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Flashcards in Neoplasia Deck (55):
0

What is neoplasia?

When cells have undergone genetic changes to allow them to be unresponsive to their normal growth controls and expand beyond their normal anatomic boundaries.

1

What are four types of cell growth?

1) hypertrophy- cell increases in size
2) hyperplasia- increase in number
3) metaplasia- transformation of one cell type into another
4) dysplasia- abnormal pattern of tissue growth

2

What are the characteristics of a benign neoplasia?

1) well differentiated 2) uniform size and shape 3) normal nuclear morphology 4) few mitoses 5) encapsulated and expansive 6) no metastases

3

What are the characteristics of a malignant neoplasia?

1) poorly differentiated and anaplastic 2) pleomorphic- variable size and shape 3) abnormal nuclear morphology 4) increased and bizarre mitoses 5) non-encapsulated and infiltrative 6) metastasises

4

What is metastasis?

Neoplasms that are discontinuous with the original tumour.

5

How would you name a benign epithelial neoplasm?

A papilloma (surface epithelium) or an adenoma (glandular epithelium)

6

How would you name a malignant epithelial neoplasm?

carcinoma- surface ep.
adenocarcinoma- glandular ep

7

How would you name mesenchymal neoplasms?

Benign- fibroma, lipoma (-oma)
Malignant- fibrosarcoma, liposarcoma (-sarcoma)

8

What are some examples of round neoplasms?

Involving the cells of the blood e.g. lymphosarcoma, mast cell tumour, plasmacytoma, leukaemia.

9

Examples of other neoplasms?

melanoma ( not benign), meningioma
and embryological one is -blastoma

10

What are the three causes of neoplasia at a genetic level?

Single inherited mutated gene
Multiple inherited genes
Acquired somatic mutations

11

What is an example of single inherited mutated gene?

NF-1, NF-2 genes that cause neurofibroma.

12

What are the two causes of acquired somatic mutations?

1) intrinsic factors- Reactive oxygen species or DNA polymerase errors (cant prevent these)
2) extrinsic factors e.g. chemical, radiation, viruses, bracken fern, aflatoxin in fungi.

13

What are the 4 molecular determinants of neoplasia?

1) growth promoting oncogenes e.g. Ras
2) growth inhibiting tumour suppressor genes e.g. p53, RB, APC, Beta-catenin and E-cadherin
3)Apoptosis genes e.g. p53
4) DNA repair genes e.g. BRCA 1 and 2

14

What does Ras do?

It promotes growth and division so if it is mutated it promotes excessive transcription of growth factors.

15

What do p53 and RB do?

The guardians of the genome- They are both pro apoptotic genes. p53 decides what to do at G2/M. RB decides what to do at G1/S, it prevents excessive replication.

16

What is the significance of a mutation in the APC WNT-Beta-catenin pathway?

If the APC gene is mutated then it will constantly allow B-catenin into the cells to promote transcription. Often the mutation is also linked to E-cadherin which is what holds the cells to each other, if this is damaged the mutated cell can grow beyond its own boundaries and even move.

17

Why is angiogenesis important for the neoplastic cell?

Neoplasms cannot grow more than 1-2mm diameter without their own blood supply. They alter the balance between pro-angiogenic and anti-angiogenic substances to promote blood vessel growth.

18

Where can a neoplastic cell get its blood supply from?

It can recruit from bone marrow cells and make its own new blood vessel or it will cause vessels to sprout from existing ones.

19

What are the three different routes of metastasis?

1) Haematogenous spread- via the blood e.g. scarcoma. They will enter the veins and go to the lung/liver.
2) Lymphatic e.g. carcinoma
3) Transcoelomic- seed into body cavities e.g. ovarian adenocarcinomas

20

What is crucial for a neoplastic cell to successfully metastasise?

It needs to have the metastatic signature- it needs to express or suppress genes that are specifically involved in metastasis. This can be used to predict the metastatic potential of a tumour.

21

What immune cells are involved to fight neoplastic cells?

CD8+ T cells, MHC, NK cells and macrophages

22

What is the stem cell theory of cancer?

Stochastic theory- all cells within a tumour can maintain tumour growth.
Stem cell theory- only a minority of the cells within a tumour are capable of sustaining tumour growth. These are known as cancer stem cells or tumour-initiating stem cells (target these).

23

What are the direct effects of neoplasia?

compress tissue, compress blood vessels, block tubular structures, organ rupture, haemorrhage, tumour emboli leading to infarcts.

24

What are the indirect effects of neoplasia?

cachexia, hypercalcaemia, hypoglycaemia, hypertrophic oesteopathy feline paraneoplastic alopecia, hepatocuntaneous syndorme

25

How does neoplasia cause hypercalcaemia?

neoplastic cells produce PTH-like substances that cause the release of calcium from bone by activating osteoclasts.

26

What are the clinical signs of hypoglycaemia?

muscle weakness, lethargy, seizure, incoordination

27

What is hypertrophic osteopathy?

Rare- it is extensive new bone growth at the periosteum in the forelimbs causing lameness. Possibly due to a lesion in the chest that takes up space-unsure...

28

What is feline paraneoplastic syndrome?

Rare- it is symmetrical alopecia of the ventrum, legs and footpads due to inactive follicles, indicated neoplasms of the pancreas.

29

What is hepatocutaneous syndrome?

Seen in dogs- It is associated with liver diseases and causes scaly erythmatous lesions on the skin.

30

Where would you find a canine mast cell tumour?

It occurs in the dermis and subcutaneous tissues. Found on the trunk, less common on the extremities, head or neck and rarely on the scrotum, tail or back. Non-cutaneous- conjunctiva, salivary gland, oral cavity or GI tract.

31

Which breeds are predisposed to canine mast cells tumours?

boxer, boston terrier, bull terrier, bull mastiff, cocker spaniel, labrador retriever, golden retriever.

32

What is the possible cause of a canine mast cell tumour?

Mutation in the c-kit gene that encodes for the KIT protein. KIT is a cell surface growth factor receptor which causes cells to proliferate. 15-40% of cmct have mutated c-kit.

33

What is the Patnaik grading system?

The grading system for mast cell tumour on their severity, It goes from I (benign) to III (malignant). It is based on their histological appearance and is used to estimate their behaviour.

34

What criteria is needed for a Patnaik grade I?

Dermis, monomorphic round cells, medium sized granules, round nucleus, no mitoses.

35

What criteria is needed for a Patnaik grade II?

Dermis and subcutis, moderately pleomorphic round to ovoid cells, fine granules, round to indented nucleus, some with double nucleus, rare mitoses.

36

What criteria are needed for a Patnaik grade III?

Dermis, subcutis and deep tissues, pleomorphic round to ovoid to spindle shaped cells, fine to no granules, indented and vesiculated nuclei, some multinucleate cells, mitoses are common

37

What other method can be used to grade a mast cells tumour?

immunohistochemistry- Ki-67 is normally expressed on actively dividing cells and over-expressed on neoplastic cell tumours. So the number of Ki-67 positive cells can be used as a diagnostic.

38

What danger do the contents of neoplastic mast cells present?

They contain far more heparin and histamine than normal. Histamine binds to H2 receptors in the stomach= gastric acid secretion, in neoplastic cells= gastric ulceration. Potential anaphylactic shock if massive amount of histamine are released.
Heparin can cause local haemorrhage.

39

What is ovine pulmonary adenocarcinoma and which cells are involved?

A lung neoplasm that is caused by JSRV. The neoplastic cell is either a clara cell or a type II pneumocyte= over production of surfactant as they both produce it.

40

What are the clinical signs of OPA?

loss of body weight, exercise intolerance, the 'wheelbarrow test'- lift hind legs and frothy fluid will pour out of the nasal cavity.

41

What do the gross nodules look like in OPA?

firm, grey, variably sized nodules in the lungs.

42

What does the histology of OPA show?

clusters of neoplastic cells around the papillary and acini structures of the lungs- they are locally invasive but never metastasise.

43

How does JSRV transform normal epithelial cells?

It is a retrovirus so either: Insertional mutagenesis (viral genome upstream of an oncogene causing neoplasia). But JSRV has its own gene (env) that perhaps manipulates the proliferation pathway and causes neoplasia.

44

What is a squamous cell carcinoma and where is it found?

It is a malignant neoplasm of squamous epithelium. It is found in the skin, oral cavity, larynx, oesophagus, stomach, urinary tract, penis and vulva.

45

What are the histological and movement characteristics of squamous cell carcinoma?

They are locally invasive and do metastasise, usually to the draining lymphnode and occasionally further afield. The lesions are nodular, proliferative and ulcerated. They are made up of chords or whorls of pleomorphic epithelial cells. Sometimes they have 'keratin pearls' at the centre of the whorl.

46

What type of animal are squamous cell carcinomas found on and why?

They are found on non-pigmented or poorly pigmented and sparsely haired skin. This is due to UV light is a major cause of damage to epithelial cells which makes them become neoplastic.
e.g. white cats and ewes with their tails docked too short (vulval SCC)

47

What is squamous cell carcinoma associated with and what are the clinical signs?

They are associated with bracken fern poisoning which causes squamous cell carcinoma in the oesophagus. The clinical signs of this are: dysphagia, regurgitation and reduced body weight due to blockage of the oesophagus.

48

What is Feline Vaccine Associated Sarcoma (FVAS)?

It is a neoplasm that occurs at the vaccine injection sight of cats e.g. the interscapular region and lateral thorax of cats.

49

What type of neoplasms can arise from FVAS and what are their characteristics?

They can be fibroblastic, myoblastic, chondroblastic or osteoblastic. They are malignant, spread into surrounding tissue and can metastasise.

50

What did the US panel do in order to reduce the incidence of FVAS and what has this resulted in?

They changed vaccination region from the interscapular region (due to difficult mass removal), e.g. Rabies in R rear leg and FeLV in L rear leg and others in the shoulder region. This has changed the distribution of the neoplasms seen to these regions.

51

What is the suggested cause of FVAS?

Some say that the rabies and FeLV vaccines are the cause while others say that it is the adjuvant that is used.

52

What is Tasmanian devil facial tumour and what is it?

It is poorly differentiated, highly pleomorphic, malignant Schwann cells (surrounds peripheral nerves and produces myelin)
The transmission of a tumour cells between devils meaning that all of the tumours have the same karyotype. It is known as an allograft cancer.

53

What is the reason for the tumour cells not being recognised?

There is no recognition of the different MHC molecules on the tumour cells. This may be due to the lack of genetic diversity in the devil population.

54

What is a teratoma?

A neoplasm that arises from a multipotent cell e.g. a cell from more than on germ layer. This causes a neoplasm with mixed tissues that is always benign and they are very very rare.