Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Loren Joseph
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, L. Joseph wrote the following 4 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Guideline Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: the Papanicolaou Society of Cytopathology guidelines for pancreatobiliary cytology. 2014

Layfield, Lester J / Ehya, Hormoz / Filie, Armando C / Hruban, Ralph H / Jhala, Nirag / Joseph, Loren / Vielh, Philippe / Pitman, Martha B / Anonymous3080788. ·Department of Pathology and Anatomical Sciences, University of Missouri, Columbia, Missouri. ·Diagn Cytopathol · Pubmed #24639398.

ABSTRACT: The Papanicolaou Society of Cytopathology has developed a set of guidelines for pancreatobiliary cytology including indications for endoscopic ultrasound-guided fine-needle aspiration, terminology and nomenclature of pancreatobiliary disease, ancillary testing, and post-biopsy management. All documents are based on the expertise of the authors, a review of the literature, discussions of the draft document at several national and international meetings, and synthesis of selected online comments of the draft document. This document presents the results of these discussions regarding the use of ancillary testing in the cytologic diagnosis of biliary and pancreatic lesions. Currently, fluorescence in situ hybridization (FISH) appears to be the most clinically relevant ancillary technique for cytology of bile duct strictures. The addition of FISH analysis to routine cytologic evaluation appears to yield the highest sensitivity without loss in specificity. Loss of immunohistochemical staining for the protein product of the SMAD4 gene and positive staining for mesothelin support a diagnosis of ductal adenocarcinoma. Immunohistochemical markers for endocrine and exocrine differentiation are sufficient for a diagnosis of endocrine and acinar tumors. Nuclear staining for beta-catenin supports a diagnosis of solid-pseudopapilary neoplasm. Cyst fluid analysis for amylase and carcinoembryonic antigen aids in the preoperative classification of pancreatic cysts. Many gene mutations (KRAS, GNAS, VHL, RNF43, and CTNNB1) may be of aid in the diagnosis of cystic neoplasms. Other ancillary techniques do not appear to improve diagnostic sensitivity sufficiently to justify their increased costs.

2 Article Telomere Diagnostics for Pancreatic Neoplasms and Cysts. 2018

Joseph, Loren. ·Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. Electronic address: ljjoseph@bidmc.harvard.edu. ·J Mol Diagn · Pubmed #29155048.

ABSTRACT: This commentary highlights the article by Hata et al that examines markers for assessing pancreatic neoplastic progression.

3 Article Transcriptional regulation of fibronectin by p21-activated kinase-1 modulates pancreatic tumorigenesis. 2015

Jagadeeshan, S / Krishnamoorthy, Y R / Singhal, M / Subramanian, A / Mavuluri, J / Lakshmi, A / Roshini, A / Baskar, G / Ravi, M / Joseph, L D / Sadasivan, K / Krishnan, A / Nair, A S / Venkatraman, G / Rayala, S K. ·Department of Biotechnology, Indian Institute of Technology Madras (IITM), Chennai, India. · Department of Human Genetics, Sri Ramachandra University, Chennai, India. · Department of Pathology, Sri Ramachandra University, Chennai, India. · Department of Plastic and Reconstructive Surgery, Government Medical College, Thiruvananthapuram, India. · Rajiv Gandhi Centre for Biotechnology (RGCB), Thiruvananthapuram, India. ·Oncogene · Pubmed #24561527.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is the eighth largest cause of cancer-related mortality across the world, with a median 5-year survival rate of less than 3.5%. This is partly because the molecules and the molecular mechanisms that contribute to PDAC are not well understood. Our goal is to understand the role of p21-activated kinase 1 (Pak1) signaling axis in the progression of PDAC. Pak1, a serine/threonine kinase, is a well-known regulator of cytoskeletal remodeling, cell motility, cell proliferation and cell survival. Recent reports suggest that Pak1 by itself can have an oncogenic role in a wide variety of cancers. In this study, we analyzed the expression of Pak1 in human pancreatic cancer tissues and found that Pak1 levels are significantly upregulated in PDAC samples as compared with adjacent normals. Further, to study the functional role of Pak1 in pancreatic cancer model systems, we developed stable overexpression and lentiviral short hairpin RNA-mediated knockdown (KD) clones of Pak1 and studied the changes in transforming properties of the cells. We also observed that Pak1 KD clones failed to form tumors in nude mice. By adopting a quantitative PCR array-based approach, we identified fibronectin, a component of the extracellular matrix and a mesenchymal marker, as a transcriptional target of Pak1 signaling. The underlying molecular mechanism of Pak1-mediated transformation includes its nuclear import and recruitment to the fibronectin promoter via interaction with nuclear factor-κB (NF-κB)-p65 complex. To our knowledge, this is the first study illustrating Pak1-NF-κB-p65-mediated fibronectin regulation as a potent tumor-promoting mechanism in KRAS intact model.

4 Article Pancreatic ductal adenocarcinoma with autoimmune pancreatitis-like histologic and immunohistochemical features. 2014

Zhang, Xuefeng / Liu, Xiuli / Joseph, Loren / Zhao, Lei / Hart, John / Xiao, Shu-Yuan. ·Department of Pathology, University of Chicago Medical Center, 5841S Maryland Ave, Chicago, IL 60605, USA. · Department of Pathology, Cleveland Clinics, Cleveland, OH 55195, USA. · Department of Pathology, University of Chicago Medical Center, 5841S Maryland Ave, Chicago, IL 60605, USA. Electronic address: sxiao@bsd.uchicago.edu. ·Hum Pathol · Pubmed #24457081.

ABSTRACT: Autoimmune pancreatitis (AIP) often manifests as a mass lesion causing obstructive jaundice, clinically mimicking pancreatic carcinoma. A diagnosis of AIP may obviate the need for surgical resection, as most patients respond to steroid treatment. However, it is not clear whether these 2 conditions can coexist. In this study, 105 specimens resected for pancreatic ductal adenocarcinoma (PDAC) that also have changes of chronic pancreatitis were examined for features considered to be characteristic of AIP. Of 105 cases of PDAC with changes of chronic pancreatitis, 10 (9.5%) exhibited histologic features of AIP, including exuberant fibrosis, lymphoplasmacytic infiltration, obliterative phlebitis, or granulocytic epithelial lesions. Of these 10 cases, 7 had more than 20 immunoglobulin G4+ plasma cells per high-power field. Of these 7 cases, 5 were analyzed for Kirsten rat sarcoma viral oncogene mutation and SMAD4 expression. Three cases showed K-ras mutation and/or loss of SMAD4 expression in benign AIP-like areas. These findings suggest 2 possibilities: first, AIP-like lesions may occur in a small but significant portion of PDAC cases; second, some PDACs may arise in a background of AIP. Therefore, caution is necessary when making a diagnosis of AIP by needle biopsy of a mass lesion, and patients with a tentative AIP diagnosis should be closely followed up clinically.