Latest Research
All publications from the Cancer3.AI database, newest first.
Incidence and survival of epithelial salivary glands cancer by tumor site and histology in Tarragona and Girona, Catalonia, Spain.
Rubió-Casadevall J, et al
Researchers from Spain conducted a retrospective population-based study analyzing 301 cases of epithelial salivary gland cancer diagnosed between 1994 and 2018 in the provinces of Tarragona and Girona, Catalonia, drawing on data from two regional cancer registries. The study examined incidence rates, survival outcomes, and trends across more than 24 distinct histological subtypes of these rare and biologically heterogeneous tumors. Squamous cell carcinoma was the most common subtype (17.9%), followed by mucoepidermoid carcinoma (16.9%), and 76.1% of all tumors arose in the parotid gland, the largest salivary gland in the body. The overall incidence was 9.2 cases per million person-years, with a declining trend over the study period that may reflect improved diagnostic accuracy and reduced exposure to risk factors such as smoking. The 10-year net survival rate for the entire cohort reached 55.5%, with acinar cell carcinoma demonstrating the most favorable long-term prognosis among all histological subtypes. These findings provide important epidemiological benchmarks for clinicians and public health planners managing this rare but diverse group of cancers in Southern Europe.
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
Source →Association of serum biomarkers, immunohistochemical profiles, and preoperative clinical manifestations in patients undergoing endoscopic endonasal resection of pituitary neuroendocrine tumors.
Ordonez-Rubiano EG, et al
This study investigated the associations between serum biomarkers, immunohistochemical tumor profiles, and preoperative clinical manifestations in patients who underwent endoscopic endonasal resection of pituitary neuroendocrine tumors (PitNETs). By integrating blood-based marker data, tissue staining characteristics, and clinical symptom profiles, researchers aimed to build a more comprehensive preoperative picture of tumor biology in this patient population. Such multifactorial analysis is particularly timely given the recent reclassification of pituitary adenomas as neuroendocrine tumors, which has heightened demand for refined diagnostic and prognostic tools. Correlating serum markers with immunohistochemical findings and clinical presentation may help surgeons better stratify patients and anticipate tumor behavior prior to minimally invasive endonasal surgery. These findings contribute to an evolving evidence base supporting an integrated, biomarker-informed approach to the management of pituitary neuroendocrine tumors in neurosurgical practice.
Neurosurgical review
Source →Resection and permanent intracranial brachytherapy using modular, biocompatible cesium-131 implants for recurrent aggressive meningiomas: 5-year results from a prospective phase 2 trial.
Lee KE, et al
A prospective phase 2 clinical trial evaluated the efficacy of surgical resection combined with permanent cesium-131 collagen tile brachytherapy (Cs-131 CTBT) in 27 patients harboring 29 recurrent aggressive meningiomas, a notoriously difficult-to-treat brain tumor. After a median radiographic follow-up of nearly three years, local tumor control at 48 and 60 months reached 73% and 48%, respectively, with the combined treatment — a dramatic improvement over the 21% and 17% local control rates achieved by prior treatments at the same sites. The hazard ratio of 0.145 (p < 0.001) confirms a highly significant reduction in the risk of local tumor progression when Cs-131 brachytherapy is added to surgery. Complications were manageable: surgery-related issues occurred in 14% of cases, and radiation-induced brain injury was observed in another 14% of patients, with all cases resolving following medical treatment. These five-year results indicate that permanently implanted Cs-131 tiles placed at the time of tumor removal represent a meaningful advance in the management of recurrent aggressive meningiomas, offering clinicians a more effective strategy for local disease control in this challenging patient population.
Journal of neurosurgery
Source →PFOA Exposure Elicits Quantitative Lipidomic Changes in the Pancreas in a Mouse Model of Pancreatic Cancer.
Hocevar BA, et al
Researchers used a genetically engineered mouse model of pancreatic cancer to investigate how exposure to perfluorooctanoic acid (PFOA) — a persistent environmental chemical found in non-stick cookware coatings and firefighting foams — alters the lipid composition of pancreatic tissue. Mice were exposed to 1 or 5 parts per million of PFOA for six months, after which comprehensive lipidomic profiling of pancreatic tissue was performed. The study found significant increases in acylcarnitine and ceramide lipid species alongside decreases in phosphatidylcholines, phosphatidylethanolamines, and phosphatidylserines, all of which are lipid changes previously linked to mitochondrial dysfunction, obesity, and chronic inflammation. Most strikingly, thromboxane B2, a potent pro-inflammatory signaling lipid, was elevated roughly 12-fold at the lower dose and 31-fold at the higher dose, pointing to a strong inflammatory response in pancreatic tissue. These findings suggest that PFOA-driven disruption of pancreatic lipid metabolism may be a critical biological pathway connecting environmental chemical exposure to diabetes and pancreatic cancer, a disease projected to become the second leading cause of cancer death in the United States by 2030.
Environmental toxicology
Source →Epigenetic adaptation of beta cells across lifespan and disease.
Manduchi E, et al
Researchers investigated genome-wide DNA methylation (DNAm) patterns in pancreatic beta and alpha cells across the human lifespan and in type 2 diabetes (T2D), using cell-type-specific epigenomic data from the Human Pancreas Analysis Program. In healthy donors, beta cells show a progressive, age-related loss of DNA methylation concentrated at regulatory regions governing beta cell identity and function, while alpha cells display the opposite trend — subtle gains in methylation over time. Strikingly, beta cells from people with T2D exhibited even greater demethylation than those from healthy controls of comparable age, whereas alpha cells showed no such disease-associated change, highlighting a unique epigenetic plasticity specific to beta cells. These findings suggest that DNA methylation remodeling in healthy beta cells represents a lifelong adaptive response to increasing metabolic demand, and that in T2D this process is accelerated as part of a compensatory effort that ultimately fails under prolonged insulin resistance. For clinicians and researchers, this work reframes T2D-associated beta cell dysfunction not merely as damage but as an adaptive epigenetic program gone awry, opening potential avenues for epigenetic biomarkers and targeted therapeutic strategies to preserve beta cell function.
Nature metabolism
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