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Tumor lysis syndrome (TLS) is an oncologic emergency that is usually associated with hematologic malignancies either spontaneously or following early chemotherapy and is caused by massive tumor cell lysis. However, it has been rarely reported in solid tumors. We report a case of 25-year-old lady recently diagnosed with metastatic gastric adenocarcinoma who developed TLS after the fourth cycle of chemoimmunotherapy (FOLFOX plus Nivolumab). She presented with abdominal pain, decrease in oral intake and decreased urine output. Laboratory studies showed acute kidney injury with electrolyte disturbances and was diagnosed initially with autoimmune nephritis secondary to Nivolumab but was later found to have TLS and recovered after appropriate treatment. Soon after this complication, our patient was found to have disease progression on imaging which makes the incidence of TLS an indicator of disease progression.
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http://dx.doi.org/10.1177/11795476221129238 | DOI Listing |
J Alzheimers Dis
September 2025
Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psychiatry, Università Campus Bio-Medico di Roma, Roma, Italy.
BackgroundAlzheimer's disease (AD) is the most common neurodegenerative disorder. While AD diagnosis traditionally relies on clinical criteria, recent trends favor a precise biological definition. Existing biomarkers efficiently detect AD pathology but inadequately reflect the extent of cognitive impairment or disease heterogeneity.
View Article and Find Full Text PDFSci Prog
September 2025
Shenzhen University Sixth Affiliated Hospital, Shenzhen Nanshan People's Hospital, Shenzhen, China.
Colorectal cancer ranks among the most prevalent and lethal malignant tumors globally. Historically, the incidence of colorectal cancer in China has been lower than that in developed European and American countries; however, recent trends indicate a rising incidence due to changes in dietary patterns and lifestyle. Lipids serve critical roles in human physiology, such as energy provision, cell membrane formation, signaling molecule function, and hormone synthesis.
View Article and Find Full Text PDFMed Oncol
September 2025
Division of Hematology and Blood Bank, Department of Medical Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Acute Myeloid Leukemia (AML) patient-derived Mesenchymal Stem Cells (MSCs) behave differently than normal ones, creating a more protective environment for leukemia cells, making relapse harder to prevent. This study aimed to identify prognostic biomarkers and elucidate relevant biological pathways in AML by leveraging microarray data and advanced bioinformatics techniques. We retrieved the GSE122917 dataset from the NCBI Gene Expression Omnibus and performed differential expression analysis (DEA) within R Studio to identify differentially expressed genes (DEGs) among healthy donors, newly diagnosed AML patients, and relapsed AML patients.
View Article and Find Full Text PDFJ Nephrol
September 2025
Department of Psychology, Institute of Psychiatry, Psychology & Neuroscience, Health Psychology Section, King's College London, 5th Floor Bermondsey Wing, Guy's Campus, London Bridge, London, SE1 9RT, UK.
Background: Depression and anxiety are common in chronic kidney disease (CKD) and worsen clinical outcomes. Psycho-behavioural interventions offer a promising, non-pharmacological approach. However, most evidence comes from people with kidney failure with distinct treatment needs, limiting relevance to earlier stages of CKD, where timely support may enhance self-management and slow progression.
View Article and Find Full Text PDFInflammopharmacology
September 2025
Centre for Research Impact & Outcome, Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India.
The NOD‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a key molecular complex that amplifies inflammatory cascades by maturing interleukin‑1 beta (IL-1β) and interleukin‑18 (IL-18) and inducing pyroptosis. It serves as a major driver and co-driver of numerous diseases associated with chronic inflammation. Dysregulated NLRP3 activation contributes to the progression of disorders such as rheumatoid arthritis, inflammatory bowel disease, neurodegenerative diseases and atherosclerosis.
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