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Transcript
Lymphoma
DR: Gehan Mohamed
Learning objectives
•
•
•
•
important types of lymphoma
Clinical presentation
Diagnosis
Staging
ALL
CLL
Lymphomas
Myeloma
naïve
B-lymphocytes
Lymphoid
progenitor
AML
Hematopoietic
stem cell
Myeloid
progenitor
Plasma
cells
T-lymphocytes
Myeloproliferative disorders
Neutrophils
Eosinophils
Basophils
Monocytes
Platelets
Red cells
Normal structure of reactive
lymph node
Microscopic picture of reactive
lymphoid follicles
lymphoma
• Definition : malignant neoplasm of lymphoid
origin, typically causing solid tissue mass usually
in form of lymphadenopathy but may be
presented as extra nodal mass as in brain or
intestine.
Epidemiology of lymphomas
• 5th most frequently diagnosed cancer in
both sexes
• males > females
Causes of lymphoma
• Genetic alterations causing mutations in
chromosomes.
• Infection specially with viruses as
Human T- cell leukemia Lymphoma
virus , Epestein Bar virus.
• Immunosuppression
Pathogenesis of lymphoma
• There is monoclonal expansions of
lymphocytic cells at certain developmental
stages either of the :
(1)immature type which arise from lymphoblast
.
(2) the mature type which arise from
lymphocyte.
WHO classification of
lymphoid neoplasms
• B cell neoplasm.
• T cell neoplasm.
• Hodgkin lymphoma.
B-CELL NEOPLASMS
(A)Precursor B cell Iymphoblastic leukemia/
Iymphoma
(B)Peripheral B-Cell Neoplasms
• B-cell chronic Iymphocytic leukemia/small Iymphocytic
Iymphoma .
• lymphoplasmacytic lymphoma
• Mantle cell Iymphoma:
• Follicular Iymphoma
• Marginal Zone B-cell Lymphoma of mucosa-associated
Iymphoid tissue (MALT) type
• Hairy cell leukemia
• Burkitt Iymphoma
T-CELL NEOPLASMS
(A)Precursor T cell lymphoblastic
leukemia/lymphoma .
(B)Peripheral T-cell and NK-cell neoplasms
• Aggressive NK cell leukemia
• Nasal and nasal-type NK/T cell Iymphoma.
• Mycosis fungoides .
• Angio-immunoblastic T-cell Iymphoma.
• Adult T-cell leukemia/lymphoma (HTLV1+).
• anaplastic large cell Iymphoma (ALCL) .
Lymphoma are classified according to the
presence or absence of Reed sternberg cell
(R.S)into:
• (1) Hodgkin lymphoma which have R.S
cell.
• (2) Non Hodgkin lymphoma which have
no R.S cell.
Reed-Sternberg cell
Risk factors for NHL
•
•
•
•
immunosuppression or immunodeficiency
family history of lymphoma
infectious agents
ionizing radiation
Sites for non Hodgkin
lymphoma
• A- Nodal lymphoma start in the lymph
nodes.
• B-extra nodal lymphoma:
- intestine
- Central nervous system
- Skin
- Brain
- testis
- spleen
- ovary
Clinical manifestations
• Variable
• severity: range from asymptomatic to extremely ill.
• Systemic manifestations
• weight loss, anorexia.
• Local manifestations
• lymphadenopathy, splenomegaly most common
• any tissue potentially can be infiltrated
Diagnosis of lymphoma
• A- gross examination
• B- microscopic examination: requires
an adequate biopsy before treatment is
initiated So we do :
- Haematoxylin and eosin stained sections.
- immunohistochemical stained sections using tumor
markers.
Gross picture for intestinal
lymphoma
Microscopic picture of Non
Hodgkin lymphoma
• Lost normal histologic architecture of the lymph
nodes.
• Diffuse infiltration of the lymph node by
monoclonal type of malignant lymphocytes.
• Immunohistochemical staining can help in the
diagnosis as:
- T cell lymphoma are +ve for CD3.
- B cell Lymphoma are +ve for CD20
Microscopic picture of reactive
lymphoid follicles
Non Hodgkin Lymphoma
(H&E)
Both c&d show little inflammatory cell infiltrate in the intestinal
mucosa associating intestinal inflammation
Intestinal lymphoma
Immuno-histochemical diagnosis for NHL using
CD20 for B cell lymphoma
Hodgkin lymphoma
Thomas Hodgkin
(1798-1866)
Classical Hodgkin Lymphoma
Epidemiology
• less frequent than non-Hodgkin
lymphoma
• overall M>F
• peak incidence in 3rd decade
Associated (etiological?)
factors
• Epestein Bar Virus infection.
• May associate Human Immunodeficiency Virus
infection.
• possible genetic predisposition.
Hodgkin lymphoma
• cell of origin: B-lymphocyte present in germinal
centre can change to Reed-Sternberg cells (or
RS variants) which is the malignant cells but
the other surrounding white blood cells in the
affected lymph node are reactive cells
( polyclonal) not neoplastic cells.
Hodgkin lymphoma
Reed-Sternberg cell
A possible model of
pathogenesis
transforming
event(s)
EBV?
loss of apoptosis
cytokines
germinal
centre
B cell
RS cell
inflammatory
response
Microscopic picture of
Hodgkin lymphoma
• Lost normal histologic architecture of the lymph
nodes.
• The only malignant cells is the classic Reed
sternberg cell or one of its variants.
• But the surrounding cells for the RS cells are
reactive and not malignant.
• Immunohistochemical staining can help in the
diagnosis as:
- R.S cell is +ve for CD15, CD30.
HODGKIN LYMPHOMA
(Hodgkin's Disease) are
further subclassified into :
(A)Nodular lymphocyte predominance Hodgkin
Iymphoma.
(B) Classical Hodgkin Iymphoma which include:
• Nodular sclerosis .
• Classical Hodgkin lymphoma, lymphocyte-rich.
• lymphocyte depleted.
• Mixed cellularity type.
RS cell and variants
classic RS cell
lacunar cell
(mixed cellularity
Hodgkin lymphoma)
(nodular sclerosis
Hodgkin lymphoma)
popcorn cell
(lymphocyte
Predominance
Hodgkin lymphoma)
Clinical manifestations:
• lymphadenopathy
• extranodal sites relatively uncommon
except in advanced disease
Staging of lymphoma to identify the degree
of spread of Hodgkin lymphoma
Stage I
Stage II
Stage III
Stage IV
A: absence of B symptoms
B: fever, night sweats, weight loss
complications of lymphoma
• bone marrow failure due to infiltration.
• CNS infiltration
• compression of structures (e.g spinal
cord, ureters)