WSC 20-21 Conf 6 Illustrated Results

Total Page:16

File Type:pdf, Size:1020Kb

WSC 20-21 Conf 6 Illustrated Results Joint Pathology CenterJoint Pathology Center Veterinary PathologyVeterinary Services Pathology Services WEDNESDAY SLIDE CONFERENCE 2020-2021 WEDNESDAY SLIDE CONFERENCE 2019-2020 Conference 6 C o n f e r e n c e 16 29 January 2020 30 September 2020 Dr. Ingeborg Langohr, DVM, PhD, DACVP Professor Department of Pathobiological Sciences Louisiana State University School of Veterinary Medicine Joint Pathology Center Baton Rouge, LA Silver Spring, Maryland CASE I: CASE S1809996 1: N16 (JPC-032 4135077(4084301).-00 ) Microscopic2.2x1.5x2 Description: cm firm mass The originatinginterstitium from the dura within themater section (meningioma). is diffusely infiltrated by Signalment:Signalment: A 3-month 13- old,yrs male,of age, mixed spayed- female,moderate to large numbers of predominantly breed pigGolden (Sus scrofa Retriever,) Canis lupus familiaris, caninemononuclear. Laboratory cells along results: with edema. There is abundantCytology: type II pneumocyteIt was reported hyperplasia that ante -mortem History: This pig had no previous signs of History: lining alveolarcytology septae of blood and manysmears of from the this animal were illness, andIt waswas reportedfound dead. that the patient had decreased consistent with lymphoid leukemia. appetite and lethargy for the past 1-2 weeks andalveolar spacesSpecial have staining: central Under areas polarized of light, Congo Gross Pathologyhad diarrhea: Approximately for ~1 day. She70% had of a history ofnecrotic macrophagesRed special admixedstain withrevealed other apple-green the lungs,seizures primarily for thein the past cranial ~3 years; regions her last of seizure wasmononuclear birefringence cells and of fewer material neutrophils. effacing glomeruli and the lobes,1 were month patchy ago. darkThe red,patient and hadfirm a generalizedOccasionally cardiac there vessel is free. nuclear basophilic comparedlymphadenopathy to the more normal (lymphoma). areas of lung.Patient was on phenobarbital, was obese and was 5-7% Microscopic description: Laboratorydehydrated. results: Porcine reproductive The microscopic findings for the submitted and respiratory syndrome (PRRS) PCR was tissues are: positive fromGross splenic Pathology: tissue, and PRRS IHC was stronglyRelevant immunoreactive gross patholog withinic findingsthe included: Kidneys: Glomeruli are diffusely and globally cytoplasmMultiple of macrophages (n=10) well in the-demarcated, affected unattached, obscured and expanded by amorphous lung tissue.soft, Porcine white, influenzalipid-like massesvirus PCR, (lipomas) ranging homogenous pale eosinophilic to amphophilic from 4-20 cm in diameter, were present in the material (amyloid). Bowman's capsules are porcine circovirus – 2 IHC, and subcutis. There was generalized enlargement of variably thickened and there is marked synechia Mycoplasmaperipheral hyopneumoniae lymph nodes IHC ~4 were times all larger than negative. norSmallmal. numbers The left caudal of E. lungcoli lobewere had a 1 cm focal isolated fromfirm, thedark cranioventral red area of lung depression. with The right aerobic culture.ventricular free wall was 3 mm and the left was 7 Lung, pig (HE, 6X). There is diffuse consolidation of mm (right:left ratio of 1:2.3). The right and leftthe lung. At low magnification, airway are filled with kidney contained innumerable miliary white fociexudate and the pleura and interlobular connective throughout the cortical parenchyma. A 3mm cysttissue are mildly expanded. was present on the cortical surface of the right kidney. The parietal lobe of the left cerebral Kidney, heart, dog. One section of kidney and heart are hemisphere was depressed by an approximately submitted for examination. (HE, 5X) 1 Kidney, dog. Glomeruli are diffusely and globally expanded by amyloid, and there is a marked loss of tubules within the intervening parenchyma. Moderate numbers of the lymphocytes and plasma cells are present within the interstitium. (HE, 100X) formation. The interstitium is diffusely infiltrated Meninges: Meningioma with small to moderate amounts of lymphocytes Brain: Meningioma-associated cerebrocortical and plasma cells. compression with locally extensive astrocytosis, oligodendrogliosis, neuronal satellitosis and Heart: Arteries and arterioles throughout the periglial edema myocardium frequently have transmural Lymph node and Spleen: Metastasis of lymphoid thickening of the vessel wall by amorphous pale leukemia amphophilic material (amyloid). Affected vessels Lung: Focal bronchioloalveolar carcinoma, well- often have recanalization characterized by differentiated multiple small caliber spaces. There is marked endocardial fibrosis and few scattered multifocal Contributor’s comment: areas of mild to moderate interstitial fibrosis; The animal in this case had multiple neoplastic associated cardiac myocytes are shrunken and processes. The neoplastic leukemic lymphoid fragmented (degeneration). There are also a few cells were effacing the lymph nodes, in multifocally extensive areas of myocardial loss pericapsular vessels associated with lymph nodes and replacement by adipose tissue and scattered and multifocally present in the spleen. This macrophages, lymphocytes and plasma cells. neoplasm is considered the primary cause of illness in this case. The meningioma and its Contributor’s morphologic diagnosis: compression against the parietal lobe of the brain Kidney: Severe diffuse global glomerular resulted in seizures. There was also a well- amyloidosis differentiated bronchioloalveolar carcinoma Heart: Submassive severe coronary arterial wall identified in one site in the lung. amyloidosis with recanalization Heart: Moderate multifocal interstitial Amyloidosis can be secondary to chronic myocardial fibrosis and fatty infiltration with inflammatory or neoplastic processes; myocardial degeneration. considering the multiple neoplasms in this case, Morphologic diagnoses for tissues not submitted: Heart, dog. The walls of myocardial arteries are multifocally expanded by amyloid which encroaches on the lumen. There is moderate fibroplasia of the adjacent arterial wall and periarteriolar fibrosis. There is loss of myofibers and replacement fibrosis in the adjacent myocardium. (HE, 97X) including lymphoid leukemia, it is likely that the associated with the amyloid light chain (AL amyloid deposition in the kidney, and possible form), is the most common form in humans, the myocardial vasculature as well, was while secondary amyloidosis, which is associated secondary to other disease processes going on. with the amyloid-associated (AA) form, is most The amyloid deposition in the vessels of the heart common in animals. may also be secondary to aging, as senile amyloid plaques have been reported in muscular arteries The AL form is immunoglobulin-derived and can of the myocardium, lungs, and spleen of old dogs. be deposited by B lymphocytes as well as plasma The cause of the myocardial lesions may be cells and result from immunocyte dyscrasias. The secondary to the vascular amyloidosis in the heart AA form of amyloidosis is derived from the and impaired oxygenation of the associated musculature. The term amyloid refers to a group of glycoproteins whose protein components represent β-pleated sheet patterns. In a healthy patient, the immune system is usually able to either repair (chaperones) or degrade (ubiquitin- proteosome pathway) these proteins. However, if the body is unable to perform such feats, one can end up with amyloidosis. These proteins deposit into organs and result in pressure atrophy of adjacent cells as they accumulate. Kidney, dog. Under polarized light, Congo Red Amyloidosis can be classified into systemic histochemical stain reveals apple-green birefringence of (amyloid deposits in multiple organs) and amyloid effacing glomeruli. (Congo Red, 10X) (Photo: localized (single organ) amyloidosis, and further Courtesy of Tuskegee University College of Veterinary categorized into primary and secondary Medicine) amyloidosis. Primary amyloidosis, which is The amyloid that was found in the cardiac vessels of this animal may be due to the systemic disease affecting this dog but may also be associated to aging. Cardiac amyloidosis has been reported in dogs ≥7 years and is somewhat comparable to the senile cardiac amyloidosis of humans, which is seen in those age 70 and greater. A prominent difference is that amyloid builds up in the atria and ventricles of the heart in humans, while studies show that it primarily only affects arterioles in dogs.2 Heart dog. A Masson’s trichrome demonstrates the mural Grossly, amyloidosis can be diagnosed by using fibroplasia surrounding amyloid plaques in affected Lugol's agent followed by diluted sulfuric acid. If arterioles. (Masson’s trichrome, 100X) the tissue becomes a purple to dark blue tinge, it is positive for amyloidosis. Microscopically, one precursor serum-amyloid associated (SAA) could use Congo Red stain as well as thioflavine- protein. This precursor is synthesized in the liver T. The stain itself is not taken up by the protein, and its production is increased in pro- but rather caught in the β-pleated sheet. Under inflammatory states such as chronic polarized light, the amyloid proteins emit an inflammation and neoplasia. With the lack of apple-green birefringence with the Congo Red. In proteolytic action on these proteins, amyloidosis the case of AA amyloidosis, the addition of can result. Humans have these same two forms, potassium permanganate results in the loss of the as well as the β-amyloid form (Aβ) which is Congo Red stain, enabling
Recommended publications
  • Endogenous Dendritic Cells from the Tumor Microenvironment Support T
    Endogenous dendritic cells from the tumor PNAS PLUS microenvironment support T-ALL growth via IGF1R activation Todd A. Tripletta, Kim T. Cardenasa,1, Jessica N. Lancastera, Zicheng Hua, Hilary J. Seldena, Guadalupe J. Jassoa, Sadhana Balasubramanyama, Kathy Chana, LiQi Lib, Xi Chenc,d, Andrea N. Marcogliesee, Utpal P. Davéf, Paul E. Loveb, and Lauren I. R. Ehrlicha,2 aDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712; bSection on Hematopoiesis and Lymphocyte Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892; cDivision of Biostatistics, Department of Health Sciences, University of Miami Miller School of Medicine, Miami, FL 33136; dSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136; eDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030; and fDivision of Hematology/Oncology, Tennessee Valley Healthcare System and Vanderbilt University Medical Center, Nashville, TN 37232 Edited by Zena Werb, University of California, San Francisco, CA, and approved January 14, 2016 (received for review October 15, 2015) Primary T-cell acute lymphoblastic leukemia (T-ALL) cells require tumor growth and metastasis (3). Tumor-associated macrophages stromal-derived signals to survive. Although many studies have (TAMs), which resemble alternatively activated (M2) macro- identified cell-intrinsic alterations in signaling pathways that promote phages (4), also support tumor growth. TAMs suppress antitumor T-ALL growth, the identity of endogenous stromal cells and their immune responses, promote tumor invasion and angiogenesis, and associated signals in the tumor microenvironment that support T-ALL are negatively associated with clinical outcomes (5).
    [Show full text]
  • Transplantation Antitumor Activity After Bone Marrow Graft-Versus-Host
    The Journal of Immunology Host NKT Cells Can Prevent Graft-versus-Host Disease and Permit Graft Antitumor Activity after Bone Marrow Transplantation1 Asha B. Pillai,* Tracy I. George,† Suparna Dutt,* Pearline Teo,* and Samuel Strober2* Allogeneic bone marrow transplantation is a curative treatment for leukemia and lymphoma, but graft-vs-host disease (GVHD) remains a major complication. Using a GVHD protective nonmyeloablative conditioning regimen of total lymphoid irradiation and antithymocyte serum (TLI/ATS) in mice that has been recently adapted to clinical studies, we show that regulatory host NKT cells prevent the expansion and tissue inflammation induced by donor T cells, but allow retention of the killing activity of donor T cells against the BCL1 B cell lymphoma. Whereas wild-type hosts given transplants from wild-type donors were protected against progressive tumor growth and lethal GVHD, NKT cell-deficient CD1d؊/؊ and J␣-18؊/؊ host mice given wild-type transplants cleared the tumor cells but died of GVHD. In contrast, wild-type hosts given transplants from CD8؊/؊ or perforin؊/؊ donors had progressive tumor growth without GVHD. Injection of host-type NKT cells into J␣-18؊/؊ host mice conditioned with TLI/ATS markedly reduced the early expansion and colon injury induced by donor T cells. In conclusion, after TLI/ATS host conditioning and allogeneic bone marrow transplantation, host NKT cells can separate the proinflammatory and tumor cytolytic functions of donor T cells. The Journal of Immunology, 2007, 178: 6242–6251. raft-vs-host disease (GVHD)3 remains a major compli- taining antitumor activity. Preclinical studies of a TLI and anti- cation of human hemopoietic cell transplantation in the thymocyte serum (ATS) regimen in mice showed that the G treatment of leukemia and lymphoma (1).
    [Show full text]
  • Post-Splenectomy Sepsis: a Review of the Literature
    Open Access Review Article DOI: 10.7759/cureus.6898 Post-splenectomy Sepsis: A Review of the Literature Faryal Tahir 1 , Jawad Ahmed 1 , Farheen Malik 2 1. Internal Medicine, Dow University of Health Sciences, Karachi, PAK 2. Pediatrics, Dow University of Health Sciences, Karachi, PAK Corresponding author: Jawad Ahmed, [email protected] Abstract The spleen is an intraperitoneal organ that performs vital hematological and immunological functions. It maintains both innate and adaptive immunity and protects the body from microbial infections. The removal of the spleen as a treatment method was initiated from the early 1500s for traumatic injuries, even before the physiology of spleen was properly understood. Splenectomy has therapeutic effects in many conditions such as sickle cell anemia, thalassemia, idiopathic thrombocytopenic purpura (ITP), Hodgkin’s disease, and lymphoma. However, it increases the risk of infections and, in some cases, can lead to a case of severe sepsis known as overwhelming post-splenectomy infection (OPSI), which has a very high mortality rate. Encapsulated bacteria form a major proportion of the invading organisms, of which the most common is Streptococcus pneumoniae. OPSI is a medical emergency that requires prompt diagnosis (with blood cultures and sensitivity, blood glucose levels, renal function tests, and electrolyte levels) and management with fluid resuscitation along with immediate administration of empirical antimicrobials. OPSI can be prevented by educating patients, vaccination, and antibiotic prophylaxis.
    [Show full text]
  • Color Atlas of Hematology
    i ii iii Color Atlas of Hematology Practical Microscopic and Clinical Diagnosis Harald Theml, M.D. Professor, Private Practice Hematology/Oncology Munich, Germany Heinz Diem, M.D. Klinikum Grosshadern Institute of Clinical Chemistry Munich, Germany Torsten Haferlach, M.D. Professor, Klinikum Grosshadern Laboratory for Leukemia Diagnostics Munich, Germany 2nd revised edition 262 color illustrations 32 tables Thieme Stuttgart · New York iv Library of Congress Cataloging-in-Publica- Important note: Medicine is an ever- tion Data is available from the publisher changing science undergoing continual development. Research and clinical ex- perience are continually expanding our knowledge, in particular our knowledge of This book is an authorized revised proper treatment and drug therapy. Insofar translation of the 5th German edition as this book mentions any dosage or appli- published and copyrighted 2002 by cation, readers may rest assured that the Thieme Verlag, Stuttgart, Germany. authors, editors, and publishers have made Title of the German edition: every effort to ensure that such references Taschenatlas der Hämatologie are in accordance with the state of knowl- edge at the time of production of the book. Translator: Ursula Peter-Czichi PhD, Nevertheless, this does not involve, imply, Atlanta, GA, USA or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of appli- 1st German edition 1983 cations stated in the book. Every user is re- 2nd German edition 1986 quested to examine carefully the manu- 3rd German edition 1991 facturers’ leaflets accompanying each drug 4th German edition 1998 and to check, if necessary in consultation 5th German edition 2002 with a physician or specialist, whether the 1st English edition 1985 dosage schedules mentioned therein or the 1st French edition 1985 contraindications stated by the manufac- 2nd French edition 2000 turers differ from the statements made in 1st Indonesion edition 1989 the present book.
    [Show full text]
  • Neurofibromin and IL-4 As Regulators of T Cell Development, Function, and Homeostasis
    Neurofibromin and IL-4 as Regulators of T Cell Development, Function, and Homeostasis by Jennifer Anne Oliver A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Immunology) in The University of Michigan 2012 Doctoral Committee: Associate Professor Philip D. King, Chair Professor Cheong-Hee Chang Professor Wesley Dunnick Professor Joel A. Swanson Associate Professor Yuan Zhu © Jennifer Anne Oliver 2012 Acknowledgements There are so many people who have helped and supported me while I completed this dissertation. The following is my attempt to acknowledge and thank them all. First, I thank my advisor, Phil King, for teaching me to approach research critically and to communicate my work clearly and concisely, for interesting, and often humorous conversation, for fostering a friendly and cooperative work environment, and for providing me with the opportunity to work on a dream project. In the same vein, I thank my current lab mates, Phil Lapinski, Beth Lubeck, and Melissa Meyer and honorary lab mate Natasha Del Cid, as well as past lab mate Tim Bauler, for assistance with research, help with the navigation of graduate school, and their invaluable friendship. I was proud to work with all of them in the King lab. Next, I would like to thank all of my committee members for their careful attention to my research projects and for their helpful comments and suggestions. I would also like to thank various members of the Chang, Dunnick, Zhu, Chensue, Laouar, O‟Riordan, Zhang, Fox, and Raghavan labs at the University of Michigan for their assistance with experimental design, implementation, and analysis.
    [Show full text]
  • Contribution of Defective Cytotoxicity to Development Of
    CONTRIBUTION OF DEFECTIVE CYTOTOXICITY TO DEVELOPMENT OF CANINE HEMOPHAGOCYTIC HISTIOCYTIC SARCOMA A Thesis Presented to The Faculty of Graduate Studies of The University of Guelph by MICHAL NETA In partial fulfillment of requirements for the degree of Doctor of Philosophy September, 2011 © Michal Neta, 2011 ABSTRACT CONTRIBUTION OF DEFECTIVE CYTOTOXICITY TO DEVELOPMENT OF CANINE HEMOPHAGOCYTIC HISTIOCYTIC SARCOMA Michal Neta Advisor: University of Guelph, 2011 Professor Robert M. Jacobs Canine Hemophagocytic Histiocytic Sarcoma (CHHS) is an aggressive neoplasm of macrophages with local lymphocytic reaction. Similarities exist between CHHS and Familial Hemophagocytic Lymphohistiocytosis (FHL), a complex of histiocytic diseases in children, which is attributable to various defects in granule dependent killing (GDK). This led to the hypothesis that defective GDK compromises lymphocyte homeostasis and anti-tumor immunity which results in CHHS. The sequence of canine perforin, a key effector molecule of GDK, was determined by RT-PCR and RACE. Genomic DNA from healthy and CHHS-affected dogs was sequenced and analyzed, but mutations with functional implications were not identified. Subsequently, tumor infiltrating lymphocytes (TIL) of CHHS were examined for GDK functionality. CHHS-TIL were compared to their functional counterparts in canine cutaneous histiocytoma (CCH), a benign histiocytic tumor in dogs, known to regress via lymphocytic reaction. To facilitate such comparison, functionality of CCH-TIL was studied by immunohistochemistry and confocal microscopy and quantified by image analysis applications. This provided novel insights regarding the physiology of TIL in tumor microenvironment and further characterizing CCH as a model for anti-tumor immunity. The comparison revealed a clear, and highly significant structural difference in polarization and degranulation of CHHS-TIL which likely hampers GDK.
    [Show full text]
  • Biomarkers and Genetics of Canine Visceral Haemangiosarcoma
    Biomarkers and genetics of canine visceral haemangiosarcoma Patharee Oungsakul Doctor of Veterinary Medicine, Master of Veterinary Studies 0000-0003-4523-3484 A thesis submitted for the degree of Doctor of Philosophy at The University of Queensland in Year 2020 School of Veterinary Science Abstract Visceral haemangiosarcoma (HSA) is a vascular endothelial cell cancer that arises in internal organs, especially in the spleen. HSA carries a very poor prognosis but is also difficult to diagnose. Therefore, dogs with HSA symptoms are often euthanized without full investigation. The goal of the thesis was to improve the diagnosis and prevention of this cancer by exploring several HSA biomarkers. The thesis comprises four independent biomarker studies regarding glycoproteins, genetics and Infrared spectral markers. The aim of the first study (chapter 2) was to validate the candidates for canine visceral HSA serum biomarkers, by performing tissue immuno- and lectin-labelling of HSA (n = 32) and HSA-like (n=26) formalin-fixed paraffin-embedded (FFPE) tissues with C7 (component complement 7), MGAM (maltase-glucoamylase), VTN (vitronectin) antibodies and DSA (Datura stramonium), WGA (Wheat germ agglutinin), SNA (Sambucus nigra) and PSA (Pisum sativum)lectins. The results showed lectin/immuno-positive signal on HSA cells, endothelial cell of the veins and arteries. IHC and LHC signal intensities were heterogeneous across the tissue types, diagnosis groups (HSA vs HSA-like) and tissue markers. A semi-quantitative assay was applied to assess and compare the levels of IHC/LHC signal intensities of each marker. Among the candidates tested, complement component 7 (C7) and DSA binding glycoproteins were considered the most promising tissue markers as they demonstrated the ability to distinguish HSA tissue from HSA-like tissues (e.g.
    [Show full text]
  • A Focal Extramedullary Hematopoiesis of the Spleen in a Patient With
    Hosoda et al. surg case rep (2021) 7:33 https://doi.org/10.1186/s40792-021-01119-5 CASE REPORT Open Access A focal extramedullary hematopoiesis of the spleen in a patient with essential thrombocythemia presenting with a complicated postoperative course: a case report Kiyotaka Hosoda* , Akira Shimizu, Koji Kubota, Tsuyoshi Notake, Shinsuke Sugenoya, Koya Yasukawa, Hikaru Hayashi, Ryoichiro Kobayashi and Yuji Soejima Abstract Background: Extramedullary hematopoiesis is a compensatory response occurring secondary to inadequate bone marrow function and is occasionally observed in essential thrombocythemia (ET). This disease usually presents as multifocal masses in the paravertebral or intra-abdominal region; however, formation of a focal mass in the liver or spleen is rare. In addition, ET is characterized by increased platelet count and shows a tendency toward thrombosis and, occasionally, bleeding. Serious bleeding is common in ET patients, caused by the decrease in or abnormalities of von Willebrand factor (vWF) as a consequence of the precipitous rise in platelets. Therefore, strict management of platelet count using medication is crucial in patients with ET who require invasive procedures, especially splenectomy. Case presentation: A 68-year-old man with ET was found to have an enlargement of a focal splenic tumor. Imag- ing fndings revealed that the tumor was likely a hemangioma or hamartoma; however, the possibility of malignant disease could not be completely ruled out because of short-term tumor enlargement, and we conducted a splenec- tomy. The surgery was uneventful, but the patient presented with severe polycythemia and vWF abnormalities post- operatively, which resulted in bleeding from the drain insertion site and wound, epistaxis, and hemorrhoidal bleeding.
    [Show full text]
  • Dcbl2 Haemopoet Tumours and Splenic Dis-2010
    HHaemopoeaemopoetticic neopneopllasmsasms andand spspllenenicic disdisrroorrdedersrs ooff DDogsogs andand CCaatsts Peter Vajdovich Szent István University, Faculty of Veterinary Science, Department of Internal Medicine and Clinics Tumorgenesis Oncogene 1910. Rous–filtrableagent–avianleukosisvirus(retrovirus) „viraloncogen” (v-onc). Inthecells-„cellularoncogens” (c-onc). Theseare„proto-oncogens”-theyarechangablegenomsandcan be transformedtobe oncogenic. Protooncogen Oncogen The tumorgenesis is passive accumulation of genetic impairments. Normal gene dysregulation – proto-oncogenes (signal transduction /cell signaling/, proliferation, differentiation) The proto-oncogenes key genoms, they control the cellular proliferation, differentiation and apoptosis. The major funcfunctions are: Growth factors Growth factor receptors Protein kinases Signal transducers NuNucclear proteins and transcription factors Life of the cells Birth Proliferation Arrest in growing Differentiation Death (apoptosis) M Mitosis and cytokinesis Prophase Metaphase Anaphase Telophase Rb Cell cycle G1 willstart, when phosph. M thechromosomas mitosis and cytokinesis areseparatedto the Meta- mitoticspindle Pro- Ana- Telo- phase phase phasepahes M-delaying factors disappear, DNA-replik. block, G1 Chromos. condens. G0 Intermediate phase G2 Resting Biosynth.: prot, RNS Premitotic phase phase Restriction point 8 h-1 year Rb dephosph . S DNA-synth. Apoptosis (double starnd DNA-production, two identic chromatid) www2.nano.physik.uni-muenchen.de/research/rep03/ Cyklin/CDK INK, KIP
    [Show full text]
  • Lymphatic Leukemia
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Lymphatic leukemia Blair S. Adams University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Adams, Blair S., "Lymphatic leukemia" (1935). MD Theses. 367. https://digitalcommons.unmc.edu/mdtheses/367 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. LYMPHATIC LEUKEMIA BY BLAIR STONE ADAMS SENIOR THESIS UNIVERSITY OF NEBRASKA COLLEGE OF MEDICINE 1935 480666 The various blood dyscrasias have always fascinated me. More than a year ago, at the Douglas County Hospital, an autopsy-v.erified case of acute IJmphatic leukemia which had previously been diagnosed as 1. bronchopneumonia, and 2. en­ cephalitis lethargica, furthered my interest, and subsequent­ ly prompted me to make thiS rather comprehensive but far from exhaustive review of the literature on lymphatic leukemia. DEFINITION Leukemia is a systemic disease characterized by a hyper­ plasia of the leucocyt-producing tissues, and accompanied by a secondary disturbance of the composition of the blood, which manifests itself in alterations in the relative pro­ portions of the leucocytes; the appearance of forms not normally found in the peripheral circulation. and usually by an increase in the total number of white cells.
    [Show full text]
  • Splenic Angiosarcoma: a Clinicopathologic and Immunophenotypic Study of 28 Cases Thomas S
    Splenic Angiosarcoma: A Clinicopathologic and Immunophenotypic Study of 28 Cases Thomas S. Neuhauser, M.D., Gregory A. Derringer, M.D., Lester D. R. Thompson, M.D., Julie C. Fanburg-Smith, M.D., Markku Miettinen, M.D., Anne Saaristo, M.B., Susan L. Abbondanzo, M.D. Departments of Hematopathology (TSN, GAD, SLA), Endocrine and Otorhinolaryngic-Head & Neck Pathology (LDRT), Soft Tissue Pathology (JCF-S, MM), Armed Forces Institute of Pathology, Washington, DC; Molecular/Cancer Biology Laboratory, Haartman Institute, University of Helsinki, Finland (AS); Wilford Hall Medical Center, Lackland AFB, Texas (TSN) entiation (CD34, FVIIIRAg, VEGFR3, and CD31) Primary angiosarcoma of the spleen is a rare neo- and at least one marker of histiocytic differen- plasm that has not been well characterized. We de- tiation (CD68 and/or lysozyme). Metastases de- scribe the clinical, morphologic, and immunophe- veloped in 100% of patients during the course of notypic findings of 28 cases of primary splenic their disease. Twenty-six patients died of dis- angiosarcoma, including one case that shares fea- ease despite aggressive therapy, whereas only tures of lymphangioma/lymphangiosarcoma. The two patients are alive at last follow-up, one with patients included 16 men and 12 women, aged 29 to disease at 8 years and the other without disease 85 years, with a mean of 59 years and median of 63 at 10 years. In conclusion, primary splenic an- years. The majority of patients (75%) complained of giosarcoma is an extremely aggressive neo- abdominal pain, and 25% presented with splenic plasm that is almost universally fatal. The ma- rupture. The most common physical finding was jority of splenic angiosarcomas coexpress splenomegaly (71%).
    [Show full text]
  • NF-Κb Dysregulation in Microrna-146A–Deficient Mice
    NF-κB dysregulation in microRNA-146a–deficient mice drives the development of myeloid malignancies Jimmy L. Zhaoa,1, Dinesh S. Raoa,b,1, Mark P. Boldinc, Konstantin D. Taganovd, Ryan M. O’Connella, and David Baltimorea,2 aDivision of Biology, California Institute of Technology, Pasadena, CA 91125; bDepartment of Pathology and Laboratory Medicine, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095; cDepartment of Molecular and Cellular Biology, Beckman Research Institute, City of Hope, Duarte, CA 91010; and dRegulus Therapeutics Inc., San Diego, CA 92121 Contributed by David Baltimore, April 25, 2011 (sent for review February 28, 2011) − − MicroRNA miR-146a has been implicated as a negative feedback tumor phenotype in miR-146a / mice and NF-κB dysregulation regulator of NF-κB activation. Knockout of the miR-146a gene in was uncertain because of the multiple potential targets of miR- C57BL/6 mice leads to histologically and immunophenotypically 146a in different molecular pathways. Here, we focus on char- defined myeloid sarcomas and some lymphomas. The sarcomas acterizing the incidence, cellular lineage, and transplantability of are transplantable to immunologically compromised hosts, show- the tumors, and to understand the molecular basis of oncogenesis. We have found that when they are allowed to age naturally, ing that they are true malignancies. The animals also exhibit −/− chronic myeloproliferation in their bone marrow. Spleen and mar- miR-146a mice on a pure C57BL/6 background develop a fl row cells show increased transcription of NF-κB–regulated genes chronic in ammatory phenotype with progressive myeloprolif- and tumors have higher nuclear p65.
    [Show full text]