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Concerns Regarding the Utility of High-Risk Pancreatic Cancer Surveillance—Reply
In Reply In our recent study, we compared the survival of patients who developed pancreatic cancer under pancreas surveillance to that of a matched US cohort. Many of the questions asked by Dasaro and Prasad we address in previous publications, cited in the article, including imaging findings and surgical pathologic findings, and an estimate of the overall risk of pancreatic cancer in the cohort (1 per 194 patient-years). We have also reported on outcomes of surgical treatment of suspicious pancreatic lesions. Very few pancreatic imaging abnormalities raise concern or need biopsy or surgical resection.
Standard di cura del Diabete 2025
E’ stata pubblicata l’ultima edizione degli Standard of Care in Diabetes dell’American […]
Primo studio clinico di successo per un farmaco contro l’Alzheimer
I ricercatori del Warren Center for Neuroscience Drug Discovery, un […]
Approcci pratici per il monitoraggio dell’aritmia dopo un ictus
L’American College of Cardiology ha pubblicato un percorso decisionale sugli approcci […]
Autismo, scoperto gene con un ruolo importante nella malattia
Potrebbe spiegare perché colpisce di più maschi
Evoluzioni per la gestione del tumore del pancreas
Domani ad Ancona congresso scientifico alla Politecnica Marche
Nel 2024 in Italia 390mila casi di tumore. Oncologi, 'la metà potrà guarire'
Report ‘I numeri del cancro’, -46% di decessi nelle donne per quello al polmone
Nel 2024 in Italia 390mila casi di tumore, 'la metà guarirà'
Report ‘I numeri del cancro’, -46% di decessi nelle donne per il polmone
Strategie e criteri per la diagnosi e la gestione della miocardite
Questo documento fornisce le linee guida dell’American College of Cardiology […]
Unghie al top, come evitare i rischi della manicure semi-permanente
Aideco, ‘il trattamento nasconde insidie se non è eseguito bene’
Unghie al top, come evitare i rischi della manicure semi-permanente
Aideco, ‘il trattamento nasconde insidie se non è eseguito bene’
Fuori Regione 670 mila ricoveri, cure cancro e protesi
Emilia più attrattiva. Cittadinanzattiva, nodo malattie croniche
Fuori Regione 670 mila ricoveri, per cure cancro e protesi
Emilia più attrattiva. Cittadinanzattiva, nodo malattie croniche
Epidemiology of gastrointestinal cancers: a systematic analysis from the Global Burden of Disease Study 2021
Background
Gastrointestinal cancers comprise nearly one-third of global mortality from cancer, yet the comprehensive global burden of these cancers remains uninvestigated.
Objective
We aimed to assess the global, regional and national burden of gastrointestinal cancers.
Designs
Data on oesophagus, gastric, colorectal, liver, pancreas and biliary tract cancers were extracted from the Global Burden of Disease 2021 database. Age-standardised incidence rate (ASIR) and age-standardised death rate (ASDR) were calculated by sex, region and Sociodemographic Index (SDI).
Results
In 2021, there were 5.26 million incidences and 3.70 million deaths from gastrointestinal cancer. The greatest burden is from colorectal, followed by gastric, oesophageal, pancreatic, liver and biliary tract cancer. We noted geographical and socioeconomic differences in ASIR and ASDR across all types of cancers. From 2000 to 2021, ASIR increased for colorectal cancer (annual percent change (APC): 0.10%, 95% CI 0.05% to 0.14%), pancreatic cancer (APC: 0.27%, 95% CI 0.14% to 0.41%), and liver cancer from metabolic dysfunction-associated steatotic liver disease (APC: 0.62%, 95% CI 0.58% to 0.67%) and alcohol-related liver disease (APC: 0.26%, 95% CI 0.22% to 0.30%). ASDR increased for pancreatic cancer (APC: 0.18%, 95% CI 0.02% to 0.34%). Higher SDI countries had higher incidence rates for most types of gastrointestinal cancer.
Conclusions
Although the ASIR of oesophageal, gastric and biliary tract cancer has decreased, the ASIR still increased in colorectal, pancreatic and liver cancer from steatotic liver disease. Public policies are important for controlling gastrointestinal cancers—most importantly, reducing alcohol consumption, hepatitis B immunisation and tackling the burden of metabolic diseases.
Metabolic reprogramming by mutant GNAS creates an actionable dependency in intraductal papillary mucinous neoplasms of the pancreas
Background
Oncogenic ‘hotspot’ mutations of KRAS and GNAS are two major driver alterations in intraductal papillary mucinous neoplasms (IPMNs), which are bona fide precursors to pancreatic ductal adenocarcinoma. We previously reported that pancreas-specific Kras G12D and Gnas R201C co-expression in p48Cre; KrasLSL-G12D; Rosa26LSL-rtTA; Tg (TetO-GnasR201C) mice (‘Kras;Gnas’ mice) caused development of cystic lesions recapitulating IPMNs.
Objective
We aim to unveil the consequences of mutant Gnas R201C expression on phenotype, transcriptomic profile and genomic dependencies.
Design
We performed multimodal transcriptional profiling (bulk RNA sequencing, single-cell RNA sequencing and spatial transcriptomics) in the ‘Kras;Gnas’ autochthonous model and tumour-derived cell lines (Kras;Gnas cells), where Gnas R201C expression is inducible. A genome-wide CRISPR/Cas9 screen was conducted to identify potential vulnerabilities in KrasG12D;GnasR201C co-expressing cells.
Results
Induction of Gnas R201C—and resulting G(s)alpha signalling—leads to the emergence of a gene signature of gastric (pyloric type) metaplasia in pancreatic neoplastic epithelial cells. CRISPR screening identified the synthetic essentiality of glycolysis-related genes Gpi1 and Slc2a1 in Kras G12D;Gnas R201C co-expressing cells. Real-time metabolic analyses in Kras;Gnas cells and autochthonous Kras;Gnas model confirmed enhanced glycolysis on Gnas R201C induction. Induction of Gnas R201C made Kras G12D expressing cells more dependent on glycolysis for their survival. Protein kinase A-dependent phosphorylation of the glycolytic intermediate enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) was a driver of increased glycolysis on Gnas R201C induction.
Conclusion
Multiple orthogonal approaches demonstrate that Kras G12D and Gnas R201C co-expression results in a gene signature of gastric pyloric metaplasia and glycolytic dependency during IPMN pathogenesis. The observed metabolic reprogramming may provide a potential target for therapeutics and interception of IPMNs.