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Kawamoto S.,Johns Hopkins Hospital | Johnson P.T.,Johns Hopkins Hospital | Hruban R.H.,Sol Goldman Pancreatic Cancer Research Center | Fishman E.K.,Johns Hopkins Hospital
Abdominal Imaging | Year: 2012

Although autopsy studies report that the second most common site of the accessory spleen is in the tail of the pancreas, intrapancreatic accessory spleens (IPASs) are rarely recognized radiologically. With recent improvements in imaging techniques, IPASs are more commonly detected on imaging studies. IPAS can be mistaken for other type of mass-forming lesions in the tail of the pancreas, particularly an asymptomatic small neuroendocrine neoplasm. Rarely, an epidermoid cyst originating from IPAS may simulate other cystic pancreatic lesion. Accurate preoperative diagnosis would obviate unnecessary surgery. IPAS should be considered when a hypervascular mass is seen in the tail of the pancreas on CT. Typical location, similar attenuation of the lesion to the spleen on noncontrast, and postcontrast CT at different phases are helpful to make diagnosis of IPAS. In particular, characteristic heterogeneous contrast enhancement of IPAS on the arterial phase may be helpful for correct diagnosis. However, when it remains difficult to exclude the other diagnosis, 99mTc labeled heat-damaged red blood cell scintigraphy or superparamagnetic iron oxide-enhanced MRI can be used to confirm the diagnosis of IPAS. © Springer Science+Business Media, LLC 2012. Source

Klein A.P.,Sol Goldman Pancreatic Cancer Research Center
Nature Reviews Cancer | Year: 2013

Pancreatic cancer is a leading cause of cancer death, and it has the poorest prognosis of any major tumour type. Familial pancreatic cancer registries are important for investigating the genetic aetiology of this devastating disease. Using data from our familial pancreatic cancer registry and other registries, this Review discusses the usefulness of family registries in the study of pancreatic and other cancers, and also how such registries provide a unique opportunity for laboratory, population and clinical research. © 2013 Macmillan Publishers Limited. All rights reserved. Source

Dutta P.,H. Lee Moffitt Cancer Center and Research Institute | Le A.,Sol Goldman Pancreatic Cancer Research Center | Vander Jagt D.L.,University of New Mexico | Tsukamoto T.,Johns Hopkins University | And 3 more authors.
Cancer Research | Year: 2013

Hyperpolarized 13C magnetic resonance spectroscopy provides a unique opportunity to detect real-time metabolic fluxes as a means to measure metabolic treatment responses in vivo. Here, we show that pharmacologic inhibition of lactate dehydrogenase-A suppressed the conversion of hyperpolarized 13C-pyruvate to lactate in murine xenografts of P493 human lymphoma. In contrast, a glutaminase inhibitor reduced conversion of 13C-pyruvate to alanine without affecting conversion of pyruvate to lactate. These results illustrate the ability to monitor biomarkers for responses to antimetabolic therapy in real-time, paving the way for clinical development of imaging biomarkers to monitor metabolic pharmacodynamics. © 2013 AACR. Source

Carter H.,Institute for Computational Medicine | Samayoa J.,Institute for Computational Medicine | Hruban R.H.,Sol Goldman Pancreatic Cancer Research Center | Karchin R.,Institute for Computational Medicine
Cancer Biology and Therapy | Year: 2010

Over 20,000 genes were recently sequenced in a series of 24 pancreatic cancers. We applied CHASM (Cancer-specific High-throughput Annotation of Somatic Mutations) to 963 of the missense somatic missense mutations discovered in these 24 cancers. CHASM identified putative driver mutations (false discovery rate ≤0.3) in three known pancreatic cancer driver genes (P53, SMAD4, CDKN2A). An additional 15 genes with putative driver mutations include genes coding for kinases (PIK3CG, DGKA, STK33, TTK and PRKCG), for cell cycle related proteins (NEK8), and for proteins involved in cell adhesion (CMAS, PCDHB2). These and other mutations identified by CHASM point to potential "driver genes" in pancreatic cancer that should be prioritized for additional follow-up. © 2010 Landes Bioscience. Source

Yachida S.,Sol Goldman Pancreatic Cancer Research Center | Yachida S.,National Cancer Center Research Institute | White C.M.,Sol Goldman Pancreatic Cancer Research Center | Naito Y.,Sol Goldman Pancreatic Cancer Research Center | And 14 more authors.
Clinical Cancer Research | Year: 2012

Purpose: Genetic alterations of KRAS, CDKN2A, TP53, and SMAD4 are the most frequent events in pancreatic cancer. We determined the extent to which these 4 alterations are coexistent in the same carcinoma, and their impact on patient outcome. Experimental Design: Pancreatic cancer patients who underwent an autopsy were studied (n = 79). Matched primary and metastasis tissues were evaluated for intragenic mutations in KRAS, CDKN2A, and TP53 and immunolabeled for CDKN2A, TP53, and SMAD4 protein products. The number of altered driver genes in each carcinoma was correlated to clinicopathologic features. Kaplan-Meier estimates were used to determine median disease free and overall survival, and a Cox proportional hazards model used to compare risk factors. Results: The number of genetically altered driver genes in a carcinoma was variable, with only 29 patients (37%) having an alteration in all 4 genes analyzed. The number of altered driver genes was significantly correlated with disease free survival (P = 0.008), overall survival (P = 0.041), and metastatic burden at autopsy (P = 0.002). On multivariate analysis, the number of driver gene alterations in a pancreatic carcinoma remained independently associated with overall survival (P = 0.046). Carcinomas with only 1 to 2 driver alterations were enriched for those patients with the longest survival (median 23 months, range 1 to 53). Conclusions: Determinations of the status of the 4 major driver genes in pancreatic cancer, and specifically the extent to which they are coexistent in an individual patients cancer, provides distinct information regarding disease progression and survival that is independent of clinical stage and treatment status. ©2012 AACR. Source

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