Relationship Between Clonal Evolution and Drug Resistance in Bladder Cancer: A Genomic Research Review.

Bladder cancer stands as a prevalent global malignancy, exhibiting notable sex-based variations in both incidence and prognosis. Despite substantial strides in therapeutic approaches, the formidable challenge of drug resistance persists. The genomic landscape of bladder cancer, characterized by intricate clonal heterogeneity, emerges as a pivotal determinant in fostering this resistance. Clonal evolution, encapsulating the dynamic transformations within subpopulations of tumor cells over time, is implicated in the emergence of drug-resistant traits. Within this review, we illuminate contemporary insights into the role of clonal evolution in bladder cancer, elucidating its influence as a driver in tumor initiation, disease progression, and the formidable obstacle of therapy resistance.

Interactions between oxidative stress and senescence in cancer: Mechanisms, therapeutic implications, and future perspectives.

BACKGROUND: Recently, numerous studies have reported the interaction between senescence and oxidative stress in cancer. However, there is a lack of a comprehensive understanding of the precise mechanisms involved. AIM: Therefore, our review aims to summarize the current findings and elucidate by presenting specific mechanisms that encompass functional pathways, target genes, and related aspects. METHODS: Pubmed and Web of Science databases were retrieved to search studies about the interaction between senescence and oxidative stress in cancer. Relevant publications in the reference list of enrolled studies were also checked. RESULTS: In carcinogenesis, oxidative stress-induced cellular senescence acts as a barrier against the transformation of stimulated cells into cancer cells. However, the senescence-associated secretory phenotype (SASP) is positively linked to tumorigenesis. In the cancer progression stage, targeting specific genes or pathways that promote oxidative stress-induced cellular senescence can suppress cancer progression. In terms of treatment, many current clinical therapies combine with novel drugs to overcome resistance and reduce side effects by attenuating oxidative stress-induced senescence. Notably, emerging drugs control cancer development by enhancing oxidative stress-induced senescence. These studies highlight the complacted effects of the interplay between oxidative stress and senescence at different cancer stages and among distinct cell populations. Future research should focus on characterizing the roles of distinct senescent cell types in various tumor stages and identifying the specific components of SASP. CONCLUDSION: We've summarized the mechanisms of senescence and oxidative stress in cancer and provided illustrative figures to guide future research in this area.

Assessment of hepatic functions, hematopoietic cytokines and haematological parameters in people occupationally exposed to volatile petroleum hydrocarbons.

Humans are occupationally exposed to volatile petroleum hydrocarbons through inhalation and ingestion. To access the effect of exposure to volatile hydrocarbons, hematopoietic cytokines, haematological parameters and hepatic functions were assayed for in 100 subjects. Male participants showed significant increase (p < 0.05) in erythropoietin, interleukin-3, alanine transaminase (ALT), alkaline phosphatase (ALP), mean cell hemoglobin concentration (MCHC), mean cell volume (MCV) and significant decrease (p < 0.05) in mean cell hemoglobin (MCH). Female participants showed significant increase (p < 0.05) in interleukin-3, ALT, AST, ALP, MCHC, MCV and significant decrease (p < 0.05) in MCH, platelets, hemoglobin and hematocrit compared to their controls. Exposure to volatile petroleum hydrocarbons raised the absolute red blood cell indices and liver enzymes and could stimulate combined increase in the release of erythropoietin and interleukin-3 leading to ineffective hematopoiesis.

Methodology for processing mastectomy and cryopreservation of breast cancer tissue in a resource- poor setting: A pilot study.

BACKGROUND: There is scarcity of breast cancer tissues derived from women of African origin available for patient - derived xenograft and organoid models. OBJECTIVE: We aim to create a versatile protocol for processing mastectomy and cryopreservation of breast cancer tissue. METHODOLOGY: An immediate collection of breast cancer tissue from mastectomy was bathed in 4 °C HBSS and immediately transferred to 4 °C RPMI1640 containing HEPES, 10% FBS, Streptomycin and Penicillin. Tissues were processed over ice yielding nine samples of cold ischemic time (20-45 min) stored at 3 min interval. Cut samples were transferred into cryovials containing 4 °C cryoprotectant agent (90% FBS +10% Me2SO) before snap -freezing in liquid Nitrogen vapour and final short-term storage in -80 °C Freezer. The histomorphology, tissue and molecular viability were assessed. RESULTS: The cold ischemic times had no detrimental effect to the nine samples despite being processed in a resource poor setting, hence providing a reproducible and reliable protocol.