0000000000331391
AUTHOR
Guido Adler
StellaTUM: current consensus and discussion on pancreatic stellate cell research
The field of pancreatic stellate cell (PSC) biology is very young, as the essential in-vitro tools to study these cells (ie, methods to isolate and culture PSC) were only developed as recently as in 1998. Nonetheless, there has been an exponential increase in research output in this field over the past decade, with numerous research groups around the world focusing their energies into elucidating the biology and function of these cells. It is now well established that PSC are responsible for producing the stromal reaction (fibrosis) of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. Despite exponentially increasing data, the methods for studying PSC remain var…
Monitoring of Enzyme Substitution Using the Cholesteryl Octanoate Breath Test
The efficiency of enzyme replacement therapy in pancreatic insufficiency is usually judged on the grounds of clinical improvement and the effect on steatorrhea: treatment is thought to be successful if steatorrhea is abolished or, at least, reduced. In the majority of patients, the amount of enzyme necessary to alleviate steatorrhea can be reduced if lipase is protected against acidic inactivation either by blocking H2 secretion of the stomach or by protecting enzymes by pH-sensitive enteric coating. However, steatorrhea is frequently not abolished and a differential treatment may be necessary in each patient.
Pattern of secondary genomic changes in pancreatic tumors ofTgfα/Trp53+/−transgenic mice
Trp53+/− mice overexpressing Tgfα in a pancreas-specific manner represent a well-established animal model for pancreatic cancer. In this study we analyzed 38 pancreatic adenocarcinomas of these mice for secondary genomic changes by comparative genomic hybridization (CGH), loss of heterozygosity (LOH) analysis, real-time PCR, and methylation-specific analysis. CGH screening of the tumors revealed a recurrent pattern of genomic changes. In more than 50% of the tumors, chromosome 11 was affected. The gain of the proximal part spans about 16 cM, including the genes for Egfr, Rel, and Stk10. The distal part of chromosome 11, which contains the Trp53 locus, was deleted. LOH analysis proved that a…