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1068491
Introduction to lymphomas and CLL
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Hematology Mind Map on Introduction to lymphomas and CLL, created by LewisLewis on 07/13/2014.
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hematology
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LewisLewis
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LewisLewis
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Resource summary
Introduction to lymphomas and CLL
Hodgkin lymphoma
WHO classes
Nodular, lymphocytic predominance (20%)
Classic (80%)
Nodular sclerosis
(these 3 are classified according to relative proportion of Reed-Sternberg cells)
Mixed cellularity
Lymphocytic rich
Lymphocyte depletion
Neoplastic cells are by far the minority of cells you find in lymph nodes
With a storm of signals they favor the accumulation of non-neoplastic cells around them
Final diagnosis cannot be obtained if you don't find the neoplastic cells
CLL
Characterized by lymphocytosis
3 steps required to produce a CLL
Transformation
Accumulation
Autonomous growth
Clonal B cell malignancy (most often CD+ B lymphocytes)
Epidemiology
Most common in adults >50 years
Many patients have comorbidities
Etiology
Unkown
No established viral etiology
Genetic factors
Nearly 9% of patients have a familial history of CLL
Increased incidence in farmers, rubber manufactory workers and asbestos workers
Cytogenetics
50% have clonal chromosomal abnormalities
Patients with an abnormal karyotype have a worse prognosis
Development of CLL is strangely linked to monoclonal B cell-lymphocytosis (MBL)
In MBL there is a 2-5% risk to develop CLL
Risk depends on the degree of lymphocytosis
If B cell count <5000/µl, risk is <2%
If B cell count >5000µl, risk is >5%
Molecular features
Clinical features
Signs
Lymphadenopathy
Splenomegaly
Hepatomegaly
Other organs
Paraneoplastic phenomenon
Investigations
Pretreatment studies
CBC
Lymphocytosis (>5000/µl)
Cytopenias
Anemia
Thrombocytopenia
Neutropenia
Peripheral blood smear
Reticulocyte count
Coomb's test
Renal and liver function tests
Serum protein electrophoresis
Immunoglobulin level
Hypogammaglobulinemia, observed in 80% of patients
Autoimmune disorders
Plasma beta2 microglobulin test
Immunophenotyping if available
Immunophenotype of CLL is: CD5+, CD20+, CD23+
CD38 is a prognostic factor
CD38-: less aggressive behavior
CD38+: aggressive behavior
Histopathology
Bone marrow biopsy
It can show a nodular pattern or a diffuse pattern
Lymph node: typically completely infiltrated by the disease
Differential diagnosis
Infection
Malignant causes
T cell CLL (<1% cases)
B cell
Leukemic phase of NHL
Hairy cell leukemia
Waldenstrom macroglobulinemia
Staging systems
Ray staging system
Binet staging system
Prognostic markers
Features suggestive of poor prognosis
17p deletion: bad prognosis
Ig mutations: better prognosis
Transformation
Diffuse large B cell lymphoma (Richter syndrome) accounts for almost 80% of cases of transformation
Pro-lymphocytic leukemia (20%)
Hodgkin disease
Multiple myeloma
Acute leukemia
Treatment
Cure is not the goal (not a curable disorder)
Reserved for patients with low or intermediate risk disease who are asymptomatic or have a progressive disease
Indications to start treatment
Follow-up: evaluation
Lymphocytosis
Lymphocyte doubling time
Anemia and thrombocytopenia
Evaluating response to treatment
Complete response, defined as:
Free of the clinical problems for which the treatment was initiated
No constitutional symptoms
Normal blood counts and Hb
No organomegaly
No bone marrow infiltration by lymphocyte nodules and marrow lymphocytosis <30%
Minimal residual disease (MRD)
Progressive disease
50% increase in lymphocyte count
Transformation to aggressive histology
Increase in spleen or lymph node size
Appearance of new lymph nodes
Treatment strategy
Alkylating agents
Chlorambucil
Cyclophosphamide
Bendamustine
Nucleoside analogues
Combination
CHOP regimen
Monoclonal antibodies
Rituximab, Alentuzumab
Immunomodulators (lenalidomide)
Drugs acting on the signaling pathways of BCR
p3K inhibitor
BTK inhibitors
To recognize a particular stage of development we need
Morphology
Tissue architecture
Relationship with capsule
Growth pattern
Cytological properties (cell size, nuclear/cytoplasmic ratio, nuclear irregularity...)
Immunophenotypes
B vs T
Maturation stage level markers
Immunohistoshemistry cannot be used as 1st method for classification, first you need morphology
Frequency of WHO histotypes
50% by 2 entities
Diffuse large B cell lymphomas (30%)
Follicular lymphomas (22%)
The remaining are fragmented in many entities
Concepts specific for lymphomas
Concept of dysplasia is not part of the spectrum of these malignancies
Grading is not reliable
Only exception is follicular lymphoma
Spreading of the tumor through the body is called "localization", not metastasis
Sometimes the definition between lymphoma and leukemia is quantitative
Steps in the classification of lymphomas
1966: Henry Rappaport's AFIP Classification
Kiel classification (1974)
Working formulation (1982)
Updated Kiel classification (1988)
For the first time lymphomas were classified not only by morphology but also by immunohistochemistry
Revised European American Lymphoma (REAL) Classification
Media attachments
Investigation (image/jpg)
provision_proton_therapy_hodgkin_lymphoma_1 (image/jpg)
zf_differential (image/jpg)
transformers8-hi (image/jpg)
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