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Rare, older than 30s with anemia, thrombocytopenia. Aggressive < 1 year survival affecting blood (>100K). Diffuse involvement of marrow and nodes, spleen (red pulp) and sometimes skin + or pleural effusion. Blood vessels invasion common. Proliferation medium sized lymphos with oval or round nucleus, nucleoli, basophilic cyto and blebs. Rare variants cerebriform cells (Sezary like) or small cells without nucleoli.

Immunohistochemistry, molecular and genetics:
Positive IHC: mature post-thymic: CD2+, 7+, 52+, CD3+ (if membranous weak) and TCL1 (antiapoptoic oncogene with px value to detect residual disease) . Negative: Tdt, CD1a. Most CD4+/Cd8-. Some CD4-/CD8+ or 4+/8+. TCR gene rearrangements clonal for the γ and B found. Abnormalities chromo 14, 8 or 11q23 by FISH(same of ataxia telangiectasia). Target therapy anti CD52 or transplant possible. 


Rare and indolent. Patient dies after many years due to neutropenia. Common in autoimmune disorders like reumatoid arthritis with abscence of homeostatic apoptosis and increase in FAS and seric FASL. Dx > 6 months blood clonal increase of large granular lymphocytes (LGL), between 2K and 20K, cytopenias, anemia and hepatospleno (red pulp involved). Rarely nodes +. Marrow may be hypo, normo or hypercellular with some reticulin fibrosis but < 50% cells are LGL. You also see frequent B cells surrounded by rims of CD4+ T cells. Look for abundant cyto with azurophilic granules containing perforins and granzymes. Differential dx: clonal expansion of LGL in HCL, CLL and after BM transplant.

Immunohistochemistry, molecular and genetics:
Most: 3+, 16+, 57+ (interstitial pattern in marrow). Other than CD8+, other markers showing cytotoxic phenotype are TCR alpha or B, TIA1, granzymes B and M. Common: CD94/KIR family, surrogate of clonality. Negative or weak: 5, 7. If CD8 neg may be rare phenotypes as gamma delta. Abnormal chromo: Nothing typical .


> 6 months with 2 -20K increase in NK cells without known cause. EBV should be neg (rule out virus, EBV, autoimmune, vasculitis, neuropathy, splenectomy and other solid or hematologic malignancy). Nk cells show increase basophilic cyto with azurophilic granules and look clear and interstitial in bone marrow, best seen with IHC. Most adults asymptomatic with only involvement of blood and marrow (cytopenias, hepatospleno, adenopathies or skin are rare).

Immunohistochemistry, molecular and genetics:
Most: cCD3, 8+,16+, 5+ (aberrant), 56+ (weak), CD94f/NKG2A, cytotoxic markers (TIA1, granzyme B and M ) Negative or weak: surface CD3, 2, 7, 57, 161, KIR family of NK cell receptors, EBV. Genetics: normal. No rearrengement of T cell receptors.


Fulminant EBV + process with 2 months survival. Common in middle age Asians with fever, high LDH and abnormal variable increase of abnormal cells in blood smears, often monotonous with some enlargement and folding in nucleus, basophilic cyto and azurophilic granules (rarely pleomorphic). Sometimes multiorgan failure with coagolopathy and hemophagocytic (look for histiocytes in marrow). Although suggested that this disease may be the aggresive counterpart of Extranodal NK/T cell lymphoma, skin involvement is rare, patients are younger with common marrow +, spleen + and CD16+.

Immunohistochemistry, molecular and genetics:
Common: CD2+, 56+, 11b, CD3Epsilon +, FAS ligand, TIA-1+, perforin+, granzyme B + ( in granules), 16+ (negative in Extranodal NK/T cell lymphoma), EBV+ by IHC (LMP-1) or ISH
Negative: CD5, 57,surface CD3. NK markers are non specific, so dx only possible after T cell excluded.
Genetics: Clonal EBV + disorder confirmed with X chromososme inactivation in female. Many cytogenetic abnormalities described. 


Previously healthy kid from Asia, Central or South America after primary acute or chronic EBV infection with mononucleolsis like syndrome for > 6 months and higher titers of capsid and early antigen to EBV. Probably due to genetic predisoposition. After oligoclonal expansion of NK cells (rarely showing important cytologic atypia), presents with fever and in few weeks fulminant systemic disease with hepatospleno, liver failure, adenopathy, marrow involvement, multiorgan failure, and sepsis. Liver and spleen involvement is sinusoidal and steatosis and necrosis possible in liver. Lymph nodes show sinus histiocytosis. Histiocytic hyperplasia and hemophagocytosis present in marrow and other organs.

Immunohistochemistry, molecular and genetics:
Common: 2+, 3+, TIA1+, CD8+ (after acute EBV infection), CD4+ after Chronic EBV infection. EBER +, LMP1 +, ISH EBER+. Rarely 4+/8+.
Negative: 56 -,
Genetics: Monoclonal rearrengment TCR. No typical chromosomal abnormalities.

Hydroa vacciniforme lymphoma like disease in kids.

Same geographic areas, genetically predisposed, with papulovesicular eruption in sun exposed areas. T cells and NK cells EBV infected. Sun predispose. Mosquito hypersensitivity. Very mild atypia in neoplastic cells. May persist for many years and evolve to systemic disease. Phenotype and genetic is similar.  


Adquired from blood and breast feeding and develop fter 20 y of latency. HTLV1+. Japan and Caribbean. May be acute, systemic and leukemic with marked leukocytosis and atypical cells, eosinophilia, rash, generalized adenopathy, hepatospleno, lytic bones, high LDH, pneumocystis or strongiloides. Lymphomatous, without leukaemia, only adenoapthies and rash. Chronic with only exema + mild lymphocytosis . Smoldering with normal WBC but > 5% neoplastic cells. High Calcium seen in acute form.
In chronic and smoldering form, lymphos appear almost normal. In acute and lymphomatous varies from small pleomorphic cells to large pleomorphic with anaplastic, lobulated, cerebriform, flower like or giant cells, with basophilic cyto. Lymph nodes may appear similar to Hodgkin. Skin look for perivascular with pautrier microabcesses. Most organs infiltration is diffuse. BM may be patchy. Short survival of months in acute and lymphomatous. Long survival of years in chronic and smoldering (may transform).

Immunohistochemistry, molecular and genetics:

Most: 2+, 3+, 5+, 4+, 30+(in large pleomorphic cells), FOXP3 + (regulatory T cell marker). Common: EBV+. Negative: CD7, 8, ALK. Rare: 4-/8+.
Genetics: T cell clonal rearrengement. Clonal integration of HTLV virus in disease. No integration in carrier. 


Asian, central or south american patient, some immunosupressed with NK or T cytotoxic phenotype (CD8) with high blood DNA titer for EBV (EBV+ type II latency pattern). Sites: Most extranodal with letal destruction an ulceration of midline involving nasal, paranasal, palate. Skin or GI ulcers and testes possible. Rarely disseminate to nodal or marrow with hemophagocytic. Bx look for angiocentric, angiodestructive, coagulative necrosis, apoptoic bodies. Neoplastic cells are mixed of small lymphos, plasma cells, eos, medium cells lymphoid cells with azurophilic granules and pleomorphic large cells. Marked pseudoepiteliomatous hyperplasia. Px variable, if extranasal or advanced stage. Very aggresive.

Immunohistochemistry, molecular and genetics:

Most: CD2+, CD3 Epsilon by IHC, CD56, EBER ISH +. Granular stain for TIA-1+, perforin+, granzyme B. Common: 43, 45RO, 25, 30, 7, HLA-DR, FAS ligand. Negative: surfaceCD3, cCD3, 4, 5, 8, 16, 57. Genetics: No specific abnormalities. TCR clonal rearrangement only in rare cases with cytotoxic T lymphocyte derivation. Remember that NK tumors are CD4−CD8− or rarely CD4−CD8+ (cytotoxic T lymphocyte derivation).

CD56 generally positive in NK cells. However:
Tumors CD3 epsilon +/CD56-/EBV+ is dx for extranodal NK.
Tumors CD3 epsilon +/CD56+/EBV - is a peripheral T cell lymphoma.
In other words, do not accept NK if EBER ISH negative, even if CD56+. EBER should be positive in most nuclei. 


Classic EATCL affect atrophic jejuno ilieum with celiac disease, most european patients HLA DQ2 +, ulcerated masses, perforation and abdominal pain. Large or middle size pleomorphic intraepitehelial lymphos with eosinophilic or clear cyto, background with eos, common necrosis. Type II enteropathy associated T cell lymphoma is a rare lymphoma not associated with celiac disease or DQ2, showing small round monomorphic cells and background withouth eos or necrosis. Both forms poor px.

Immunohistochemistry,molecular and genetics:

Positive in classic variant: CD3, 7, 30, 103 Negative: CD8, 56, 5, 4 Positive in type II variant: CD8, 56, 3 Negative in type II: CD4. All intraepithelial lymphos in adjacent mucosa share phenotype in both variants.

Genetics: Most type II and some classic are TCRB+. Many chromosomal abnormalities seen mainly in chromo 9 and 1.  


Very rare lymphoma in immunosupressed young adults (frequently posttransplant) with monotonous medium sized gamma delta cytotoxic T lymphos showing pale cyto, liver +, spleen sinusoids +(red pulp) and marrow +. No adenopathies. Anemia, leucopenia, thrombocytopenia, hepatomegaly, not necessarily spleno.

Immunohistochemistry, molecular and genetics:
Most:CD3+, TIA-1, granzyme M. Common: CD56. Negative: CD5, granzyme B. γδ T-cell tumors are CD4−CD8−or CD4−CD8+.
Genetics: Most are γδ T-cell origin. PCR used to evaluate γδ receptor ( not good by IHC). Rare cases are alpha beta. Common chromosomal abnormalities affect chromo 7


Very rare, young with subcutaneous nodules in extremities, some with lupus. Mixed cytopenias and hemophagocytic. No adenopathies. Hepatospleno possible. Atypical medium or large size T cell cytotoxic cells with pale cyto mixed with plasma cell and histios, infiltrating subcutaneous fat, similar to lobular panniculitis (not septal). Necrosis and apoptosis important features.

Immunohistochemistry, molecular and genetics:
Positive: CD8, granzyme B, perforin B, TIA1, T cell receptor alpha. Negative: EBV, CD56.
Differences with gamma delta T cell lymphoma : this tumor is alpha beta positive, gamma delta negative, CD56 negative, does not involve dermis and px is poor (however better than cutaneous gamma delta). 


Any age. Initially multiple indolent skin patches, then plaques and then nodules or tumors for years. In stage of plaque small to medium size cerebriform lymphos surrounded by halos along dermal epidermal junction and pautrier microabscesses (specific but least sensitive). In stage of nodule px is poor and shows diffuse dermal infiltration with or without epidermotrophism and mixed transformed large cells. Enlarge lymph nodes commonly show dermatophatic lymphadenopathy but early neoplastic infiltrate may happen. Rarely extension liver, spleen, lung.
Variants: 1) Folliculotropic variant around follicles head and neck worse px than early plaque. 2) Pagetoid reticulosis show plaques with loclaized dermoepidermal medium to large cerebriform cells CD4 or 8+ and CD30 often +. 3) Granulomatous slack skin: Indolent course with CD4+ cerebriform dermoepidermal cells + granulomas, most axilla and groin.

Immunohistochemistry, molecular and genetics:
Positive: CD4 and CD2. Variable loss of CD3, 7 and 5 (3 or 5 more significant and supportive of a T-cell neo than 7). Few CD30+ large transformed cells appear in tumoral stage . Strong CD30 in 20% of large cell transformation of MF. Rarely may be CD8+. Genetics: clonal T cell receptors in some. Variable chromosomal abnormalities.

Diff dxl: Primary Cutaneous CD4 positive small/medium T cell lymphoma: main difference with M Fungoides. Solitary plaque in head, neck or upper trunk without the characteristic patches of MF and it is more common in dermis or subcutis, rarely with minimal epidermotropism. Cells are small to median size with mild pleomorphism, mixed with some large cells, histiocytes and plasma cells.


Everything similar to Mycosis Fungoides including histology, phenotype and genetics. Differences: most in elderly, erythroderma (common involvement palm-plants-scalp), generalized adenopathy, visceral involvement, PB >1000 sezary cells/mm (cerebriform cells), CD4/8 ratio > 10/1. Marrow not always + or subtle interstitial infiltrate.  


Cutaneous anaplastic larce cell lymphoma (CALCL) favorable px, elderly, rare in kids. Do not include CD30+ transformation of mycosis fungoides or systemic ALCL involving skin. Solitary or multiple nodules anywhere in the skin. Rarely nodes +. Most anaplastic pleomorphic cells with eosinophilic cyto. If ulcerated, malignant CD30+ cells are isolated in rich infiltrate of PMNs, eos, histiocytes. IHC: Positive: CD4 and cutaneous lymphocyte antigen/CLA (neg in ALCL). Common: granzyme B, TIA1, perforin, 56+. Rare: CD8+. Negative: 2, 5, 3, 15, EMA, ALK. EMA and ALK + in ALCL. ALK neg in CALCL (chromo 2 translocation absent). Genetics: clonal T cell receptor rearrangement present in most.

Lymphomatoid Papulosis (LP) Adult with nodules anywhere (may include oral), self healing in 1 to 3 months, composed of small clusters of large cerebriform Hodkin CD30 cells mixed with PMNs, eos, histio and lymphos, or only large clusters of CD30+ without inflammatory background. Rarely epidermotrophic.

IHC: Both CALCL and LP CD3+, 4+, 30+. Most CD8 neg (rare CD8+). Genetics : Common clonal rearrengment of T cell receptors. t(2;5) not detected.


Rare. B symptoms and generalized tumors anywhere in skin or oral (common in extremities), medium to large lymphos dermoepidermal, dermal or subcutaneous panniculitis but gamma delta T cell receptors. Rarely extranodal. Hemophagocytic syndrome common. Px is poor, worst if subcutaneous.

Immunohistochemistry, Molecular and Genetics:
Positive:CD3, 2, 56. Negative: Both CD4 and 8, CD5 and 7, EBV, BF1 (beta F1).
Genetics: TCR gamma by IHC or PCR. May be infered with IHC showing abscence of BF1


Very rare in adults, agressive, poor px. Pagetoid with marked epidermotrophism and epidermal necrosis, ulceration, blisters. Tumoral cells may have any size from small to large. Angiocentricity .
IHC: Positive: CD8, 3, granzyme, perforin, TIA1. Variable +/-: CD45RA, CD2, 7. Negative: CD4, CD5, CD45RO, EBV. Genetics: T Cell Receptor rearrangements.


Adults. Poor px. Worse if EBV +. Wastebasket cathegory, for cases not classificable anywhere. Most systemic and advanced with fever, multiple nodes +, liver+, spleen + (red pulp), marrow +. PB may be +. If skin + dermoepidermal, dermal or subcutis. Hemophagocytic common. Diffuse proliferation of large pleomorphic or lobulated lymphos with clear cyto and abundant mitosis, mixed with inflammatory background with lymphos, plasma cells and eos ( if RS like cells present Hodgkin is in the diff dx). Vascular proliferation common. Abundant mitosis. Rarely, abundants epithelioid histiocytes obscure neoplastic cells.
IHC: Positive: Most are CD4+ but any combination of CD4/8 is possible. Ki-67 is high and BF1 +. Common: CD56 +. If CD30 positive, CD15 is expected negative. Commonly negative: CD5 and 7 downregulated. CD52 neg Rare: aberrant CD20 or 79a+. Diff dx with Angioimmunoblastic (AITL): AITL has follicuar T helper phenotype
clonal for T cell receptor Beta (correlate with IHC positive for BF1). Many chromosomal gains and deletions.

3 Variants of PTCL NOS:Lymphoepithelioid (Lennert) small irregular neoplastic CD8+ cells, mixed with clusters of interfollicular epithelioid histios and RS like, EBV+ Follicular variant: Paracortical, perifollicular of intrafollicular nodules . T Zone Variant: small paracortical lymphos with minimal atypia, CD3 and 4 + with downregulation of CD5 and 7. Diff dx with paracortical hyperplasia.

For more information about PTCL read chapter of comments below. 


It is common aggresive peripheral T cell lymphoma in midddle age. Related to PTCL NOS with similar histology and behavior. Fever, multiple nodes +, liver +, spleen + (red pulp), marrow +, PB may be + and sometimes skin. It may shows reumathoid factor +, arthritis, pleuritis, ascitis, hypergama, cold agglutinins and hemolityc anemia. Micro is polymorphic, paricortical with proliferation of endothelial veins and atypical cells with clear cyto in inflammatory background including eos.

IHC: Positive: CD4+, 2, 5. Follicular T helper phenotype with CD10+, BCL6+, and CXCL-13+ (perivascular and perifolicular). CXCL-13 also positive in reactive paracortical and follicular T cells, dendritic cells, histiocytes. FDC meshworks expanded (CD21, CD23, or CD35+). AILT may have some CD20+ large B cells RS like (hodgkin is in the differential). EBER is positive but not in neoplastic T cells (+ in CD79a cells). Negative: CD8. Reactive CD8+ cells present. Genetics: Clonal T cells rearrengement in some. Some trisomies and other alterations described.


Young patients with advanced systemic disease and fever. Common nodes+, skin+, bones+, soft tissue+, lung+, liver+. Rare CNS and mediastinum. 1/3 marrow +. Most common pattern show diffuse or sinusoidal multiple hallmark pleomorphic cells with kidney or horshoe nuclei and eosinophilic region near nucleus. Nuclear inclusions are common artefact. Other variant is lymphohisitocytic with rare hallmark cells mixed with abundant hystios and plasma cells. Another subtype show predominant small cells mixed with only rare perivascular CD30+ hallmark cells (blood may be + in this variant). Some cases resemble nodular sclerosis Hodgkin with fibrotic bands. Composite cases show mixture of patterns. Mulcinucleated pleomorphic, sarcomatoid or signet ring cells described.

IHC: Positive: EMA+, TIA-1+, granzyme B+, CD4+, 2, 5, 43 (CD2, 4 and 5 generally positive but Pan T loss possible). Strong and membranous monoclonal CD30 (membrane and cyto dot like golgi). ALK + generally nuclear and cyto if classic t(2;5) with NPM partner. If other partners (many variants) positivity may only be diffuse cytoplasmic. Common: CD45+, CD45RO+, CD15+. Negative: CD8, BCL2, EBV, CD3.
Comments: Some Immunoblastic DLBCL may be ALK + and EMA+ but they are CD30 neg. If marrow + bad px, seen in 15% ALCL (50% in small cell variants). Marrow + histology is subtle and require CD30+ and ALK-1+ to detect scattered tumor cells. ALK tests possible by IHC or FISH. Genetics:αβ TCR lost in ALCL. T(2;5). Other variant transslocations seen.


Similarities with ALK positive: Similar clinic and morpholoy (small cell variant not recognized). Positive in both: clonal T cell rearrengement, even if PanT markers lost. TIA-1 and perforin +, CD4+, 2+ , 5+ and 43+. CD30 + in both membranous and cytoplasmic. Lost in both: CD8. CD15 may be positive.

Differences with ALK positive:
Alk negative seen in older patients, maybe more pleomorphic with some eos in background, very difficult to differentiate from PTCL NOS. CD3 lost in most ALK positive but present in most ALK negative. EMA positive in most ALK +, negative in most ALK neg. Definitely worse px in ALK neg.

Comment: Some PTCL NOS may be CD30+ but not membranous in every single neoplastic cells. However differential dx between ALCL ALK negative and PTCL NOS is very difficult.


T Cell Phenotype: IHC αβ TCR + is dx of T cell and rule out NK. TCR gene rearrangement by PCR also differentiate cytotoxic T-cell and a NK. 15% T-cell neo lack TCR gene. Lack of TCR is not indication of NK.

EBV: Not only for NK cell leukemia. Important in PTLD, mononucleosis, immunoblastic/plasmablastic tumors, Burkitt, HL and AILT. IH detect latent membrane protein (LMP-1) and Epstein-Barr nuclear antigen (EBNA-2); ISH detect EBV-encoded RNA (EBER). In BL EBER is + but LMP-1 and EBNA-2 negative (type I latency). In HL EBER and LMP-1 are + and EBNA-2 negative (type II latency). In PTLD all markers + (type III latency). IH for LMP is specific but not a sensitive as ISH for EBV (best method). LMP or EBNA-2 are not required for EBV diagnosis.

CD7 : CD7 may be decreased or absent in Adult T cell lymphoma leukaemia, MF and skin reactive conditions. Normally expression of CD7 in paraffin is weaker than other T-cell antigens. Loss of CD3 or CD5 more significant and supportive of a T-cell or NK neoplasm.

15% T-cell neo lack TCR gene rearrangement. See Molecular genetic notes for T cell receptor alpha and gamma evaluation.

Clues to suspect T cell lymphoma? If CD3+ T cells increased, order CD4, CD8, CD2, CD5, and CD7. Markedly skewed CD4/CD8 ratio in absence of HIV or virus may indicate T cell lymphoma. Also loss of pan–T (CD2, CD3, CD5, CD7) and lack or dual CD4/CD8 expression.

Why T cell and NK cell neo is a difficult dx? Rare (only 10% of lymphomas), frequently extranodal with reactive look and mixture of large and small lymphos with inflammatory cells. No dx morphology or specific markers of T-cell clonality. Clonality may be attempted by IHC (TCR-Vβ gene by flow may suggest clonality but not widely used)

Definite evidence of T cell: CD3 best pan–T, + in and after 2nd stage of thymic differentiation. NK cells may express epsilon chain of CD3; expression of cytoplasmic CD3 not always evidence of T-cell . Surface CD3 by flow is definitive evidence of T-cell or + TCR protein αβ by β-F1 by IHC.

T cell subsets: CD4 (helper) and CD8 (suppressor, cytotoxic ) normal ratio is CD4/ CD8 = 1.5–3:1. In reactive lesions CD4 predominate. In HIV – patients or negative for viral infection, consider T-cell or NK-cell neo if extranodal site and marked increase of CD8+. CD5 is a pan–T, negative in NK. CD5 is not lineage specific, seen in some normal B cells, MCL, and B-cell tumors. If CD5 is + in B cell areas, rule out small B-cell neo. If CD5 – in T cell areas, rule out T-cell or NK lymphoma. Rare PTCLs CD20 + and/or CD79a +.

Immature T cell proliferation? Lack of TdT or CD34 . Precursor T-ALL/LBL CD10+ in 60% and some CD1a+ (second stage of thymic differentiation).

CD7: Some lymphomas like adult T cell leukemia/lymphoma and mycosis fungoides show lost of CD7, but this marker is also decreased in some skin reactive conditions. Normally expression of CD7 in paraffin weaker than other T-cell antigens. Loss of CD3 or CD5 more significant and supportive of a T-cell or NK neo.

CD4 and CD8 expression: Most T-cell lymphomas: MF, adult T-cell leukemia/lymphoma, AILT, ALCL, and PTCL are CD4+. Some CD4+ lymphomas (MF, ALCL) may be CD8+ . IHC panel for CD8 tumors is CD56, CD57, TIA-1, granzyme B, the αβ TCR protein (detected by β-F1) and EBER

CD4 CD8 negative γδ T-cell lymphoma, precursor T-ALL/LBL and rare T-cell lymphomas with aberrant T cell antigen loss. Autoimmune lymphoproliferative syndrome is a reactive polyclonal expansion of double negative T cells. There is no IHC antibody to detects γδ TCR protein. Absence of the αβ TCR protein (IHC negative for β-F1) is evidence of γδ. TCR gene rearrangement confirms a T-cell lineage. Both NK-cell and γδ T-cell malignancies are CD56+ and cyttoxic granule protein TIA-1+. Hepatosplenic γδ T-cell lymphoma lacks granzyme B due to nonactivated cytotoxic T-cell phenotype (granzyme B + in NK cell tumors).

CD30 and CD15: Neos expressing both CD30 and CD15 may be ALCL, ALK positive or negative, PTCL NOS or CHL. EBER + favor Hodgkin. CD30only may be + in infectious mono, drugs, bug bites, AITL, transformed MF, some DLBCL, HL, embryonal or pancreatic CA, mesothelioma. Most NHL some CD30+ cells. Melanoma and AML may be CD30 + but cytoplasmic (not membranous).

IH in necrotic tissues is not adequate for classification of lymphomas, it is reported that IH may be reliable in necrotic tissue only in some CD3+ lymphomas

Main References:
WHO classification of tumors of hematopoietic and lymphoid tissues
Russell A.Higgins, MD; Jennifer E Blankenship, MD; Marsha C Kinney, MD.Application of Immunohistochemistry in the Diagnosis of NonHodgkin and Hodgkin Lymphoma. Arch Pathol Lab Med. 2008; 132: 441-462
AFIP Atlas of Bone Marrow Tumors
AFIP Atlas of Lymph Node and Spleen Tumors
Other multiple sources