Neoplastic proliferation arising from white blood cells. Introductory remarks. Classification
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1 Neoplastic proliferation arising from white blood cells Lymphoproliferative and myeloproliferative diseases and syndromes Oliver Rácz, Introductory remarks Leukemia and lymphoma are old descriptive terms On the other side the new classification is also descriptive and not fully rational. High number of subtypes in most group. Typisation is based on new knowledge histology, surface antigens (imunochemistry, flow cytometry) and genetics Not without purpose different treatment regimes 2 Classification LYMPHOID NEOPLASMS Hodgkin, non-hodgkin ALL, CLL CHAOS TILL 1994 REAL, 1997 WHO Immunochemical and genetic characteristics MYELOID NEOPLASMS Acute AML Chronic CML Myelodysplastic syndromes 3 1
2 LYMPHOID NEOPLASMS, B;T; HODGKIN 1. Precursor B cell neoplasms (1) 2. Peripheral B cell neoplasms (12) why? Hairy cell leukemia, plasmocytoma, Burkitt lymphoma 3. Precursor T cell neoplasms (1) 4. Peripheral T and NK cell neoplasms (12) why? 5. Hodgkin lymphoma (5 subtypes) 4 LYMPHOID NEOPLASMS, B;T; HODGKIN 1. Precursor B cell neoplasms (1) 2. Peripheral B cell neoplasms (12) why? Hairy cell leukemia, plasmocytoma, Burkitt lymphoma 3. Precursor T cell neoplasms (1) 4. Peripheral T and NK cell neoplasms (12) why? WHY 1:12? There is only one precursor but many development stages 5 6 2
3 LYMPHOID NEOPLASMS, B;T; HODGKIN 1. Precursor B cell neoplasms (1) NHL 2. Peripheral B cell neoplasms (12) NHL 3. Precursor T cell neoplasms (1) NHL 4. Peripheral T and NK cell neoplasms (12) NHL 5. Hodgkin lymphoma (5 subtypes) HL CLINICAL PICTURE NODAL ENLARGEMENT IN 80% NHL, ALL HL SUPRESSION OF NORMAL HEMATOPOIESIS SPLEEN AND LIVER INFILTRATION IMMUNE SYSTEM DYSFUNCTION SPECIFIC OR also NOTHING 7 LYMPHOID NEOPLASMS, B;T; HODGKIN 1. Precursor B cell neoplasms (1) NHL 2. Peripheral B cell neoplasms (12) NHL 3. Precursor T cell neoplasms (1) NHL 4. Peripheral T and NK cell neoplasms (12) NHL 5. Hodgkin lymphoma (5 subtypes) HL LABORATORY PICTURE PERIPHERAL BLOOD NEOPLASM BIOPSY ANTIGEN RECEPTORS AND OTHER SURFACE PROTEINS (CD1 79) PRESENT ALSO ON NORMAL CELLS FLOW CYTOMETRY CHROMOSOME AND GENE ANALYSIS 8 Hodgkin: Reed-Sternberg cells 9 3
4 Hodgkin: Reed-Sternberg cells Size between microns; Amphofilic, finely granular/homogenous cytoplasm; Two mirror-image nuclei ("owl eyes") each with an eosinophilic nucleolus and a thick nuclear membrane (chromatin is distributed on the inner surface of the nuclear membrane, generating a halo image around the nucleolus). 10 Hodgkin: Clinical picture 5 subtypes according Ly morphology and tumor histology, 1 4 is the same, 5 (nodular lymphocyte predominant Hodgkin disease; NLPHD) is a separate disease Enlargement of one ore more lymphatic nodes, without pain, mostly in the cervical or mediastinal region Fever, sweat, quiver, weight loss (or no) Later dissemination to other organs 11 The Reed-Sternberg cells affect the immune system! 12 4
5 Non-Hodgkins: More frequent B >> T (80-85 vs %) Associated with (cause???) Epstein Barr virus (Africa, Burkitt) HTLV human T-cell Lymphotropic (Japan) HIV Posttransplantation (immunosupression?) Helicobacter MALT lymphoma? 13 Non-Hodgkins B >> T (80-85 vs %) V(D)J recombinations and regulated somatic hypermutations higher possibility of mistakes 14 Non-Hodgkins: Symptoms, prognosis More generalized as HL Enlarged L.N., no pain Many types, for general medicine is enough Low grade Aggressive Very aggressive (but radio-chemosenzitive) During disease the aggresivity can increase Therapy with monoclonal antibodies rituximab against CD20 (B) with 90 Y Transplantation of stem cells or bone marrow 15 5
6 Lymphoid and myeloid leukemias ABNORMAL PROLIFERATION OF CELLS, CIRCULATING IN BLOOD, INFILTRATING ORGANS IN AGE 1 14 YEARS LEADING CAUSE OFMORTALITY, DESPITE THE FACT THAT LEUKÉMIA IS 10-TIMES MORE REQUENT IN ADULTS ALL children, 2 4 y. CLL older, m > w AML adults CML 30 50, and also children 16 Etiology in general Radiation Hiroshima, Tchernobyl and? Aromatic substances Antitumor drugs!!! Down (RR 10), Recklinghausen, Fanconi, Bloom > 500 different translocations and other chromosomal aberrations (Philadelphia) 17 Philadelphia chromosome, chronic myeloid leukemia (CML) 9 22 bcr abl-bcr hybrid gene p210 tyrosinkinase with increased activity abl 18 6
7 Neurofibromatosis 1 Recklinghausen (and Genersich) Tumor supressor gene on 17th ch. (NF1) Risk of other malignities, too AD, 1/ Acute lymphatic leukemia Children, boys > girls Whites > nonwhites (2x) preb > > pret, B earlier, T later Blood cell morphology makes possible differential dg ofall and AML, further immunophenotypisation Chromosomes: hyperploidia (> 50), polyploidia, Philadelphia and other translocations Microchip technology specific patterns of abnormal gene expression 20 Symptoms (common for ALL, AML) Rapid onset of symptoms (weeks) Anaemia, fatigue, fever, bleeding Bone pain Generalised lymphadenopatia, splenomegaly, hepatomegaly ALL > AML, sometimes testes (ALL) Headache, cramps (ALL) THE PROGNOSIS IS IMPROVING 21 7
8 Chronic lymphatic leukemia, CLL Most frequent from all Manifestation in age over 50, M > W Ly > 4000/µl, sometimes /µl Prolymphocytes in LN, high number of mitoses In blood small Ly, small amount of cytoplazma, fragile smudge cells. Ly in bone marrow and other tissues Special immunophenotype Low number of chromosomal abnormalities Often asymptomatic Danger of increase in degree of malignancy 22 Myeloid neoplasma types in general From developmemtal stages of these cells Less infiltrate spleen, liver and L.N. AML cells are nondifferentiated, haematopoesis blocked CML differentiated cells Myelodysplastic syndromes Danger of transformation towards more agressive forms 23 AML Mostly in young adults The maturation is blocked!!! Blasts /µl Frequent chromosomal aberrations (up to 90 % with modern technology) The prognosis is not very good 24 8
9 AML Classification M0 M7, mostly 1 and 2, AML without and with maturation, but also erytro... (M6) a megakaryo... (M7) M3 often associated with DIC (acute promyelocyte L) WHO classification according to chromosomal aberrations 25 Symptoms (common for ALL, AML) Rapid onset of symptoms (weeks) Anaemia, fatigue, fever, bleeding Bone pain Generalised lymphadenopatia, splenomegaly, hepatomegaly ALL > AML, sometimes testes (ALL) Headache, cramps (ALL) THE PROGNOSIS IS IMPROVING 26 Chronic myeloid leukemia, CML Philadelphia chromosome in 90 %, with special methods the hybrid gene can be identified also in the remaining 10 % Uncontrolled proliferation of cells, inhibition of apoptosis Bone marrow is 100 % cellular (n: 50%) Peripheral blood up to granulocytes, myelocytes, metamyelocytes Often high number of eosinophiles and bazophiles Thrombocytosis Extramedullan haematopoesis 27 9
10 Chronic myeloid leukemia, CML Slow nonspecific onset Fatigue, anorexia, weight loss Splenomegaly Cca after 3 years often acceleration New chromosomal abnormalities Blast crises Therapy: Inhibition of BCR-ABL kinase Bone marrow transplantation 28 Myelodysplastic syndromes Pimary or in association with the therapy of other leukemias After 60 Ineffective and abnormal haematopoesis, apoptosis Pancytopenia Transformation into AML 29 Other Polycytaemia vera Also platelets increased, ht up to 60 Flebotomy as therapy Essencial thrombocytosis (up to ) Primary myelofibrosis cytopenia and compensatory extramedullar haematopoesis 30 10
11 31 References Robbins Cotran: Pathologic basis of disease, 7th Ed. (Kumar-Abbas-Fausto) Elsevier 2005 Aster: Diseases of white blood cells Porth: Essentials of Pathophysiology, 2nd Ed., Lippincott 2007 Gaspard: Disorders of white blood cells and lymphoid tissues 32 11
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