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Principles of Science Strand > Principles of Oncology > Flashcards

Principles of Oncology Flashcards

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1
Q

Neoplastic Predisposition:

Boxers

A
  • MCT
  • Lymphoma
  • others
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2
Q

Neoplastic Predisposition:

Flat Coat Retrievers

A

soft tissue sarcomas

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3
Q

Neoplastic Predisposition:

Irish Wolfhound

A
  • osteosarcoma
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4
Q

Neoplastic Predisposition:

GSD

A
  • Haemangiosarcoma
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5
Q

Give examples of hormonal factors in the aetiology of cancer

A

Steroid hormones oestrogen and progesterone in females

  • Mammary tumours

Androgens in males

  • Prostate carcinoma
  • Perianal adenoma
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6
Q

Give examples of exposure to biological agents (oncogenic pathogens) as an environmental factor in the aetiology of cancer

A
  • Retroviruses (e.g. FeLV causing lymphoma in cats)
  • Poxviruses (e.g. BPV which also causes equine sarcoids)
  • Others (Helicobacter pylori and gastric carcinoma) - Helicobacter pylori (H. pylori) is a type of bacteria. These germs can enter your body and live in your digestive tract. After many years, they can cause sores, called ulcers, in the lining of your stomach or the upper part of your small intestine
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7
Q

Describe proto-oncogenes

A
  • Genes whose normal function is to promote cell growth/proliferation or inhibit apoptosis
  • Activated during certain specific periods of tissue development (e.g. foetal growth) or remodelling + repair
  • Tightly controlled expression
  • Loss of control following mutation = oncogene
  • Some viruses contain oncogenes
  • These accelerate proliferatiion
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8
Q

Describe tumour suppressor genes

A

Prevent cancer

e.g. p53 and retinoblastoma protein (Rb)

  • Normally act to prevent uncontrolled prolferation
  • Cause cell cycle arrest and programmed cell death if the cell is damaged
  • Eradicate pre=-malignant cell from body
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9
Q

What are the hallmarks of cancer

(6)

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Activating invasion + metastasis
  • Enabling replicative immortality
  • Inducing angogenesis
  • Resisting cell death
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10
Q

How can tumour cells become self-sufficient?

A
  • Synthesising own growth factors

E.g. Epidermal growth factor

Autocrine + paracrine

Altering receptors

Activating mutations so receptor is always on even without ligand OR

Overexpression of receptor to respond to relatively low levels of ligand (breast example)

Mutation of signalling molecules

Activating mutations switch on proliferation in absence of receptor ligation e.g. Ras, Raf

a chain of proteins in the cell that communicates a signal from a receptor on the surface of the cell to the DNA in the nucleus of the cell.

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11
Q

Describe mast cell tumours and mutations in KIT (stem cell factor receptor)

A
  • SCF acts through KIT (c-kit) receptor, which has tyrosine kinase activity
  • KIT gene mutations found in 30-50% of canine mast cell tumours
  • Presence of mutation seems to be associated with more aggressive disease
  • Normally: binding of ligand –> phopshorylation –> cell signalling pathways - survival + proliferation
  • Abnormal: mutation in juxtamembrane region: receptor autophosphorylates - constantly signalling survival + proliferation
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12
Q

Describe treatment of canine mast cell tumour

A

Receptor tyrosine kinase inhibitors

  • Toceranib (Palladia)
  • Masitinib (Masivet)

Withdraw ability of survival and proliferation from mutant cell

-also have off-target effect on angiogenesis of the tumor (as VEGF receptor is a tyrosine kinase)

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13
Q

germline mutation in Bull Mastiff

A
  • Eg germline p53 mutation in bull mastiff - breed predisposed to lymphoid neoplasia e.g. lymphoma - polymorphisms in tumour suppressor genes which increase risk of mutation
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14
Q

Describe the initiation of cell death in a normal cell

A
  • Castpase cascade facilitates cell death
  • Extrinsic pathway by death receptors on surface - caspase 8
  • Intrinsic pathway from DNA damage - mitochondria release cytochrome C
  • Either pathway enabled caspase casade which cause apoptosis
  • Can take advantage by using chemotoxic agents to try and stimulate intrinsic pathways to drive cell into programmed cell death
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15
Q

How can tumour cells avoid apoptosis

A
  • No expression of death receptor - block extrinsic pathway
  • Over-expression of molecules which inhibit caspase cascade
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16
Q

How do tumour cells avoid senescence

A
  • Most cells can only undergo limited number of divisions before they become sensecent + die
  • Cancer cells must achieve immortality
  • Telomeres at the end of chromosomes become eroded after each cell division
  • Once they are critically shortened the cell undergoes apoptosis
  • Telomerase enzyme adds new telomeres + is often upregulated in cancer cells - typically only expressed in germline cells
  • Telomerase inhibitors now in clinical trials
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17
Q

Describe tissue invasion + metastasis

A
  • More malignant tumours can invade local tissues + metastasise to distant sites via lymphatics or blood
  • They can do this due to…
  • Matric metalloproteinases to disrupt surrounding tissues: “melts” ECM and allows growth into tissue
  • Alteration in cell adhesion molecules to detach + migrate (e.g. decreased E-cadherin in canine mammary tumours)
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18
Q

What possible mechanisms can tumours use to avoid detection by the immune system?

(4)

A
  • Downregulate immunogenic antigens
  • Kill tumour infiltrating lymphocytes
  • Produce immunosuppressive mediators
  • Induce tolerance
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19
Q

Describe possible mechanisms to counter a tumour avoiding immune destruction

A
  • Anti-cancer vaccines: stimulate immune system to target the tumour
  • Monoclonal antibodies

E.g. combination anti CTLA-4 (prevents tolerance tumour cell) with anti PD-1 (blocks death recpetor that tumour cells use to kill lymphocytes)

  • Immune modulators
20
Q

Describe how we can target tumour-promoting inflammation to tackle cancer

A
  • Anti-inflammatory drugs
  • E.g. Cox2 inhibitors in bladder cancer
  • Remove -ve inflammatory reaction = good
21
Q

Describe staging of cancer patients

(TNM)

A
  • After making diagnosis of cancer
  • Staging assesses extent of disease in body
  • Performed by clinican
  • Assess

Primary tumour (T) - T3 = greater than 5cm, T2 = 3-5 cm

Drainage lymph node (N)= N0 = no metastasis, N1 = evidence of

Distant metastasis (M) = M0, M1

Important for treatment planning, prognosis and communication

**Some tumors don’t fit into the TNM system -> lymphoma

22
Q

Give examples of cancer staging systems

(2)

A
  • TMN system
  • WHO system (ex: lymphomas)
23
Q

Describe the WHO system for cancer staging

A

For some types of tumour TMN does not work - WHO system used for staging lymphoma

In stages

  • Stage 1: single LN involved
  • Stage 2: regional area (one side of the diaphragm)
  • Stage 3: generalised lymphadenomegaly (both sides of diaphragm)
  • Stage 4: liver + spleen involvement
  • Stage 5: involvement of BM or other organ systems (e.g. CNS or kidney)
24
Q

Give examples of baseline test that can be used to asses the cancer patient

A
  • Haematology/CBC
  • Biochemistry
  • Urinalysis
25
Q

Decribe the use of biochemistry as a baseline test to asses a cancer patient

A
  • Geneal health screen
  • Assess organ damage/fucntion

Prior to GA

Asses drug metabolism (liver/kidneys)

Affects choice + dose of drugs

  • for paraneoplastic effects e.g. hypercalcaemia due to PTH-rp secretion
26
Q

Give examples of coagulopathies due to tumours

A
  • E.g. bleeding tendencies
  • Hyper or hyocoagulable
  • Thrombocytopenia e.g if bone marrow involvement/DIC

e.g. dog with mast cell tumour releasing heparin

Heparin is made by the liver, lungs, and other tissues in the body and can also made in the laboratory

27
Q
A
  • Hypercalcaemia

PD/PU/ lethargy, anorexia, depression, vomiting, weakness, bradycardia

  • Hypoglycaemia

Weakness, collapse, seizures

E.g. insulinoma or secretion of insulin-like substances

  • Hyperviscosity with hyperglobulinaemia, polycytheamia

Neurological signs, retinal detachment, seizures

E.g. antibody production from myeloma

28
Q

What approaches are available to address cancer?

A
  • Surgery
  • Radiation Treatment
  • Chemotherapy
  • Novel treatment options
  • (+supportive care)
29
Q

Describe surgery used against cancers

A

Treatment of choice for many primary carcinomas and sarcomas, mast cell tumours

May be sole treatment modality but often used in combination wtih radiation or chemotherapy

30
Q

Describe chemotherapy for cancer

A

Disseminated disease/tumours with high metaststic potential

  • Haematopoetic tumours e.g. lymphoma, leukemias
  • Systemic/high grade mast cell tumours
  • Adjunctive treatment for highly metastatic tumours e.g. OSA, HSA, high grade STS
  • Situations where Sx or radiation treatment is not possible
31
Q

Give an example of an adverse effect of cancer therapy and how this can be prevented

A

GI problems

  • H2 blockers/sucralfate/omeprazole
  • Anti-emetics e.g. maropitant, ondasetron
  • Appetite stimulants - mirtazepine
32
Q

Some alternative Tx to SCC

(2)

A
  • Plesiotherapy
  • Photodynamic therapy - Give patient photosensitizing chemical that gets localized in tumor then expose to light and causes oxidizin damage to the tumor
33
Q

Give examples of supportive care for cancer therapy patients

A

Antibiotics if chemotherapy causes neutropenia

Analgesics

  • NSAIDs
  • Opiods e.g. tramadol, buprenorphine
  • Gabapentin
  • Paracetamol

Physiotherapy - keep petient mobile + active

34
Q

How can inflammation caused by injection lead to cancer?

A
  • Chronic inflammation can lead to cell mutation
  • Tumour microenvironment is rich in fibroblast-like cells and inflammatory cells (cytokine + growth factor release)
  • Tumour infiltrating lymphoytes can produce PDFG
  • ISS cells have growth factor receptors

Proliferation

Angiogenesis

Metastasis

35
Q

FISS

A
  • Vaccine-associated sarcomas consist of cells that are morphologically and immunohistochemically compatible with fibroblasts and myofibroblasts.
  • Stimulation of these cells by highly immunogenic and persistent adjuvants or other vaccine components resulting in inflammation that alone or in association with unidentified carcinogens or oncogenes leads to neoplastic transformation and tumor development
36
Q

What cell type are ISSs typically

A

Vaccine associated sarcomas in cats are most often fibrosarcomas but many other types of sarcomas have also been reported.

Sarcomas in the cats are usually characterized by:

  • Cellular pleomorphism
  • High mitotic activity
  • Large central zones of necrosis
  • Features consistent with an aggressive biological behavior
  • Highly locally invasive + v infiltrative
  • Can be cystic
37
Q

Describe the advantages and disadvantages of cytology as a diagnostic approach to injection site sarcoma

A
  • Not as accurate as biopsy - histo is the gold standard
  • Often diagnostic, though difficult if lots of inflammation or mass it cycstic (may just get fuid which is not representative)
  • Cheap, quick, no anaesthesia required
  • No information on grade
38
Q

Describe the advantages and disadvantages of incisional biopsy (wedge) as a diagnostic approach to injection site sarcoma

A

More accurate, allows appropriate treatment

Gives grading information, does not change prognosis

More expensive, require anesthesia

Can make later treatment more difficult

39
Q

Describe the advantages and disadvantages of excisional biopsy as a diagnostic approach to injection site sarcoma

A
  • More accurate
  • Gives grading information, impairs patients prognosis! (if you need to do a second one then it becomes much more extensive … for insistence if you send it off and then it comes back saying that all your margins are infected then you have to do it again and remove the whole scar … hard!)
  • More expensive, requires anesthesia
  • Can make successful later treatment impossible
40
Q

OUt of cytology, incisional biopsy and excisional biopsy, which would you use to investigate injection site sarcoma in the cat

A
  • Cytology
  • Folowed by incisional biopsy
41
Q

1,2,3 rule for FIIS

When should you always incisional biopsy a suspected injection site sarcoma?

A
42
Q

FIIS: How big does a long nodule have to be to be seen on x ray?

CT?

A

8 mm … less than this you wont see on x ray versus

on CT 2 or 3 mm are visible on CT

43
Q

Tx for ISS

A
  • Aggressive multi-modality treatment
  • Radical surgery necessary at initial excision

Amputation if poss

+/- dorsal spinous processes, dorsal scapula

Wide + deep surfical margins (3cm minimum)

  • Adjuvant radiation therapy (after resection)
  • Wai 10-14d post op
  • RT protocols

Hyperfractionated (curative) small doses frequently

Hypofractionated (palliative) large doses weekly)

Chemotherapy

44
Q

Comment on the use of pre-op radiotherapy for injection site sarcoma

A
  • Very select cases
  • Increases risk of wound dehiscence
  • Makes tissue abmormal
  • RT more effective against microscopic disease
45
Q

ISS: Cytotoxic Chemo

high grade, aggressve behavior or metastatic

A

AC protocol (3 wk cycle)

  • Doxorubicin (main drug used)
  • Cyclophosphamide

Carboplatin

4-6 cycles

46
Q

Comment on future possible therapies to target injection site sarcomas

A

Use of targeted therapy

  • Metronomic chemotherapy
  • Cox inhibitors
  • Tyrosine kinase inhibitors
  • Electrochemotherapy
  • Immunotherapy - melanin vaccines
47
Q

Give examples of injection site guidlines for rabies, FeLV and FVRCP+/-C

A

Rabies: distal right hindlimb (51.7%)

FeLV: distal left hindlimb (28.6%)

FVRCP: distal right forelimb

**Or at base of tail

Principles of Science Strand (11 decks)

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