Mast cell tumours Flashcards

1
Q

Outline the make up of mast cell tumours

A

 Start as CD34+ progenitor’s in bone marrow
 Mature in peripheral tissue
 Barrier’s – GIT, skin, lungs
 Granules contain
▪ Histamine and heparin amongst others
▪ Released due to trauma, heat, IgE binding

MCT granules can be stained after released into periphery, not before
Can use Touridine blue stain for histo.

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2
Q

Where do you get MCTs?

A

 Most commonly cutaneous
 Occasionally mucocutaneous
 Rarely visceral,GI or bone marrow

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3
Q

What are the common breeds for MCT

A

 Brachycephalics,GRT and Labs predisposed.
▪ Boxers and Pugs mostly low grade
▪ Sharpei’s more aggressive disease

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4
Q

What is darier’s sign?

A

A wheal around the tumour

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5
Q

How common is it to get more than one tumour?

A

10-20% dogs will have more than 1 at dx

40% will get more than one in life

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6
Q

Compare FNAs and biopsies

A
 FNA
 Round cell (fried egg) with variable numbers of
granules
 Some correlation with grade but biopsy better
 Biopsy – incisional
 Grading information
 MI
 Can measure proliferation indices
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7
Q

What are the main grading systems?

A

 Patnaik currently currently most used
 Good differentiation between high and low
 Grade 2 problematic

 Kiupel
 Two grade system
 Some improvement in performance

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8
Q

What is the use of proliferation indices?

A
 MI
▪ >5 is bad
▪ No additional cost
▪ Good link with prognosis prognosis
 Ki67
▪ Independent risk factor for recurrence, metastasis and death
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9
Q

How does grade reflect metastatic rate?

A
Metastatic rates
 Grade 1 – 10 % or less
 Grade 2 – 22% or less
 Grade 3 ~ 80%
 Therefore I discuss staging for all MCTs and recommend staging for:
 all G2 and G3 tumours
 all tumours with aggressive appearance or behaviour
 all recurrences – upstaging?

Assume all grade 3s have spread

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10
Q

What staging should be done?

A

 Aspiration of local lymph nodes
 Thoracic radiographs
 Tumours located in areas that drain to thoracic lymph
nodes
 Abdominal ultrasound
 Aspiration of spleen and liver
 There can be metastatic disease in the liver without
ultrasonographic structural abnormalities

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11
Q

What factors affect prognosis?

A

 Possibly breed  Appearance  Location
 Controversial but possibly scrotal or inguinal worse
 Recurrence after surgery
 LN and distant metastasis
 Grade  High proliferation markers  Kit mutation
 Poor response to medical therapy

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12
Q

What is the order of preference for local treatment of MCTs?

A

 Surgery
 Neoadjuvant medical therapy then surgery
▪ Surgery and RT
▪ rTKI
 Other medical therapy
rTKI inhibitors are not a substitute for surgical excision

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13
Q

Outline the use of Sx in MCT tx

A

 Treatment of choice for localised non‐metastasised
MCTs
 Loco‐regional control improves outcome even in higher grade disease
 Combination of surgery and radiation therapy effective forG1 and 2 tumours with nodal metastasis
 Manipulation carries a risk of degranulation
 Gentle handling
 Consider pre and perioperative anti‐histamines

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14
Q

How radical does surgery need to be?

A

 Grade is known
 ‘Concerning’ grade 2 and grade 3
▪ 3 cm laterally and 1 fascial plane/muscle layer deep to the deepest tumour tissue
 Grade 2 or 1
▪ 2 cm laterally and at least 1 fascial plane
 Grade unknown
 3 cm laterally and 1 fascial plane/ muscle layer deep to the deepest tumour tissue

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15
Q

What are the options if you are not confident in getting a good margin?

A
 Refer to a soft tissue surgeon
 Surgery alone
▪ Surgery followed by radiation therapy
 Neoadjuvant treatment
 Prednisolone
 VBL + Prednisolone
 Tyrosine kinase inhibitor (licenced)
▪ Masitinib /Toceranib
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16
Q

Outline the use of neoadjuvant therapy

A
 Aim – to shrink a non‐resectable tumour
sufficiently to allow resection
 Prednisolone
▪ 2.2 mg/kg for 10 days OOR of 70%
▪ mean 50% reduction in size
 Vinblastine and prednisolone
▪ no more than 2 cycles
▪ Also thought to reduce size indicated in high risk
tumours as adjuvant therapy
17
Q

Outline the use of tyrosine kinase inhibitors in gross disease

A

 Mastinib
 50% have ~ 50% reduction in tumour size within 6
months
 Toceranib
 ~ 40% response rate in ‘non‐resectable disease’
BUT HOW LONGUNTIL MAXIMUM EFFECT?
BUTWHEN DOYOU STOP?

18
Q

What are the indications for adjunctive therapy?

A
 Confirmed metastasis
 High k ris tumours
 Grade 3
 Other grade with high MI
▪ Other grade with high KI 67
19
Q

Outline the use of prednisolone and vinblastine

A
 8 cycle protocol
 Staging before first and after last treatment.
 Haematology before each treatment
 Adjuvant treatment
 All tumours MST > 570 days
 Grade III – MST 330 days
20
Q

How often should follow up/ staging be performed?

A

 Regular follow up is indicated for all tumours
 Re‐staging based upon risk
 At the end of treatment
 One month after the end of treatment
 Then every 3 months for at least a year
 Then every 6 months to a year
 If the patient is unwell

21
Q

Outline oral/ perioral MCTs

A

 Comparatively rare presentation
 Cutaneous grading scheme does not apply
 MST prolonged prolonged – 52 mths
 But shorter with nodal metastasis – 14 mths

22
Q

Outline subcutaneous MCTs

A
 Cutaneous grading systems unproven
 Combination of following predictive of outcome
▪ MI
▪ Ki‐67
▪ KIT cellular localisation
23
Q

Outline multiple cutaneous MCTs

A

 Not clear whether these are metastatic or not
 Prognosis for multiple MCTs treated with surgery
is not necessarily worse than single MCTs
 However
 High rate of de novo appearance of new tumours
▪ Often low grade
 Treatment
 Repeat surgeries
 Short course of chemotherapy

24
Q

Outline BM/ visceral/ GI MCTs

A

 Rare in dogs  GI disease poorly reported
 Prognosis seems to be variable
 Visceral disease
 Reported MST of 90 days
 Newer / more aggressive adjuvant therapy may improve
this
 Bone Marrow
 Poor survival ~ 45 days
 Poor response to conventionaltreatments