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Small Animal Medicine II > Mast Cell Tumors > Flashcards

Mast Cell Tumors Flashcards

1
Q

Where do mast cells arise from? What are 4 functions?

A

BM hematopoietic precursors under the influence of stem cell factor

  1. wound healing
  2. induction of innate immune response
  3. antiparasite activity
  4. modulation of reaction to insect and spider venoms
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2
Q

What 4 substances are found in the granules of mast cells?

A
  1. heparin - bruising
  2. histamine - irritation, ulceration
  3. TNFa
  4. proteases - chymase, tryptase
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3
Q

What is the most common cutaneous tumor? What are some breeds with predisposition?

A

mast cell tumors

  • Bulldogs
  • Labs
  • Goldens
  • Cockers
  • Schnauzers
  • Pitbulls
  • Beagles
  • Shar-Peis
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4
Q

How do mast cell tumors arise?

A

normal KIT receptor for stem cell factor become dysregulated and aberrantly located, leading to abnormal growth and aggressive biologic tendencies

  • stem cell factor independent activation and unregulated KIT signal transduction
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5
Q

What are common locations of MCTs?

A
  • conjunctiva (benign)
  • nasopharynx
  • larynx
  • oral cavity (malignant)
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6
Q

How are MCTs commonly diagnosed? Graded? Staged?

A

cytology - Wright-Giemsa or toluidine blue can stain granules when Romanowsky stains fail

histopathology with IHC of vimentin, tryptase, and CD117 (for KIT)

abdominal U/S, three-view chest radiographs, LN evaluation, BM cytology, buffy coat more useful in cats

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7
Q

What is a more accurate indication of mast cell tumor metastasis through lymph nodes?

A

clustering and aggregates —> most likely need to remove node for histologic confirmation

  • mast cells are normally found in LNs in smaller amounts and can increase in the presence of infection and ulceration
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8
Q

What are the 4 stages of MCTs according to the Weishaar Nodal Classification System?

A
  1. HN0 - no metastasis
  2. HN1 - pre-metastatic
  3. HN2 - early metastasis
  4. HM3 - overt metastasis

HN2 and HN3 are clinically relevant with decreased MST

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9
Q

When is U/S guided aspiration of liver and spleen indicated for staging MCTs?

A

only if they seem abnormal

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10
Q

What are some prognostic factors affecting MCTs?

A
  • histologic grade
  • clinical stage
  • location - SQ, conjunctival > oral, sublingual, MM preputial, scrotal, muzzle
  • cell proliferation rate - mitotic index (MI), AgNOR, Ki67
  • recurrence
  • systemic signs
  • breed - brachycephalic > Shar-Peis
  • tumor size - bigger = harder to get good margins
  • C-kit mutations
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11
Q

What are the 3 grades of the Patnaik grading scheme?

A
  • Grade I = well-differentiated, 80-100% survival with surgery
  • Grade II = 44%
  • Grade III = 6-7%
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12
Q

What is a new method of grading MCTs? How is this becoming difficult?

A

2 tiered - high vs low grade

  • Grade II tumors have been classified as low-grade (16.5%) and high-grade (83.5%) and using the 2-tiered system did not seem to overcome this issue
  • there have been high numbers of Grade II tumors not being cured with wide excision and new targeted chemotherapy drugs are being introduced
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13
Q

What is the most common treatments that lead to a cure of Grade II (less than 4 cm) MCTs?

A

surgical excision alone with appropriate margins

  • must be non-metastatic
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14
Q

What is the point of the mast cell tumor proliferation panel? What 4 proteins are evaluated?

A

provides and objective way of grading Grade II MCTs to determine if additional systemic therapy is required after adequate local control

  1. Ki67 (IHC) - proliferation marker only located in dividing cells
  2. AgNORs - indicative of cell turn over (protein synthesis)
  3. KIT (IHC) - location within cell
  4. C-kit mutational status (PCR)
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15
Q

What are implication of positives seen on the MCT panels? What treatment will they require?

A
  • high AgNOR and Ki67 indicate high proliferation rate = chemotherapy
  • abnormal localization of KIT = targeted Palladia
  • C-kit mutation positive = targeted Palladia
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16
Q

What are 4 treatment options for MCTs?

A
  1. surgery
  2. radiation - definitive or palliative coarse fractionated
  3. chemotherapy - Vinblastine, Lomustine (CCNU)
  4. small-molecule targeted therapy - Palladia (toceranib phosphate)
17
Q

What margins are preferred for excision of MCTs?

A

proportional margins based on the widest diameter + one well-defined fascial plane (clean margin = >1mm)

  • 1.5 cm length = 1.5 cm margin
  • 6 cm length = 6 cm margin
18
Q

What can be added to the treatment plan to decrease recurrence rates of Grade II MCTs following surgical removal?

A

neoadjuvant prednisone until size decreases to one good enough for clean margins

19
Q

What treatment is recommended for Grade II MCTs with lymph node metastasis?

A

surgical removal with removal of metastatic lymph node to increase survival

  • overall, regional LN status does not predict survival in dogs with Grade II MCTs
20
Q

What treatment is recommended for SQ MCTs?

A

surgical excision

  • tend to behave less aggressively than dermal variety due to the fat surrounding it creating a barrier
21
Q

When is definitive radiation therapy recommended for MCTs? What treatment plan is recommended?

A

areas where total excision is not an option, like the distal antebrachium

Mon-Fri daily treatments for a total of 18 treatments (3gy x 18 = 54gy)

22
Q

How does the result of definitive radiation therapy compare in incompletely excised Grade II MCTs, Grade II MCTs with LN metastasis, and Grade III MCTs?

A

~90% disease free 1-5 years with survival 2-5 years (median disease free interval = 54 months)

radiation therapy to primary site and regional lymph node = median disease free interval of 1240 days

median duration of remission = 27.7 months, MST = 28 month

23
Q

How often is coarse fractionated radiation therapy given? In what cases is it recommended? What is commonly added?

A

8gy x 4 doses = MST of 1872

when Prednisone and surgery do not work

Palladia

24
Q

What 4 pre-meds are recommended before starting chemotherapy for MCTs?

A
  1. Prednisone
  2. Diphenhydramine (Benadryl) - blocks H1 receptors
  3. Famotidine - blocks H2 receptors
  4. Omeprazole - recommended for large tumor burdens to avoid GI ulceration
25
Q

What 3 combinations of chemotherapies are used for MCTs? What else is commonly added?

A
  1. Vinblastine - 47% response (MST = 154 days)
  2. Vinblastine + Cyclophosphamide - MST = 145 days
  3. CCNU - 42% response (MST = 79 days)

Palladia - 40% shrinkage, 60% biologically stable disease

26
Q

When is adjuvant chemotherapy recommended? What is commonly used?

A

higher risk Grade II MCT with LN metastasis or location at mucocutaneous junctions / Grade III MCTs

Vinblastine/Prednisone

27
Q

What is Palladia? What 3 results does it action end in?

A

small molecule receptor tyrosine kinase inhibitor - blocks VEGFR-2 (blood vessels), PDGFR, and KIT (on mast cell)

  1. blocks ATP binding site in receptors, which blocks phosphorylation and downstream signal transduction of KIT = stops proliferation
  2. inhibits tumor angiogenesis
  3. regulatory T-cell inhibition
28
Q

What is mutated KIT associated with in mast cells? How does this occur?

A

higher chance of recurrence and metastasis

internal tandem duplication of exons 11 or 12, resulting in a constantly turned on KIT, leading to autophosphorylation without presence of stem cell factor —> continuous proliferation

29
Q

What is Palladia labeled for use in? What response is expected?

A

recurrent Grade II or III canine mast cell tumors with or without LN metastasis

  • objective response = 42.8%
  • biologic response = 59.5%
30
Q

What 5 adverse effects are expected with the use of Palladia? When should it not be given?

A
  1. diarrhea
  2. weight loss
  3. hematochezia, melena
  4. neutropenia
  5. lameness

on the same day as NSAIDs or steroids - avoids GI upset

31
Q

How can the adverse effects of Palladia be managed?

A
  • drug holiday/discontinuation
  • dose reduction
  • change dose frequency
  • supportive medications - Famotidine, Diphenhydramine, Omeprazole, Sucralfate, Cerenia, ONdansetron, Metoclopramide, Metronidazole, Loperamide
32
Q

How do feline MCTs compare to canine MCT?

A
  • multiple, benign cutaneous MCT common
  • no established histologic grading —> well-differentiated vs. anaplastic may have prognostic significance
  • staged with abdominal U/S and chest radiographs
33
Q

What are the 2 most common visceral MCTs seen in cats?

A
  1. splenic
  2. GI
34
Q

How do most cats present with splenic MCTs? What treatment is recommended?

A
  • typical differential for splenic disease + involvement of other organs (liver, LNs, BM, and blood common)
  • concurrent cutaneous involvement not common

surgery (splenectomy) even in the face of disseminated disease + post-op Palladia, since most cats have active mutations in c-kit

(MST = 1-1.5 years)

35
Q

What is the prognosis of feline GI MCT like? What treatment is recommended?

A

poor - high metastatic rate at the time of diagnosis (>80%, MST = 2 months to 1.5 years)

  • NO DISSEMINATION = surgery + post-op adjuvant chemotherapy or targeted therapy
  • DISSEMINATION = chemotherapy/targeted therapy

Small Animal Medicine II (57 decks)

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