Surgical Pathology Criteria

Diffuse Large B Cell Lymphoma

Differential Diagnosis

Reactive immunoblastic processes may simulate DLBCL


Kikuchi lymphadenitis may simulate DLBCL


Burkitt Lymphoma Diffuse Large B Cell Lymphoma
Starry sky macrophages present Starry sky pattern infrequent
Fine chromatin Vesicular chromatin
Multiple small nucleoli Few, prominent nucleoli
Uniform cells Heterogeneous cells
Ki67 nearly 100% Ki67 moderately high
Translocation involving myc gene 15% of cases have myc translocation
Generally only a problem if cytologic detail is obscured by processing related artifacts


Lymphoblastic Lymphoma, B or T DLBCL
Median age 17-20 years Median age 60 years
90% T lineage, 10% B lineage B lineage
Starry sky macrophages present Starry sky pattern infrequent
Fine chromatin Vesicular chromatin
None or small nucleoli May have prominent nucleoli
Uniform cells Heterogeneous cells
Generally only a problem in suboptimally processed specimens


Diffuse Mixed Lymphoma DLBCL
50-75% of cells are small atypical B cells Over 50% large atypical B cells
No confluent foci of large cells Confluent foci of large cells
In T cell rich B cell lymphoma, the background small cells are T lineage


Diffuse Large B Cell Lymphoma Paraimmunoblastic SLL/CLL
Nuclear shape variable Nuclei round, uniform
Nucleoli frequently multiple Nucleoli single
Cytoplasm may be basophilic Cytoplasm pale
Node capsule frequently destroyed Node capsule preserved even if overrun
CD5 rare CD5 80%


Sporadic Diffuse Large B Cell Lymphoma SLL/CLL with Large Cell Transformation
No history of SLL/CLL History or concurrent SLL/CLL
CD23 negative CD23 85%
CD5 negative CD5 80%
CD43 rare CD43 60-80%


Plasmablastic Lymphoma Immunoblastic DLBCL
Typically oral cavity mass in HIV+ patient Wide variety of presentations, including HIV
LCA negative or minimal + LCA >90%
CD20 minimal to negative, CD79a positive Both CD20 and CD79a >90%
Ki67 >95% Ki67 moderately high, variable
EBV in situ 50% EBV in situ rare in de novo cases; frequent in immunodeficiency cases
CD138 positive CD138 negative
Amphophilic cytoplasm and pleomorphic nuclei with prominent nucleoli may cause difficulty with distinction of plasmablastic lymphoma from immunoblastic large B cell lymphoma


Both may partially replace the node and be negative or minimally reactive for CD20 and CD45RB
Diffuse Large B Cell Lymphoma KSHV-associated Germinotropic Lymphoproliferative Disorder
Typically effaced architecture Overall nodal architecture preserved
Typically sheets of large atypical cells Follicular pattern
HHV8 and EBV negative except in immunosuppressed patients HHV8 and EBV positive


Diffuse Large B Cell Lymphoma True Histiocytic Lymphoma
Variable cytoplasm Abundant cytoplasm with erythrophagocytosis
Most over 30 years of age Most under 30 years
CD20, CD79a positive CD20, CD79a negative
CD68, CD15, CD163, Lysozyme, CD138 negative or rare CD138+ or at least two of: CD68, CD15, CD163, Lysozyme


Classical Hodgkin Lymphoma Diffuse Large B Cell Lymphoma
CD45RB, CD20 and CD79a 10-20% CD45RB, CD20 and CD79a >90%
CD15 80% CD15 5%
CD30 90% CD30 30%
Light chains polytypic or negative Light chains monotypic or negative
Reed-Sternberg cells are frequently positive for both kappa and lambda, apparently due to nonspecific uptake of serum immunoglobulin


Lymphocyte Predominant Hodgkin Lymphoma Diffuse Large B Cell Lymphoma, T Cell Rich B Cell Variant
Background small cells B lineage Background small cells T lineage
CD57+ small cells increased No increase in CD57+ small cells
CD57+ rosettes around large cells No CD57+ rosettes
Large cells EMA 50% Large cells EMA negative


Primary Systemic Anaplastic Large Cell Lymphoma Anaplastic Variant Large B Cell Lymphoma ALK Positive Large B Cell Lymphoma
Marked anaplasia Marked anaplasia Monomorphic with round nuclei
Frequently sinusoidal Frequently sinusoidal Frequently sinusoidal
CD30 >90% CD30 variable CD30 negative
EMA 60% EMA 33% EMA positive
T lineage B lineage B lineage
ALK immunohistology 60-85% positive ALK immunohistology negative ALK immunohistology 100% positive
Majority of ALK positive cases show ALK translocation such as t(2;5) or t(1:2) Lack ALK translocation Rare cases reported with clathrin-ALK t(2:17) gene rearrangement
ALCL may lack T markers and require genetic analysis to determine lineage

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