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Part 2 Nhl
 

Part 2 Nhl

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    Part 2 Nhl Part 2 Nhl Presentation Transcript

    • Peripheral B cell Neoplasm Neoplasm of Mature B cells
    • FOLLICULAR LYMPHOMA
    • FEATURES
      Follicular lymphoma is the most common form of indolent NHL in the United States
      Middle age men and women equally.
      Arise from germinal center B cells.
      Strongly associated with translocation involving BCL2
    • hallmark
      Translocation( 14; 18)
      This translocation is seen in most but not all follicular lymphomas
      Leads to overexpression of BCL2 protein.
      BCL2, = is an antagonist of apoptotic cell death and appears to promote the survival of follicular lymphoma cells.
    • Features
      10% show Peripheral blood involvement sufficient to produce lymphocytosis
      (usually <20,000/mm3 )
      85% have Bone marrow involvement
      Paratrabecularlymphoid aggregates.
      Splenic white pulp and hepatic portal triads are also frequently involved.
    • Reactive LymphoidFollicular Lymphoma Hyperplasia
      Majority Small cleaved cells
      Form Follicles
    • BCL2 Immunostain
      7
    • Immunophenotype and Genetics
      Express CD19, CD20, CD10
      Like Normal follicular center B cells,
      CD5 is NOT Expressed
      In contrast to CLL and SLL and mantle cell lymphoma, CD5 is expressed.
      OverExpression of BCL2 protein - > 90%
      Versus Normal Follicular center B cells, which are BCL2 negative
    • Clinical Features.
      Painless lymphadenopathy, which is frequently generalized.
      Uncommon Involvement of extranodalsites
      GIT, CNS, Testis
      Often follows an indolent waxing and waning course.
    • Survival
      Overall median survival is 7 to 9 years
      Is not improved by aggressive therapy
      The usual clinical approach is to palliate patients with low-dose chemotherapy or radiation when they become symptomatic.
    • Transformation
      Retain t(14;18)
      Somatic Hypermutation promote transformation
      Occurs in 30 to 50% of follicular lymphomas,
      Most commonly to diffuse large B-cell lymphoma.
      Median survival is less than 1 year after transformation.
    • DIFFUSE LARGE CELL LYMPHOMA
    • Most common form of NHL
      60-70%
      Aggressive lymphoid neoplasm
      M>F , Median age 60y/o
      DIFFUSE LARGE B-CELL LYMPHOMA
    • Features
      Rapidly enlarging mass
      Often Symptomatic
      Arise in any site
      Waldeyerring, Oropharyngeal LN, Tonsils
      Liver, spleen
      Localized Disease with extranodal involvement
      Rarely present as leukemia
    • Immunophenotype
      Mature B cell
      Express CD19 & CD20
      Variably Express Germinal Center Markers
      Have surface Ig
      Negative Tdt
    • Molecular Pathogenesis
      30% Dysregulation of BCL6
      Repress germinal center B-cell Differentiation  Growth Arrest  Holds cell in Undifferentiated Proliferative state
      Silence the expression of p53
      Prevent the activation of DNA repair mechanism
    • Liver -DLCL
    • Morphology
      Diffuse pattern of growth
      Large Neoplastic cells
      4-5x small lymphocytes
      DIFFUSE LARGE CELL LYMPHOMA
    • Diffuse Large Cell
    • Therapy
      60-80% Complete remission with combination Chemotherapy
      50% remain free from disease for years
      Immunotherapy with Anti-CD20 improves outcome especially elderly
    • Subtype
      Immunedeficiency-associated large B cell Lymphoma
      T cell immunodeficiency ( HIV )
      (+) EBV Neoplastic B cell
      Restoration of immunity
      Regression of proliferation
    • BURKITTS LYMPHOMA
    • BURKITTS LYMPHOMA
      3 TYPES
      1. African ( Endemic )
      2. Sporadic ( Non-endemic )
      3. Aggressive lymphoma occuring in HIV patients
      • Histologically identical
      • Genotype & virologic difference
      • CD10 Usually seen
    • Features
      • Cell of origin
      • Germinal center Bcell
      • African  LATENTLY INFECTED w/ EBV
      • All forms associated
      • Translocations c-myc gene on Chromosome 8 with IgH [t(8,14)]
      • Commonly
    • Clinical features
      Adolescent or Young Adult w/ jaw or extranodal abdominal mass
      Very aggressive
      Respond well to chemotx
      Outcome guarded in Older adults
      UNCOMMON BM or peripheral blood
    • Clinical features
      Endemic
      Often as Abdominal Mass
      Ileocecal
      Peritoneum
      Often Mandibular mass
      Unusual predilection to abdominal viscera
      Kidneys
      Ovary
      Adrenals
      Sporadic
    • Morphology
      Starry sky pattern
      High mitotic activity
    • BurkittsLymphomaStarry sky pattern
    • High Mitotic IndexMonotonous Cells
    • Marginal Zone Lymphomas
    • Features
      LOW grade lesions
      Encompass a heterogenous group of B cell tumors
      Arise in LN, Spleen, Extranodal Tissues
      Tumor cell resemble normal Marginal Zone B cells
      Initially recognized at mucosal sites
      MALTOMA
    • Unusual Pathogenesis
      1. Often arise – Chronic Inflammatory D/O
      Autoimmune
      Sjogrens – Salivary gland
      Hashimotos - Thyroid
      Infectious
      Helicobacter pylori- Stomach
    • Unusual Pathogenesis
      2. Remain localized for prolonged periods – Spread late
      3. May regress if inciting agent is eradictaed – H. pylori
    • GIT- Maltoma
    • MULTIPLE MYELOMA
    • Multiple bone involvement
      Can also spread to LN & Extranodal
      1% in Western countries
      Higher incidence
      Men>Women
      Older Patients
      Radiation exposure
      African decent
      MULTIPLE MYELOMA
    • Pathogenesis
      IL-6
      Proliferation of tumor cells are DEPENDENT on Cytokione
      Active Disease and Poor Prognosis
      MIP 1 alpha & RANK Ligand
      Mediate Bone Destruction
      Karyotyping
      Deletions of 13q
      IgH
      MULTIPLE MYELOMA
    • X-ray
      Multiple lyticlesions
      Punch out lesions
      Axial Skeleton
      Starts at Medullary
      Gelatinous , soft tumor
      MULTIPLE MYELOMA
    • Mutiple Myeloma
    • Laboratory
      High M proteins  Rouleaux
      55% IgG Monoclonal Ab
      Proliferation of Neoplastic plasma cells
      30% of bone marrow cellularity
      (Plasma cell Leukemia )
      Bence Jones proteins in urine
      Myeloma kidney
      Seen in 60-80%
      ClinicopathologicDx
      Correlation of X-ray & Laboratory Findings
      MULTIPLE MYELOMA
    • BM aspirate- Myeloma
    • Electrophoresis
      IgG k M protein
    • Clinical Features
      Bone pain – axial skeleton (Vertebrae)
      Hypercalcemia ( 25%)
      Renal Failure (30-50%)
      Myeloma kidney
      Proteinacious tubular cast
      Nephrocalcinosis ( metastatic calcification)
    • Clinical Features
      Hematologic findings
      Normocytic anemia with rouleaux
      Prolonged bleeding due to defect in platelet aggregation
      Radiculopathy due to bone compression and vertebral fracture
      Recurrent infection – Most common cause of death
    • Prognosis
      Variable but Generally Poor
      Median survival is 6 months without treatment
    • SOLITARY MYELOMA
    • Solitary Myeloma
      Lesions either in the Bone or Soft Tissue
      Axial Skeleton
      Lungs, Oropharynx, Nasal Sinuses
      Minority show (+) M protein
      Progression to Multiple Myeloma
      Common in solitary Osseous myeloma
      ( 10-20 yrs)
      Less common in Extraosseous
    • PERIPHERAL T-CELL and NK-CELL NEOPLASMS
      NEOPLASM OF MATURE T CELLS AND NK CELLS
    • EXTRANODAL NK/T-CELL LYMPHOMA
    • EXTRANODAL NK/T-CELL LYMPHOMA
      PREVIOUSLY MIDLINE GRANULOMA
      3% OF NHL IN ASIA
      DESTRUCTIVE MIDLINE MASS  INVADE SMALL VESSELS  EXTENSIVE ISCHEMIC NECROSIS
      NEOPLASTIC ELEMENTS
      MIXTURE OF SMALL & LARGE LYMPHOID CELLS
    • Mycosis fungoides