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ESA 2 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is a neoplasm?

A

Abnormal growth of cells that persists after the initial stimulus has been removed

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2
Q

What is a malignant neoplasm

A

Abnormal growth of cells that persist after stimulus removed AND invades surrounding tissue with potential to spread to distant sites

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3
Q

What’s a tumour

A

Clincally detectable lump or swelling

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4
Q

What is a cancer

A

Malignant neoplasm

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5
Q

What’s a metastisis

A

A malignant neoplasm that has spread from its original site to a new non contiguous site

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6
Q

What’s dysplasia

A

Pre neoplastic alteration in which cells show disordered tissue organisation. NOT neoplastic as this is reversible

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7
Q

What do benign tumours do re site?

A

Remain confined to site of origin

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8
Q

Describe the appearance of a benign tumour

A

Confined to local area with pushing outer margin

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9
Q

Describe a malignant tumour

A

Irregular outer margi and sharp and may show areas of necrosis and ulceration

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10
Q

What do benign neoplastic cells show under micoscope

A

Cells that closely resemble parent tissue (well differentiated )

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11
Q

What do malignant neoplasms look like under microscope

A

Well to poorly differentiated cells, all the way up to anaplastic cells

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12
Q

What’s a aplasia

A

Cells with no resemblance to parent tissue

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13
Q

What comes with worsening differntiation of individual cells?

A 
Increasing nuclear size 
Increased nuclear to cytoplasm ratio
More mitotic figures
Hyperchromasia
Increased variation in size and shape (pleomorphism)
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14
Q

What does the term grade indicate

A

Differentiation

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15
Q

What’s dysplasia

A

Altered differentiation

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16
Q

What causes mutations and what caused cell proliferation in regards to neoplasm

A

Initiations are mutagenic

Promoters are causing proliferation

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17
Q

The population of mutant cells are derived from one cell therefore

A

Monoclonal

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18
Q

What occurs after initiation and promotion

A

Progression

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19
Q

How do we know neoplasms are monoclonal?

A

Study of X linked G6PDH in women where lyonisation has occurred. Normal tissue would be patchwork. Cancer one cell type

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20
Q

What genetic alterations occur (type of gene) to promote neoplasm

A

Proto-oncogenes become abnormally activated
Tumour suppressor genes become inactivated

Both favour neoplasm

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21
Q

What do benign neoplasms end in

A

Oma

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22
Q

What does a epithelial malignant neoplasm end in

A

Carcinoma (90% of malignant tumours)

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23
Q

What does a sarcoma mean

A

It’s malignant and from some type of connective tissue

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24
Q

What is leukaemia

A

Malignant neoplasm of blood forming cells arising in the bone marrow

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25
Q

What is lymphoma

A

Malignant neoplasm of lymphocytes mainly affecting lymph nodes

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26
Q

What is myeloma

A

Malignant neoplasm of plasma cells

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27
Q

What’s a blastoma

A

Malignant neoplasm from immature precursor cells

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28
Q

What (generally) does invasion and mets lead to

A

Increased tumour burden

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29
Q

What are the 3 steps that need to occur for invasion and mets to be successful

A
  1. Grow and invade primary site
  2. Enter a transport system
  3. Grow at secondary (collinisation)

At all points avoiding immune system

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30
Q

What 3 changes are needed for invasion to be possible

A

Altered adhesion
Stromal proteolysis
Motility

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31
Q

If the 3 alterations of a carcinoma has occurred whats it called?

A

Epithelial to mesenchymal transition- new cell phenotype more like a mesencymal cell

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32
Q

What does altered adhesion between malignant cells require?

A

Reduction in E cadherin

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33
Q

What does altered adhesion between malignant cels and stromal proteins require?

A

Changes in integrin expression

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34
Q

What is needed for cells to degrade basement membrane and stroma to invade>

A

Expression of proteases notable matrix metalloproteinases MMP

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35
Q

How is altered motility achieved in cancer cells trying to invade

A

Changes in actin cytoskeleton

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36
Q

What’s a cancer niche?

A

Malignant cells taking advantage of nearby cells growth factors and proteases

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37
Q

How is signalling achieved in malignant cells?

A

Through integrins via small G proteins such as Rho family

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38
Q

What 3 roots can malignant cancers use?

A

Blood vessels
Lymphatic
Fluid in cavities- transcoelomic spread

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39
Q

What’s the greatest barrier to successful formation of mets

A

Failed collinisation

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40
Q

How can you explain the phenomenon of tumour dormancy

A

Micrometastases remain in disease free people

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41
Q

What determines the site of secondary?

A
  1. Regional drainage of blood, lymph of coelomic fluid

2. Seed and soil phenomenon

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42
Q

How do carcinomas typically spread

A

Via lymphatics initially

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43
Q

How do sarcomas tend to spread?

A

Via blood initially

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44
Q

What are common sites of blood borne mets?

A

Lung, liver, Bone, brain

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45
Q

What neoplasms most frequently spread to bone?

A

Breast, bronchus, kidney, thyroid, prostate

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46
Q

What is likelihood of mets determined by

A

Relative size of primary

47
Q

What are the 2 classifications of effects caused by neoplasms

A

Direct local and systemic

48
Q

What are paraneoplastic syndromes

A

Indirect systemic effects of neoplasm

49
Q

What are the 3 main types of systemic effects of neoplasm (classes)

A

Tumour burden
Hormone secretion
Misc

50
Q

What are 4 main local effects of primary and secondary neoplasm

A

Direct invasion and destruction of normal tissue
Ulceration leading to bleeding
Compression of adjacent structures
Blocking of tubes and orrifices

51
Q

What is the parasitic effect of neoplasm

A

Tumour using a lot of energy
Secreted factors such as cytokines causing reduced apetite and weight loss
Malaise
Immunosupression if bone marrow infiltrated
Thrombosis

52
Q

What neoplasms tend to secrete hormones and why?

A

Benign as normally well differentiated, malignant can also eg bronchial SCC

53
Q

What are some of the miscellaneous systemic effects of neoplasia

A 
Neuropathies
Skin issues like pyuritis
Pigmentation
Fever
Finger clubbing
Myositis
54
Q

What are the 5 leading behavioural and dietary risks that attribute to 30% of cancer deaths

A 
High BMI
Lowe fruit and veg
Lack of physical activity 
Tobacco use
Alcohol use
55
Q

What are the 3 main extrinsic factor categories and to what level are they the causes of cancer

A

Chemical, radiation and infections

85%

56
Q

What did the malignant neoplasms caused by 2-napthylamine show us?

A

There is a long delay (sometimes decades between exposure and onset
Risk dependent on dose
Sometimes organ specific

57
Q

What is critical in the adminisirisation of promoters and initiators

A

The sequence, initiator->promoter ++

58
Q

What does Ames test show is?

A

Initiators are mutagens while promoters cause prolonged proliferation of target tissues

59
Q

After promoters what is needed for a monoclonal cell to become fully malignant

A

Progression

60
Q

Mutagenic chemical carcinogens can be what?

A 
Polycyclic aromatic hydrocarbons
Aromatic amines
N nitroso compounds
Alkylation get agents 
Diverse natural products
61
Q

What’s a pro-carcinogen

A

One that is converted by the liver into carcinogen

62
Q

What’s a complete carcinogen

A

One that acts as both initatior and promotor

63
Q

How far does UV light penetrate

A

No deeper than the skin

64
Q

How does ionising radiation damage cells

A

Strips them of electrons. Damage either direct or through free radical production

65
Q

What does nuclear radiation comprise of?

A

Alpha+beta particles

Gamma rays

66
Q

Where is most people exposure to ionising radiation coming from?

A

Background radiation from radon

67
Q

How does ionising radiation directly damage cells

A

DNA bases damaged causing single and double strand breaks

68
Q

What are the two main ways infections can be carcinogenic

A

Direct affect on genes controlling cell growth

Indirect by causing chronic tissue injury

69
Q

How does chronic tissue injury from infection cause neoplasms

A

Regeneration that can act as a promotor for existing mutaton or new mutations through dna replication errors

70
Q

How does HPV have such a link with cervical carcinoma?

A

Direct carcinogen as it inhibts p53 and pRB

71
Q

How does hep B or C have an association with liver neoplasia

A

Liver cell injury and regeneration

72
Q

What is Knudsons 2 hit hypothesis

A

The thought that 2 mutations are required for something that has 2 alleles coding for it. Explains why genetic predispositions arise as these have germ line 1 hit.

73
Q

What do tumour suppressor genes code for

A

Things that inhibit neoplastic growth

74
Q

What are oncogenes

A

Genes that enhance neoplastic growth (abnormally activated versions of proto-oncogenes)

75
Q

Whats the difference between TSG and POG in regards to mutations

A

Only one hit of POG required to promote tumour growth, where as TSG requires 2

76
Q

What is RAS (mutated in 1/3 of all malignant neoplasm)

A

Encodes a small G protein that relays signals to push cell past cell cycle restriction point
Mutant RAS encodes protein always active

77
Q

What does the RB gene code for?

A

Restrains cell proliferation by inhibiting passage through the restriction point (inactivation of both alleles required)

78
Q

What types of things can protooncogenes encode?

A

Growth factors, growth factor receptors, plasma membrane signal transducers, intracellular kinases, transcription factors, cell cycle regulators, apoptosis regulators

79
Q

What do tumour suppressor genes encode

A

Proteins in the same pathways as proto-oncogenes but instead they have anti growth effects

80
Q

What is Xeroderma pigementosum a mutation in? What doe sit lead to?

A

One of the 7 genes of DNA nucleotide excision repair

Very sensitive to UV damage therefore skin cancer at young age

81
Q

What is hereditary non polyposis colon cancer a mutation in

A

One of several DNA mismatch repair genes

82
Q

Familial breast carcinoma is associated with what? What is there normal purpose

A

BRCA1 BRCA2 important in repair of dna double strand breaks

83
Q

What are caretaker genes

A

Tumour suppressor genes that maintain genetic stability

84
Q

What does the adenocarcinoma sequence illustrate?

A

Multiple accumulation of mutations required to process to malignant neoplasm

85
Q

What is the stead accumulation of multiple mutations termed?

A

Progression

86
Q

What are the 6 hallmarks of cancer

A
  1. Self sufficient in growth signals
  2. Resistance to growth stop signals
  3. No limit in times it can divide (immortalisation)
  4. Sustained ability to produce blood vessels (angiogenessis)
  5. Resistant to apoptosis
  6. Ability to invade and metastisis
87
Q

What is a summary of the cancer pathogenesis

A

Somatic cells exposed to carcinogens (initiator and promoter)
Monocloncal population (inherited mutation may be present)
Hallmark changes occur
Genetic instability

88
Q

What cancers account for over half of all new cancers in the uk

A

Breast, lung, prostate, bowel

89
Q

Children younger than 14 are more likely to have what cancers

A

Leukaemia
Central nervous system tumours
Lymphomas

90
Q

What’s the biggest cause of cancer deaths in the uk

A

Lung

91
Q

What are some predicting outcome for cancer

A 
Tumour type
Grade
Stage
Treatments
Age and general health
92
Q

What does the TNM staging describe

A

T is size of primary 1-4
N is mets to lymph 0-3
M is distant mets 0-1

93
Q

How is cancer staging worked out generally

A 
Conversion of TNM to stage
1- local small
2- local big
3-node mets
4- distant mets
94
Q

What staging does lymphoma have? What is it

A

Ann Arbor

  1. single node
  2. 2 nodes one side of diaphragm
  3. Spread to both sides of diagram
  4. Spread to extra lymphatic organs like bone or lung
95
Q

What is Dukes staging used in? What is it

A 
Colorectal carcinoma
A- invasion but not through bowel
B- invasion through bowel wall
C- involvement of lymph nodes
D- distant mets
96
Q

What are the tumour grades?

A

G1- well differntiatied
G2- moderately differentiated
G3- poorly differentiated
G4 anaplastic

97
Q

When is grading used a lot in neoplasms

A

Squamous cell and colorectal

98
Q

What grading system is used for breast cancer

A

Bloom-Richardson- looks at tubule formation, nuclear variation, number of mitosis

99
Q

When can tumour grade be more important than stage

A

Soft tissue sarcoma, primary brain tumours, lymphomas, breast and prostate

100
Q

What are some cancer treatments

A 
Surgery
Chemo
Hormone
Radio
Targeted treatment
101
Q

What’s an adjuvant treatment

A

Given after surgical removal to eliminate sub-clinical disease

102
Q

What’s neoadjuvant treatment

A

Pre surgery to reduce size of primary prior to surgery

103
Q

How does radiation therapy work

A

Kills proliferating cells by triggering apoptosis or interfering with mitosis

104
Q

Why is a fractioned dose of radiotherapy given

A

Minimise normal tissue damage

105
Q

How does ionising radiation preferential kill dividing cells

A

Direct or free radical dna damage detected by cell cycle checkpoints triggering apoptosis s

106
Q

What are 4 types of chemo?

A

Antimetabolites
Alkylating
Antibiotics
Plant derived

107
Q

What’s an issue with chemotherapy

A

Affects proliferating cells but is non specific

108
Q

When is tamoxifen used? What is it an example of?

A

Hormone receptor positive breast cancer
Blocks oestrogen binding
Hormone therapy

109
Q

When is herceptin used? How does it work?

A

Used for breast cancer with over expression of her 2 receptor
Her Epstein blocks its signalling (oncogene targeting)

110
Q

When is imatinib used?

A

In chronic myeloid leukaemia, it inhibits the fusion of protein

111
Q

What are tumour markers main use?

A

Monitoring tumour burden

Also have a role in diagnosis

112
Q

What are some types of tumour markers

A

Hormones, onvogetal antigens, specific proteins and mucins

113
Q

What are screening programs looking for in cancer?

A

Early signs in healthy people when curative chance is highest

114
Q

What are some problems with cancer screening

A

Lead time biase, length bias and overdiagnosis

ESA 2 (10 decks)

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