Neoplasia Flashcards

1
Q

What is a neoplasm? Compared to hyperplasia or regeneration?

A

Neoplasm is an abnormal growth that continues to proliferate in the absence of a stimulus. Both hyperplasia and regeneration have a stimulus (growth factor) - and stop on removal of this stimulus

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2
Q

What is a malignant neoplasm?

A

An abnormal growth that invades surrounding tissue with potential to spread to distant sites

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3
Q

What is the difference between a neoplasm, tumour and cancer?

A

A tumour is any growth- detectable lump or swelling
A neoplasm is a type of tumour
Cancer is a malignant neoplasm

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4
Q

Why is dysplasia not neoplastic?

A

Because it is reversible. It has the potential to become neoplastic and malignant - and often is pre-neoplastic

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5
Q

What are the macroscopic differences between a benign tumour and malignant tumour and why?

A

Benign - usually defined outer margin and refined to a local area - smoother

Malignant - usually rough outer edges - may have necrosis/ulceration

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6
Q

Why might malignant tumours show necrosis?

A

Because some areas of the tumour may not have angiogenesis - necrosis. Or tumour is growing faster than angiogenesis can provide blood supply - necrosis.

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7
Q

Does a well differentiated neoplasm always mean it is benign?

A

No some malignant neoplasms are well differentiated. But benign neoplasms are always well differentiated.

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8
Q

Can malignant tumours be any of: poorly, moderately and well differentiated?

A

Yes

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9
Q

What is an anaplastic tissue?

A

One that has no resemblance to any tissue

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10
Q

Which 4 microscopic features correlate with a poor differentiated tissue?

A
  • Mitosis seen (sometimes abnormal forms - aneuploidy)
  • Cellular and nuclear size size variation
  • Nuclear hyperchromasia
  • Increased nuclear:cytoplasm ratio
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11
Q

What is nuclear hyperchromasia?

A

Nucleus stains more deeply than normal

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12
Q

What is pleomorphism?

A

Variation in size and shape of cells and nuclei

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13
Q

Is high grade tumour poorly or well differentiated?

A

High grade tumour is poorly differentiated

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14
Q

Does grade of cancer correlated with prognosis? What 3 factors do clinicians look at in the cell when grading a breast cancer for example (think microscopic features)?

A

Yes - grade 3 much less survival, and grade 2 less survival than 1.

Look at 1) Amount of tubules 2) Mitotic figures 3) Nuclear pleomorphism - then Grade either 1, 2, 3 depending on how differentiated the malignant neoplasm is.

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15
Q

Is a carcinoma in situ a reversible growth?

A

No. Once a growth goes from dysplasia to carcinoma in situ it is irreversible.

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16
Q

When looking at skin dysplasia - what is reduced keratin evidence of?

A

Reduced differentiation —> dysplasia —> often preceded malignant tumour. Dysplasia is characterised by abnormal differentiation.

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17
Q

When does an in situ tumour become an invasive tumour?

A

When it breaks through the basement membrane

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18
Q

Are most cancers initiated by intrinsic or extrinsic risk factors?

A

85% are extrinsic risk factors, 15% thought to be genetic. Get information by looking at ethnic migrant groups and comparing.

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19
Q

What are initiators and promotors? What is the relevance of them?

A

Initiators are mutagens that can cause cancer, promotors cause the cell proliferation. You need an initiator followed by prolonged promotor exposure to proliferate.

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20
Q

How does a monoclonal pre-neoplastic growth become polyclonal? What is this process termed? Are mutagens intrinsic/extrinsic/both?

A

Accumulation of more mutagens - called progression. Mutagens can be both intrinsic and extrinsic

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21
Q

What is the definition of monoclonal?

A

A group of cells that are originated from the same founding cell.

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22
Q

What is lyonisation?

A

X-linked inactivation of one allele in every female cell. Occurs in early embryogenesis.

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23
Q

What are oncogenes compared to proto-oncogenes?

A

Porto-Oncogenes are normal genes that code for proteins involved in cell growth. When photo-oncogenes become abnormally activated they become oncogenes.

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24
Q

What occurs with tumour suppressor genes in cancer?

A

They normally suppress neoplasm growth - they can become inactivated - favouring neoplastic growth

25
Q

What is the difference between leukaemia, lymphoma, myeloma?

A

Leukaemia - malignant neoplasm of WB cells from bone marrow
Lymphoma - malignant neoplasm of lymphocytes, mainly lymph nodes
Myeloma - malignant neoplasm of plasma cells

26
Q

What is pluripotent? Compared to totipotent?

A

Stem cells that can produce any cell in the body (but not placental or extra embryonic cells as with totipotent).

27
Q

Do blastomas mainly occur in adults or children? What does it blastoma usually mean?

A

Mainly children - derived from immature precursor cells

28
Q

What are the chances of survival with a stage 1 compared to stage 4 cancer? Why less chance of survival with stage 4 cancer?

A

Stage 1 - 95%
Stage 5 - 10%

Because of the huge tumour burden on metabolic resources - less for organs/body

29
Q

What are the most lethal actions of neoplastic tumours?

A

Invasion and Metastasis

30
Q

Can tumour metastases give off metastases themselves? Do benign tumours metastasise?

A

Yes

No

31
Q

What are the three steps to invasion and metastases? Does the immune system attack all steps? Which of these steps are the main limiters to metastases and why?

A

1) Grow and invade primary site
2) Be transported to new secondary site and lodge
3) Be able to grow at secondary site

Yes immune system attempts to stop all stages

Main limiting stages are 2 and 3 - as many cancer cells get lodged/damaged/broken in transport system where they then cannot grow. 3 is the biggest barrier to cancer cells because many can lodge in a site but don’t proliferate there so don’t form metastases.

32
Q

What is the term used to describe growth of tumour cells at a secondary site?

A

Colonisation

33
Q

Why do you usually need a substantial sized primary tumour for metastases to develop?

A

Because metastases formation is an inefficiency process that requires enough cells to break off from the primary tumour and travel elsewhere in the body to be able to form a secondary tumour

34
Q

Are most cancer cells epithelial?

A

Yes

35
Q

What are mesenchymal cells?

A

Multipotent stromal (connective tissue) cells that can differentiate into many cells e.g. chondrocytes/myocytes/adipocytes/osteoblasts etc.

36
Q

What 3 cellular alterations are needed for invasion of malignant neoplasm into surrounding tissue? Explain them. What is this alteration process called?

A

1) Altered adhesion - changes in cadherins & integrins
2) Stromal proteolysis - MMPs
3) Motility - Actin

called epithelial-to-mesenchymal transition (EMT)

37
Q

What is the role of E-cadherin in general and what happens in malignant cells? What is the role of integrins and what happens in malignant cells? What are the role of MMPs in invasion?

A

‘Calcium dependent adhesion’ in epithelial cells - keep cells together with adherins - in malignant cells there is a reduction in E-Cadherin expression so they can invade.

Integrins - bind cell to extracellular matrix - in malignant cells these are altered to allow invasion through basement membrane/stroma etc

MMPs - degrade extracellular matrix to allow invasion (proteolysis)

38
Q

How do cancer cells create their own niche?

A

Use cells surrounding e.g. fibroblasts, endothelial cells, inflammatory cells - these cells even release growth factors and proteases that are then used by the cancer cells to degrade ECM

39
Q

Why does E-cadherin and Integrin expression decrease and increase in malignant invasion/metastases?

A

Because expression reduces when malignant cells are breaking away from each other to be able to invade and enter a transport system (e.g. blood) - then once in a location need to increase expression to be able to bind to each other and the endothelium again.

40
Q

What does transcoelomic spread mean?

A

Spread of metastases through cavities e.g. peritoneal, pericardial, pleural, in brain

41
Q

Which 3 transport routes do cancer cells have to metastasise?

A

Blood
Lymphatic system
Transcoelomic

42
Q

What are micrometastases?

A

Microcolonies of cancer cells that have failed to grow into metastases at their secondary site (biggest barrier to cancer cells)

43
Q

What can cause tumour dormancy (3)

A
  • Hostile secondary site
  • Immune system
  • Failed angiogenesis
44
Q

What is tumour dormancy and what does it have to do with cancer relapses?

A

Tumour dormancy is many micrometastases in an apparantly disease-free person. When relapses occur it is typically due to one or more micro metastases starting to grow

45
Q

What two things determine the secondary site of a tumour?

A

1) Mode of transport - predict where it will go from blood compared to lymph/transcoelomic
2) ‘Niche’ in new location - whether environment is favourable

46
Q

Where would cancers likely spread if travelling via lymphatics, blood, transcoelomic?

A

Lymphatics - Lymph nodes
Blood - normally next capillary bed - liver/lungs
Transcoelemic - somewhere close in that space

47
Q

Carcinomas normally spread via _____ then ______ and sarcomas normally spread via ________

A

Lymphatic then blood

Blood

48
Q

What are common secondary sites for blood borne metastases (4)?

A

Lung bone liver brain

49
Q

Breast bronchus kidney, thyroid and prostate most commonly metastasis to _________

A

Bone

50
Q

Is small cell bronchial carcinoma aggressive or not in terms of metastases? Compared to basal cell carcinoma of the skin?

A

It metastasises early so is aggressive. Basal cell carcinoma almost never does.

51
Q

The likelihood of metastases is related to the ______ of primary tumour

A

Size

52
Q

What is paraneoplastic syndrome as opposed to local effect’?

A

Paraneoplastic syndrome is a collection of signs/symptoms due to systemic effect son cancer e.g. burden, hormones etc whereas local effect is the effect on the local tissue e.g. compression.

53
Q

Local effects and hormonal effects are common for which type of neoplasm?

A

Benign

54
Q

What 4 ways can a tumour affect the tissue surrounding it locally (local effect) ?

A
  • Invasion and destruction
  • Form ulcers that may bleed
  • Compress structures
  • Blocking tubes/orrifices
55
Q

Give 4 examples of systemic signs/symptoms of tumour

A
  • Cachexia/Anorexia
  • Immunosuppression
  • Malaise
  • Thrombosis - hypercoaguable
56
Q

Are benign tumours of endocrine glands well differentiated? What does this lead to? Are these the only type of tumours that can produce hormones?

A

Yes means they can secrete hormones - ed thyroid adenoma. No other malignant tumours can produce hormones e.g. small cell bronchial carcinoma/bronchial squamous cell carcinoma

57
Q

What hormones do small cell bronchial carcinoma/bronchial squamous cell carcinoma produce?

A

small cell bronchial carcinoma can produce ACTH as it is a neuroendocrine carcinoma, bronchial squamous cell carcinoma can produce PTH-like hormone

58
Q

What other miscellaneous systemic effects can occur?

A

Neuropathies affecting brain/peripheral nerves, skin problems such a pruritis and abnormal pigmentation, fever, finger clubbing and myositis (inflammation of muscles)