1. Lymphoma
DR: Gehan Mohamed

2. Learning objectives important types of lymphoma Clinical presentation
Diagnosis
Staging

3. Myeloproliferative disorders
ALL
Myeloma
CLL
Lymphomas
naïve
germinal center
B-lymphocytes
Plasma
cells
Lymphoid
progenitor
T-lymphocytes
Hematopoietic
stem cell
AML
Myeloproliferative disorders
Neutrophils
Eosinophils
Basophils
Monocytes
Platelets
Red cells
Myeloid
progenitor

4. Normal structure of reactive lymph node

5. Microscopic picture of reactive lymphoid follicles

6. 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.

7. Epidemiology of lymphomas
5th most frequently diagnosed cancer in both sexes
males > females

8. Causes of lymphoma
Genetic alterations causing mutations in chromosomes.
Infection specially with viruses as Human T- cell leukemia Lymphoma virus , Epestein Bar virus.
Immunosuppression

9. Pathogenesis of lymphoma
There is monoclonal expansions of lymphocytic cells at certain developmental stages either of the :
immature type which arise from lymphoblast .
the mature type which arise from lymphocyte.

10. WHO classification of lymphoid neoplasms
B cell neoplasm.
T cell neoplasm.
Hodgkin lymphoma.

11. 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

12. 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) .

13. 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.

14. Reed-Sternberg cell

15. Risk factors for NHL immunosuppression or immunodeficiency
family history of lymphoma
infectious agents
ionizing radiation

16. 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

17. 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

18. 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.

19. Gross picture for intestinal lymphoma

20. 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

21. Microscopic picture of reactive lymphoid follicles

22. Non Hodgkin Lymphoma (H&E)

23. Both c&d show little inflammatory cell infiltrate in the intestinal mucosa associating intestinal inflammation

24. Intestinal lymphoma

25. Immuno-histochemical diagnosis for NHL using CD20 for B cell lymphoma

26. Hodgkin lymphoma
Thomas Hodgkin
( )

27. Classical Hodgkin Lymphoma

28. Epidemiology less frequent than non-Hodgkin lymphoma overall M>F
peak incidence in 3rd decade

29. Associated (etiological?) factors
Epestein Bar Virus infection.
May associate Human Immunodeficiency Virus infection.
possible genetic predisposition.

30. 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.

31. Hodgkin lymphoma

32. Reed-Sternberg cell

33. A possible model of pathogenesis
loss of apoptosis
transforming
event(s)
EBV?
cytokines
germinal
centre
B cell
RS cell
inflammatory
response

34. 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.

35. 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.

36. RS cell and variants classic RS cell lacunar cell popcorn cell
(lymphocyte
Predominance
Hodgkin lymphoma)
(mixed cellularity
Hodgkin lymphoma)
(nodular sclerosis
Hodgkin lymphoma)

37. Clinical manifestations:
lymphadenopathy
extranodal sites relatively uncommon except in advanced disease

38. 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

39. complications of lymphoma
bone marrow failure due to infiltration.
CNS infiltration
compression of structures (e.g spinal cord, ureters)