DOCSLIB.ORG

Immunophenotypic Identification of Acute Myeloid Leukemia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Immunophenotypic Identification of Acute Myeloid Leukemia Letters to the Editor 1321 pluripotent stem cell. However, the fact that not all CD34- Bobigny, France; 5 positive or all BFU-E or CFU-GM colonies are positive for Third Department of Internal Medicine, Semmelweis University, Budapest, Hungary; V617F suggests that the bone marrow of this patient is not 6 monoclonal with respect to the JAK2 mutation. Department of Haematology, University Hospital Linko¨ping, Linko¨ping, Sweden; In summary, the JAK2 V617F mutation was detected in a 7Genomics center, School of Biomedical and Health Sciences, cohort of patients with 5qÀ syndrome and a hypercellular Kings College London, London, UK; marrow. Despite no statistical difference, a higher median 8National Health Centre, Semmelweis University, platelet count was observed in the mutant cases with 50% (3/6) Budapest, Hungary; showing a platelet count 4700 Â 109/l compared with only 3% 9Institute of Pathology and Cancer Research, Semmelweis (3/91) in the wild-type cases. The lack of clinical response to University, Budapest, Hungary and 10 erythropoietin in the two cases described fails to support Department of Oncology and Clinical Immunology, previous in vitro studies documenting hypersensitivity to St-Johannes-Hospital, Duisburg, Germany erythropoietin in the presence of the mutation. E-mail: [email protected] 11These authors contributed equally to this work Whether the JAK2 mutation occurs as an early or late event during the disease course is unclear. We detected the JAK2 mutation both at time of diagnosis and at a follow-up of 132 References months in one case analysed, suggesting that the mutation occurred as an early event. Longer follow-up is however 1 James C, Ugo V, Le Couedic JP, Staerk J, Delhommeau F, Lacout C necessary to determine the prognostic significance of JAK2 et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 434: 1144– mutation and in particular, whether these cases will show 1148. favourable response to lenalidomide as previously demonstrated 2 Levine RL, Wadleigh M, Cools J, Ebert BL, Wernig G, Huntly BJ in 5qÀ chromosomal abnormalities.8 et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell 2005; 7: 387–397. Acknowledgements 3 Kralovics R, Passamonti F, Buser AS, Teo SS, Tiedt R, Passweg JR et al. A gain-of-function mutation of JAK2 in myeloproliferative W Ingram is supported by the Leukaemia Research Fund, UK. disorders. N Engl J Med 2005; 352: 1779–1790. 4 Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S et al. Acquired mutation of the tyrosine kinase JAK2 in human W Ingram1,11, NC Lea1,11, J Cervera2, U Germing3, P Fenaux4, myeloproliferative disorders. Lancet 2005; 365: 1054–1061. B Cassinat4, JJ Kiladjian4, J Varkonyi5, P Antunovic6, 5 Steensma DP, Dewald GW, Lasho TL, Powell HL, McClure RF, NB Westwood1, MJ Arno7, A Mohamedali1, J Gaken1, Levine RL et al. The JAK2 V617F activating tyrosine kinase T Kontou1, BH Czepulkowski1, NA Twine1, J Tamaska8, mutation is an infrequent event in both ‘atypical’ myeloprolife- J Csomer9, S Benedek5, N Gattermann3, E Zipperer3, rative disorders and myelodysplastic syndromes. Blood 2005; 106: 1207–1209. A Giagounidis10, Z Garcia-Casado2, G Sanz2 and GJ Mufti1 1 6 Jones AV, Kreil S, Zoi K, Waghorn K, Curtis C, Zhang L et al. Department of Haematological Medicine, Kings College Widespread occurrence of the JAK2 V617F mutation in chronic Hospital and Kings College London, London, UK; 2 myeloproliferative disorders. Blood 2005; 106: 2162–2168. The Servicio de Hematologia y Hemoterapia, Hospital 7 James C, Delhommeau F, Marzac C, Teyssandier I, Couedic JP, Universitario La Fe, Valencia, Spain; 3 Giraudier S et al. Detection of JAK2 V617F as a first intention Department of Haematology, Oncology and Clinical diagnostic test for erythrocytosis. Leukemia 2006; 20: 350–353. Immunology, Heinrich-Heine-University, 8 List A, Kurtin S, Roe DJ, Buresh A, Mahadevan D, Fuchs D et al. Du¨sseldorf, Germany; Efficacy of lenalidomide in myelodysplastic syndromes. N Engl J 4Hematology Department at Hopital Avicenne, Med 2005; 352: 549–557. Immunophenotypic identification of acute myeloid leukemia with monocytic differentiation Leukemia (2006) 20, 1321–1324. doi:10.1038/sj.leu.2404242; biologic diversity within FAB AML subtypes led to the World published online 27 April 2006 Health Organization (WHO) classification of AML, published in 2001, in which morphologic, immunophenotypic, genetic, and clinical features of AML were included in defining disease In 1976, the French-American-British (FAB) Cooperative entities.3 By WHO criteria, cases previously diagnosed as FAB Group published a morphologic classification of acute myeloid M4 or M5 may be classified as AML with recurrent cytogenetic leukemia (AML).1 A revision of this classification published in abnormalities (inv(16)(p13q22)/t(16;16)(p13;q22)(CBFb/MYH11), 1985 was widely used and recognized as the standard for AML 11q23(MLL), or t(8;21)(q22;q22)(AML1/ETO)), AML with multi- classification for over 15 years.2 Included in the FAB classifica- lineage dysplasia, therapy related AML, and AMML or AMoL tion were two groups of AML that exhibited monocytic subtypes of AML not otherwise categorized (NOC). Appropriate differentiation, acute myelomonocytic leukemia (AMML; M4), classification of AML is important for clinical management and and acute monoblastic/monocytic leukemia (AMoL; M5). A allows for future studies to expand and refine our understanding subset of M4 with abnormal and increased eosinophils (M4EO) of these diseases. was found to be associated with chromosome 16 abnormalities, While immunophenotypic features are included in the WHO either inv(16)(p13q22) or t(16;16)(p13;q22). Recognition of the classification of AML, immunophenotypic criteria for monocytic Leukemia Letters to the Editor 1322 54 Figure 1 Frequency of antigen expression in blasts of acute HLA-DR 100 monoblastic/monocytic leukemia (AMoL) (n ¼ 23) and nonmonocytic 60 leukemia (NM-AML) (n ¼ 72). Solid bars: AMoL; open bars: CD64 100 NM ¼ AML. 26 CD56 85 17 AML have not been clearly defined. A high level of expression of CD36 06 CD14 is a specific feature of mature monocytes, but this antigen 68 CD34 is frequently absent or underexpressed on immature monocytic 17 cells. Furthermore, other antigens that are generally considered 94 to be monocyte-associated may be expressed in other types of CD33 100 AML. The goals of the present study were to identify 0 immunophenotypic patterns that reliably characterize mono- Antigens CD16 38 cytic AMLs and to explore their immunophenotypic 74 heterogeneity in relationship to morphologic and cytogenetic CD15 100 subgroups. 0 A total of 126 cases of de novo AML diagnosed and analyzed CD14 61 with 4-color flow cytometry at our institution from 1998 to 2004 100 were included in the study. All cases were classified according CD13 83 to FAB criteria2 based on morphology and cytochemical 33 reactivity for myeloperoxidase and alpha naphthyl butyrate CD11b 100 esterase (ANBE), and also according to WHO criteria3 based on 30 clinical, morphologic, immunophenotypic, and cytogenetic CD4 100 features. By FAB criteria, 54 exhibited morphologic and cytochemical features of monocytic AML, including 31 cases 020406080 100 120 of M4 and 23 cases of M5 (15 monoblastic and eight Antigen Expression in % monocytic). Those 54 cases were classified by WHO criteria Figure 2 Expression patterns of CD36 in blasts of acute myeloid leukemia (AML) with monocytic differentiation. (a) Blasts (red) in acute monoblastic leukemia coexpressed CD36 and CD64. (b) Group 1 acute myelomonocytic leukemia (AMML) with one population (red) in the blast/ monocytic region, which showed a spectrum of CD36 and CD64. The least differentiated blasts were CD36(À) and CD45(moderate), followed by acquisition of CD36, and finally progression to bright CD45 expression. (c) Group 2 AMML with distinct population of blasts (red) and monocytes (blue) in the CD5/SSC dot plot. Both populations formed distinct clusters in the expression of CD36 and CD64. Green: granulocytes. Leukemia Letters to the Editor 1323 as AML with t(8;21) (3), inv(16)/t(16;16) (7), or 11q23 (11); However, all AMoLs in our series were positive for CD11b AML with multilineage dysplasia (3); or AML NOC (30). Of and HLA-DR, while none of the APLs expressed both antigens the 30 AML NOC cases, 17 were classified as AMML and 13 (data not shown). Furthermore, intense myeloperoxidase ex- as AMoL. pression, either by cytochemistry or flow cytometry, should help By flow cytometric analysis, blasts and monocytes were to distinguish microgranular APL from AMoL. identified using CD45/side scatter (SSC)/forward scatter (FSC) Cases of FAB M4 AML could be divided into two groups characteristics in combination with various cell surface anti- based on the definitive separation of discrete subpopulation of gens. The frequency of antigen expression in 23 AMoLs was blasts and monocytic cells in the analysis of CD45 and light compared to 72 nonmonocytic AMLs (NM-AML) (Figure 1). scatter (Figure 2b and c). One group showed a single Overall, the blasts in AMoL more frequently expressed CD4, (indistinguishable) population composed of both blasts and CD11b, CD14, CD16, CD36, CD56, CD64, and HLA-DR, and monocytic cells (designated group 1; 11 cases) (Figure 2b). The less often expressed CD34 compared to NM-AMLs (each immature cells in all cases of group 1 coexpressed CD36 and Po0.01). As single markers, none of these were sufficiently CD64. Thus, immunophenotypically, these closely resembled sensitive and specific for identifying monocytic AML. CD14 the AMoLs in our series, but were distinguished by a substantial expression in the blast/immature monocytic population was population of maturing granulocytes. Although discrete popula- seen in all eight cases of acute monocytic leukemia, but in eight tion of blasts and monocytic cells could not be discriminated in of 15 cases of acute monoblastic leukemia (P ¼ 0.021).
Load more

Recommended publications
  • 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
    [Show full text]
  • The Clinical Management of Chronic Myelomonocytic Leukemia Eric Padron, MD, Rami Komrokji, and Alan F
    The Clinical Management of Chronic Myelomonocytic Leukemia Eric Padron, MD, Rami Komrokji, and Alan F. List, MD Dr Padron is an assistant member, Dr Abstract: Chronic myelomonocytic leukemia (CMML) is an Komrokji is an associate member, and Dr aggressive malignancy characterized by peripheral monocytosis List is a senior member in the Department and ineffective hematopoiesis. It has been historically classified of Malignant Hematology at the H. Lee as a subtype of the myelodysplastic syndromes (MDSs) but was Moffitt Cancer Center & Research Institute in Tampa, Florida. recently demonstrated to be a distinct entity with a distinct natu- ral history. Nonetheless, clinical practice guidelines for CMML Address correspondence to: have been inferred from studies designed for MDSs. It is impera- Eric Padron, MD tive that clinicians understand which elements of MDS clinical Assistant Member practice are translatable to CMML, including which evidence has Malignant Hematology been generated from CMML-specific studies and which has not. H. Lee Moffitt Cancer Center & Research Institute This allows for an evidence-based approach to the treatment of 12902 Magnolia Drive CMML and identifies knowledge gaps in need of further study in Tampa, Florida 33612 a disease-specific manner. This review discusses the diagnosis, E-mail: [email protected] prognosis, and treatment of CMML, with the task of divorcing aspects of MDS practice that have not been demonstrated to be applicable to CMML and merging those that have been shown to be clinically similar. Introduction Chronic myelomonocytic leukemia (CMML) is a clonal hemato- logic malignancy characterized by absolute peripheral monocytosis, ineffective hematopoiesis, and an increased risk of transformation to acute myeloid leukemia.
    [Show full text]
  • Acute Monocytic Leukemia Linked to Pulmonary Infiltrates and the Importance of Early Induction Chemotherapy
    http://jhm.sciedupress.com Journal of Hematological Malignancies, 2018, Vol. 4, No. 1 CASE REPORT Acute Monocytic Leukemia Linked to Pulmonary Infiltrates and the Importance of Early Induction Chemotherapy Yvonne Chu1, Umit Tapan2, Adam Lerner2 1 Department of Medicine, Boston Medical Center, Boston, U.S.A. 2 Section of Hematology and Oncology, Boston Medical Center, Boston, U.S.A. Correspondence: Yvonne Chu, Department of Medicine, Boston Medical Center, Boston, U.S.A. E-mail: [email protected] Received: February 28, 2018 Accepted: May 3, 2018 Online Published: June 9, 2018 DOI: 10.5430/jhm.v4n1p1 URL: https://doi.org/10.5430/jhm.v4n1p1 Abstract Currently there is no consensus on the approach to evaluating lung infiltrates in patients with newly diagnosed acute myeloid leukemia (AML), a rare disease with an incidence of 3-4 cases per 100,000 people. The CT findings of pulmonary infiltrates in patients with AML are nonspecific and can range from confluent air-space opacities with patchy consolidation to interstitial markings and multiple subpleural small nodules. Biopsy will most often reveal bacterial or fungal infection and rarely malignant infiltrates. Here is a case of a patient with newly diagnosed AML, specifically of the monoblastic subtype, who was admitted to the hospital for induction chemotherapy and underwent transthoracic lung biopsy that confirmed monoblastic leukemic infiltrates. Following chemotherapy there was complete resolution of the lung infiltrates. Key Words AML, Acute myeloid leukemia, Acute monocytic leukemia, Acute monoblastic leukemia, Leukemic lung infiltrate 1. Introduction Currently there is no consensus on the approach to evaluating lung infiltrates in patients with newly diagnosed acute myeloid leukemia (AML), a rare disease with an incidence of 3-4 cases per 100,000 people.
    [Show full text]
  • Mirna182 Regulates Percentage of Myeloid and Erythroid Cells in Chronic Myeloid Leukemia
    Citation: Cell Death and Disease (2017) 8, e2547; doi:10.1038/cddis.2016.471 OPEN Official journal of the Cell Death Differentiation Association www.nature.com/cddis MiRNA182 regulates percentage of myeloid and erythroid cells in chronic myeloid leukemia Deepak Arya1,2, Sasikala P Sachithanandan1, Cecil Ross3, Dasaradhi Palakodeti4, Shang Li5 and Sudhir Krishna*,1 The deregulation of lineage control programs is often associated with the progression of haematological malignancies. The molecular regulators of lineage choices in the context of tyrosine kinase inhibitor (TKI) resistance remain poorly understood in chronic myeloid leukemia (CML). To find a potential molecular regulator contributing to lineage distribution and TKI resistance, we undertook an RNA-sequencing approach for identifying microRNAs (miRNAs). Following an unbiased screen, elevated miRNA182-5p levels were detected in Bcr-Abl-inhibited K562 cells (CML blast crisis cell line) and in a panel of CML patients. Earlier, miRNA182-5p upregulation was reported in several solid tumours and haematological malignancies. We undertook a strategy involving transient modulation and CRISPR/Cas9 (clustered regularly interspersed short palindromic repeats)-mediated knockout of the MIR182 locus in CML cells. The lineage contribution was assessed by methylcellulose colony formation assay. The transient modulation of miRNA182-5p revealed a biased phenotype. Strikingly, Δ182 cells (homozygous deletion of MIR182 locus) produced a marked shift in lineage distribution. The phenotype was rescued by ectopic expression of miRNA182-5p in Δ182 cells. A bioinformatic analysis and Hes1 modulation data suggested that Hes1 could be a putative target of miRNA182-5p. A reciprocal relationship between miRNA182-5p and Hes1 was seen in the context of TK inhibition.
    [Show full text]
  • Leukemia Cutis in a Patient with Acute Myelogenous Leukemia: a Case Report and Review of the Literature
    CONTINUING MEDICAL EDUCATION Leukemia Cutis in a Patient With Acute Myelogenous Leukemia: A Case Report and Review of the Literature Shino Bay Aguilera, DO; Matthew Zarraga, DO; Les Rosen, MD RELEASE DATE: January 2010 TERMINATION DATE: January 2011 The estimated time to complete this activity is 1 hour. GOAL To understand leukemia cutis and acute myelogenous leukemia (AML) to better manage patients with these conditions LEARNING OBJECTIVES Upon completion of this activity, you will be able to: 1. Recognize the clinical presentation of AML. 2. Discuss the classification of AML based on the French-American-British system and the World Health Organization system. 3. Manage the induction of remission and prevention of relapse of leukemia cutis in patients with AML. INTENDED AUDIENCE This CME activity is designed for dermatologists and general practitioners. CME Test and Instructions on page 12. This article has been peer reviewed and approved by College of Medicine is accredited by the ACCME to provide Michael Fisher, MD, Professor of Medicine, Albert Einstein continuing medical education for physicians. College of Medicine. Review date: December 2009. Albert Einstein College of Medicine designates this edu- This activity has been planned and implemented in cational activity for a maximum of 1 AMA PRA Category 1 accordance with the Essential Areas and Policies of the Credit TM. Physicians should only claim credit commensurate Accreditation Council for Continuing Medical Education with the extent of their participation in the activity. through the joint sponsorship of Albert Einstein College of This activity has been planned and produced in accor- Medicine and Quadrant HealthCom, Inc.
    [Show full text]
  • Mutations and Prognosis in Primary Myelofibrosis
    Leukemia (2013) 27, 1861–1869 & 2013 Macmillan Publishers Limited All rights reserved 0887-6924/13 www.nature.com/leu ORIGINAL ARTICLE Mutations and prognosis in primary myelofibrosis AM Vannucchi1, TL Lasho2, P Guglielmelli1, F Biamonte1, A Pardanani2, A Pereira3, C Finke2, J Score4, N Gangat2, C Mannarelli1, RP Ketterling5, G Rotunno1, RA Knudson5, MC Susini1, RR Laborde5, A Spolverini1, A Pancrazzi1, L Pieri1, R Manfredini6, E Tagliafico7, R Zini6, A Jones4, K Zoi8, A Reiter9, A Duncombe10, D Pietra11, E Rumi11, F Cervantes12, G Barosi13, M Cazzola11, NCP Cross4 and A Tefferi2 Patient outcome in primary myelofibrosis (PMF) is significantly influenced by karyotype. We studied 879 PMF patients to determine the individual and combinatorial prognostic relevance of somatic mutations. Analysis was performed in 483 European patients and the seminal observations were validated in 396 Mayo Clinic patients. Samples from the European cohort, collected at time of diagnosis, were analyzed for mutations in ASXL1, SRSF2, EZH2, TET2, DNMT3A, CBL, IDH1, IDH2, MPL and JAK2. Of these, ASXL1, SRSF2 and EZH2 mutations inter-independently predicted shortened survival. However, only ASXL1 mutations (HR: 2.02; Po0.001) remained significant in the context of the International Prognostic Scoring System (IPSS). These observations were validated in the Mayo Clinic cohort where mutation and survival analyses were performed from time of referral. ASXL1, SRSF2 and EZH2 mutations were independently associated with poor survival, but only ASXL1 mutations held their prognostic relevance (HR: 1.4; P ¼ 0.04) independent of the Dynamic IPSS (DIPSS)-plus model, which incorporates cytogenetic risk. In the European cohort, leukemia-free survival was negatively affected by IDH1/2, SRSF2 and ASXL1 mutations and in the Mayo cohort by IDH1 and SRSF2 mutations.
    [Show full text]
  • The AML Guide Information for Patients and Caregivers Acute Myeloid Leukemia
    The AML Guide Information for Patients and Caregivers Acute Myeloid Leukemia Emily, AML survivor Revised 2012 Inside Front Cover A Message from Louis J. DeGennaro, PhD President and CEO of The Leukemia & Lymphoma Society The Leukemia & Lymphoma Society (LLS) wants to bring you the most up-to-date blood cancer information. We know how important it is for you to understand your treatment and support options. With this knowledge, you can work with members of your healthcare team to move forward with the hope of remission and recovery. Our vision is that one day most people who have been diagnosed with acute myeloid leukemia (AML) will be cured or will be able to manage their disease and have a good quality of life. We hope that the information in this Guide will help you along your journey. LLS is the world’s largest voluntary health organization dedicated to funding blood cancer research, advocacy and patient services. Since the first funding in 1954, LLS has invested more than $814 million in research specifically targeting blood cancers. We will continue to invest in research for cures and in programs and services that improve the quality of life for people who have AML and their families. We wish you well. Louis J. DeGennaro, PhD President and Chief Executive Officer The Leukemia & Lymphoma Society Inside This Guide 2 Introduction 3 Here to Help 6 Part 1—Understanding AML About Marrow, Blood and Blood Cells About AML Diagnosis Types of AML 11 Part 2—Treatment Choosing a Specialist Ask Your Doctor Treatment Planning About AML Treatments Relapsed or Refractory AML Stem Cell Transplantation Acute Promyelocytic Leukemia (APL) Treatment Acute Monocytic Leukemia Treatment AML Treatment in Children AML Treatment in Older Patients 24 Part 3—About Clinical Trials 25 Part 4—Side Effects and Follow-Up Care Side Effects of AML Treatment Long-Term and Late Effects Follow-up Care Tracking Your AML Tests 30 Take Care of Yourself 31 Medical Terms This LLS Guide about AML is for information only.
    [Show full text]
  • Myelodysplastic Syndromes Overview and Types
    cancer.org | 1.800.227.2345 About Myelodysplastic Syndromes Overview and Types If you have been diagnosed with a myelodysplastic syndrome or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Are Myelodysplastic Syndromes? ● Types of Myelodysplastic Syndromes Research and Statistics See the latest estimates for new cases of myelodysplastic syndromes in the US and what research is currently being done. ● Key Statistics for Myelodysplastic Syndromes ● What's New in Myelodysplastic Syndrome Research? What Are Myelodysplastic Syndromes? Myelodysplastic syndromes (MDS) are conditions that can occur when the blood- forming cells in the bone marrow become abnormal. This leads to low numbers of one or more types of blood cells. MDS is considered a type of cancer1. Normal bone marrow 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Bone marrow is found in the middle of certain bones. It is made up of blood-forming cells, fat cells, and supporting tissues. A small fraction of the blood-forming cells are blood stem cells. Stem cells are needed to make new blood cells. There are 3 main types of blood cells: red blood cells, white blood cells, and platelets. Red blood cells pick up oxygen in the lungs and carry it to the rest of the body. These cells also bring carbon dioxide back to the lungs. Having too few red blood cells is called anemia. It can make a person feel tired and weak and look pale. Severe anemia can cause shortness of breath. White blood cells (also known as leukocytes) are important in defending the body against infection.
    [Show full text]
  • Hematology Liquid Biopsy
    17527 Technology Dr, Suite 100 Irvine, CA 92618 Tel: 1-949-450-9421 genomictestingcooperative.com Hematology Liquid Biopsy Patient Name: Ordered By Date of Birth: Ordering Physician: Gender (M/F): Physician ID: Client: Accession #: Case #: Specimen Type: Body Site: Specimen ID: _____________________________________________________________________________________________ Ethnicity: Family History: MRN: Indication for Testing: Collected Time Reason for Malignant Neoplasm of Lung Date: : Referral: Received Time Tumor Type: Lung Date: : Reported Time Stage: T2B Date: : Test Description: This is a next generation sequencing (NGS) test performed on cell-free DNA (cfDNA) to identify molecular abnormalities in 177 genes implicated in hematologic neoplasms, including leukemia, lymphoma, myeloma and MDS. Whenever possible, clinical relevance and implications of detected abnormalities are described below. Detected Genomic Alterations FLT3-ITD IDH2 TET2 DNMT3A NRAS Heterogeneity IDH1 mutation is detected in very small subclone when compared with the rest of the mutations Diagnostic Implications Acute Leukemia Consistent with Acute Myeloid Leukemia (AML), but NRAS mutation suggests AMML, likely evolving from CMML background. MDS N/A Lymphoma N/A Myeloma N/A Other N/A Therapeutic Implications FLT3-ITD Rydapt (Midostaurin) IDH2 (Subclone) Idhifa (Enasidenib) Prognostic Implications FLT3-ITD Poor The professional and technical components of this assay were performed at Genomic Testing Cooperative, LCA, 27 Technology Drive, Suite 100, Irvine, CA 92618 (CLIA ID: 05D2111917). The assay is FDA cleared and the performance characteristics were established at this location and was .... 27 Technology Dr, Suite 100 Irvine, CA 92618 Tel: 1-949-450-9421 genomictestingcooperative.com IDH2 Neutral TET2 Neutral DNMT3A Poor NRAS Neutral Overall Poor Relevant Genes with No Alteration NPM1 Results Summary ▪ There are mutations in FLT3-ITD, TET2, IDH2, DNMT3A, NRAS genes.
    [Show full text]
  • In Vitro Induction of Granulocyte Differentiation in Hematopoietic
    Proceeding8 of the National Academy of Sciences Vol. 67, No. 3, pp. 1542-1549, November 1970 In Vitro Induction of Granulocyte Differentiation in Hematopoietic Cells from Leukemic and Non-Leukemic Patients Michael Paran, Leo Sachs, Yigal Barak*, and Peretz Resnitzky* DEPARTMENT OF GENETICS, WEIZMANN INSTITUTE OF SCIENCE, REHOVOT, ISRAEL, AND KAPLAN HOSPITAL*, REHOVOT, ISRAEL Communicated by Albert B. Sabin, August 17, 1970 Abstract. Human spleen-conditioned medium can induce the formation in vitro of large granulocyte colonies from normal human bone marrow cells. The granulocyte colonies contained cells in various stages of differentiation, from myeloblasts to mature neutrophile granulocytes. Human spleen-conditioned medium also induced colony formation with rodent bone-marrow cells, whereas rodent spleen-conditioned medium induced colony formation with rodent bone marrow but not with human cells. This in vitro system has been used to determine the potentialities for cell differentiation in bone-marrow and peripheral blood cells from patients with a block in granulocyte differentiation in vivo. The cloning efficiency, colony size, and number of mature granulocytes in bone-marrow colonies from patients with congenital neutropenia, whose bone marrow contained only 1% mature granulo- cytes, were not less than in people whose bone marrow had the normal level of about 40% mature granulocytes. The cloning efficiency of peripheral blood cells from patients with acute myeloid leukemia was 350 times higher, with 10 times larger colonies, than the cloning efficiency of peripheral blood cells from normal people. The cytochemical properties and number of mature granulocytes in colonies from the leukemic patients were the same as in colonies from non- leukemic people.
    [Show full text]
  • Chronic Myeloid Leukemia Mimicking Primary Myelofibrosis: a Case Report
    ISSN: 2640-7914 DOI: https://dx.doi.org/10.17352/ahcrr CLINICAL GROUP Received: 02 November, 2020 Case Report Accepted: 01 February, 2021 Published: 02 February, 2021 *Corresponding author: Anju S, Junior Resident, Gov- Chronic myeloid leukemia ernment Medical College, Kottayam, Kerala, India, Tel: 91 9496057350; E-mail: mimicking primary Keywords: Chronic myeloid leukemia; Primary myelo- fi brosis; Blast crisis; Myeloproliferative neoplasms myelofi brosis: A case report https://www.peertechz.com Anju S*, Jayalakshmy PL and Sankar Sundaram Junior Resident, Government Medical College, Kottayam, Kerala, India Abstract Bone marrow fi brosis leading to dry tap aspiration and often associated with blast crisis has previously been reported in both Chronic myeloid leukemia and Primary myelofi brosis. The similarities between these two conditions in terms of clinical presentation and morphology can really create a diagnostic dilemma. Here we present a case of Chronic myeloid leukemia in fi brosis and blast crisis in a 32 year old lady which closely resembled Primary myelofi brosis in transformation. All myeloproliferative neoplasms can undergo blast transformation. In this case, the detection of Philadelphia chromosome helped to distinguish Chronic myeloid leukemia from other myeloproliferative neoplasms. Introduction diffi cult to distinguish the different MPNs especially those in blast crisis and fi brosis. The treatment of CML involves targeted Myeloproliferative Neoplasm (MPN) results from therapy namely, Imatinib mesylate, which is a tyrosine kinase unchecked proliferation of the cellular elements in the bone inhibitor. Also, JAK1/2 inhibitors administered in PMF patients marrow characterized by panmyelosis and accompanied by show clinical improvement [2]. So, it is Important to distinguish erythrocytosis, granulocytosis, and/or thrombocytosis in every MPNs even in their blastic phase as they have different the peripheral blood.
    [Show full text]
  • Acute Myeloid Leukemia and Related L Id L Myeloid Neoplasms
    Acute myeloid leukemia and related myelidloid neoplasms: WHO 2008 brings us closer to understanding clinical behavior No conflicts of interest to disclose Steven Devine, MD The Ohio Sta te UiUnivers ity Common Presentations of AML • vague history of chronic progressive lethargy • 1/3 of patients with acute leukemia will be acutely ill with significant skin, soft tissue, or respiratory infection. • Petechiae with or without bleedinggy may be present • Leu kem ias w ith a monocy tic componen t may have gingival hypertrophy from leukemia infiltration/ extramedullary involvement (of CNS, gums, skin, other) Lab Findings in AML • The hematocrit is generally low but severe anemia is uncommon • The peripheral white blood cell count may be increased, decreased, or normal. – Approximately 35% of all AML patients will have ANC < 1,000/uL; circulating blast cells may be absent 15% of the time • Disseminated intravascular coagulation (DIC) is common, it is nearly universal in acute promyelocytic leukemia • Thrombocytopenia is frequently observed-- platelet counts <20,000/uL are common, often leads to bruising or blee ding (gums, pe tec hiae ) Basics of AML • Approximately 9,000 new cases yr in US • Incidence of AML rises with advancinggg age • The median age is 65 – Most children with leukemia have ALL (not AML) • AML is about 80% of adult acute leukemias But usuallyyy we don’t know why… • An increased incidence of AML is associated with certain conggyyenital conditions like Down syndrome, Bloom's syndrome, Fanconi's anemia • Patients with acquired
    [Show full text]