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      Pineal Diffuse Large B-Cell Lymphoma Concomitant With Pituitary Prolactinoma: Possible Correlation Between 2 Distinguished Pathologies : A Case Report

      case-report
      , MD, , MD, PhD, , MD, PhD, , MD, PhD, , MD, , MD, PhD, , MD, PhD, , MD, PhD
      Medicine
      Wolters Kluwer Health

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          Abstract

          This is the first reported case of pineal lymphoma with concomitant prolactin-producing pituitary adenoma.

          A 51-year-old male experienced worsening headaches accompanied by nausea, diplopia, and memory loss for 1 month. Cranial nerve examination revealed bilateral upward gaze limitation with convergence impairment, which is known as Parinaud syndrome. Magnetic resonance images revealed a mass in the pineal gland with a coexisting mass within the enlarged sella fossa. Hormone analysis revealed hyperprolactinemia. The pineal mass was removed without injuring the hypothalamus, brain stem, or any neighboring vessels. Pathology examination confirmed the diagnosis of diffuse large B-cell lymphoma (DLBCL) involving the pineal gland. After further studies, the pineal lymphoma was determined to be a secondary tumor from a gastric primary tumor. The patient died 6 months after diagnosis due to systemic progression of DLBCL.

          Although the mechanistic link between hyperprolactinemia and lymphoma progression has not been clarified on a clinical basis, high prolactin levels may contribute to the rapid progression and therapeutic resistance of the lymphoma.

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          Most cited references45

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          Extrapituitary prolactin: distribution, regulation, functions, and clinical aspects.

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            High incidence of occult leptomeningeal disease detected by flow cytometry in newly diagnosed aggressive B-cell lymphomas at risk for central nervous system involvement: the role of flow cytometry versus cytology.

            We assessed the cerebrospinal fluid (CSF) by flow cytometry and cytology in 51 newly diagnosed and 9 treated aggressive B-cell lymphomas at risk for central nervous system (CNS) involvement to examine the utility of flow cytometry, incidence of CSF disease, and clinical surrogates of CNS spread. Multicolor flow cytometry using multiple antibody panels for light chains and B- and T-cell antigens identified neoplastic clones that constituted as little as 0.2% of total CSF lymphocytes. Among 51 newly diagnosed patients, 11 (22%) had occult CSF involvement. All 11 were detected by flow cytometry but only 1 by cytology (P = .002). Among 9 treated patients, CSF involvement was detected by flow cytometry alone in 2 and also by cytology in 1 case. CSF chemistry and cell counts were similar in patients with and without CSF lymphoma. Only the number of extranodal sites was associated with occult CSF lymphoma in newly diagnosed patients by univariate (P = .006) or logistic regression analysis (P = .012). We hypothesize that the biologic phenotype associated with colonization of extranodal sites leads to CNS spread, possibly related to the microenvironment. Patients at risk for CNS spread should undergo staging CSF evaluation by flow cytometry.
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              KITENIN promotes glioma invasiveness and progression, associated with the induction of EMT and stemness markers

              KITENIN (KAI1 COOH-terminal interacting tetraspanin) promotes tumor invasion and metastasis in various cancers. This study assessed the association between KITENIN expression and advanced glioma grade in patients. In vitro assays revealed that KITENIN knockdown inhibited the invasion and migration of glioma cells, whereas KITENIN overexpression promoted their invasion and migration. In orthotopic mouse tumor models, mice transplanted with KITENIN-transfected glioma cells had significantly shorter survival than mice transplanted with mock-transfected cells. Patients with low KITENIN expression showed a significantly longer progression-free survival than patients with high KITENIN expression. KITENIN induced the expression of the epithelial-mesenchymal transition (EMT) markers (N-cadherin, ZEB1, ZEB2, SNAIL and SLUG) as well as the glioma stemness markers (CD133, ALDH1 and EPH-B1). Taken together, these findings showed that high levels of KITENIN increased glioma invasiveness and progression, associated with the up-regulation of EMT and stemness markers.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                February 2016
                03 March 2016
                : 95
                : 8
                : e2923
                Affiliations
                From the Department of Neurosurgery (Y-JK, SJ, K-SM); Department of Internal Medicine (HKK, D-HY); and Departments of Pathology, Chonnam National University Research Institute of Medical Sciences (M-GN, J-HL, K-HL), Chonnam National University Hwasun Hospital and Medical School, Hwasun-gun, Jeollanamdo, South Korea.
                Author notes
                Correspondence: Kyung-Sub Moon, Department of Neurosurgery, Brain Tumor Clinic and Gamma Knife Center, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Hwasun-gun, Jeollanam-do 519-763, South Korea (e-mail: moonks@ 123456chonnam.ac.kr ).
                Kyung-Hwa Lee, Department of Pathology, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Hwasun-gun, Jeollanam-do 519-763, South Korea (e-mail: mdkaylee@ 123456jnu.ac.kr ).
                Article
                02923
                10.1097/MD.0000000000002923
                4779034
                26937937
                90c49858-31f2-4a9f-8cb5-e2cd97a0aa3a
                Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

                This is an open access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0, where it is permissible to download, share and reproduce the work in any medium, provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                : 1 December 2015
                : 1 February 2016
                : 2 February 2016
                Categories
                5700
                Research Article
                Clinical Case Report
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