A Case of Ductal Dysplasia of the Pancreas A Possible Prerequisite for Pancreatic Cancer

The precise pathobiology of precursor lesions, which develop into pancreatic adenocarcinoma, remains controversial. Recently, we encountered a patient with dysplastic lesion of the pancreas; a case in which a precursor lesion of the pancreatic carcinoma may have been documented. The patient was a 73-year-old female with epigastric discomfort. As part of a general check-up, she underwent abdominal ultrasound, which revealed the pancreatic duct in the pancreatic body to be slightly indented. Computed tomography (CT) scan revealed mild dilatation of the main pancreatic duct and a small low-density area (less than 1 cm in diameter). Endoscopic retrograde cholangiopancreatography (ERCP) showed the irregularity in the body of the main pancreatic duct. Under general anesthesia, resection of the distal portion of the pancreas was performed with splenic conservation. Pathological examination revealed focal hyperplastic epithelium of the pancreatic duct with moderate dysplasia. Expression of the proliferating cell nuclear antigen (PCNA) in the lesion was observed, indicating a slightly proliferative nature. Mutant p53 protein was slightly expressed in the lesion. As is seen in this case, ductal hyperplasia of the pancreas might represent precursor lesions, and constitute part of a continuous development spectrum evolving into ductal adenocarcinoma of the pancreas with accumulation of genetic alterations

Literature survey on epidemiology and pathology of cardiac fibroma

<p>Abstract</p> <p>Background</p> <p>Although cardiac fibroma has been regarded as benign tumor, it presents various symptoms and may lead to death. Unfortunately, only a few studies have reported the epidemiology, embryology, and histopathology of the tumor, and the factors predicting poorer outcome are still obscured.</p> <p>Methods</p> <p>In July 2011 we searched for English and Japanese cases of cardiac fibroma using the PubMed and IgakuChuoZasshi databases. We then extracted and sampled raw data from the selected publications in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) style as much as was possible.</p> <p>Results</p> <p>Details of a total of 178 patients with cardiac fibroma were retrieved. The mean age was 11.4 years (median: 2.8 years). Tumor sizes ranged from 8.0 to 150.0 mm (mean 53.1 mm). The left ventricle was found to be the most common site associated with the tumor at a rate of 57.3%, followed by the right ventricle, and interventricular septum. The highest mortality was found in patients with septal involvement (58.6%). In all, 111 patients survived among the 160 patients with a recorded outcome. A younger age of the patient at the time of diagnosis was associated with a decreased survival rate. In addition, a significant positive association was found between ages for patients younger than 17 years of age and the diameter of the tumor at the time of diagnosis (r = 0.341, <it>P </it>= 0.006).</p> <p>Conclusions</p> <p>Both the younger age of patients at the time of diagnosis and septal involvement can be regarded as factors significantly indicating a poor prognosis. Furthermore, our statistical analyses support the following hypotheses. First, the high ratio of tumor-to-heart size may generate low cardiac output and therefore lead to poor outcome. Second, the ratio of the sites where cardiac fibroma occurred corresponds with the ratio of the muscular weight of the cardiac chamber. Third, cardiac fibroma involving the interventricular septum more frequently induces conduction system disease.</p

Gene Expression Analysis of a Murine Model with Pulmonary Vascular Remodeling Compared to End-Stage IPAH Lungs

BACKGROUND: Idiopathic pulmonary arterial hypertension (IPAH) continues to be one of the most serious intractable diseases that might start with activation of several triggers representing the genetic susceptibility of a patient. To elucidate what essentially contributes to the onset and progression of IPAH, we investigated factors playing an important role in IPAH by searching discrepant or controversial expression patterns between our murine model and those previously published for human IPAH. We employed the mouse model, which induced muscularization of pulmonary artery leading to hypertension by repeated intratracheal injection of Stachybotrys chartarum, a member of nonpathogenic and ubiquitous fungus in our envelopment. METHODS: Microarray assays with ontology and pathway analyses were performed with the lungs of mice. A comparison was made of the expression patterns of biological pathways between our model and those published for IPAH. RESULTS: Some pathways in our model showed the same expression patterns in IPAH, which included bone morphogenetic protein (BMP) signaling with down-regulation of BMP receptor type 2, activin-like kinase type 1, and endoglin. On the other hand, both Wnt/planar cell polarity (PCP) signaling and its downstream Rho/ROCK signaling were found alone to be activated in IPAH and not in our model. CONCLUSIONS: Activation of Wnt/PCP signaling, in upstream positions of the pathway, found alone in lungs from end stage IPAH may play essential roles in the pathogenesis of the disease