Lymphoproliferative Disorders
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IRF4/DUSP22 Gene Rearrangement by FISH
IRF4/DUSP22 Gene Rearrangement by FISH The IRF4/DUSP22 locus is rearranged in a newly recognized subtype of non-Hodgkin lymphoma, large B-cell lymphoma with IRF4 rearrangement. These lymphomas are uncommon, but are clinically distinct from morphologically similar lymphomas, Tests to Consider including diffuse large B-cell lymphoma, high-grade follicular lymphoma, and pediatric- type follicular lymphoma. The IRF4/DUSP22 locus is also rearranged in a subset of ALK- IRF4/DUSP22 (6p25) Gene Rearrangement negative anaplastic large cell lymphomas (ALCL), where this rearrangement is associated by FISH 3001568 with a signicantly better prognosis. Method: Fluorescence in situ Hybridization (FISH) Test is useful in identifying ALK-negative anaplastic large cell lymphomas and large B- Disease Overview cell lymphoma with IRF4 rearrangement The rearrangement is associated with an improved prognosis Incidence See Related Tests Large B-cell lymphoma with IRF4 rearrangement accounts for <1% of all non-Hodgkin B-cell lymphomas overall More common in younger patients, with an incidence of 5-6% under age 18 IRF4/DUSP22 rearrangement is found in 30% of ALK-negative ALCLs Symptoms/Findings Large B-cell lymphoma with IRF4 rearrangement typically presents with limited stage disease in the head and neck, while the presentation of ALK-negative ALCLs is variable. Disease-Oriented Information Patients with large B-cell lymphoma with IRF4 rearrangement typically have a favorable outcome after treatment. Rearrangement of the IRF4/DUSP22 locus in ALK-negative ALCL is associated with a better prognosis than ALK-negative ALCL without this rearrangement. Test Interpretation Analytical Sensitivity The limit of detection (LOD) for the IRF4/DUSP22 probe was established by calculating the upper limit of the abnormal signal pattern in normal cells using the Microsoft Excel BETAINV function. -
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. -
The Lymphoma and Multiple Myeloma Center
The Lymphoma and Multiple Myeloma Center What Sets Us Apart We provide multidisciplinary • Experienced, nationally and internationally recognized physicians dedicated exclusively to treating patients with lymphoid treatment for optimal survival or plasma cell malignancies and quality of life for patients • Cellular therapies such as Chimeric Antigen T-Cell (CAR T) therapy for relapsed/refractory disease with all types and stages of • Specialized diagnostic laboratories—flow cytometry, cytogenetics, and molecular diagnostic facilities—focusing on the latest testing lymphoma, chronic lymphocytic that identifies patients with high-risk lymphoid malignancies or plasma cell dyscrasias, which require more aggresive treatment leukemia, multiple myeloma and • Novel targeted therapies or intensified regimens based on the other plasma cell disorders. cancer’s genetic and molecular profile • Transplant & Cellular Therapy program ranked among the top 10% nationally in patient outcomes for allogeneic transplant • Clinical trials that offer tomorrow’s treatments today www.roswellpark.org/partners-in-practice Partners In Practice medical information for physicians by physicians We want to give every patient their very best chance for cure, and that means choosing Roswell Park Pathology—Taking the best and Diagnosis to a New Level “ optimal front-line Lymphoma and myeloma are a diverse and heterogeneous group of treatment.” malignancies. Lymphoid malignancy classification currently includes nearly 60 different variants, each with distinct pathophysiology, clinical behavior, response to treatment and prognosis. Our diagnostic approach in hematopathology includes the comprehensive examination of lymph node, bone marrow, blood and other extranodal and extramedullary tissue samples, and integrates clinical and diagnostic information, using a complex array of diagnostics from the following support laboratories: • Bone marrow laboratory — Francisco J. -
Quantitative Analysis of Bcl-2 Expression in Normal and Leukemic Human B-Cell Differentiation
Leukemia (2004) 18, 491–498 & 2004 Nature Publishing Group All rights reserved 0887-6924/04 $25.00 www.nature.com/leu Quantitative analysis of bcl-2 expression in normal and leukemic human B-cell differentiation P Menendez1,2, A Vargas3, C Bueno1,2, S Barrena1,2, J Almeida1,2 M de Santiago1,2,ALo´pez1,2, S Roa2, JF San Miguel2,4 and A Orfao1,2 1Servicio General de Citometrı´a, Universidad de Salamanca, Salamanca, Spain; 2Departamento de Medicina and Centro de Investigacio´n del Ca´ncer, Universidad de Salamanca, Salamanca, Spain; 3Servicio de Inmunodiagno´stico, Departamento de Patologı´a Clı´nica, Hospital Nacional Edgardo Rebagliati Martins, Lima, Peru´, ; and 4Servicio de Hematologı´a, Hospital Universitario, Salamanca, Spain Lack of apoptosis has been linked to prolonged survival of results in the overexpression of the bcl-2 protein and it malignant B cells expressing bcl-2. The aim of the present represented the first clear example of a common step in study was to analyze the amount of bcl-2 protein expressed 9,10 along normal human B-cell maturation and to establish the oncogenesis mediated by decreased cell death. Currently, frequency of aberrant bcl-2 expression in B-cell malignancies. the exact antiapoptotic pathways through which bcl-2 exerts its In normal bone marrow (n ¼ 11), bcl-2 expression obtained by role are only partially understood, involving decreased mito- quantitative multiparametric flow cytometry was highly vari- chondrial release of cytochrome c, which in turn is required for þ À able: very low in both CD34 and CD34 B-cell precursors, high the activation of procaspase-9 and the subsequent initiation of in mature B-lymphocytes and very high in plasma cells. -
Therapeutic Effect and Mechanism of Ibrutinib Combined with Dexametha- Sone on Multiple Myeloma
ORIGINAL ARTICLES Hematology Department of The Second Hospital1, Cheeloo College of Medicine, Shandong University; Department of Hematology of Jining No. 1 People’s Hospital2; Institute of Biotherapy for Hematological Malignancies of Shandong University3; Shandong University-Karolinska Institute Collaborative Laboratory for Stem Cell Research4; Hematology Department of Linyi Central Hospital5; Hematology Department of Binzhou Medical University Hospital6; Institute of Medical Sciences, The Second Hospital, Cheeloo College of Medicine, Shandong University7, Jinan, Shandong, China Therapeutic effect and mechanism of ibrutinib combined with dexametha- sone on multiple myeloma SHENGLI LI1,2, LIKUN SUN1,3,4, QIAN ZHOU1,5, SHUO LI1,6, XIAOLI LIU1,3,4, JUAN XIAO1,3,4, YAQI XU1,3,4, FANG WANG7, YANG JIANG1,3,4,*, CHENGYUN ZHENG1,3,4 Received November 14, 2020, accepted December 2020 *Correspondence author: Yang Jiang, Hematology Department, the Second Hospital of Shandong University, 247th of Beiyuan Rd., Jinan, Shandong, China [email protected] Pharmazie 76: 92-96 (2021) doi: 10.1691/ph.2021.0917 Ibrutinib is an irreversible inhibitor of Bruton’s tyrosine kinase and has proven to be an effective agent for B-cell-mediated hematological malignancies, including multiple myeloma (MM). Several clinical trials of ibrutinib treatment combined with dexamethasone (DXMS) for relapsed MM have demonstrated high response rates, however, the mechanism still remains unclear. In this study, we explored the therapeutic effect and mechanism of ibrutinib combined with DXMS on MM in vitro and vivo. The apoptosis of MM cell lines and mononuclear cells from MM patients’ bone marrow induced by ibrutinib combined with DXMS was detected by flow cytometry and the expression of apoptosis-related proteins were detected by Western blot. -
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. -
What Is Multiple Myeloma?
cancer.org | 1.800.227.2345 About Multiple Myeloma Overview If you have been diagnosed with multiple myeloma or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Is Multiple Myeloma? Research and Statistics See the latest estimates for new cases of multiple myeloma and deaths in the US and what research is currently being done. ● Key Statistics About Multiple Myeloma ● What’s New in Multiple Myeloma Research? What Is Multiple Myeloma? Cancer starts when cells begin to grow out of control. Cells in nearly any part of the body can become cancer, and can spread to other areas. To learn more about how cancers start and spread, see What Is Cancer?1 Multiple myeloma is a cancer of plasma cells. Normal plasma cells are found in the bone marrow and are an important part of the immune system. The immune system is made up of several types of cells that work together to fight infections and other 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 diseases. Lymphocytes (lymph cells) are one of the main types of white blood cells in the immune system and include T cells and B cells. Lymphocytes are in many areas of the body, such as lymph nodes, the bone marrow, the intestines, and the bloodstream. When B cells respond to an infection, they mature and change into plasma cells. Plasma cells make the antibodies (also called immunoglobulins) that help the body attack and kill germs. Plasma cells, are found mainly in the bone marrow. -
SNF Mobility Model: ICD-10 HCC Crosswalk, V. 3.0.1
The mapping below corresponds to NQF #2634 and NQF #2636. HCC # ICD-10 Code ICD-10 Code Category This is a filter ceThis is a filter cellThis is a filter cell 3 A0101 Typhoid meningitis 3 A0221 Salmonella meningitis 3 A066 Amebic brain abscess 3 A170 Tuberculous meningitis 3 A171 Meningeal tuberculoma 3 A1781 Tuberculoma of brain and spinal cord 3 A1782 Tuberculous meningoencephalitis 3 A1783 Tuberculous neuritis 3 A1789 Other tuberculosis of nervous system 3 A179 Tuberculosis of nervous system, unspecified 3 A203 Plague meningitis 3 A2781 Aseptic meningitis in leptospirosis 3 A3211 Listerial meningitis 3 A3212 Listerial meningoencephalitis 3 A34 Obstetrical tetanus 3 A35 Other tetanus 3 A390 Meningococcal meningitis 3 A3981 Meningococcal encephalitis 3 A4281 Actinomycotic meningitis 3 A4282 Actinomycotic encephalitis 3 A5040 Late congenital neurosyphilis, unspecified 3 A5041 Late congenital syphilitic meningitis 3 A5042 Late congenital syphilitic encephalitis 3 A5043 Late congenital syphilitic polyneuropathy 3 A5044 Late congenital syphilitic optic nerve atrophy 3 A5045 Juvenile general paresis 3 A5049 Other late congenital neurosyphilis 3 A5141 Secondary syphilitic meningitis 3 A5210 Symptomatic neurosyphilis, unspecified 3 A5211 Tabes dorsalis 3 A5212 Other cerebrospinal syphilis 3 A5213 Late syphilitic meningitis 3 A5214 Late syphilitic encephalitis 3 A5215 Late syphilitic neuropathy 3 A5216 Charcot's arthropathy (tabetic) 3 A5217 General paresis 3 A5219 Other symptomatic neurosyphilis 3 A522 Asymptomatic neurosyphilis 3 A523 Neurosyphilis, -
Allogeneic Stem Cell Transplantation for Multiple Myeloma and Myelofibrosis Version Date: 29JAN2019 Principal Investigator: Catherine J
Protocol name: Allogeneic Stem Cell Transplantation for Multiple Myeloma and Myelofibrosis Version Date: 29JAN2019 Principal Investigator: Catherine J. Lee, MD Allogeneic Stem Cell Transplantation for Multiple Myeloma and Myelofibrosis Lead Org. ID: HCI98381/IRB# 98381 CTO#HCI-17-HEME-07 ClinicalTrials.gov ID – NCT03303950 Principal Investigator Catherine J. Lee, MD Blood & Marrow Transplant Program University of Utah 2000 Circle of Hope, Rm 2152 Salt Lake City, UT 84132 Phone: (801) 587-0231 Email: [email protected] Sub-investigator(s) Douglas Sborov, MD Clinical Instructor, Department of Medicine Phone: (801) 581-8394 Email: [email protected] Vedran Radojcic, MD Assistant Professor, Department of Medicine Phone: (801) 213-6109 Email: [email protected] Daniel R. Couriel, MD, MS Director, Blood & Marrow Transplant Program Professor, Department of Medicine Phone: (801) 587-4056 Email: [email protected] Jo-Anna Reems, PhD (Laboratory) Scientific Director, Cell Therapy & Regenerative Medicine Research Professor, Department of Medicine Phone: (801) 585-6262 Email: [email protected] Protocol name: Allogeneic Stem Cell Transplantation for Multiple Myeloma and Myelofibrosis Version Date: 29JAN2019 Principal Investigator: Catherine J. Lee, MD Michael Boyer, MD Associate Professor, Department of Medicine Phone: (801) 585-3229 Email: [email protected] Josef Prchal, MD Professor, Department of Medicine Phone: (801) 585-3229 Email: [email protected] Tibor Kovacsovics, MD Associate Professor, -
Non-Hodgkin and Hodgkin Lymphomas Select for Overexpression of BCLW Clare M
Published OnlineFirst August 29, 2017; DOI: 10.1158/1078-0432.CCR-17-1144 Biology of Human Tumors Clinical Cancer Research Non-Hodgkin and Hodgkin Lymphomas Select for Overexpression of BCLW Clare M. Adams1, Ramkrishna Mitra1, Jerald Z. Gong2, and Christine M. Eischen1 Abstract Purpose: B-cell lymphomas must acquire resistance to apopto- follicular, mantle cell, marginal zone, and Hodgkin lymphomas. sis during their development. We recently discovered BCLW, an Notably, BCLW was preferentially overexpressed over that of antiapoptotic BCL2 family member thought only to contribute to BCL2 and negatively correlated with BCL2 in specific lymphomas. spermatogenesis, was overexpressed in diffuse large B-cell lym- Unexpectedly, BCLW was overexpressed as frequently as BCL2 in phoma (DLBCL) and Burkitt lymphoma. To gain insight into the follicular lymphoma. Evaluation of all five antiapoptotic BCL2 contribution of BCLW to B-cell lymphomas and its potential to family members in six types of B-cell lymphoma revealed that confer resistance to BCL2 inhibitors, we investigated the expres- BCL2, BCLW, and BCLX were consistently overexpressed, whereas sion of BCLW and the other antiapoptotic BCL2 family members MCL1 and A1 were not. In addition, individual lymphomas in six different B-cell lymphomas. frequently overexpressed more than one antiapoptotic BCL2 Experimental Design: We performed a large-scale gene family member. expression analysis of datasets comprising approximately Conclusions: Our comprehensive analysis indicates B-cell 2,300 lymphoma patient samples, including non-Hodgkin lymphomas commonly select for BCLW overexpression in andHodgkinlymphomasaswellasindolentandaggressive combination with or instead of other antiapoptotic BCL2 lymphomas. Data were validated experimentally with qRT- family members. Our results suggest BCLW may be equally as PCR and IHC. -
Non-Hodgkin Lymphoma
Non-Hodgkin Lymphoma Rick, non-Hodgkin lymphoma survivor This publication was supported in part by grants from Revised 2013 A Message From John Walter President and CEO of The Leukemia & Lymphoma Society The Leukemia & Lymphoma Society (LLS) believes we are living at an extraordinary moment. LLS is committed to bringing you the most up-to-date blood cancer information. We know how important it is for you to have an accurate understanding of your diagnosis, treatment and support options. An important part of our mission is bringing you the latest information about advances in treatment for non-Hodgkin lymphoma, so you can work with your healthcare team to determine the best options for the best outcomes. Our vision is that one day the great majority of people who have been diagnosed with non-Hodgkin lymphoma will be cured or will be able to manage their disease with a good quality of life. We hope that the information in this publication will help you along your journey. LLS is the world’s largest voluntary health organization dedicated to funding blood cancer research, education and patient services. Since 1954, LLS has been a driving force behind almost every treatment breakthrough for patients with blood cancers, and we have awarded almost $1 billion to fund blood cancer research. Our commitment to pioneering science has contributed to an unprecedented rise in survival rates for people with many different blood cancers. Until there is a cure, LLS will continue to invest in research, patient support programs and services that improve the quality of life for patients and families. -
Transformation of Follicular Lymphoma to Acute Lymphoblastic Leukemia
Transformation of Follicular Lymphoma to Acute Lymphoblastic Leukemia Xiaoping Sun, MD, PhD; Leo I. Gordon, MD; LoAnn C. Peterson, MD n March 1994, a 56-year-old man underwent lobectomy sies showed a single paratrabecular lymphoid aggregate I of the upper lobe of the right lung and lymph node that suggested involvement by the follicular lymphoma. dissection for poorly differentiated adenocarcinoma. Ma- During the next 6 years, the patient underwent 2 biopsies lignant lymphoma, follicular, small cleaved was identi®ed and 2 ®ne-needle aspiration biopsies of lymph nodes from in multiple paratracheal and hilar lymph nodes. Hema- different sites, and the results of all of these biopsies were toxylin-eosin±stained sections of the lymph nodes showed consistent with the initial diagnosis. Flow cytometric im- a follicular pattern and a predominance of small cleaved munophenotyping was performed on 3 of the lymph node lymphoma cells (Figure, A). Bilateral bone marrow biop- specimens, and all contained CD101 and CD52 clonal B cells (CD191 and CD201) with l surface immunoglobulin light chain restriction. In August of 1999, 5 years after the Accepted for publication March 1, 2002. initial diagnosis, repeated bilateral bone marrow biopsies From the Department of Pathology, Northwestern University Medical School, Chicago, Ill. showed a normocellular bone marrow with 2 nonparatra- Reprints: LoAnn C. Peterson, MD, Department of Pathology, North- becular lymphoid aggregates; these ®ndings were not di- western University Medical School, Feinberg Pavilion, Room 7-344, agnostic for lymphoma. Flow cytometry studies of the 251 East Huron St, Chicago, IL 60611 (e-mail: [email protected]). bone marrow showed no evidence of B-cell clonality.