Lymphoma is a cancer of lymphocytes. The most common place for abnormal lymphocytes is in lymph nodes (glands) particularly under the arms, in the neck and in the groin. Lymphoma is solid tumors of the immune system arising from cells of lymphoid tissues; lymphocytes, histiocytes, and reticulum cells. It can happen anywhere in the immune system, but usually in lymph nodes, spleen, marrow, and tonsils. Location and the behavior of lymphomas separate them from leukemia.The malignancy starts and restricted to lymphoid tissues and progress to involve the BM and appears in PB, at this stage it may be named, “lymphosarcoma cell leukemia.

1. By
Mojgan Talebian
1

2.  Solid tumors of the immune system
 Arise from cells of lymphoid tissues;
lymphocytes, histiocytes, and reticulum cells
 Anywhere in the immune system, but usually
in lymph nodes, spleen, marrow, and tonsils
 Location and the behavior of lymphomas
separate them from leukemias
 The malignancy starts and restricted to
lymphoid tissues and progress to involve the
BM and appears in PB, at this stage it may be
named, “lymphosarcoma cell leukemia”
2

3. A heterogeneous disorder
• Hodgkin lymphoma or Hodgkin disease
• Lymphocytic lymphomas or referred to as non-
Hodgkin’s lymphoma (NHL’s), most cases are fatal
3

4. Based on the following categories
• Physical examination, measurement of the
enlarged lymph node/spleen
• Bone marrow examination, Aspirate/biopsy
• Radiology studies/CT scans
• Hematology studies
• Chemistry tests; pr electrophoresis, kidney and
liver function tests
• Lapratomy to determine the spread of the disease
• Lymph node biopsy/histological features
4

5.  Stage I
 only 1 lymph node area or lymphoid organ (I)
 1 area of a single organ outside of the lymph system (IE)
 Stage II
 on the same side of the diaphragm(above or below)
 in 2 or more groups of lymph nodes ( II)
 extends from a single group of lymph node(s) into a nearby organ
(IIE)
 Stage III
 in lymph node areas on both sides of (above and below) the
diaphragm
 It may also have spread into an area or organ next to the lymph
nodes (IIIE), into the spleen (IIIS), or both (IIISE).
 Stage IV
 spread outside the lymph system into an organ that is not right next
to an involved node.
 spread to the bone marrow(IVM ) , liver ( IVL), brain or spinal cord, or
the pleura (thin lining of the lungs
5

6. A, asymptomatic
B, presence of any or all of the following
signs:
• Greater than 10% of total body weight loss in the
last 6 months
• Unexplained fever above 38° C, night sweats
6

7.  A malignant lymphoma with clonal proliferation
 Unknown etiology
• majority of cases both classical HL(CHL) and nodular
lymphocyte predominant HL(NLPHL) are clonal
proliferation of B cells
• may caused by infectious transmission in the host:
 Epidemiologic evidence
 Presence of two peaks period of onset
 Recovery of the EB Virus DNA from “lesions of approximately
80% of cases of HL”
 certain RNA tumor viruses
 CMV, herpes virus 6
 Presence of Reed-Sternberg cells accompanied
with H-cells (malignant histiocytes), these cells are
surrounded by lymphocytes, plasma cells, and
eosinophils
7

8.  The hallmark of the HL
 Very large cells, 50 -100 µm, irregular with
abundant pale acidophilic cytoplasm, usually
with 2 lobulated nuclei each contains a
gigantic azurophilic nucleolus with a
perinuclear halo
 The usual immunophenotypes: CD45-
,CD30+, CD15+
 These cells can be found in other diseases:
Rubella, EBV, IMN, Toxoplasmosis, T-cell
lymphoma, multiple myeloma
8

9.  Classical
 Lacunar
 Popcorn cells
 Sarcomatous
 Each type of these variants is associated with a specific histological type of
HL
 Immunophenotypes:
• More types of RS cells are HLA-DR + expressing T-cell null lineage
 receptors for IL-2(CD25+),
 CD13 +, CD15+, CD45-,CD30+
 Not reactive to B-cell antigens
 Clonal T-cell rearrangement
 T zone distribution
 Lymphocyte predominant form of HD
• RS variant typically displays Pan B-cell antigens, tendency of invasion to
B-cell area
• Some RS variants have feature of monocyte-macrophage lineage;
phagocytic and contain lysozyme and alpha -naphthyl esterase
9

10. 10
Mononuclear Hodgkin cell
L& H (popcorn cell)
Characteristic cell in NLPHL
Pleomorphic Reed-Sternberg cell
Lacunar cell

11.  Histological classification of HD is based on
histological examination of a lymph node
 Rye classification system is a modification of
Lukes and Butler system
• Lymphocyte predominant, * WHO recognizes it as a
distinct form of HD
• Nodular sclerosing
• Mixed cellularity
• Lymphocyte depleted
* Each classification is based on: the amount of
Lymphocyte presents, the type of RS cells, and the
degree of fibrosis
11

12. Lymphocyte predominant
Classic HD
• Nodular sclerosing
• Mixed cellularity
• Lymphocyte rich
• Lymphocyte depletion
12

13.  Patients: usually young, asymptomatic and commonly in stage I or II,
good prognosis
 The lymph node:
• Small lymphocytes, mature B-cells
• Varying number of histiocytes
• A few plasma cells
• There is no: neutrophils, eosinophils, necrosis and fibrosis
• RS variant cells: Popcorn cells/L&H cells in large numbers:
small cells with lobulated nuclei and small nucleoli
• L&H cells relates to proliferating germinal center (centroblast)
cells
• Intra-follicular pattern
• B cells; CD30+ and CD15-
13

14.  Two types of LP
• Nodular pattern
 Malignant cells surrounded by lymphocytes
 Male predominant
 In younger patients
• Diffuse pattern
 Cluster of malignant cells surrounded by loosely arranged
non- malignant reactive T cells
14
NLPHL
http://www.pathpedia.com/

15.  Common type of HD, 60% to 80% cases of HL
 More common in female patient less than 50
 Invasion to mediastinum
 Good prognosis because of the patient’s fibrogenic defense
 Lymph node:
• Histological pattern: follicular, birefringent collagenous sclerosis
• Nodules of H-cells
• Variable number of lymphocytes separated by thick bands of collagen
• T, B, Null cells; CD30+ and CD15+
• Classic Reed-Sternberg cells
• Lacunar RS cells
 An empty space /lacuna around the nucleus
Because of cytoplasm shrinkage during
formalin fixation
15

16. 16
Nodular Sclerosis HL, Collagen bands between the lymphoid tissue

17. • 15% to 30% cases of HL
• Patients usually present in stage III or IV, poor prognosis
 Heterogeneous mixed Cellularity:
• Diffuse or follicular histologic pattern
• Neoplastic cells outnumber the reactive cells
• Numerous classical RS and RS variants
(mononuclear)
• Lymphocytes, macrophages, eosinophils and plasma
cells, histiocytes
• Presence of fibrosis but no collagen
• T, B and Null cells;CD30+ and CD15+
17
MCHL

18. 5% of HL cases
Rich in small lymphocytes
• Small numbers of classic RS and H cells
• Clinical and pathological features more close to
Mixed Cellularity HD
18

19.  Rarest (<1%) and the most aggressive form of HD
 In older patients or HIV Positive, median age 35
 Presents in stage III or IV, the poorest prognosis
 Lymph node:
• Diffuse and fibrotic pattern
• Large numbers of RS (sarcomatous variants) and H cells
• Rare lymphocytes in fibrotic stroma
• Large and bizarre neoplastic cells
• Irregular sclerosis
• Unknown cells; CD30+ and CD15+
19

20.  In young adult and after the age of 60:
• Lymphadenopathy
 Non-painful lymph node swelling
• Weight loss
• Fever, night sweats, fatigue
• Mediastinal involvement, in 60% of cases
• Supraclavicular area invasion; distension of the neck
• Pruritus and purpura; less common
• Paralysis as a result of spinal/nerve compression
• Suppressed cellular immunity because of the disease
and therapy; viral, fungal and protozoan infections
• Extranodal involvement is common in
• and NSHL
20

21. Normochromic normocytic, mild anemia,
sometimes development of autoimmune
hemolytic anemia
Slightly increased leukocyte, neutrophilia
Lymphopenia is common
Increased ESR
BM involvement is focal and associated
with fibrosis, more seen in advanced
stages
21

22.  Significant percentage of patients treated successfully
 Chemotherapy
• for patient in stage II and above or not cured by radiotherapy
 Radiation therapy
• Best choice for patients with good prognosis; localized lesions,
asymptomatic ,and at stage IA
 Mantle field
 Inverted Y field
 Combination of mantle and inverted Y, Total Nodal Irradiation TNI
22

23.  Most commonly chemotherapeutic regime used:
ABVD
 Adriamycin, inhibiting replication and transcription
of DNA
 Bleomycin, breaking single and double stranded
DNA
 Vinblastine, disrupting mitotic spindles; BM
suppression
 Dacarbazine, interfering with DNA synthesis
• 4 cycles of ABVD for patients with early stages
• 6 to 8 cycles of ABVD for more advance disease
• For lesions greater than 10cm a combination of
ABVD and radiotherapy
23

24.  Solid tumors of the immune system
 Mostly B-cell lineage (in the follicles of the
lymph nodes),85% to 90% of lymphomas
 T-cell/NK about 10% to 15% lymphomas
 Histiocytic/dendritic cell lineage about <1%
 3-5% of all malignancies in modern countries,
seventh most common malignancy
 Average age 60 yrs-old, more common in
men
24

25.  Three major anatomical regions of a lymph node: Cortex,
paracortex, and medulla
 Cortex: B-cells, macrophages, plasma cells, and reticular cells
• Primary follicles, predominant cells are small B cells
• in response to antigenic stimulation primary follicles convert to
Secondary follicles (germinal center surrounded by a crescent of B
cells named mantle zone):
 Germinal center : centrocytes (resting B cells), centroblasts ( proliferating B
cells), dendritic cells, and histiocytes/macrophages
 Starry sky of the germinal center is because of the pale large macrophages
 Paracortex: mostly T cells, endothelial venules for entry of
circulating lymphocytes into the lymph node parenchyma
 Medulla: T cells, B cells, macrophages, and plasma cells
25

26. 26

27.  Well differentiated lymphocytes
• T or B-cells
• Small cells
• Small non-cleaved; plasmacytoid B-cells, B-
centrocytes
• Small and large cleaved cells
 Poorly differentiated lymphocytes
• T or B-cells, immunoblasts
• T or B-cells, centroblasts
• B-cell large non-cleaved cells
 Macrophages
27

28.  Classification is based on:
• Histologic pattern
• cell size
• Nuclear characteristics; cleaved or non-cleaved, convoluted or cerebriform
• Immunophenotypes
 Keil classification
• Morphology
• Immunophenotyping
 Luke and Collins system
• Immunophenotyping
 The Rappaport system
• Growth pattern
• cytological characteristics
 Revised European/American Lymphoma or REAL classification
• Clinical features
• Immunophenotypes
• Genotypic features
 WHO classification of tumors of lymphoid tissues
• Modified form of the REAL classification
• The classification includes NHLs, and all lymphoid neoplasms ; leukemias, HD and
plasma cell dyscrasia
28

29.  B cell Neoplasms
• Precursor B cell neoplasm
 Precursor B lymphoblastic leukemia/lymphoma
• Mature B-cell neoplasms
• B cell proliferations of uncertain malignant potential
 T-cell and NK-cell neoplasms
• Precursor T cell neoplasms
 Precursor T lymphoblastic leukemia/lymphoma
• Mature T cell and natural killer neoplasms
• T cell proliferation of uncertain malignant potential
 Hodgkin Lymphoma
 Histiocytic and dendritic cell neoplasms
 Posttransplantation lymphoproliferative disorders (PTLDs)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109529/table/T1/
29

30.  The majority of lymphoblastic lymphomas are T cell type (85%
to 90%)
 Solid tumor most commonly relative to T-cell ALL, small
percentage as pre-B cells
 Mostly in older male children, young male adults
 Lymph node involvement and < 25% blasts in bone marrow
 Malignant cells at early stage of thymic T-cell differentiation;
TdT+, CD7+, CD2+, CD5+, CD4+/CD8+
 CD3 expression is lineage specific
 Non- T-cell Ags expression:CD79a, CD13, and CD33
 A high risk disease
 Mediastinal involvement is common
 Infiltration to BM and CNS is common
 Bone lytic lesions is common in B- cell LBL
30

31.  B cell lymphomas
• Precursor B cell lymphomas , uncommon (<1% of
NHLs)
• Mature B cell lymphomas, 90% of all lymphoid
neoplasms
 Most common in developed countries
 Predominant in older adults, 60 yrs
 Some of the subtypes of Mature B cell lymphomas :
 Follicular lymphoma
 Diffuse large B cell lymphoma
 Burkitt lymphoma
 CLL/Small Lymphocytic lymphoma
 Marginal Zone lymphomas (MALT lymphomas)
31

32.  40% of NHLs and majority of low grade lymphomas
 (partially) follicular growth pattern with two principal cell types in the
germinal center:
• Centrocytes (cleaved cells)
• Centroblasts (large noncleaved cells)
• the malignant follicle
 the absence of a well- developed mantle zone
 the absence of tingible body macrophages
32
Secondary follicle (benign)
Dark and Light Zone, Mantle Zone
Tingible body macrophages
(arrows)
Follicular Lymphoma
Poorly defined mantle zone
Lack of polarization into
dark and light zones

33. Chromosomal Translocation:
• t(14;18) in 70% to 95% of cases of follicular
lymphoma, involving BCL2 and IgH gene
Immunophenotype of follicular lymphoma:
• sIg+
• B cell associated Antigens: CD19+, CD20+, BCL-
6+, CD10+, CD5-, CD23-, CD43-, CD11c-,
33

34.  The most common type of NHL worldwide 30%
 Starts de novo or as an advanced phase of a pre-
existing B-cell lymphoma; cloned B cells of large
size
 Patients average age; 50 yrs old, male/female
 At the time of diagnosis the disease is mostly
limited to one side of the diaphragm, but has the
ability to infiltrate to extranodal sites
(gastrointestinal tract)
 Presence of sclerosis in cleaved cell variant
 Large mononuclear cells
• Mostly B cell centroblast; CD5-, CD10-
• Large nucleus cleaved or non-cleaved
34
DLBCL a mixture of large B cells: Centroblastic,
immunoblastic , and pleomorphic morphology

35.  Highly aggressive and rapidly fatal but potentially curable
 the doubling time of the lymphoma is the highest of any tumor
 chromosomal rearrangements of the c-myc oncogene
 Associated with AIDS and transplant recipients
 Median age 7 yrs old, male-to female ratio approximately 2.5 to 1
• Translocation of t(8;14) in majority of cases
 Two forms of the disease;
• Endemic, tropical Africa and New Guinea, cells are positive for EBV genome, accompanied by
tumors in the face and jaw, an early B cell origin of the lymphoma cells
• Non-endemic/sporadic, median age of 11 yrs old, negative for EBV genome, and in
immunocompromised patients (AIDS),tendency to Payer's patches and abdominal areas
(abdominal mass), the latter stage of B cell development
 Burkitt’s lymphocytes:
• Moderate size cells with small uniform nuclei and many prominent nucleoli
• High mitotic rate
• Lipid vacuoles in the cytoplasm on smears or imprint of the tissue
• “Starry sky” pattern is because of phagocytosis of apoptotic debris
• Morphology of the cell types in Romanowsky staining is ALL L3
• Immunophenotype : CD10+, sIgM+, CD5-, CD23-, Bcl-2-, TdT-
35

36. • Solid state version of B cell CLL
• B cell lineage with surface IgM; CD5+ (a T-cell Ag), CD19+,
CD20+, CD22+, CD23+, CD43+
• B-cell SLL cells with plasmacytoid differentiation lack CD5
• 80% of SLL exhibit clonal cytogenetic abnormality, del
13q14 (50%)
*presence of CD5 distinguishes these lymphomas from the
follicular type,
• Malignant cells spread to other parts of body through
bloodstream, BM involvement seen
• tendency to turn into more aggressive lymphoma
• Growth centers (pseudofollicular pattern) are composed of
prolymphocytes and paraimmunoblasts cells
36

37.  Median age 60 yrs old, more common in females
 A low grade neoplasm, localized at the time of diagnosis
 The extranodal MZL; lung, stomach, thyroid, eyes, lungs, salivary glands,
stomach; lymphomas of mucosal-associated lymphoid tissue (MALT),
associated with chronic Ag stimulation; autoimmune disease (Hashimoto's
thyroiditis, and Sjogren's syndrome) or infections like Helicobacter pylori
gastritis
 Lymph node-based MZL: in patients with autoimmune disorders e.g.
Sjogren’s syndrome or coexistent extranodal type of marginal zone
lymphoma
 Lymphoepithelial lesions is a constant feature of this lymphoma
 Follicular colonization, the neoplastic cells infiltrate the reactive follicules
 B- cells
• Marginal zone B-cells, centrocyte-like cells (small cleaved cells)
• monocytoid lymphocytes: in lymphoid sinuses and paracortex of some reactive lymph
nodes but not normal lymph nodes
• Plasma cell differentiation is common
• Cells are; sIg+, cIg+, CD10-, CD19+,CD23- and CD43+
37

38.  Mostly in elderly male patients
 Involvement of lymph nodes and spleen
 Aggressive neoplasm
 Lymphomatous polyposis:
• Presentation of MCL in intestine
 Small to medium size B- cells
• originate at germinal center
• Forma a mantle zone around the benign germinal
center
• sIg+, CD19+, CD5+, and CD43+, CD10-
• Translocation of t(11;14)in most cases, involving the
BCL1 proto-oncogene and immunoglobulin heavy-
chain gene
38
Normal lymph node

39.  12% of NHLs worldwide
 Among the most aggressive of hematolymphoid
malignancies
 Divided to mature and precursor types; precursor T-
cell lymphoma is identical to T-cell acute lymphoblastic
leukemia
 Mature T-cell/NK cell lymphomas, the mature T-cells
are mostly differentiate into CD4+ or CD8+
• Three patterns of clinical features in mature T/NK cell lymphoma:
 Nodal presentation e.g.:
 Peripheral T-cell lymphoma, not otherwise specified
 Anaplastic large cell lymphoma
 Extranodal presentation e.g.:
 Primary cutaneous anaplastic large cell lymphoma
 Leukemic/disseminated
39

40. • 50% of the mature T/NK cell lymphomas
• A disease of adults but some cases is in childhood
• Predominantly nodal presentation, with
extranodal sites involvement
• Lymphoma cells
 Polymorphous mixture of atypical small, medium, and
large sized cells mix with variable numbers of reactive
cells ( Eos, plasma cells and macrophage)
 Mature T-helper phenotype:CD3+, TdT-, CD4+, and
CD8-, however some phenotypes show CD8+ with
CD4+/-
40

41. • Mostly in children and young adults
• A nodal based lymphoma
• Rare CD30+ (Ki-1ag) lymphoma cells
• Translocation t(2;5) leads to expression of the ALK-
NPM protein
• Expression of epithelial membrane antigen (EMA)
leads to confusion with carcinoma
• Clonal rearrangement of T cell receptor, in 90% of
cases
• Heterogenous cells with variable number of distinctive
kidney/horseshoe-shaped large cells and
juxtanuclear eosinophilic inclusion – like zone next to
the nucleus
41http://imagebank.hematology.org/

42. Dysplastic and malignant T-cell
proliferations
A tendency for infiltration of the skin
Disorders:
• Mycosis fungoides and Sezary syndrome:
 Infiltration of the dermis and epidermis by malignant T-
cells with cerebriform nucleus
• Lymphomatoid papulosis
• Primary cutaneous anaplastic large-cell lymphoma
42

43. Three clinical phases:
• Premycotic (erythroderma) phase, 6 months to 50
yrs, with eczematous dermatosis because of T-cell
infiltrate
• Formation of plaques, plaque stage
• Tumor nodules, tumor stage
Systemic dissemination develops in the later stages
As a terminal event transformation to a large cell
lymphoma
Prognosis is good and > 10 yrs, except for
extracutaneous spread with a survival rate <1 year
43

44. In the early erythroderma stage, leukemia
of the cerebriform T cells (Sezary cells)
Tumor stage is unusual in Sezary
syndrome
44

45.  Two types of Sezary cells;
1. Larger than mature small lymphocytes, dense chromatin
pattern, cerebriform, is deeply creased or grooved, and
lumpy
2. Atypical Sezary cell, large with convoluted nucleus ringed
by a string of cytoplasmic vacuoles
• Phenotyping; in 90% of cases Pan T +, CD4+, CD8-, in 10%
of cases CD8+, monoclonal TCR gene rearrangements
• Cytogenetic abnormalities present but not specific
45

46.  In early stages; patchy, scaly or generalized
reddening areas of skin, itching
 Skin infections (fungal) secondary to
scratching and ulceration
 Tumor like lesions, plaques (raised circular
patches of skin)
 Diagnosis
• Histology of the infiltrated skin areas: malignant
Sezary cells in clusters known as Pautrier’s
microabsecesses
• Presence of Sezary cells in PB
• Lymph node biopsy in the case of lymphadenopathy
46

47. Topical chemotherapy ( nitrogen mustard ,
steroid creams)
Radiation therapy, electron beam
irradiations
Photo chemotherapy, psoralin
(methoxsalen), UVA
For advanced stages of the disease;
topical therapeutic combined with
systematic chemotherapy
47

48.  Infiltrating the skin, most often head and neck as red and
purple nodules
 Lung
 Gastrointestinal involvement in lymphomas around abdominal
area, mostly in stomach and the small intestine; vomiting,
abdominal mass, diarrhea, GI bleeding, and obstruction;
diffuse large cell lymphomas
 Waldeyer’s ring; the oral cavity, maxillary sinuses, nasal
cavities
 Liver involvement
 Spleen, splenomegaly and as a result pancytopenia
 BM involvement, but lytic lesions of the bone is not common
 CNS involvement in high grade lymphomas, in Burkitt’s
lymphoma CNS involvement rate is high
48

49.  Blood cell counts normal
 Anemia due to replacement of marrow cells,
hypersplenism, AHA, GI bleeding, and therapy
effects
 Thrombocytopenia secondary to the above causes
 Lymphocytopenia depending to the stage of the
disease
 Invasion of lymphoma cells in 10% lymphomas
leads to absolute lymphocyte counts of 15.0 to
40.0 X 109 /L; usually in diffuse, small lymphocytic,
and the lymphoblastic lymphomas
49

50. Positive biopsy of BM indicates stage IV
BM involvement mostly in:
• Small cleaved cell lymphoma
• Mixed small cleaved lymphoma
• Large cell lymphoma
• Lymphoblastic lymphoma; nodular or focal pattern
50

51. Radiotherapy, most of lymphomas are
sensitive
• Hodgkin disease
• NHL
• Low grade lymphomas in the early stages
• Lymphomas in stage I
Chemotherapy
• CVP/CHOP ( Cyclophosphamide, Adriamycin,
Oncovin, vincristine, and prednisone)
51

52. 1. The tissue equivalent of CLL?
a. Diffuse large B cell lymphoma
b. Small lymphocytic lymphoma
c. Lymphoblastic lymphoma, precursor T cell
d. Lymphoblastic lymphoma precursor B cell
2.. Monocytoid B cells in the reactive lymph nodes particularly common in:
a. The HIV infection
b. Toxoplasmosis
c. MZL
d. All of the above
3. An anterior Mediastinal mass is often present in:
3. NSHL
4. NLPHL
5. MCHL
6. LR
4.The most aggressive form of HL:
a. Lymphocyte depletion
b. Lymphocyte predominant
c. Mixed cellularity
d. Nodular sclerosing
5. Identification of reed-Sternberg cell
a. Seen in a variety of malignant and benign conditions
b. With immunophenotyping techniques is no more a requirement
c. Finding the cells suggests the possibility of HL
d. All of the above
52

53. 6. Leukemia and lymphoma are in different categories because of their:
a. Location
b. behavior
c. a and b
d. non of the above
7. Which of the followings are hematologic finding in HD?
a. Eosinophilia
b. Neutrophilia
c. Lymphopenia
d. all of the above
8. In MALT lymphomas:
a. the malignant cells are T- cells
b. the malignant cells are monocytoid lymphocytes c. there is extranodal
presentation
d. b and C
9. In Burkitt’s lymphoma:
a. cell type is that of L3
b. Is EBV positive in sporadic form
c. Is HIV positive in endemic form
d. a and c
10. Sezary cells:
a. seen in PB of mycosis fungoides patients
b. Pan T +, CD4+, CD8-, monoclonal TCR gene rearrangements
c. Pan T +, CD4+, CD8-, poly clonal TCR gene rearrangements
d. a and b
53

54. 11. Infection commonly related to Hodgkin’s lymphoma:
a. Herpes
b. EBV
C. H. pylori
d. CMV
12. Cell feature in all types of classic Hodgkin’s lymphoma:
a. Sezary cell
b. Lacunar cell
c. Histiocytes
d. Reed-Sternberg cell
13. Asymptomatic Mediastinal mass is common in:
a. LD
b. MC
c. LP
d. NS
14. Small Lymphocytic Lymphoma is characterized by all of the followings except:
a. the tissue equivalent of CLL
b. growth centers
c. prolymphocytes and paraimmunoblasts are common
d. CD19+, CD20+, CD5-
15. BCl1 proto-oncogene AND IgH genes are associated to :
a. Mantle cell Lymphoma
b. Marginal Zone lymphoma
c. SLL
d. Burkitt lymphoma
54

55. 16.Burkitt’s lymphoma is histological characterized by:
a. Starry sky
b. high proliferation rate
c. uniform nuclei
d. a and b and c
17. A lymphoma of monoclonal B cells expressing CD10 and BCL2 gene is from:
a. mantle cells
b. marginal zone cells
c. inter-follicular cells
d. follicular center cells
18. Which one of the following is not a T cell disorder:
a. mycosis fungoides
b. Sezary syndrome
c. Burkitt’s lymphoma
d. Anaplastic Large cell lymphoma
19. Lymphoblastic Lymphomas are related to all the following except:
a. development to ALL
b. mostly are B-cell phenotype
c. potentially curable in young patients
d. Mediastinal mass
55

56. 20. The staging system for Hodgkin’s lymphoma and NHLs is:
a. Duke’s staging system
b. Rye staging system
c. Ann Arbor staging system
d. Working Formulation
21. Reed- Sternberg cells’ immunophenotyping:
a. CD45+, CD30+, CD15+
b. CD45+, CD30+, CD15-
c. CD45-, CD30+, CD15+
d. CD45-, CD30-, CD15+
22. The bone marrow involvement indicates which stage of lymphoma:
a. Stage II
b. stage IIIE
c. stage IIIS
d. stage IV
56

57.  1. b
 2. d
 3. a
 4. a
 5. d
 6. c
 7. d
 8. d
 9. a
 10. b
 11. b
 12. d
 13.d
 14. d
 15. a
 16. d
 17. d
 18. c
 19. b
 20. c
 21. c
 22. d
57

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