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Principles of Disease > Disorders of Cell Growth > Flashcards

Disorders of Cell Growth Flashcards

1
Q

What is the commonest type of carcinoma in men in the UK?

A

Prostate cancer.

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2
Q

How are tumours classified?

A

Based in tissue origin and whether benign or malignant.

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3
Q

What is an adenocarcinoma?

A

Malignant epithelial tumour of glandular tissue.

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4
Q

What is the name for a benign tumour of glandular epithelial tissue?

A

Adenoma

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5
Q

What is the name for a malignant tumour of the CNS?

A

Astrocytoma

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6
Q

What is the name for a benign tumour of squamous epithelia?

A

Squamous papilloma

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7
Q

What is the name for a malignant tumour of squamous epithelia?

A

Squamous-carcinoma

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8
Q

What is leukaemia?

A

A malignant tumour of white blood cells.

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9
Q

What is a lipocarcinoma?

A

A malignant tumour of fatty tissue.

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10
Q

What is lymphoma?

A

A malignant tumour in the lymphoid tissue.

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11
Q

What is the name of a malignant tumour in the peripheral nervous system?

A

Schwannoma

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12
Q

What is a melanocyte naevus?

A

A benign tumour of melanocytes.

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13
Q

What is the name of a malignant tumour of melanocytes?

A

Melanoma

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14
Q

What are seminomas and teratomas?

A

Malignant tumours of germ cells.

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15
Q

What is a fibro-sarcoma?

A

A malignant tumour of fibrous connective tissue.

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16
Q

What is the name for a benign tumour of fibrous connective tissue?

A

Fibroma

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17
Q

What is a lipoma?

A

A benign tumour of connective fat tissue.

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18
Q

What is the name for a malignant tumour of connective fat tissue?

A

Lipo-sarcoma

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19
Q

What is an osteo-sarcoma?

A

A malignant tumour of bone connective tissue.

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20
Q

what is the name for a benign tumour of connective tissue in bone?

A

Osteoma.

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21
Q

What is a tumour?

A

An abnormal growing mass of tissue which is uncoordinated and autonomous growth (irreversible change)

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22
Q

Describe the characteristics of malignant tumours.

A
  • invasive
  • no-capsule
  • capsule breached by tumour cells
  • cells abnormal
  • poorly differentiated
  • evidence of spread of cancer
  • frequently cause death
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23
Q

Describe the characteristics of malignant tumours.

A
  • non-invasive
  • capsule
  • no invasion
  • cells similar to normal cells
  • well-differentiated tumours
  • similar functions to normal
  • rarely cause death
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24
Q

the momentum is a common site of metastasis in?

A

Ovarian cancer

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25
Q

What is the primary genetic cause of retinoblastoma?

A

Loss of tumour suppressor genes.

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26
Q

What is a retinoblastoma?

A

Malignant tumour of the retina. Development is a multistep process, which is true for ALL tumours.

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27
Q

What are the properties of cancer cells?

A
  • Cellular and nuclear pleomorphisms
  • Loss of tumour suppressor genes
  • Gain of function of oncogenes
  • Altered cellular function
  • Abnormal morphology
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28
Q

What are tumour biomarkers used for?

A
  • Screening
  • Diagnosis
  • Prognosis
  • Predictive (e.g Kras for colorectal cancer)
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29
Q

Give examples of tumour biomarkers.

A

Alpha-fetoprotein, carcino-embryonic antigen, oestrogen receptor, prostate specific antigen

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30
Q

What is alpha-fetoprotein used as a marker for?

A

Teratoma of testis

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31
Q

What is carcino-embryonic antigen (CEA) used as a marker for?

A

Colorectal cancer

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32
Q

What is the oestrogen receptor used as a marker for?

A

Breast cancer

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33
Q

What is the prostate specific antigen used as a marker for?

A

Prostate cancer

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34
Q

Describe the spread of cancer.

A

Invasion and metastasis (multi-step)

Increase matrix degradation by proteolytic enzymes and altered cell-to-cell and cell-matrix adhesion.

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35
Q

What are the modes of spread of cancer?

A

Local, Lymphatic, Blood, Trans-coelemic

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36
Q

What is trans-coelomic spread and give examples?

A

Spread across body cavities e.g across pleural and peritoneal cavities from tumours in lungs, stomach and ovaries.

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37
Q

What does metastasis depend on?

A

Metastatic niche (tumour and tissue related factors)

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38
Q

List some uncommon sites of metastasis.

A

Spleen, Kidneys, Skeletal muscle, Heart

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39
Q

List the local effects of cancer.

A 
POT BEP
Pressure
Obstruction
Tissue destruction
Bleeding
Pain
Effects of treatment
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40
Q

List the systemic effects of cancer.

A

Weight loss - cancer cachexia, secretion of hormones, paraneoplastic syndromes, effects of treatment

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41
Q

Define dysplasia.

A

Pre-malignant change which is the earliest change in the process of malignancy that can be visualised and can progress to cancer.

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42
Q

What are the features of dysplasia?

A
  1. No invasion

2. Disorganisation of cells (increase in nuclear size, mitotic activity and abnormal mitoses)

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43
Q

Define ints-epithelial neoplasms.

A

Development of benign neoplasms or high-grade dysplasia in epithelium. Associated with high risk of developing cancer.

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44
Q

Give an example of an intra-epithelia neoplasm (IEN).

A

Cervical IEN - potentially pre-malignant transformation and abnormal growth of squamous cells on surface of cervix cause by HPV.

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45
Q

What are the benefits of early detection of cancer?

A

Decrease or prevent morbidity and mortality.

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46
Q

Describe interphase in normal cells.

A 
G1 = cells respond to external signals ready for DNA replication.
S = DNA synthesis and replication
G2 = preparation for mitosis
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47
Q

Describe the cell cycle of normal cells.

A

G1, S, G2, M

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48
Q

What is G0?

A

Variable e.g cardiac myocytes.

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49
Q

How is the cell cycle controlled?

A
  1. External factors (hormones, growth factors, cytokines, stroma)
  2. Intrinsic factors (checkpoints and restriction points
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50
Q

What does progress through G1 depend on?

A

External stimuli up to restriction point and after that, progression is autonomous.

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51
Q

What are cell cycle checkpoints?

A

System of enzymatic switches.

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52
Q

Name two of the main checkpoints.

A
  1. Cyclin-dependent kinases (phosphorylates target proteins, activate/inactivate substrates and regulate events in next phase)
  2. p53 (maintains genomic integrity)
53
Q

Outline the process of carcinogenesis.

A

Uncontrolled proliferation via cell cycle dysregulation (also balance between proliferation and apoptosis)

54
Q

What are the two frequently disrupted pathways in carcinogenesis?

A
  1. Cyclin D-pRb-E2F pathway

2. p53 pathway

55
Q

At what stage in the cell cycle are virtually all cancers dysregulated at?

A

G1-S

56
Q

List the four main mutated cell cycle regulated genes.

A
  1. cyclin D (cyclin D/CDK complexes phosphorylate pRb)
  2. CDK4
  3. p16
  4. pRb
57
Q

What are CDKIs?

A

cell cycle inhibitors which inhibit molecules binding to CDK/cyclin complexes (INK41 and CIP?KIP gene families)

58
Q

Discuss the pRb gene.

A

Most important target for E2F transcription factors.
ACTIVE pRb - inactivates E2F
INACTIVE pRb - loses affinity for E2F.

59
Q

Discuss E2F.

A

Free form activates vital target genes and patent stimulator for cell cycle entry.

60
Q

Discuss p53.

A

Maintains genomic integrity and induces cell arrest at G1 and facilitates DNA repair.
Mutated p53 = cells do not G1 arrest or repair damaged DNA therefore, cell proliferates and malignant neoplasms form.

61
Q

List the etiological agents of cancer.

A
  1. Environmental (chemicals, radiation, oncogenic viruses)
  2. Inherited (inherited cancer syndromes or familial cancers)
  3. Age
  4. Geography
62
Q

What are the effects of chemical agents?

A

Purine and pyrimidine bases damaged.

DNA adduction from chemical carcinogens and active metabolites reacting with DNA and forming covalently bound products.

63
Q

What are the effects of radiation?

A

Purine and pyrimidine damage.

No p53 or G1 arrest therefore, mitotic failure, cell death, division with mutation and aneuploidy.

64
Q

Give examples of oncogenic viruses.

A
  1. HPV (cervical cancer)
  2. EBV (Burkitt’s lymphoma)
  3. Hep B (liver cancer)
65
Q

Give and example of an autosomal dominant inheritance of a single mutant gene.

A

Familial retinoblastoma.

66
Q

Describe familial cancers.

A

Family clustering but individual predisposition unclear, multifactorial inheritance e.g some breast and ovarian cancers.

67
Q

What are tumour suppressor genes?

A

Anti-oncogenes.
Mutations cause loss of function.
Discourage cell growth or temporarily halt cell division to carry out DNA repair.

68
Q

What are proto-oncogenes?

A

Promote cell growth and mitosis.

69
Q

What are oncogenes?

A

Cancer causing and derived from proto-oncogenes with ‘gain of function’.

70
Q

What are oncogenes activated by?

A
  1. Alteration of porto-oncogene structure (point mutations, chromosome rearrangements, translocations etc)
  2. Dysregulation of proto-oncogene expression (gene amplification and over expression)
71
Q

Give an example of a cancer that results in over expression/ activation of oncogenes.

A

Burkitt’s Lymphoma

72
Q

Give an example of a tumour that results from recombination to form chimeric proteins.

A

Chronic myeloid leukaemia

73
Q

What is the “two-hit hypothesis” of oncogenesis.

A

Inactivation/ loss of BOTH normal allelic copies give rise to cancer.

  1. Inherited form (one inherited copy of pRb and somatic point mutation of another copy)
  2. Sporadic form ( both hits occur in a single gene)
74
Q

Why is tumour formation a multi step process.

A

Activation of several oncogenes and loss of two or more tumour suppressor genes occur in most cancers.

75
Q

Where can mutations occur?

A
  1. DNA damaging environment agents.
  2. Inherited mutations in genes affecting DNA repair
  3. Inherited mutations in genes affecting proliferation or apoptosis
  4. Activation of growth promoting oncogenes.
76
Q

What imaging techniques arecommonly used in diagnosis, staging and treatment of cancer?

A

MRI, CT and PET.

77
Q

What is the scientific basis of MRI?

A

Strong magnetic field aligns protons (H+) in body in one direction, radio frequency pulses displace portions and images created by displaying time taken for protons to ‘relax’ back to original.

78
Q

Give examples of the behaviour of different molecules in MRI.

A

Fat molecules don’t rotate for long because of their high molecular weight whereas water takes longer to reach alignment because of smaller molecular weight.

79
Q

What are the indications for use of MRI?

A

Excellent bone/ soft tissue detail, vessels can be seen, vascular lesions and more tumours easily seen with contrast.

80
Q

What are the contraindications for MRI?

A

Claustrophobia, motion artefact, pacemakers, aneurysms and clips.

81
Q

What IV contrast medium is used in MRI?

A

Gadolinium DTPA (causes change in local magnetic field so alters tissue signal). Not to be used in patients with kidney or liver disease/failure.

82
Q

Discuss patient safety issues with MRI.

A
  • radio-frequency field risk only encountered in infants
  • remove metallic belongings and make-up etc with metal particles.
  • only non-ferromagnetic items in room
83
Q

Wjhat is the diagnosis staging based on?

A

Tumour, Node and Metastasis

84
Q

Describe the use of basic statistical concepts that can help to decide which radiological treatment would be most useful.

A
  1. Sensitive (how many patients with the disease test positive?)
  2. Specificity (how many patients without the disease test negative?)
  3. Positive predictive values (how many patients testing positive do have the disease?)
  4. Negative predictive values (how many patients testing negative don’t have the disease?)
85
Q

What is the positive predictive value affected by?

A

Prevalence of disease.

86
Q

Describe the pros of population screening with radiological testing?

A
  • diagnose at early stage
  • more likely to cure cancer
  • high sensitivity and specificity
    e. g mammography for breast cancer.
87
Q

Describe the cons of population screening for breast cancer.

A

Overdiagnosis, unnecessary treatment, radiation exposure, pain/incovenience, cost

88
Q

What are the WHO principles of screening?

A

Should be acceptable tp population, should be important health problem, should be latent stage of disease, should be a treatment fo condition, facilities required for diagnosis and treatment

89
Q

Describe the principles of staging in cancer.

A

Carcinogen, initiation, promotion, tumour growth and progression (clinical cancer)

90
Q

What causes the initiation of cancer.

A

Chemical, physical or viral

91
Q

What causes the promotion of cancer.

A

Oncogenes, growth factors, stimulation may be autocrine or paracrine.

92
Q

What system is used to stage cancer?

A

TNM system (tumour, node, metastasis)

93
Q

Discuss anti-VEGF therapy?

A

Anti-VEGF antibody Avastin binds VEGF

  • prevents interaction with receptors and activation of downstream signalling molecules.
  • Ultimately leads to decrease in microvascular growth, inhibit progression of metastatic disease and tumour dormant.
94
Q

Where are VEGF receptors (1 and 2) located?

A

On vascular endothelial cell walls.

95
Q

Discuss cancer and the immune system.

A

PD1 (programmed death receptor) present on T lymphocytes.
PDL-1 (ligand) on tumour cells.
Interaction of both, suppress T cell action and cancer cells “hide” from immune system.

96
Q

What is the immunotherapy potential for cancer treatment?

A

Block PD1 or PDL-1.

97
Q

What was the first successful PD1 inhibitor on the market?

A

Nivolumab

98
Q

Discuss the steps of metastasis.

A
  1. Tumour invades through basement membrane
  2. Moves into ECM/CT/surrounding cells and invades blood vessels
  3. Many enzymes involved
  4. Angiogenesis (key to maintenance and progression of malignant tumours to exceed 2mm in diameter)
99
Q

Name two local treatments of cancer.

A
  1. Surgery (needs anatomical clearance)

2. Radiotherapy (needs anatomical coverage)

100
Q

What are the 5 R’s of radiotherapy?

A
  1. Radiosensitivity
  2. Repair
  3. Re-population
  4. Re-oxygenetaion
  5. Re-assortment
101
Q

Define ‘designer therapies’ and give two examples.

A

‘Specific’ based on molecular science - inytracellular growth control points e.g imatinib (blocks tyrosine kinase) and ZD1839 ( EGFR inhibitor)

102
Q

What is systemic treatment useful for?

A

Wide-spread disease, potential to be very specific and can be used within therapeutic index.
E.g hormonal therapy, chemotherapy, immunotherapy.

103
Q

Describe the two modalities of therapy currently available.

A
  1. Local/regional

2. Systemic

104
Q

What are indications of use of cytotoxic drugs?

A

Curative, palliative, adjuvant, neoadjuvant

105
Q

Give examples of hormonal drugs that act as a targeted therapy.

A

Anti-oestrogen (tamoxifen) - aromatase inhibitor for breast cancer

106
Q

Give examples of targets for targeted chemotherapy drugs.

A

EGFR, VEGF, KRAS (no current drug available) etc.

107
Q

What is CTLA4 inhibitor (ipilimumab) an example of?

A

Immunotherapy drug.

108
Q

What are the side-effects of immunotherapy?

A

Colitis, pneumonitis, endocrinopathies (due to over-stimulation of immune system).

109
Q

List some side-effects associated with chemotherapy.

A

Nausea/vomitting, alopecia, diarrhoea, SOB, difficulty sleeping, tiredness, diarrhoea, cardiotoxicity etc.

110
Q

Describe systemic chemotherapy.

A

Delivered IV or orally in regular cycles with timings dependent on pharmacokinetic findings. Delay in treatment if toxicities develop.

111
Q

What are the methods used to assess drug delivery?

A

Advanced disease = CT, PET abd or clinical examination (RECIST criteria in radiology)
overall survival, progression-free survival, improved QOL, adjuvant treatment, neoadjuvant treatment.

112
Q

What are the 7 main classes of chemotherapy drugs?

A
  1. Alkylating agents e.g cisplatin
  2. Antimetabolites
  3. Vinca alkaloids
  4. Texans
  5. Antimitotic antibiotics
  6. Mitotic inhibiters
  7. Combination therapy
113
Q

Describe the mechanism of action of the alkylating agents.

A

DNA helix cross-links intra- and inter strands therefore, cannot act as templates for new DNA formation.

  • decrease entry or increase exit of agent
  • inactivation of agent in cell
  • enhanced repair of DNA lesions produced by alkylation.
114
Q

Describe the mechanism of action of antimetabolites.

A

May be incorporated into new nuclear material or bind irreversibly with vital enzymes to inhibit cell division.

115
Q

Describe the mechanism of action of vinca alkaloids.

A

Metaphase arrest agents (bind to tubulin and block microtubule formation and spindle formation)

116
Q

Describe the mechanism of action of taxanes.

A

Promote spindles and ‘freeze’ cells at that stage of the cycle.

117
Q

Describe the mechanism of action of antibiotic antimitotics.

A

Anthracylines and non-anthracyclines (intercalate and inhibit DNA and RNA synthesis, membrane binding to increase permeability to various ions, free radicals disrupt DNA chain and prevent mitosis.

118
Q

Describe combination therapy.

A
  • Can be synergistic or additive
  • Reduce risk of developing resistance
  • Aim to increase efficacy
  • Must have different mechanisms of resistance and compatible side-effects.
119
Q

At what phases of the cell cycle does the alkylating agents act?

A

G1, S, G2 and M

120
Q

At what phase of the cell cycle does the vinca alkaloids and taxanes act?

A

M phase

121
Q

At what phase of the cell cycle does the antimetabolites act?

A

S phase

122
Q

At what phases of the cell cycle does the antibiotics act?

A

G1, S and G2

123
Q

Do slow or fast growing tumours respond best to cytotoxic chemotherapy?

A

Fast growing.

124
Q

What are more common point mutations or frame-shift mutations?

A

Point mutations.

125
Q

What are the functions of MMR genes?

A

MMR (mismatch repair) genes correct errors that spontaneously occur during DNA replication.

126
Q

What percentage of colorectal cancers are familial?

A

Approximately 30% (60% are sporadic).

127
Q

What type of mutation does sickle cell haemoglobin arise from?

A

Point mutation.

128
Q

What are BRCA1 and BRCA2 examples of?

A

Tumour suppressor genes.

Principles of Disease (9 decks)

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