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PVS > Oncology > Flashcards

Oncology Flashcards

1
Q

Define neoplasia

A

New growth, the abnormal proliferation of cells. A neoplasm is an abnormal mass of tissue that occurs as a result of abnormal cell proliferation

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2
Q

What is meant by a benign neoplasia?

A

Nevi or skin moles

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3
Q

What is a malignant neoplasia?

A

Cancer

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4
Q

What is a pre-mallignant neoplasia?

A

Carcinoma in situ. Some changes to become abnormal but not quite cancer

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5
Q

What are the 2 potential primary tumour types?

A

Monoclonal (one cell type) or polyclonal (more than one cell type)

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6
Q

How is neoplasia related to the cell cycle?

A

Cell division is a basic property of cells, but aberrant cell division is likely to create risk of cancer in any individual

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7
Q

What 2 groups of factors are involved in cancer?

A
  • Genetic factors (predisposition)

- Environmental (epigenetic)

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8
Q

Genetic factors may leadto cancer?

A
  • Chemical and physical carcinogens
  • Point mutations
  • Chromosomal alterations
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9
Q

Outline what chromosomal alterations may lead to cancer

A
  • Change in composition of a chromosome
  • Change in chromosome number
  • Can involve all chromosomes (damaged, replaced) and can be inherited
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10
Q

How do epigenetic regulations occur in cells?

A

Modifications of histones and methylation of DNA in the chromatin

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11
Q

How may epigenetic alterations lead to cancer?

A
  • DNA methylation and histone modification can be altered in cancer
  • Do not alter the composition of the DNA, but alter the expression
  • e.g. DNA methylation can silence DNA
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12
Q

What is the multiple-hit hypothesis in cancer?

A
  • One mutation (genetic or epigenetic) is not sufficient to produce cancer
  • Few forms only arise from 1 genetic modification
  • Therefore require multiple alterations to lose cellular control
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13
Q

List the hallmarks of cancer

A
  • Self sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Limitless replicative potential
  • Evasion of apoptosis
  • Sustained angiogenesis
  • Tissue invasion and metastasis
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14
Q

Explain the self-sufficiency in growth signals in cancer

A
  • Normally tissues have hormones and growth factors that control proliferation. repair and replacement
  • Cancer cells become autonomous and grow/replicate without these
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15
Q

Explain the insensitivity to anti-growth signals in cancer cells

A
  • Normally have mechanisms that halt cell cycle and decide to continue or apoptose
  • Cancer cells are non-responsive to these
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16
Q

Explain the sustained angiogenesis in cancer cells

A
  • Secrete factors involved in tissue regeneration

- Induces new blood vessel growth ensuring own blood supply

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17
Q

How do the hallmarks of cancer aid the development of cancer?

A
  • Allows cell survival in an environment unfavourable to other cells
  • Continue to develop
  • When cellular clones within tumour acquire another modification, allows improved survival and proliferation, and so make up the majority of that tissue/tumour
  • Continue to accumulate hallmarks until optimal survival characteristics are acheived
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18
Q

What are oncogenes?

A

Genes that promote cancer

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19
Q

What are tumour suppressor genes?

A

Genes that prevent aberrant cell proliferation

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20
Q

What is the relationship between oncogenes and tumour suppressor genes?

A

Imbalance between these genes leads to neoplasia

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21
Q

How are the oncogenes expressed in mammals?

A

c-Src, are proto-oncogenes, over-expression and sustained activity (i.e. gain of function) converts proto-oncogenes into oncogenes

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22
Q

How can mammalian proto-oncogenes gain function?

A
  • Mutation

- Translocation

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23
Q

How do proto-oncogenes gain function by mutation?

A
  • Ras and activation of MAPK

- Many tumours

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24
Q

Outline how self-sufficiency in growth signals leads to deregulation of receptor signalling

A
  • Over expression of receptors on the membrane

- Alteration in protein structure (and so signalling without the ligand)

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25
Q

What allows cancer cells to have limitless replicative potential?

A
  • In normal replication, telomere shortens with each replication and undergoes apoptosis when gets too short
  • Express telomesase, and so maintain long telomeres
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26
Q

How are tumour suppressor genes involved in cancer and give examples?

A
  • Loss of function induces caners through mutation, deletion or DNA methylation
  • E.g. regulators of apoptosis (p53), inhibitors of cell cycle (p16m, p21, Rb), DNA repair genes
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27
Q

What are the 3 main pre-neoplastic changes?

A
  • Hyperplasia
  • Metaplasia
  • Dysplasia
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28
Q

What histological features are indicative of neoplasia?

A
  • Increased cellularity
  • Increased nuclear to cytoplasmic ratio (bigger nucleus)
  • Variation in cell and nuclear size between cells
  • Nuclear morphology altered
  • Necrosis
  • Mitotic discs
  • Cells separate from stroma (individualised)
  • Invasive cells
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29
Q

What are some histological features of benign neoplasms?

A
  • Well differentiated mass
  • Good demarcation from surrounding tissue
  • Low mitotic rate
  • Minimal nuclear or cell pleomorphism (more similar to normal tissue)
  • Minimal necrosis
  • Low haematotic rate
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30
Q

What are some histological features of a malignant neoplasm?

A
  • Invasive to surrounding tissues incl. blood/lymph vessels
  • Disorganisation of tissue
  • Increased nuclear or cell pleomorphism
  • Large/multiple nuclei
  • High mitotic rate
  • Necrosis
  • High cellularity, minimal stroma
  • Scirrhous or desmoplastic region
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31
Q

Compare the growth rate of benign and malignant tumours

A
  • Benign: slow, progressive, rare mitotic figures, normal mitotic figures
  • Malignant:slow to rapid growth, many mitotic figures, abnormal mitotic figures
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32
Q

Compare metastasis of benign and malignant neoplasms

A
  • Benign: no metastasis

- Malignant: frequent metastasis

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33
Q

Compare the host consequences of benign and malignant neoplasms

A
  • Benign: space occupying lesion, consequence depends on location (e.g. spine may be dangerous)
  • Malignant: life threatening
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34
Q

What is an adenoma?

A

Benign glandular epithelial neoplasm

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35
Q

What is a papilloma?

A

Benign protective epithelium (squamous or transitional) neoplasm

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36
Q

What is the suffix for a benign mesenchymal or nervous tissue neoplasm?

A
  • Oma
  • Fibrous tissue = fibroma, fat tissue = lipoma
  • Astrocytes = astrocytoma
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37
Q

What is an adenocarcinoma?

A

A malignant tumour of the glandular epithelium

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38
Q

What is a carcinoma?

A

A malignant tumour of the protective epithelium (squamous or transitional)

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39
Q

What is the suffix for a malignant mesenchymal neoplasm?

A
  • Sarcoma
  • Fibrous tissue: fibrosacoma
  • Fat tissue: liposarcoma
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40
Q

How are malignant tumours of nervous tissue and round cells named?

A

Use the word malignant or specific names

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41
Q

What do the letters of TNM staging stand for?

A
  • T: size of primary tumour
  • N: degree of lymph node involvement
  • M: extent of metastasis
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42
Q

Outline tumour grading

A
  • Indicates how similar/dissimilar a neoplasm is to normal tissue
  • Higher grade = more dissimilar
  • Linked to prognosis and response to therapy
  • Indicates biological behaviour
43
Q

What is tumour grading affected by?

A
  • Tissue type

- i.e. skin tumour grade 2 does not correspond to glandular tumour type 2

44
Q

What are the tumour grades?

A

I: well differentiated
II: moderately differentiated
III: poorly differentiated/anaplastic

45
Q

What is tumour staging?

A
  • Gives indication of extend of growth and spread

- Guides clinician in developing a therapeutic plan and prognosis

46
Q

Give the different categories of T in tumour staging

A

T0-T4, small to large

47
Q

Give the categories of N in tumour staging

A

N0: no LN involvement
N1: regional LN involvement
N2: distant LN involvement

48
Q

Give the categories of M in tumour staging

A

M0: no detectable metastases
M1: detectable metastases

49
Q

What diagnostic techniques are required for tumour staging and grading?

A
  • Some imaging
  • Macroscopic examination
  • Microscopic examination (histopathology, mainly for diagnosis and grading)
  • Immunohistochemistry to assess molecular markers (diagnosis and predictive response to treatment)
50
Q

List some changes associated with neoplastic disease

A
  • Loss of function
  • Pain
  • Swelling and inflammation
  • Necrosis
  • Loss of normal morphology
51
Q

What are metastases?

A

Spread of the tumour

52
Q

What is the result of tumour growth?

A

Space occupying lesion with the possibility of expansion beyond the site of growth, but primary tumours are only responsible for 10% of deaths from cancer

53
Q

What are the consequences of metastases?

A
  • 90% of deaths are due to metastases
  • Changes treatment, other complications
  • Long term follow up, may not be apparent for long time after initial diagnosis and treatment of primary tumour
54
Q

Outline the linear progression model of tumour spread and metastasis

A
  • During local progression, aggressive cells selected, dissemination initiates
  • Sequential seeding of metastatic sites
  • Each metastatic site produces more seeds as it develops
55
Q

Outline the early dissemination/parallel progression model of tumour spread

A
  • Dissemination starts early
  • Different organs seeded in parallel, not sequentially
  • Growth of disseminated tumour cells may need extra factors produced by primary tumour or micro-environment
56
Q

Outline the metastatic cascade

A
  • Primary tumour formation
  • Localised invasion of lymph/blood vessels
  • Intravasation
  • Transport through circulation
  • Arrest in microvessels of various organs
  • Extravasation
  • Formation of a micrometastasis
  • Colonisation and formation of a macrometastasis
57
Q

Outline the process of invasion and intravasation of metastatic cells

A
  • Breach in basement membrane
  • Cells highly invasive through process that changes their phenotype from epithelial to mesenchymal (Epithelial to Mesenchymal transition, EMT)
58
Q

How does the breach in the basement membrane in metastasis occur?

A

Secretion from tumour cells of matrix metalloproteinases (MMPs) which degrade components of the ECM

59
Q

What are the consequences of EMT to cancer cells?

A

Acquire invasiveness, motility, heightened resistance to apoptosis

60
Q

What features of epithelial cells are lost in the process of EMT?

A
  • Cytokeratin (intermediate filament) expression
  • Epithelil adherens junction protein E-cadherin
  • Epithelial cell polarity
61
Q

What features of mesenchymal cells are acquired in the process of EMT?

A
  • Fibroblast like shape
  • Motility
  • Invasivness
  • Mesenchymal gene expression program
  • Mesenchymal adherens junction protein (N-cadherin)
  • Protease secretion (MMP-2, MMP-9)
  • Vimentir (intermediate filament) expression
  • Fibronectin secretion
  • PDGF receptor expression
  • alphavbeta6 integrin expression
62
Q

What is EMT stimulated by?

A

Stimulated factors secreted by the stroma (e.g. TGFbeta, TNFalpha). Normal epithelial cells are not usually sensitive to these, changes in cancer cells make them very sensitive

63
Q

What is intravasation stimulated by?

A

Tumour associated macrophages (TAM), recruited by tumour cells to vessels to aid intravasation of tumour cells

64
Q

Outline the process of transport and extravasation of tumour cells

A
  • Use blood or lymphatic vessels to travel to other areas of the body
  • Lodge in vessels of various tissues
  • Is a hostile environment for cancer cells and so employ either rapid or slow strategy of extravasation
65
Q

Outline the slow strategy of extravasation

A
  • Period of days

- Requires proliferation and subsequent destruction of the parenchyma

66
Q

Outline the rapid strategy of extravasation

A
  • Minutes
  • Trigger endothelial vessel wall to retract leaving space for extravasation
  • Same method as immune cells
67
Q

Outline the reversal of EMT (MET)

A
  • After extravasation
  • Switch off mesenchymal and switch on epithelial markers
  • Establish selves and colonise
68
Q

What is the consequence of EMT followed by MET?

A

The secondary tumour (metastasis) resembles the primary tumour from which it originated

69
Q

What is meant by colonisation with regards to metastases?

A

Expansion into macroscopic masses (>2mm diameter)

70
Q

When is EMT normally used in the body?

A
  • Embryogenesis

- Wound healing

71
Q

What is colonisation of a metastasis dependent on?

A

Interactions specific to a particular type of metastasising cell and microenvironment

72
Q

List the pathways of metastasis

A
  • Transcoelomic
  • Lymphatic
  • Haematogenous
73
Q

Outline the transcoelomic metastasis pathway

A
  • Cancers arise on surface of abdominal and thoracic structures (mesotheliomas, ovarian adenocarcinomas)
  • More similar to invasion, pass across structures
74
Q

Outline the lymphatic metastasis pathway

A
  • Metastatic cells travel in lymph circulation, lower pressure cf. blood
  • Lymph nodes closest to tumour colonised first and develop largest masses
75
Q

Outline the haematogenous metastasis pathway

A
  • Travel via the blood vessels
  • Most commonly veins rather than arteries
  • Ultimately enter lungs and liver
  • More commonly used by sarcomas cf. carcinomas
76
Q

What tissues do pancreatic cancers commonly metastasise in?

A
  • Mostly liver

- Some lung

77
Q

What tissues do colonic cancers commonly metastasis in?

A

Mostly liver, some bone marrow, some lung

78
Q

What tissues do mammary and prostate cancers commonly metastasise to?

A
  • Both most commonly bone
  • Breast lung, prostate liver
  • Both metastasis to lungs, brain, liver
79
Q

What does metastatic tropism depend on?

A
  • Ability of tumour cells to adapt to microenvironment of distant tissues
  • Layout of circulation
  • Will not always fit the pattern
80
Q

What is metastatic tropism?

A

Cancer cells colonise some metastatic sites more readily than others depending on the primary site

81
Q

What primary tumours commonly metastasise to the lungs?

A
  • Osteosarcoma
  • Haemagiosarcoma
  • Melanoma
  • Mammary tumours
  • Others e.g. thyroid,tonsillar, pancreatic
82
Q

What primary tumours commonly metastasise to the liver, spleen and/or kidney?

A
  • Mast cell tumours

- Haemagiosarcomas

83
Q

What primary tumours commonly metastasise to bone?

A
  • Mammary
  • Prostate
  • Bladder
84
Q

How do bone metastases develop?

A
  • Cancer cells reach bone via vessel of marrow
  • Adhere to specialised stromal cells coating bone facing marrow
  • Are attracted by growth factors contained in the ECM
  • Aids cancer proliferation
85
Q

What are the consequences of bone metastases?

A
  • Cancer cells activate osteoclasts and osteoblasts to different extents resulting in osteolytic and osteoblastic metastases
  • Lose bone strength (lysis) and get increased mineralisation (large islands of tumour cells, blastic)
86
Q

What techniques can be used in the detection of metastases?

A
  • Physical examination
  • Thoracic radiography
  • Ultrasonography
  • CT
  • MRI
87
Q

Outline thoracic radiography in the detection of metastases

A
  • Can be used to detect tumour spread via haematogenous route
  • Not very sensitive
  • Both lateral views required, collapse of lungs can hide metastases
  • Can be difficult to interpret
88
Q

Outline ultrasonography in the detection of metastases

A
  • Sensitive for lesions in liver, spleen, kidneys
  • Limited use for determining the nature of the lesion
  • Subjective to image quality and interpretation
  • Useful for guided biopsy
89
Q

Outline thoracic CT for in the detection of metastases

A

More sensitive than radiography

90
Q

Outline MRI in the detection of metastases

A
  • Good for soft tissues (brain, soft tissue sarcomas, spinal cord)
  • Useful for assessing degree of invasion
  • Slow, problems with mvoement blur, not good for all anatomical areas
91
Q

Outline methods for detecting bone metastases

A
  • Radiography: can see areas of bone lysis, production or mixed, commonly at sites typical for bone tumours
  • Scintigraphy: very sensitive, good if amputation may be required
92
Q

What are the implications on treatment due to metastases?

A
  • Surgical procedure must be followed by systemic therapy (chemo/radiotherapy)
  • Treatments may not be effective in all secondary sites
  • Poor blood flow may mean poor delivery of drugs
  • Early detection essential for good prognosis
93
Q

What are the consequneces of occult micrometastases?

A
  • Challenge for long term survival
  • Micrometastasis can be occult, result from slow proliferation and/or dormancy
  • May wait until better conditions for survival in unfavourable tissues
  • Slow or no proliferation so common anti-cancer treatments may not work
94
Q

What are the theories of occult metastases?

A
  • Cellular dormancy/quiescence

- Tumour mass dormancy: angiogenic restriction, immunesurveillance

95
Q

What breeds of dog are particularly predisposed to cancer? (in descending order of prevalence)

A
  • Irish Water Spaniel
  • Flat coated retriever
  • Hungarian wirehaired viza
  • Bernese Mountain dog
  • Rottweiler
  • Italine spinone
  • Boxer
  • Staffie
  • Welsh terrier
  • Giant schnauzer
96
Q

What are the 3 key points in the approach to cancer cases?

A
  • Establish diagnosis (type and grade of tumour)
  • Establish extent/stage of disease
  • Investigate complications
97
Q

Outline the use of FNA and cytology in the diagnosis of cancer

A
  • Quick, simple, in-house
  • Distinguish between inflammatory and neoplastic lesions
  • Cannot grade as cannot assess architecture
  • Not all tumours exfoliate cells
  • Good for mast cell tumours and lymphomas
98
Q

What methods are available for biopsy to diagnose cancer?

A
  • Needle biopsy/TruCut biopsy
  • Jamshidi bone biopsy
  • Punch biopsy
  • Excisional biopsy
  • Incisional biopsy
99
Q

Outline how staging of disease is carried out

A
  • Thorough physical examination, especially palpating LNs
  • Radiographs
  • Ultrasound
  • Advanced imaging
  • TMN
  • Stages describe the anatomical extent of tumour at a set point in time
100
Q

What methods may be used to investigate potential complications in cancer?

A
  • Blood biochemistry and haematology

- Urinalysis (paraneoplastic hypercalcaemia, hypoglycaemia, bone marrow infiltration etc.)

101
Q

What are the options following cancer diagnosis?

A
  • Do nothing
  • Euthanasia
  • Palliative care
  • Chemotherapy
  • Surgery
  • Radiotherapy
  • Anti-cancer vaccines (e.g. melanoma)
  • Photodynamic therapy for superficial cancers
  • Cryotherapy
102
Q

What is involved in palliative care of cancer patients?

A
  • Maintain quality of life
  • Balance side effects and comfort
  • Pain control, especially important with bone tumours
103
Q

What are the consequences of doing nothing following cancer diagnosis?

A
  • Tumour will grow (rate varies)

- Welfare may be compromised

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