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Lymphoma Flashcards

1
Q

Canine lymphoma accounts for what % all canine tumors?

% of all canine hematopoietic tumors?

A

7-24% of all canine tumors and 83% of all canine hematopoietic tumors

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2
Q

Median age for dogs affected by LSA?

A

Affects primarily middle-aged to older dogs (6-9 years) – dogs with T-cell LSA may be younger

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3
Q

Gender predilection?

Sex predilection?

A

None

Intact females are at lower risk similar to people

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4
Q

What are the 11 high breed associated risk?

A

Boxer, bullmastiff, Basset hound, St. Bernard, Scottish terrier, Airedale, pitbull, Briard, Irish setter, Rottweiler, bulldog

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5
Q

Name 2 canine breeds with lower risk?

A

dachshund, Pomeranian

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6
Q

Etiology for canine LSA?

A

Unknown but probably multifactorial

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7
Q

Chromosomal translocations are catalyzed by what 2 proteins which can lead to chromosomal abnormalities in LSA?

A

RAG-1 and RAG-2 proteins during V(D)J gene rearrangement to form B-cell and T-cell receptors

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8
Q

What chromosomal abnormalities are seen in canine LSA?

A

Gain of chromosomes 13, 31- Trisomy of chromosome 13 associated with better prognosis

Loss of chromosome 14

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9
Q

What 2 canine breeds get T-cell LSA?

A

Boxers, Asian/Arctic breeds

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10
Q

What 3 canine breeds get B-cell LSA?

A

Cocker spaniel, Dobermans, Bassett hounds

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11
Q

What canine breed gets T-zone LSA?

A

Golden retriever

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12
Q

How does epigenetics play a role in canine LSA?

A

Global hypomethylation of DNA seen in most lymphoma cases tested, likely plays a role in cancer progression (genomic instability).

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13
Q

Specific mutations or signaling pathway dysregulations

A

N-ras, p53, Rb, Bcl-2 family proteins, telomerase, p16, NF-kB

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14
Q

Recurrent somatic mutations found in B-cell lymphomas

A

TRAF3-MAP3K14, FBXW7, POT1

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15
Q

Infectious factors associated with canine LSA?

A

No confirmed proof of retroviral etiology as in the cat

Possible association with EBV or EBV-like herpesvirus

Possible association of H. pylori with gastric MALT lymphoma (laboratory evidence)

Fecal microbiota of dogs with LSA is significantly different from that of healthy dogs, but no proven association with lymphomagenesis

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16
Q

Environmental factors associated with canine LSA?

A

2,4-D – Highly controversial with some studies citing increased risk with exposure and others questioning these findings. However, 2,4-D exposure is also a purported risk factor in humans.

OR for LSA was 1.3 in dogs exposed to lawns treated 4 or more times per year

2,4-D detectable in urine at > 50 mg/L in dogs exposed to lawn treatment within 7 days of application

Possible increase risk with exposure to paints and solvents and residency in industrial areas.

Possible association with exposure to strong magnetic fields (high-tension wires).

Proximity to environmental waste may be a risk indicator rather than a risk factor

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17
Q

Immunologic factors associated with canine LSA?

A

Major risk factor in humans with HIV/AIDS, transplant patients, elderly

Immune system dysfunction documented in dogs with LSA

Development of LSA subsequent to previous ITP

1 case of LSA developing after cyclosporine treatment (Somewhat dubious… dog was only on cyclosporine for 4 weeks prior to diagnosis of LSA).

Immunosuppressive drug therapy is a known risk factor for lymphoma in humans and cats

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18
Q

Multicentric LSA accounts for what % of all canine LSA?

A

80%

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19
Q

Alimentary LSA accounts for what %

Most GI LSA are what immunophenotype?

What breeds are pre-disposed?

A

5-7%

T-cells

Bosers and Shar-peis

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20
Q

What % are mediastinal LSA?

Immunophenotype?

A

~5%

Usually T-cell

Hypercalcemia in 10-40% of all dogs with LSA and is most common in mediastinal form

Characterized by enlargement of craniomediastinal LN’s, thymus, or both

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21
Q

Most common cutaneous LSA?

What cell type is affected? Humans?

What is sezary syndrome?

A

Epitheliotropic cutaneous T-cell lymphoma (mycosis fungoides) is most common type of cutaneous LSA

CD8+ (cytotoxic T) in dogs (as opposed to CD4+ (helper T) in humans)

Sézary syndrome – rare form of MF characterized by generalized cutaneous involvement (diffuse erythroderma in humans) and circulating neoplastic T-cells

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22
Q

Non-epitheliotropic LSA is what cell type?

Occurs where in the skin?

Common DDx?

A

Non-epitheliotropic LSA (can be either B-cell or T-cell) usually spares epidermis/papillary dermis and occurs in mid-deep dermis to subcutis. Tends to form multifocal to coalescing tumors/crusts rather than patches/plaques.

Must DDx other cutaneous/subcutaneous round cell tumors

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23
Q

How does hepatosplenic LSA present in dogs?

What immunophenotype?

A

Characterized by lack of peripheral lymphadenomegaly in the face of hepatic, splenic and bone marrow infiltration

Usually T-cell (gd T-cells)

gd refers to the form of the T-cell receptor (TCR) displayed by these T-cells. TCRs come in 2 basic types: ab and gd.

Highly aggressive, responds poorly to therapy

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24
Q

Intravascular lymphoma (aka angiotropic LSA or angioendotheliomatosis)

Commonly affected organs?

Immunophenotype?

A

Proliferation of neoplastic lymphocytes within the lumen and wall of blood vessels in the absence of a primary extravascular mass or leukemia

Eye, CNS commonly affected

Usually T-cell or null cell in dogs (B-cell in humans)

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25
Q

Pulmonary lymphomatoid granulomatosis

A

Rare pulmonary infiltrative/nodular disorder characterized by a heterogenous accumulation of B- and T-lymphocytes with an angiocentric distribution.

Possibly a pre-lymphomatous state?

3 grades in humans, with grade 1 being most akin to “pre-lymphoma, ” grade 2 akin to T-cell rich large B-cell lymphoma, and grade 3 akin to DLBCL

Heterogeneous response to therapy (everything from durable CR to rapid death)

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26
Q

WHat are the 5 most common subtypes of LSA in decreasing order?

A

DLBCL>PTCL-NOS>TZL>T-LBL>MZL

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27
Q

What are 4 features of indolent (low grade) tumors?

A

Small mature lymphocytes

Low mitotic rate

Typically progress slowly

Long survival but survivable

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28
Q

What are 4 features of high grade (aggressive) LSA?

A

Large immature lymphocytes, high mitotic rate, likely to response to chemotherapy but rapidly progressive, potentially curable in humans (rarely in dogs)

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29
Q

How are canine LSA graded?

A

Grade in the WHO/REAL system is assigned based upon mitotic index alone (low = 0-5/hpf, intermediate = 6-10/hpf, high = >10/hpf)

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30
Q

What % are the following?

B-cell

T-cell

Mixed B/T cell

Null cell

A

60-80% of canine LSA are B-cell

10-38% are T-cell

22% Mixed B/T tumors (likely represent aberrant surface Ag expression, especially as assessed by flow cytometry)

<5% are null cell

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31
Q

High grade much more likely to have __ on chemotherapy than low-grade

T-cell LSA have ___ rate of CR, ___ remission, ___ survival time (except TZL)

A

CR

lower, shorter, shorter

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32
Q

Diffuse pulmonary infiltrates on rads in ___ % - up to ___ have lung involvement based on BAL

A

27-34%

2/3

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33
Q

Common clinical signs with GI LSA

A

GI lymphoma usually have vomiting, diarrhea, weight loss, malabsorption

May see hepatosplenomegaly, mesenteric LN enlargement

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34
Q

What is pre-caval syndrome?

A

venous or lymphatic obstruction occurs causing pitting edema of head, neck, forelimbs

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35
Q

Ocular LSA

A

Iridal thickening, hypopyon, uveitis, hyphema, posterior synechiae, glaucoma

37% of dogs with multicentric LSA had ocular involvement in 1 study

LSA accounted for 17% of uveitis cases in another study

Primary solitary ocular lymphoma (PSOL) is an entity distinct from secondary ocular lymphoma in multicentric disease.

MST for PSOL was 769 days vs. 103 days for multicentric with ocular involvement

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36
Q

Most common paraneoplastic syndrome in canine LSA?

A

anemia

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37
Q

What are the common signs exhibited in dogs with hypercalcemia?

A

Hypercalcemia depresses the activity of any excitable tissue (increases threshold potential). Many clinical signs are referable to this phenomenon:

Skeletal muscle – weakness

Smooth muscle – anorexia, vomiting

Nerve – weakness, ataxia, CNS depression, anorexia, adipsia

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38
Q

Effect of hypercalcemia on kidenys?

A

Decreased responsiveness of collecting ducts to ADH – nephrogenic DI, primary polyuria

Renal arterial vasoconstriction – ischemic injury, renal failure

Direct cytotoxic effects to renal tubular epithelium

With chronicity – Ca x P >60 leads to nephrocalcinosis

39
Q

Main cause of hypercalcemia is PTHrp, what are other causes?

A

IL-1, TNF-a, TGF-b, vitamin D analogs

40
Q
A
41
Q

Other PNS associated with canine LSA?

A

Monoclonal gammopathy/hyperglobulinemia

Neuropathies

Cancer cachexia

42
Q

DDx for lymphadenomegaly

A

bacterial, viral, protozoal, fungal disease

43
Q

What % of dogs will have ocular involvement?

A

33-50%

44
Q

What is the most common hematological abnormality in canine LSA?

A

Anemia

Usually anemia of chronic inflammatory disease but often multifactorial (hemorrhage, hemolysis, myelophthisis)

45
Q

Thrombocytopenia is seen in what % of dogs?

A

Thrombocytopenia in 30-50%

46
Q

Neutrophilia is see in what % of dogs?

A

Neutrophilia in 25-40%

47
Q

Lymphocytosis is seen in what % of dogs with canine LSA?

A

~20% (dogmatically considered an indicator of bone marrow infiltration, but circulating lymphocytes can come from anywhere).

Must DDx ALL/CLL (can usually be done with bone marrow evaluation, immunophenotyping (inc. CD34), and evaluation of clinical features)

48
Q

Hypoproteinemia common in what type of LSA?

A

alimentary LSA

49
Q

Monoclonal gammopathy in __% of dogs with LSA

A

6%

50
Q

Hypercalcemia is seen in what % of LSA?

Mediastinal LSA?

T-cell LSA?

A

15% of all LSA

30-40% of mediastinal LSA

35% of T-cell LSA

51
Q

Azotemia if _____ or _____

Increased liver enzymes or bilirubin with _____

Proteinuria, isosthenuria may be seen on UA (note: early hypercalcemia causes hyposthenuria due to nephrogenic DI. Isosthenuria occurs with progressive renal injury)

A

hypercalcemic, renal infiltration

hepatic infiltration

52
Q

Histologic and cytologic evaluation of extranodal sites

Cytologic samples acceptable for CSF, pleural effusion, intrathoracic masses

Alimentary LSAWedge biopsy of intestine that does not penetrate lumen

Adequate tissue must be obtained to DDx from LPE.

Endoscopic samples may not be adequate for Dx.

PARR may be less accurate for GI biopsies (likely due to mix of lymphoid and non-lymphoid tissue in organ sampled)

Image-guided biopsy of secondarily involved LN’s may be acceptable

Punch biopsies acceptable for cutaneous LSA

Avoid secondarily infected lesions

Biopsy disease interface with normal tissue for subtle lesions

A
53
Q

Marker for T cell?

Marker for B cell?

A

CD3 (T-cell) or CD79a (B-cell) expression

54
Q

Other markers for B cell?

A

CD20, CD21 – B cell

55
Q

Marker for Helper T-cell?

A

CD4

56
Q

Marker for Cytotoxic T-cell?

A

CD8

57
Q

_____ is a hallmark of malignancy?

A

Clonality, Theoretically, all cancers derive from a single malignant cell.

58
Q

What is the Sn and Sp for PCR in dogs?

A

Sn – 91%, Sp – 96% (Burnett RC, et al. Vet Pathol 2003;40:32-41)

59
Q

False positive for PCR can be seen with what disease?

List 5 other differential diagnoses?

A

May get FP with rickettsial disease (monoclonal gammopathies also reported with rickettsial disease) as well as other diseases

Ehrlichiosis, borreliosis, leishmaniasis, histiocytoma, myeloid leukemias

60
Q

In one study, 57% of patients had cytologic evidence of BM involvement although only 28% had circulating neoplastic cells

A
61
Q

List 3 DDx for increased numbers of large lymphocytes in BM?

A

GI parasitism

IMHA

Other immune mediated diseases

62
Q

What % of dogs will have intrathoracic radiographic abnormalities?

pulmonary infiltrate?

lymphadenomegaly?

craniomediastinal LN enlargement?

A

Approximately 60-75% of dogs with multicentric lymphoma will have intrathoracic radiographic abnormalities

1/3 will have pulmonary infiltrates

2/3 have lymphadenomegaly

20% have craniomediastinal LN enlargement

Pleural effusion also may be present

63
Q

What % of dogs show lymphadenomegaly on abdominal radiographs?

A

50% of cases will show lymphadenomegaly (mesenteric, sublumbar), hepatomegaly, and/or splenomegaly

64
Q

MST for untreated LSA?

A

Untreated LSA – MST 4-6 weeks

65
Q

CHOP-based protocol indice CR in what % of dogs?

A

80-95% of dogs

66
Q

MST with CHOP for dogs with LSA?

What % live 2 years or longer?

A

10-12 months depending on several factors

About 20-25% live 2 years or longer (free drinks from me at VCS for anyone who can find me an article from the primary literature documenting a 2-year survival rate of this magnitude. Studies incorporating radiation or hematopoietic stem cell transplantation don’t count.)

67
Q

CR associated with CHOP? MST?

A

CHOP – 80-90% CR, MST of ~12 months

68
Q

CR associated with COP? MST?

A

COP – 60-70% CR, MST of 6-7 months

69
Q

CR associated with single agent doxorubicin? MST?

A

50-75% CR, MST 6-8 months

70
Q

Remission with prednisone?

A

Single-agent prednisone – short-lived remissions of 1-2 months

71
Q

Response rate to single agent doxorubicin noted to be much poorer for T-cell than B-cell lymphoma in one study (86% CR for B-cell, 17% CR for T-cell)

A
72
Q

What is the major role of MDR?

A

MDR usually develops and PgP/ABCB1 is thought to be a major player in MDR, but there are numerous other molecular players involved

73
Q

What %of dogs experience CR second round of CHOP? How long is remission?

A

About 90% of dogs will experience CR on second go-around of CHOP, but remission usually shorter (≤50% duration of first remission)

74
Q

What is the response to rescue protocols?

Duration response?

A

Response to rescue protocols reportedly 40-90% (90% not particularly realistic if CHOP was the induction protocol) and durations of response generally 1.5-2.5 months (see Table 33.5 for rescue protocols)

75
Q

Monoclonal antibody approaches

Humans – addition of rituximab (anti-CD20 therapeutic monoclonal antibody) to CHOP significantly improves survival for many types of B-NHL

Increased cure rate for DLBCL from ~30-40% to ~50-70%

Rituximab has no activity in dogs due to inability to bind CD20 in vivo (epitope targeted by rituximab is on the intracellular surface of the canine cell membrane) on canine lymphoma cells and the inherent antigenicity of humanized monoclonal antibodies in dogs (therapeutic MoAbs for dogs need to be “caninized”)

Therapeutic moAbs developed for dogs:

Blontuvetmab (Blontress) – targeted CD20 (B-cell)

Tametuvetmab (Tactress) – targeted CD52 (T-cell)

After extensive clinical evaluation, the target specificity of these antibodies was found to be inadequate to have meaningful antitumor activity. Neither is available currently.

A
76
Q

Alimentary Lymphoma

Chemotherapy generally unrewarding

CHOP has resulted in some durable remissions

Consider surgery for rare localized alimentary lymphomas, or those presenting with obstruction/perforation

A “small cell” variant, similar to EATL type II (LGAL) seen in cats, has been described, and is associated with a favorable outcome

Colorectal B-cell LSA also seems to have a favorable clinical course

A
77
Q

Primary CNS Lymphoma

RARE – CNS involvement usually part of multicentric disease

Localized may be treated with RT

Generally poor response rate and short remission duration

A
78
Q

Of cutaneous LSA which has better outcome?

A

Mucocutaneous cases appear to have a better outcome than cutaneous cases

79
Q

Localied cutaneous LSA can be treated with?

A

RT

80
Q

Diffuse cutanoeus LSA is best treated with?

CCNU +/- pred is standard therapy, resulting in ___% ORR, but short PFS (___ months), although some durable remissions reported

A

Diffuse best treated with chemotherapyCCNU +/- pred is standard therapy, resulting in ~80% ORR, but short PFS (~3 months), although some durable remissions reported

81
Q

2 most improtant pronostic factors for canine LSA?

Extranodal LSA are commonly what immunophenotype?

What 2 factors with B cell LSA is assocaited with poor outcome?

A

-Immunophenotype – T-cell is worse and Substage b is worse

Extranodal lymphomas are commonly T-cell, and these tend to have poor prognosis overall, but less clear whether it is T-cell immunophenotype or primary anatomic location that is the most important prognostic indicator.

For B-cell tumors, low expression of B5 antigen and low expression of MHC II also predict poor outcome

82
Q

Prognosis for LSA

Stage I and II tend to be better than III-V, but the former are rare

Proliferative indices (Ki67, AgNORs, BrdU uptake) may provide some prognostic information, but study results are contradictory

Anatomic site – extranodal tends to be bad

History of chronic inflammatory disease predicted earlier relapse in 1 study

Gender

Neutered females better prognosis

Males may have higher incidence of T-cell and therefore worse Px

Serum biomarkers (see table 33.8)

LDH, TK-1, Glutathione-S-transferase, VEGF levels, CRP - require further validation

A
83
Q

The Indolent Lymphomas

Aggressive lymphomas are chemoresponsive but incurable and usually lethal

Indolent lymphomas are poorly chemoresponsive but often associated with long-term survival

One caveat is nodal MZL – PFS of 5 months and PS of 8.5 months

Substantially less than splenic MZL

NOTE: 1 study showed gene expression signatures of late stage nodal MZL to be essentially the same as those for DLBCL – maybe this isn’t always an indolent cancer…

A
84
Q

2 breeds overrepresented fot lymphocytic leukemia?

Most studies implicate what breed?

ALL is seen in ___ dogs?

CLL is seen in ____ dogs?

A

German shepherd and Golden retriever overrepresented in some studies

More recent studies implicate small breed dogs as at risk for B-CLL

ALL – often young dogs

CLL – usually older dogs

85
Q

ALL cell size?

What marker is noted in ALL?

A

ALL – intermediate to large cells

Distinguishable from myeloblasts by a more condensed chromatin pattern and less prominent nucleoli, although sometimes differentiation can be problematic without cytochemical staining or immunodiagnostics

CD34 – early myeloid and lymphoid blasts (may DDx stage V lymphoma)

Some T-ALL do not express it

CD3/CD79a – T and B-cells (may not be present on very early blasts)

ALL is usually B-cell (CD21+, CD3-, CD4-, CD8-)

<10% are T-ALL

86
Q

What cell size is CLL?

A

CLL – small cells

Morphologically indistinguishable from normal mature lymphocytes, Usually T-cell (CD8+) – LGLs

B-cell less common

NOTE – B-CLL and B-SLL are considered the same disease

CLL with atypical immunophenotypes (e.g. CD3-, CD8+) is a rare variant of CLL in dogs

Note that human CLL is essentially always a B-cell disease. T-CLL is exceptionally rare in humans.

87
Q

Clinical signs associated with CLL?

____ present in advanced disease

A

Affected dogs usually ASYPTOMATIC/May see mild lethargy, decreased appetite

Splenomegaly may be present, and can be marked in advanced disease

Mild cytopenias common – may be more pronounced as lymphocyte count exceeds 30,000/ml

Lymphocyte counts vary but may be enormous (I’ve seen ~1,000,000/ml)

Extremes in lymphocyte count like this are due to increased lymphocyte lifespan rather than massive production. Remember, this is a slowly progressive disease.

88
Q

4 paraneoplastic syndromes associated with CLL?

A

Paraneoplastic syndromes

-Monoclonal gammopathy

Macrogammaglobulinemia – production of IgA or IgM by neoplastic B-cells

Waldenstrom’s macroglobulinemia – IgM monoclonal gammopathy associated with B-CLL

  • Hyperviscosity syndrome may develop
  • IMHA
  • Pure red cell aplasia (PRCA)

Hypercalcemia (rare) – may be more common in B-CLL

89
Q

For ALL, affected dogs are ___?

Common clinical signs?

A

Affected dogs usually SICK

PU/PD, weight loss, anorexia, lethargy

Splenomegaly, hepatomegaly, lymphadenomegaly, petechial/ecchymotic hemorrhage

Cytopenias common and often pancytopenic – extensive BM infiltration is the norm

CNS signs, signs of bone pain also common

90
Q
A

Normal lymphocyte subset distribution in peripheral blood

80% T cell (CD4+ > CD8+)

15% B cell

NK cells and CD4-/CD8- T-cells account for the rest

Knowing these normal ratios is helpful when interpreting flow cytometry results in dogs with mature lymphocytosis

PARR can also help distinguish neoplastic from non-neoplastic lymphocytosis, but occasional false positives (Ehrlichiosis)

91
Q

When do you start treatment for CLL?

A

Cytopenias

Lymphocyte count >60,000 (arbitrary)

Significant lymphadenopathy or splenomegaly

Clinical signs of illness present

92
Q

CR for CLL?

What is Richters syndrome?

A

CR’s rare but MST’s usually 1-3 years due to indolent behavior

Richter’s syndrome – rapidly progressive acute phase of disease in which CLL progresses to an immunoblastic lymphoma - associated with poor Px

93
Q

Median remission/survival for CLL?

MST for T-CLL?

MST B-CLL?

MST atypical CLL?

A

Excellent for CLL

70% have normalization of CBC, some have long-term survival with no treatment

Median remissions/survivals 1-3 years are reported

Immunophenotype may be prognostic

MST T-CLL – 930 days (2.5 y)

MST B-CLL – 480 days (1.3 y)

MST atypical CLL – 22 days

Degree of lymphocytosis may also be prognostic in dogs with CD8+ T-CLL

Lymphocytes >30,000/ml – MST 131 days

Lymphocytes <30,000/ml – MST 1098 days

94
Q

MST for ALL with VCR/pred?

MST with CHOP?

MST B-ALL?

A

Very poor for ALL

MST 120 days with VCR/pred (29% ORR), almost all dogs dead by 8 months

MST 16 days in 46 dogs treated with CHOP

MST 129 days in a series of dogs with B-ALL

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