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Updates in Mastocytosis
Updates in Mastocytosis Tryptase PD-L1 Tracy I. George, M.D. Professor of Pathology 1 Disclosure: Tracy George, M.D. Research Support / Grants None Stock/Equity (any amount) None Consulting Blueprint Medicines Novartis Employment ARUP Laboratories Speakers Bureau / Honoraria None Other None Outline • Classification • Advanced mastocytosis • A case report • Clinical trials • Other potential therapies Outline • Classification • Advanced mastocytosis • A case report • Clinical trials • Other potential therapies Mastocytosis symposium and consensus meeting on classification and diagnostic criteria for mastocytosis Boston, October 25-28, 2012 2008 WHO Classification Scheme for Myeloid Neoplasms Acute Myeloid Leukemia Chronic Myelomonocytic Leukemia Atypical Chronic Myeloid Leukemia Juvenile Myelomonocytic Leukemia Myelodysplastic Syndromes MDS/MPN, unclassifiable Chronic Myelogenous Leukemia MDS/MPN Polycythemia Vera Essential Thrombocythemia Primary Myelofibrosis Myeloproliferative Neoplasms Chronic Neutrophilic Leukemia Chronic Eosinophilic Leukemia, NOS Hypereosinophilic Syndrome Mast Cell Disease MPNs, unclassifiable Myeloid or lymphoid neoplasms Myeloid neoplasms associated with PDGFRA rearrangement associated with eosinophilia and Myeloid neoplasms associated with PDGFRB abnormalities of PDGFRA, rearrangement PDGFRB, or FGFR1 Myeloid neoplasms associated with FGFR1 rearrangement (EMS) 2017 WHO Classification Scheme for Myeloid Neoplasms Chronic Myelomonocytic Leukemia Acute Myeloid Leukemia Atypical Chronic Myeloid Leukemia Juvenile Myelomonocytic -
Follicular Lymphoma
Follicular Lymphoma What is follicular lymphoma? Let us explain it to you. www.anticancerfund.org www.esmo.org ESMO/ACF Patient Guide Series based on the ESMO Clinical Practice Guidelines FOLLICULAR LYMPHOMA: A GUIDE FOR PATIENTS PATIENT INFORMATION BASED ON ESMO CLINICAL PRACTICE GUIDELINES This guide for patients has been prepared by the Anticancer Fund as a service to patients, to help patients and their relatives better understand the nature of follicular lymphoma and appreciate the best treatment choices available according to the subtype of follicular lymphoma. We recommend that patients ask their doctors about what tests or types of treatments are needed for their type and stage of disease. The medical information described in this document is based on the clinical practice guidelines of the European Society for Medical Oncology (ESMO) for the management of newly diagnosed and relapsed follicular lymphoma. This guide for patients has been produced in collaboration with ESMO and is disseminated with the permission of ESMO. It has been written by a medical doctor and reviewed by two oncologists from ESMO including the lead author of the clinical practice guidelines for professionals, as well as two oncology nurses from the European Oncology Nursing Society (EONS). It has also been reviewed by patient representatives from ESMO’s Cancer Patient Working Group. More information about the Anticancer Fund: www.anticancerfund.org More information about the European Society for Medical Oncology: www.esmo.org For words marked with an asterisk, a definition is provided at the end of the document. Follicular Lymphoma: a guide for patients - Information based on ESMO Clinical Practice Guidelines – v.2014.1 Page 1 This document is provided by the Anticancer Fund with the permission of ESMO. -
Circle) None Fever Night Sweats Wt Loss Laboratory Studies Hgb WBC Plate
LYMPHOMA STAGING DIAGRAM Instructions: boxed items must be completed History B Sx (Circle) none fever night sweats wt loss Laboratory studies Hgb WBC Plate ECOG performance status g/L x109/L x109/L LDH (patient/upper normal) / CERVICAL PRE-AURICULAR HIV antibody pos neg WALDEYER'S RING UPPER CERVICAL MEDIAN OR LOWER CERVICAL HBsAg pos neg POSTERIOR CERVICAL SUPRACLAVICULAR INFRACLAVICULAR MEDIASTINAL HBcoreAb pos neg PARATRACHEAL MEDIASTINAL AXILLARY Hep C Ab pos neg AXILLARY HILAR RETROCRURAL SPE monoclonal protein pos neg type____________ SPLEEN PARA AORTIC PARA AORTIC MESENTERIC For Hodgkin lymphoma only CELIAC COMMON ILIAC SPLENIC (HEPATIC) HILAR EXTERNAL ILIAC PORTAL Albumin g/L INGUINAL MESENTERIC Lymphs x 109/L INGUINAL FEMORAL OTHER EPITROCHLEAR POPLITEAL Treatment Largest tumor diameter (nearest whole cm) Treatment plan Initial biopsy site Date (d/m/y) / / Histologic diagnosis Doctor in Charge 1 _________________________________________ 2 Reason for referral Bone marrow pos neg not done New Recurrent Follow-up Completed by _______________ Date____________ List all other extranodal sites here 1 2 Complete if diagnosis or stage subsequently changed 3 4 Diagnosis/Stage amended to _________________________ 5 Reason__________________________________________ 6 By_______________________ Date______________ Stage (circle) 0 1 2 3 4 A B E This staging diagram can be found on NOTIFY PATIENT INFORMATION IF STAGE OR H:lym_docs\staging\lymphoma.doc DIAGNOSIS IS AMENDED Form #TH-41 Revised 26 March 2007 LYMPHOMA AND CHRONIC LYMPHOCYTIC LEUKEMIA STAGING SYSTEMS BCCA LYMPHOMA, HODGKIN AND CHRONIC LYMPHOCYTIC LEUKEMIA NON-HODGKIN 1982 STAGE FINDINGS STAGE INVOLVEMENT 0 Lymphocyte count > 5.0 x 109 /L 1 Single lymph node region (1) or one Bone marrow contains 40% extralymphatic site (1E). -
Late Effects Among Long-Term Survivors of Childhood Acute Leukemia in the Netherlands: a Dutch Childhood Leukemia Study Group Report
0031-3998/95/3805-0802$03.00/0 PEDIATRIC RESEARCH Vol. 38, No.5, 1995 Copyright © 1995 International Pediatric Research Foundation, Inc. Printed in U.S.A. Late Effects among Long-Term Survivors of Childhood Acute Leukemia in The Netherlands: A Dutch Childhood Leukemia Study Group Report A. VAN DER DOES-VAN DEN BERG, G. A. M. DE VAAN, J. F. VAN WEERDEN, K. HAHLEN, M. VAN WEEL-SIPMAN, AND A. J. P. VEERMAN Dutch Childhood Leukemia Study Group,' The Hague, The Netherlands A.8STRAC ' Late events and side effects are reported in 392 children cured urogenital, or gastrointestinal tract diseases or an increased vul of leukemia. They originated from 1193 consecutively newly nerability of the musculoskeletal system was found. However, diagnosed children between 1972 and 1982, in first continuous prolonged follow-up is necessary to study the full-scale late complete remission for at least 6 y after diagnosis, and were effects of cytostatic treatment and radiotherapy administered treated according to Dutch Childhood Leukemia Study Group during childhood. (Pediatr Res 38: 802-807, 1995) protocols (70%) or institutional protocols (30%), all including cranial irradiation for CNS prophylaxis. Data on late events (relapses, death in complete remission, and second malignancies) Abbreviations were collected prospectively after treatment; late side effects ALL, acute lymphocytic leukemia were retrospectively collected by a questionnaire, completed by ANLL, acute nonlymphocytic leukemia the responsible pediatrician. The event-free survival of the 6-y CCR, continuous first complete remission survivors at 15 y after diagnosis was 92% (±2%). Eight late DCLSG, Dutch Childhood Leukemia Study Group relapses and nine second malignancies were diagnosed, two EFS, event free survival children died in first complete remission of late toxicity of HR, high risk treatment, and one child died in a car accident. -
Hematopoietic and Lymphoid Neoplasm Coding Manual
Hematopoietic and Lymphoid Neoplasm Coding Manual Effective with Cases Diagnosed 1/1/2010 and Forward Published August 2021 Editors: Jennifer Ruhl, MSHCA, RHIT, CCS, CTR, NCI SEER Margaret (Peggy) Adamo, BS, AAS, RHIT, CTR, NCI SEER Lois Dickie, CTR, NCI SEER Serban Negoita, MD, PhD, CTR, NCI SEER Suggested citation: Ruhl J, Adamo M, Dickie L., Negoita, S. (August 2021). Hematopoietic and Lymphoid Neoplasm Coding Manual. National Cancer Institute, Bethesda, MD, 2021. Hematopoietic and Lymphoid Neoplasm Coding Manual 1 In Appreciation NCI SEER gratefully acknowledges the dedicated work of Drs, Charles Platz and Graca Dores since the inception of the Hematopoietic project. They continue to provide support. We deeply appreciate their willingness to serve as advisors for the rules within this manual. The quality of this Hematopoietic project is directly related to their commitment. NCI SEER would also like to acknowledge the following individuals who provided input on the manual and/or the database. Their contributions are greatly appreciated. • Carolyn Callaghan, CTR (SEER Seattle Registry) • Tiffany Janes, CTR (SEER Seattle Registry) We would also like to give a special thanks to the following individuals at Information Management Services, Inc. (IMS) who provide us with document support and web development. • Suzanne Adams, BS, CTR • Ginger Carter, BA • Sean Brennan, BS • Paul Stephenson, BS • Jacob Tomlinson, BS Hematopoietic and Lymphoid Neoplasm Coding Manual 2 Dedication The Hematopoietic and Lymphoid Neoplasm Coding Manual (Heme manual) and the companion Hematopoietic and Lymphoid Neoplasm Database (Heme DB) are dedicated to the hard-working cancer registrars across the world who meticulously identify, abstract, and code cancer data. -
Waldenstro¨M's Macroglobulinemia Is a Biological Syndrome Which May
Correspondence 1637 cation,10 particularly in acute promyelocytic leukemia (APL), we References searched for genomic similarities. The few specific studies in existence on sequence analysis of the PML-RAR␣ gene show that the breakpoint within the involved gene (usually the PML locus) is variably situated, 1 Saglio G, Guerrasio A, Tassinari A, Ponzetto C, Zaccaria A, Testoni and that the corresponding fusion transcript should be aberrant. The P, Celso B, Rege Cambrin G, Serra A, Pegoraro L. Variability of the ␣ resulting PML-RAR proteins contained residues not homologous with molecular defects corresponding to the presence of a Philadelphia ␣ either PML or RAR . These reported atypical breaks were very similar chromosome in human hematologic malignancies. Blood 1988; to the one recorded in our case. A second original characteristic of 72: 1203–1208. the BCR break reported by us is that an intronic sequence derived 2 Chissoe SL, Bodenteich A, Wang YF, Wang YP, Burian D, Clifton from abl intron Ib was juxtaposed to bcr exon. This is another unpre- SW, Crabtree J, Freeman A, Iyer K, Jian L. Sequence and analysis cedented feature for a CML patient, although on rare occasions it has 10 of the human ABL gene, the BCR gene, and regions involved in been reported in AML patients. So, it may be speculated that in a the Philadelphia chromosomal translocation. Genomics 1995; 27: small proportion of the DNA breaks that occurs in leukemia, a cur- 67–82. rently unknown molecular mechanism could break the coding DNA. 3 Saglio G, Guerrasio A, Rosso C, Zaccaria A, Tassinari A, Serra A, The resulting RNA remains in-frame coding an aberrant or, as in our Rege-Cambrin G, Mazza U, Gavosto F. -
Lymphoproliferative Disorders
Lymphoproliferative disorders Dr. Mansour Aljabry Definition Lymphoproliferative disorders Several clinical conditions in which lymphocytes are produced in excessive quantities ( Lymphocytosis) Lymphoma Malignant lymphoid mass involving the lymphoid tissues (± other tissues e.g : skin ,GIT ,CNS …) Lymphoid leukemia Malignant proliferation of lymphoid cells in Bone marrow and peripheral blood (± other tissues e.g : lymph nods ,spleen , skin ,GIT ,CNS …) Lymphoproliferative disorders Autoimmune Infection Malignant Lymphocytosis 1- Viral infection : •Infectious mononucleosis ,cytomegalovirus ,rubella, hepatitis, adenoviruses, varicella…. 2- Some bacterial infection: (Pertussis ,brucellosis …) 3-Immune : SLE , Allergic drug reactions 4- Other conditions:, splenectomy, dermatitis ,hyperthyroidism metastatic carcinoma….) 5- Chronic lymphocytic leukemia (CLL) 6-Other lymphomas: Mantle cell lymphoma ,Hodgkin lymphoma… Infectious mononucleosis An acute, infectious disease, caused by Epstein-Barr virus and characterized by • fever • swollen lymph nodes (painful) • Sore throat, • atypical lymphocyte • Affect young people ( usually) Malignant Lymphoproliferative Disorders ALL CLL Lymphomas MM naïve B-lymphocytes Plasma Lymphoid cells progenitor T-lymphocytes AML Myeloproliferative disorders Hematopoietic Myeloid Neutrophils stem cell progenitor Eosinophils Basophils Monocytes Platelets Red cells Malignant Lymphoproliferative disorders Immature Mature ALL Lymphoma Lymphoid leukemia CLL Hairy cell leukemia Non Hodgkin lymphoma Hodgkin lymphoma T- prolymphocytic -
The Lymphoma Guide Information for Patients and Caregivers
The Lymphoma Guide Information for Patients and Caregivers Ashton, lymphoma survivor This publication was supported by Revised 2016 Publication Update The Lymphoma Guide: Information for Patients and Caregivers The Leukemia & Lymphoma Society wants you to have the most up-to-date information about blood cancer treatment. See below for important new information that was not available at the time this publication was printed. In November 2017, the Food and Drug Administration (FDA) approved obinutuzumab (Gazyva®) in combination with chemotherapy, followed by Gazyva alone in those who responded, for people with previously untreated advanced follicular lymphoma (stage II bulky, III or IV). In November 2017, the Food and Drug Administration (FDA) approved brentuximab vedotin (Adcetris®) for treatment of adult patients with primary cutaneous anaplastic large cell lymphoma (pcALCL) or CD30- expressing mycosis fungoides (MF) who have received prior systemic therapy. In October 2017, the Food and Drug Administration (FDA) approved acalabrutinib (CalquenceTM) for the treatment of adults with mantle cell lymphoma who have received at least one prior therapy. In October 2017, the Food and Drug Administration (FDA) approved axicabtagene ciloleucel (Yescarta™) for the treatment of adult patients with relapsed or refractory large B-cell lymphoma after two or more lines of systemic therapy, including diffuse large B-cell lymphoma (DLBCL) not otherwise specified, primary mediastinal large B-cell lymphoma, high-grade B-cell lymphoma, and DLBCL arising from follicular lymphoma. Yescarta is a CD19-directed genetically modified autologous T cell immunotherapy FDA approved. Yescarta is not indicated for the treatment of patients with primary central nervous system lymphoma. In September 2017, the Food and Drug Administration (FDA) approved copanlisib (AliqopaTM) for the treatment of adult patients with relapsed follicular lymphoma (FL) who have received at least two prior systemic therapies. -
Anaplastic Large Cell Lymphoma (ALCL)
Helpline (freephone) 0808 808 5555 [email protected] www.lymphoma-action.org.uk Anaplastic large cell lymphoma (ALCL) This page is about anaplastic large-cell lymphoma (ALCL), a type of T-cell lymphoma. On this page What is ALCL? Who gets it? Symptoms Treatment Relapsed and refractory ALCL Research and targeted treatments We have separate information about the topics in bold font. Please get in touch if you’d like to request copies or if you would like further information about any aspect of lymphoma. Phone 0808 808 5555 or email [email protected]. What is ALCL? Anaplastic large cell lymphoma (ALCL) is a type of T-cell lymphoma – a non-Hodgkin lymphoma that develops from white blood cells called T cells. Under a microscope, the cancerous cells in ALCL look large, undeveloped and very abnormal (‘anaplastic’). There are four main types of ALCL. They have complicated names based on their features and the types of proteins they make: • ALK-positive ALCL (also known as ALK+ ALCL) is the most common type. In ALK-positive ALCL, the abnormal T cells have a genetic change (mutation) that means they make a protein called ‘anaplastic lymphoma kinase’ (ALK). In other words, they test positive for ALK. ALK-positive ALCL is a fast-growing (high-grade) lymphoma. Page 1 of 6 © Lymphoma Action • ALK-negative ALCL (also known as ALK- ALCL) is a high-grade lymphoma that accounts for around 3 in every 10 cases of ALCL. The abnormal T cells do not make the ALK protein – they test negative for ALK. -
| Lymphoproliferative Disorders
| Lymphoproliferative Hematology 438 teamwork disorders Color index: Red: Important Gray: notes Blue: extra Editing file Not malignant | definitions Lymphoproliferative disorders characters: -mature lymphocytes (no blasts), -lymphocytosis, Lymphoma -chronic. Lymphoid leukemia Several clinical conditions in Malignant proliferation of Malignant lymphoid mass which lymphocytes are lymphoid cells in Bone involving the lymphoid tissues produced in excessive marrow and peripheral blood (± other tissues ie; Extranodal quantities (Lymphocytosis) when the malignancy of lymphocytes reaches the lymphoma, by definition, involves sites other N.B: Lymphoproliferative disorders occur when the normal bone marrow or the peripheral blood we call it than lymph nodes, spleen, thymus and the mechanisms of control of proliferation of lymphocytes break lymphoid leukemia. pharyngeal lymphatic ring. e.g : skin down, resulting in autonomous, uncontrolled proliferation of lymphoid cells and typically leading to lymphocytosis and/or (± other tissues e.g : lymph ,GIT ,CNS) lymphadenopathy, and sometimes to involvement of extranodal sites, e.g. bone marrow. nodes ,spleen , skin ,GIT ,CNS) Autoimmune Infection Malignant Mostly virus Causes of lymphoproliferative disorder: These include (1) malignant—clonal in nature, resulting from the uncontrolled proliferation of a single transformed cell, e.g. lymphoma; (2) nonmalignant—polyclonal lymphoproliferative disorders may result from conditions including (a) infections—lymphocytosis is commonly caused by viral infections, e.g. Epsitein–Barr virus (EBV); lymphadenopathy is a common feature of a very wide variety of infections, (b) reactive—conditions such as systemic lupus erythematosus (SLE) and sarcoidosis frequently cause lymphadenopathy. | Lymphocytosis Blood film is very important, also Age is very important to expect the cause of lymphocytosis. Small lymphocytes: in non-infectious causes ●bacterial infection Some bacteria as ●Chronic lymphocytic ●Viral infection Pertussis ,brucellosis. -
CD20-Negative Diffuse Large B-Cell Lymphomas: Biology and Emerging Therapeutic Options
Expert Review of Hematology ISSN: 1747-4086 (Print) 1747-4094 (Online) Journal homepage: http://www.tandfonline.com/loi/ierr20 CD20-negative diffuse large B-cell lymphomas: biology and emerging therapeutic options Jorge J Castillo, Julio C Chavez, Francisco J Hernandez-Ilizaliturri & Santiago Montes-Moreno To cite this article: Jorge J Castillo, Julio C Chavez, Francisco J Hernandez-Ilizaliturri & Santiago Montes-Moreno (2015) CD20-negative diffuse large B-cell lymphomas: biology and emerging therapeutic options, Expert Review of Hematology, 8:3, 343-354, DOI: 10.1586/17474086.2015.1007862 To link to this article: http://dx.doi.org/10.1586/17474086.2015.1007862 Published online: 01 Feb 2015. Submit your article to this journal Article views: 165 View related articles View Crossmark data Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ierr20 Download by: [North Shore Med Ctr], [Jorge Castillo] Date: 16 March 2016, At: 07:44 Review CD20-negative diffuse large B-cell lymphomas: biology and emerging therapeutic options Expert Rev. Hematol. 8(3), 343–354 (2015) Jorge J Castillo*1, CD20-negative diffuse large B-cell lymphoma (DLBCL) is a rare and heterogeneous group of Julio C Chavez2, lymphoproliferative disorders. Known variants of CD20-negative DLBCL include plasmablastic Francisco J lymphoma, primary effusion lymphoma, large B-cell lymphoma arising in human herpesvirus 8-associated multicentric Castleman disease and anaplastic lymphoma kinase-positive DLBCL. Hernandez-Ilizaliturri3 Given the lack of CD20 expression, atypical cellular morphology and aggressive clinical and Santiago 4 behavior characterized by chemotherapy resistance and inferior survival rates, CD20-negative Montes-Moreno DLBCL represents a challenge from the diagnostic and therapeutic perspectives. -
Death from Mast Cell Leukemia: a Young Patient with Longstanding Cutaneous Mastocytosis Evolving Into Fatal Mast Cell Leukemia
CASE REPORTS Pediatric Dermatology Vol. 29 No. 5 605–609, 2012 Death from Mast Cell Leukemia: A Young Patient with Longstanding Cutaneous Mastocytosis Evolving into Fatal Mast Cell Leukemia Rattanavalai Chantorn, M.D.,*, and Tor Shwayder, M.D. *Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand, Department of Pediatric Dermatology, Henry Ford Hospital, Detroit, Michigan Abstract: Mastocytosis is a broad term used for a group of disorders characterized by accumulation of mast cells in the skin with or without extracutaneous involvement. The clinical spectrum of the disease varies from only cutaneous lesions to highly aggressive systemic involvement such as mast cell leukemia. Mastocytosis can present from birth to adult- hood. In children, mastocytosis is usually benign, and there is a good chance of spontaneous regression at puberty, unlike adult-onset disease, which is generally systemic and more severe. Moreover, individuals with systemic mastocytosis may be at risk of developing hematologic malignancies. We describe a girl who presented to us with a solitary mastocytoma at age 5 and later developed maculopapular cutaneous mastocytosis. At age 23, after an episode of anaphylactic shock, a bone marrow examination revealed mast cell leukemia. She ultimately died despite aggressive chemotherapy and bone marrow transplantation. Mastocytosis is characterized by the abnormal common forms of CM in childhood. The excoriation growth and infiltration of mast cells (MC) in various of lesions causes hives and perilesional erythema, tissues and is classified into two broad categories: which characterizes Darier’s sign (Fig. 3). SM is cutaneous mastocytosis (CM) and systemic mastocy- characterized by multifocal MC infiltrates with or tosis (SM) (1).