading to increase in mean survival time of DL mice. These findings suggest that FNC has potential therapeutic effects in mitigating DL-induced adverse effects. Conclusion: FNC represents an efficient and targeted treatment strategy against T-cell lymphoma. FNC’s proficient ability to induce apoptosis through ROS generation and MMP reduction makes it a promising candidate for developing newer and more effective anticancer therapies. Continued research could unveil FNC’s potential role in designing a better therapeutic approach against NHL.

Microplastics, ranging from 1 micron to 5 mm in size, ubiquitous environmental pollutants, arise from diverse sources such as industrial processes, personal care products, textiles, and urban runoff, permeating air, soil, freshwater, sediment, and marine environments. Human exposure occurs through ingestion, inhalation, and dermal contact, leading to health concerns including oxidative stress, metabolic disruption, and immune modulation, with potential direct links to lung, skin, and digestive cancers. While direct evidence linking microplastics to lymphoma remains elusive, therefore we hypothesized that bloodstream's immediate exposure post-entry suggests a plausible indirect link. This review explores mechanisms around our hypothesis by which microplastics might contribute to lymphoma, encompassing inflammation, oxidative stress, immune dysregulation, endocrine disruption, and genotoxicity. Understanding these pathways is crucial given lymphoma's global impact. Future research warrants comprehensive epidemiological studies and interdisciplinary approaches, integrating epidemiology, experimental research, and computational modeling to elucidate the association between microplastics and lymphoma.

Synthetic polymer debris, particularly microplastics and nanoplastics (NPs), has emerged as a structurally persistent and biologically active stressor in aquatic systems. This chapter offers an integrative synthesis of how micro-/nanoplastics interact with aquatic organisms at molecular, cellular, and systemic levels. Beyond trophic ingestion, we examine sublethal toxicodynamics, including mitochondrial collapse, oxidative stress, neurotoxicity, immunomodulation, and reproductive disruption – effects now documented across phylogenetically diverse taxa. NPs, due to their ultrafine scale and surface reactivity, exhibit disproportionate bioavailability and organotropism, making them uniquely invasive at the intracellular level. We link mechanistic laboratory evidence with field-scale ecological data to trace bioaccumulation patterns and cascading disruptions across food webs. These particles are termed “hidden poison” by our laboratory in a recent paper because their effects are often cryptic, chronic, and cumulative – rarely lethal in isolation, yet profoundly destabilizing over time. Lacking scent, taste, or visibility, they bypass organismal defenses and regulatory frameworks alike. This silent toxicity challenges conventional paradigms of aquatic health assessment. By bridging ecotoxicology with systems biology and material science, this chapter proposes a new framework for understanding polymer-driven biological stress. We conclude with a call for predictive models that integrate particle-specific traits with ecosystem-level feedback, essential for mitigating this unresolved planetary contaminant.

Lymphoma therapeutics research revealed an unsettling parallel: the plastic we consume daily might contribute to the very disease we're trying to cure. Microplastics-and particularly nanoplastics with their superior ability to enter the bloodstream-are now detected in human blood, lungs, and placentas. While direct evidence linking them to lymphoma remains absent, our recent comprehensive mechanistic review hypothesized biological plausibility through five convergent pathways-inflammation, oxidative stress, immune dysregulation, genotoxicity, and endocrine disruption. Nanoplastics, with their enhanced bioavailability and cellular penetration, may represent the primary etiological agents, though microplastics serve as the persistent environmental reservoir from which nanoplastics continuously fragment. Unlike therapeutic compounds that kill cancer cells through acute pathway activation, chronic low-dose plastic exposure may promote cancer through the same mechanisms. Critical evidence gaps exist-no studies have measured plastic particles in lymph nodes or compared exposures between lymphoma patients and controls-making urgent investigation necessary. This hypothesis, while mechanistically plausible based on our recent comprehensive review, requires rigorous testing through epidemiological studies, lymph node tissue analysis, and animal carcinogenesis bioassays before any causal claims can be made.