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Silver Spring, MD, United States

Lewis R.B.,American Institute for Radiologic Pathology | Lewis R.B.,Uniformed Services University of the Health Sciences | Mehrotra A.K.,The Joint Pathology Center | Rodriguez P.,La Princesa University Hospital | And 3 more authors.
Radiographics | Year: 2014

Gastrointestinal (GI) lymphoma encompasses a heterogeneous group of neoplasms that have a common lymphoid origin but variable pathologic and imaging features. Extranodal marginal zone B-cell lymphoma (ENMZL) and diffuse large B-cell lymphoma (DLBCL) are the most common. ENMZL usually occurs in the stomach, where it is associated with chronic infection by Helicobacter pylori, and is typically a superficial spreading lesion that causes mucosal nodularity or ulceration and mild wall thickening. DLBCL may arise de novo or from transformation of ENMZL or other low-grade lymphomas. This form of lymphoma produces extensive wall thickening or a bulky mass, but obstruction is uncommon. Mantle cell lymphoma is the classic cause of lymphomatous polyposis, but multiple polyps or nodules can also be seen with ENMZL and follicular lymphoma. Burkitt lymphoma is usually characterized by an ileocecal mass or wall thickening in the terminal ileum in young children, often in the setting of widespread disease. Primary GI Hodgkin lymphoma, which is rare, may be manifested by a variety of findings, though stenosis is more common than with non-Hodgkin lymphoma. Enteropathy-associated T-cell lymphoma is frequently associated with celiac disease and is characterized by wall thickening, ulceration, and even perforation of the jejunum. Accurate radiologic diagnosis of GI lymphoma requires a multifactorial approach based on the clinical findings, site of involvement, imaging findings, and associated complications. © RSNA, 2014. Source

Sharad S.,Uniformed Services University of the Health Sciences | Ravindranath L.,Uniformed Services University of the Health Sciences | Haffner M.C.,Johns Hopkins University | Li H.,Uniformed Services University of the Health Sciences | And 12 more authors.
Epigenetics | Year: 2014

The prostate transmembrane protein androgen induced 1 (PMEPA1) gene is highly expressed in prostate epithelial cells and is a direct transcriptional target for the androgen receptor (AR). AR protein levels are controlled by the ARPMEPA1 negative feedback loop through NEDD4-E3 ligase. Reduced expression of PMEPA1 observed in prostate tumors, suggests that loss of PMEPA1 may play critical roles in prostate tumorigenesis. This study focuses on epigenetic mechanisms of reduced PMEPA1 expression in the cancer of the prostate (CaP). Benign (n = 77) and matched malignant (n = 77) prostate epithelial cells were laser capture micro-dissected from optimum cutting temperature embedded frozen prostate sections from 42 Caucasian American (CA) and 35 African American (AA) cases. Purified DNA specimens were analyzed for CpG methylation of the PMEPA1 gene. PMEPA1 mRNA expression levels were evaluated by qRT-PCR. Analysis of PMEPA1 methylation and mRNA expression in the same tumor cell populations indicated a significant inverse correlation between mRNA expression and methylation in CaP (P = 0.0115). We noted higher frequency of CpG methylation within the evaluated first intronic region of the PMEPA1 gene in prostate tumors of CA men as compared with AA. In CaP cell lines, PMEPA1 expression was induced and AR protein levels were diminished in response to treatment with the DNA methyltransferase inhibitor, 5-aza-2′-deoxycytidine (decitabine). Cell culture-based studies demonstrated that decitabine restores PMEPA1 expression in AR-positive CaP cell lines. This report reveals the potential role of PMEPA1 gene methylation in the regulation of AR stability. Thus, downregulation of PMEPA1 may result in increased AR protein levels and function in CaP cells, contributing to prostate tumorigenesis. © 2014 Landes Bioscience. Source

Kligerman S.J.,University of Maryland Baltimore County | Franks T.J.,The Joint Pathology Center | Galvin J.R.,University of Maryland Baltimore County | Galvin J.R.,American Institute for Radiologic Pathology
Radiographics | Year: 2013

Organization, characterized by fibroblast proliferation, is a common and nearly universal response to lung injury whether it is focal or diffuse. Despite the vast range of injurious agents, the lung's response to injury is quite limited, with a similar pattern of reaction seen radiologically and histologically regardless of the underlying cause. Although there is a tendency to divide organization into distinct entities, the underlying injury to the alveolar epithelial basement membrane is a uniting factor in these processes. This pattern of lung injury is seen in the organizing phase of diffuse alveolar damage, organizing pneumonia (OP), acute fibrinous and organizing pneumonia, and certain types of fibrotic lung disease. In addition, although organization can heal without significant injury, in some instances it progresses to fibrosis, which can be severe. When fibrosis due to organization is present, other histologic and imaging patterns, such as those seen in nonspecific interstitial pneumonia, can develop, reflecting that fibrosis can be a sequela of organization. This article reviews the histologic and radiologic findings of organization in lung injury due to diffuse alveolar damage, OP, and acute fibrinous and organizing pneumonia and helps radiologists understand that the histologic and radiologic findings depend on the degree of injury and the subsequent healing response. © RSNA, 2013. Source

Butler D.A.,Medical Follow up Agency | Baker T.P.,The Joint Pathology Center
Military Medicine | Year: 2015

The Department of Defense’s Joint Pathology Center (JPC) is the world’s largest collection of human pathology specimens, comprising some 7.4 million accessions. The biorepository, which began during the Civil War as a collection of materials obtained from medical and surgical procedures performed by Army physicians, houses specimens and associated data obtained for diagnostic purposes. It also holds several collections of specimens from military personnel who shared a common, service-related exposure or medical condition. This article, which is excerpted and adapted from the 2012 Institute of Medicine report “Future Uses of the Department of Defense JPC Biorepository,”1 summarizes information on the repository, its past uses, and the future operational issues and challenges that the JPC faces as it develops a concept of operations that will allow it to move forward as a resource for researchers. © 2015 Association of Military Surgeons of the U.S. All rights reserved. Source

Rastogi A.,Uniformed Services University of the Health Sciences | Tan S.-H.,Uniformed Services University of the Health Sciences | Mohamed A.A.,Uniformed Services University of the Health Sciences | Chen Y.,Uniformed Services University of the Health Sciences | And 11 more authors.
Genes and Cancer | Year: 2014

The fusion between ERG coding sequences and the TMPRSS2 promoter is the most prevalent in prostate cancer (CaP). The presence of two main types of TMPRSS2-ERG fusion transcripts in CaP specimens, Type I and Type II, prompted us to hypothesize that the cumulative actions of different ERG variants may impact CaP development/progression. Using TMPRSS2-ERG3 (Type I) and TMPRSS2-ERG8 (Type II) expression vectors, we determined that the TMPRSS2-ERG8 encoded protein is deficient in transcriptional regulation compared to TMPRSS2-ERG3. Co-transfection of vectors resulted in decreased transcriptional regulation compared to TMPRSS2-ERG3 alone, suggesting transdominance of ERG8. Expression of exogenous ERG8 protein resulted in a decrease in endogenous ERG3 protein levels in TMPRSS2-ERG positive VCaP cells, with a concomitant decrease in C-MYC. Further, we showed a physical association between ERG3 and ERG8 in live cells by the bimolecular fluorescence complementation assay, providing a basis for the observed effects. Inhibitory effects of TMPRSS2-ERG8 on TMPRSS2-ERG3 were also corroborated by gene expression data from human prostate cancers, which showed a positive correlation between C-MYC expression and TMPRSS2-ERG3/TMPRSS2-ERG8 ratio. We propose that an elevated TMPRSS2-ERG3/TMPRSS2-ERG8 ratio results in elevated C-MYC in CaP, providing a strong rationale for the biomarker and therapeutic utility of ERG splice variants, along with C-MYC. © 2014, Impact Journals LLC. All rights reserved. Source

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