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Principles of Disease > Tumour Pathology > Flashcards

Tumour Pathology Flashcards

1
Q

What is a tumour?

A

A tumour is an abnormal mass of growing tissue

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2
Q

Describe tumour growth.

A

Growth is uncoordinated with that of the surrounding tissue and continues after the removal of any stimulus which caused it.

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3
Q

What are the two types of tumour?

A

Benign

Malignant

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4
Q

What is the difference between benign and malignant tumours?

A

Malignant tumour is able to metastasise and spread throughout the body.

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5
Q

What characterises a benign tumour?

A
  • Non-invasive growth pattern
  • Usually encapsulated
  • No invasion/metastases
  • Cells similar to normal- well differentiated
  • Function similar to that of normal tissue
  • Rarely cause mortality- unless in bad place (brain/heart etc)
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6
Q

What characterises a malignant tumour?

A
  • Invasive growth pattern
  • No capsule/or capsule is breached by tumour cell
  • Cells are abnormal- poorly differentiated
  • Loss of normal function- spread of cancer
  • Frequently cause death
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7
Q

Which type of tumour is cancer?

A

Malignant

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8
Q

Which type of tumour frequently causes death?

A

Malignant

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9
Q

What is tumour nomenclature based on?

A

The tissue of origin and whether or not it is malignant.

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10
Q

What are tumours called in glandular epithelium?

A 
Benign = Adenoma
Malignant = Carcinoma
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11
Q

What are tumours called in squamous epithelium?

A 
Benign = Squamous papilloma 
Malignant = Squamous carcinoma
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12
Q

What are tumours called in the bone?

A 
Benign = Osteoma 
Malignant = Osteosarcoma
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13
Q

What are tumours called in the fat?

A 
Benign = Lipoma 
Malignant = Lipo-sarcroma
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14
Q

What are tumours called in the fibrous tissue?

A 
Benign = Fibroma 
Malignant = Fibro-sarcroma
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15
Q

What is cancer called in the blood?

A

Only WBC, only malignant = Leukaemia

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16
Q

What is cancer called in the lymphoid tissue?

A

Only malignant = Lymphoma

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17
Q

What are tumours in the melanocyte tissue called?

A 
Benign = Naevus
Malignant = Melanoma
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18
Q

What are tumours in neural tissue called?

A 
CNS = Astrocytoma 
PNS = Schwannoma
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19
Q

What are tumours in germline cells called?

A

Teratomas- develop in gonads, composed of various tissues.

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20
Q

What are the properties of cancer cells?

A
  • Loss of tumour suppressor genes
  • Gain of oncogene function
  • Altered cellular function
  • Abnormal morphology
  • Capable of independent growth
  • Tumour biomarkers
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21
Q

Why do cancer cells lose the tissue function?

A

Loss of cell-to-cell adhesion
Altered cell-to-matrix adhesion
Production of tumour-related proteins including tumour biomarkers.

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22
Q

What are tumour biomarkers?

A

Tumour biomarkers are biochemical indications of tumour development and progression.

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23
Q

Why are tumour biomarkers utilised clinically?

A

To allow diagnosis- used in screening, prognosis and prediction.

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24
Q

What is alpha-fetoprotein a tumour biomarker for?

A 
Teratomas of testes (testicular cancer)
Hepatocellular carcinoma (liver cancer)
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25
Q

What is carcinoma-embryonic antigen (CEA) a tumour biomarker for?

A

Colorectal cancer.

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26
Q

What is oestrogen receptor a tumour biomarker for?

A

Breast cancer.

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27
Q

What is prostate specific receptor a tumour biomarker for?

A

Prostate cancer.

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28
Q

What is kRas?

A

Biomarker for colorectal cancer.

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29
Q

What is Braf?

A

Biomarker for melanoma.

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30
Q

What are EGFR/PD-L1

A

Biomarkers for lung cancer.

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31
Q

What is HER2?

A

Biomarker for breast/gastric cancer.

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32
Q

What does tumour morphology exhibit?

A

Cellular and nuclear pleomorphism (marked variation in shape and size)

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33
Q

What is tumour growth based on?

A

A balance between angiogenesis and apoptosis (new blood vessel formation and death).

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34
Q

What is angiogenesis?

A

Angiogenesis is the formation of new blood vessels by tumours. It is required in order to sustain tumour growth and provides a route for tumours to enter into the circulation. More blood vessels in a tumour leads to a poorer prognosis due to faster spread.

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35
Q

What is apoptosis?

A

Programmed cell death, active cell process which regulates cell growth, utilised in chemotherapy and radiotherapy,

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36
Q

What is metastases?

A

Spread of cancer leading to the formation of secondary tumours.

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37
Q

How does tumour invasion work?

A

It is a multi-step process with increased matrix degradation by proteolytic enzymes. There is altered cell-to-cell adhesion and cell-to-matrix adhesion.

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38
Q

What are the modes of cancer spread?

A

Local spread
Lymphatic spread
Blood spread
Trans-coelomic spread

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39
Q

Describe local spread.

A

A malignant tumour invades the connective tissue. It then enters the lymphatics or blood vessels to travel.

40
Q

Describe lymphatic metastasis.

A

A malignant tumour has adherence to the lymph vessels. There is invasion from lymphatics into the lymph nodes and metastasis is clinically evident.

41
Q

Describe circulatory metastasis.

A

A malignant tumour has adherence to the blood vessels. There is invasion from blood vessels into a tissue which can either be supportive or hostile, but metastasis will be clinically evident either way.

42
Q

Describe trans-coelomic spread.

A

Trans-coelomic spread is a specialised form of metastasis across body cavities. For example, the pleural and peritoneal cavities.

43
Q

Where do breast and prostate cancers often spread to?

A

Bone

44
Q

Where does colorectal cancer often spread to?

A

Liver

45
Q

Where does ovarian cancer often spread too?

A

Peritoneum- can go in two opposite directions due to dual vascularisation.

46
Q

What are the local effects of benign tumours?

A

Pressure, obstruction but usually not mortality unless there is an obstruction of a major organ (e.g. cardiac blockage)

47
Q

What are the local effects of malignant tumours?

A
  • Pressure
  • Obstruction
  • Tissue destruction (ulceration/infection)
  • Bleeding (anaemia/haemorrhage)
  • Pain (pressure on nerves, perineural infiltration, bone pain from pathological fractures)
  • Effects of treatment (chemotherapy, radiotherapy etc)
48
Q

What are the systemic effects of malignant tumours (cancer)?

A

Weight loss (cancer cachexia)
Secretion of hormones (normal/abnormal)
Paraneoplastic syndromes
Effects of treatment

49
Q

Describe normal/abnormal hormones secreted by a tumour.

A

Normal hormone secretion refers to secretion of hormones by a tumour of an endocrine organ. However, this still may be secreted outwith normal ranges.
Abnormal hormone secretion refers to the secretion of hormones from a tumour in a place that usually doesn’t secrete them.

50
Q

What are paraneoplastic syndromes?

A

Paraneoplastic syndromes cannot be explained by the local or metastatic effects of tumours- they relate to the immune mechanism and hormone/growth factor production.

51
Q

Why is it important to detect cancer at an early stage?

A

To reduce morbidity and mortality.

52
Q

What is particularly effective in reducing cancer mortality?

A

Detection at the pre-invasive stage.

53
Q

How is pre-invasive cancer detected?

A

Identification of dysplasia and intraepithelial neoplasia.

54
Q

What is dysplasia?

A

Dysplasia is a pre-malignant change that is the earliest form of malignancy that we can detect.

55
Q

Where is dysplasia recognised?

A

Epithelium

56
Q

What are the features of dysplasia?

A

Disorganisation of cells- increased nuclear size, increased mitotic activity, abnormal mitoses.
Graded in low-high grades.
No invasion.

57
Q

What does early detection of cancer require?

A

Effective screening programmes.

58
Q

What is the normal mechanism of cellular replication?

A

Mitosis

59
Q

What are the stages of mitosis?

A

Interphase, prophase, metaphase, anaphase, telophase followed by cytokinesis.

60
Q

What does interphase consist of?

A

G1 (Growth 1)
S (Synthesis)
G2 (Growth 2)

61
Q

Why are there “quality check” controls in cell division?

A

To ensure that both daughter cells have a complete chromosome complement and ensure that any damage is detected.

62
Q

What are control points?

A

Control points act as checkpoints/brakes and allow evaluation before the process is activated to continue. They are able to monitor and regulate progress and can prevent progression at specific points.

63
Q

What are control points usually made up of?

A

Control points are usually complexes of cyclically active/inactive enzyme switches which can control entry into phases.

64
Q

When do checkpoints occur?

A

G1 phase
S phase
Metaphase

65
Q

What is the G1 checkpoint?

A

G1 checkpoint- occurs near the end of G1 in interphase- monitors CELL SIZE- there has to be sufficient mass to form two daughter cells. This contols entry into the synthesis phase.

66
Q

What is the G2 checkpoint?

A

G2 checkpoint- occurs near the end of G2 in interphase and assesses the SUCCESS OF DNA REPLICATION to ensure that each daughter cell receives a complete DNA copy.

67
Q

What is the M (metaphase) checkpoint?

A

M checkpoint- occurs during metaphase within the mitotic phase and monitors CHROMOSOME ALIGNMENT to ensure that daughter cells receive one chromatid from each chromosome. It controls the entry into anaphase and therefore determines exit from mitosis into cytokinesis.

68
Q

What are CDK/Cyclin complexes?

A

Catalytic sub-unit cyclin-dependent kinases are activated by regulatory sub-unit cyclins. When activated, they aid the cell cycle.

69
Q

What do activated CDK/Cyclin complexes do?

A

Phosphorylates target proteins and activates them to coordinate entry into the next stage of the cell cycle.

70
Q

What are CKI’s?

A

Cyclin-dependent kinase inhibitors

These bind to CDK/Cyclin complexes and prevent them from aiding the cell cycle.

71
Q

Name two examples of CKIs.

A

INK4As, CIP/KIP.

72
Q

What is the retinoblastoma gene?

A

A gene that regulates the cell cycle- it encodes a pRb phosphoprotein expressed in nearly every human cell.

73
Q

When is the retinoblastoma gene activated?

A

Active when NOT phosphorylated.

74
Q

What does retinoblastoma actually do within the cell?

A

Inhibits transcription factors.

75
Q

How do the G1 CDKs interact with retinoblastoma?

A

G1 CDK’s phosphorylate retinoblastoma, allowing it to stay in its inactive form. This prevents it from inhibiting transcription factors and allows the promotion of transcription genes required for S-phase DNA replication.

76
Q

What does phosphorylated pRb lose affinity for?

A

E2F- a powerful signal for cell cycle activation.

77
Q

What is p53 triggered by?

A

DNA damage.

78
Q

What can p53 do?

A

Repair DNA
Arrest the cell cycle
Stimulate apoptosis

79
Q

What causes cells to lose control of proliferation?

A

Mutations in the genes regulating cell division, apoptosis, and DNA repair.

80
Q

What are two frequently disrupted control pathways?

A

Cyclin/CDK-pRb-E2F pathway

p53 pathway

81
Q

How does p53 maintain the integrity of the genome?

A

p53 maintains the integrity of the genome- cells with mutated p53 do not G1 arrest or repair damaged DNA. Genetically damaged cells proliferate and form malignant neoplasms.

82
Q

Where are most cancers dysregulated?

A

G1-S restriction point.

83
Q

What are genotoxins?

A

Toxins that cause irreversible damage to DNA.

84
Q

What are the types of genotoxin?

A

Chemical agents (NMU)
Non-chemical agents (ionising radiation/UV light)
Certain viruses can also act as genotoxins.

85
Q

What are tumour suppressor genes?

A

Anti-oncogenes.

These act as brakes to the cell cycle and function to restrain inappropriate cell growth, preventing cancer.

86
Q

What can mutations in anti-oncogenes (tumour suppressor genes) do?

A

Favour cellular proliferation and can lead to the development of cancers.

87
Q

Give an example of a tumour suppressor gene.

A

Retinoblastoma- inhibits transcription factors.

88
Q

What types of gene may be affected in hereditary cancer syndromes?

A

Tumour suppressor genes
Mismatch repair genes
Proto-oncogenes

89
Q

What are proto-oncogenes?

A

Proto-oncogenes are normal genes coding for normal growth-regulating proteins.

90
Q

What are oncogenes?

A

Oncogenes are derived from proto-oncogenes but are cancer causing. They are activated by alterations in proto-oncogene structure or dysregulation of their expression.

91
Q

In DNA, what are critical cellular targets for damage by ionising radiation/oxidising and alkylating agents?

A

Purine and pyrimidine bases- can be critically damaged by this.

92
Q

What do chemical carcinogens form when they react with DNA?

A

Covalently-bound products called ADUCTS.

Adduct formation can lead to the activation of oncogenes or the loss of anti-oncogene function.

93
Q

What kinds of higher energy radiation are also carcinogenic?

A

Gamma radiation, UV radiation and X-rays.

94
Q

How does radiation cause direct DNA damage?

A

DNA directly absorbs the UVB photon. This causes thymine base pairs to turn into thymine dimers which cannot be replicated properly.

95
Q

What are onco-viruses?

A

Carcinogenic viruses which insert their genome near a host proto-oncogene. The viral promoter will then proceed to cause over expression.

96
Q

Is carcinogenesis usually implemented through a single mutation?

A

No- it is a multi-step process. Activation of several oncogenes/deactivation of more than 2 anti-oncogenes is usually required for carcinogenic development.

Principles of Disease (22 decks)

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