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Concepts Of Disease > Cancer > Flashcards

Cancer Flashcards

1
Q

What are tumours/neoplasms

A

arise from normal tissue but are unorganised, divided into benign and malignant

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2
Q

What is a benign tumour

A

non-invasive, localised and can maintain normal function

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3
Q

What is a malignant tumour

A

invasive, metastatic so spreads to sites distant from the origin, tissues show loss of form and function

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4
Q

What are the 4 main groups of tumours and what are they classified based on

A

based on cell type of origin
epithelial
mesenchymal
hematopoietic
neuroendodermal

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5
Q

What are epithelial cells

A

line walls/cavities or form a covering like skin
secrete proteins to form the basement membrane

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6
Q

What are tumours from epithelial cells known as and what percentage of tumours form them

A

carcinomas
reponsible for 80% of known tumours

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7
Q

What are squamous cell carcinomas

A

tumours from the protective layer or epithelial cells

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8
Q

What are adenocarcinomas

A

tumours from secretory epithelial cells

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9
Q

What are mesenchymal tumours and what percentage of tumours are they

A

responsible for 1% of tumours
derived from connective tissue cell types - originally from embryonic mesoderm

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10
Q

What are sarcomas

A

a type of mesenchymal tumour. mutiple types such as osteosarcoma (from osteoblasts) and liposarcomas (from adipocyte cells)

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11
Q

What are haematopoetic tumours and 2 examples

A

derived from cell types in blood-forming tissues
around 7% of tumours
eg
leukaemia - malignant cell derivatives that move freely in the circulation
lymphoma - solid tumours of T or B cells

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12
Q

What are neuroendodermal tumours and examples

A

responsible for around 1.5% of tumours
derived from components of the CNS / PNS
such as glioblastomas, neuroblastoma, schwannomas, astrocytomas

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13
Q

What are the two of benign tumours

A

hyperplastic, metaplastic, dyplastic

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14
Q

What are hyperplastic benign tumours

A

excessive cell number, cells are nomral and form structures

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15
Q

What are metaplastic benign tumours

A

displacement of normal cells with other normal cells not found in tissue. often found in the epithelial transition zone. can be premalignant

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16
Q

What are dyplastic benign tumours

A

cytologically abnormal cells, variable shape and crowded. hyperchromatic nuclei and lack of differentiation markers. the officially the premalignant state

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17
Q

What makes a tumour malignant

A

when cells breach the basement membrane and invade the surrounding stroma. cells are abnormal with poor differentiation and spread to different sites

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18
Q

What are the two types of tumour growth

A

monoclonal = one cell is abnormal and becomes replicated
polyclonal = multiple cells are abnormal and all replicate

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19
Q

Why should we screen for cancer

A

detect cancer in early stages, makes it easier to treat and more successful treatment

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20
Q

What are the screening criteria categories by WHO

A

condition must be a major problem with risk factors
the test must be safe reliable and specific
the treatment must be effective
screening programme must reduce morbidity and be effective and viable

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21
Q

What are the changes in a cell that transform a normal cell to a cancer cell

A

proliferative signalling
evade growth suppressors
avoid immune destruction
enable replicative immortality
activating invasion and metastasis
inducing angiogenesis
resist cell death
deregulating cell energetics

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22
Q

How do cancer cells sustain proliferation via growth signal autonomy

A

enhancing external stimulation such as mutation in growth factor receptors or increased growth factors
losing dependency on growth factors by:
mutations in signal transduction components such as PI3-kinase, Ras and Raf
mutations in cell cycle components

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23
Q

How do cancer cells evade growth inhibitory or suppressive signals

A

loss of activity of tumour suppressor genes such as p53, PTEN and Rb
aberration in development of signalling pathways such as hedgehog, Wnt and TGFB which all promote growth and metastasis

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24
Q

How do cancer cells evade apoptosis

A

mutations that affect the intrinsic apoptosis pathway such as loss of p53, upregulation of anti-apoptotic members of BCL2 family, down regulation of pro-apoptotic members of the BCL-2 family
mutations that affect the extrinsic pathway such as aberrations in death receptor regulation

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25
Q

What is angiogenesis

A

the formation of new blood vessels. tumours require vascularization to grow into a mass and prevent necrotic cell death. facilitates metastasis

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26
Q

What are the stages of angiogenesis

A

dormant blood vessel
perivascular detachment and vessel dilation
beginning of angiogenic sprouting of vesssles
continuous sprouting and recruit pericytes to stabilise the new sprout
tumour vasculature

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27
Q

What is VEGF

A

a proangiogenic molecule. is a growth factor. regulated by hypoxia and oncogenic signalling pathways. result in abnormal tumour vasculature

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28
Q

How do cancer cells maintain replicative immortality

A

normal cells have telomeres that shorten and limit the divisions that can take place. cancer cells produce telomerase that maintains telomere length and immortality. excessive length in cancer cells causes instability and promotes mutations

29
Q

What are telomeres

A

composed of repetitive sequences of DNA - TTAGGG and associated proteins
protects ends of chromosomes and controls chromosome length
shorten by 100-200 bp each DNA replication round due to the limited of DNA polymerase needing an RNA primer

30
Q

What are Cancer stem cells (CSCs)?

A

Are subpopulations within a tumour that are thought to initiate and maintain the cancer.

31
Q

What are cancer stem cells responsible for?

A

Heterogeneity of tumours
Tumour plasticity
Migratory abilities

32
Q

How can cancer stem cells be identified?

A

Stem cell markers e.g CD44 (breast and pancreas), CD133 (colon, prostate, brain)

33
Q

Are cancer stem cells more likely or less likely to survive anti-cancer treatments?

A

More likely

34
Q

How cancer stem cells arise?

A

From deregulation of self-renewal pathways e.g wnt and hedgehog

35
Q

What is invasion and metastasis?

A

Cancer cells have gained the ability to invade and spread (metastasise) to distant sites by:
- Breaking cell- cell adhesion and cell- extracellular matrix (ECM) attachment
- Changing shape and becoming more motile
- degrading the ECM via proteases to allow invasion
- inducing angiogensis to support secondary tumour growth

36
Q

What is a primary tumour?

A

Site of origin

37
Q

What is a secondary tumour?

A

Metastases (traced back to primary tumour- same cell type)

38
Q

What are the sites of spread?

A

• Close proximity to primary tumour- Direction of blood flow- Tumour cells get trapped in capillary bed
• Distal/ non-obvious- Seed and soil hypotheses (Paget) (cells need to match with optimum environment)- Premetastatic niche (Lynden)
(distant site is prepared via circulating tumour derived factors)

39
Q

What are the steps involved in invasion and metastasis?

A
  1. Invasion
  2. Intravasation
  3. Transport
  4. Extravasation
  5. Metastatic colonisation
  6. Angiogenesis
40
Q

What is the role of Src?

A

Mediates breakdown of cell: cell contacts and cell: EXM contact

41
Q

What is epithelial- mesenchymal- transition (EMT):

A
  • Reversible process
  • Common in wound healing and early embryogenesis
  • Reactivated in cancer
42
Q

What are the cellular changes in EMT?

A

• Activation of transcription factors SNAIL and TWIST
• Loss of cell polarity and loss of cell adhesion molecules e.g. E-cadherin
• Changes in cell shape
• Increase in mesenchymal markers e.g. N-cadherin, vimentin
• Protease production
• Promotion of ‘stemness abilities’ i.e. early metastasising cells likely to be CSCs

43
Q

What is the rationale for cancer cells to utilise aerobic glycolysis?

A
  • Cancer cells are frequent hypoxic- Lack of oxygen for oxidative
  • Process of glycosis also generates intermediates for biosynthetic pathways such as growth
44
Q

How do cancer cells evade the immune system?

A

Loss of tumour antigens
Downregulation of antigen present molecule (APCS)
Over-expression of immune checkpoint proteins and anti-apoptotic proteins

45
Q

What is the multi-hit model and what is it supported by?

A

A cell has to acquire several mutations before it’s going to transform a normal cell into a cancer cell.

Supported by:
- Genetic homogeneity in cells from a given tumour
- Cancer incidence increase with age
- Evidence of cooperative effects of mutations

46
Q

What is a driver mutation?

A

Confers growth/ survival advanatage

47
Q

What is a carcinogenic agent and give examples?

A

• Cause damage that is not repaired- mutations survive and propagate
• Radiation
• Chemicals
• Infectious pathogens
• Endogenous reactio

48
Q

What is ionising radiation and what are the risk factors?

A

Ionising radiation e.g gamma rays , alpha and beta particles
• Direct DNA damage- ionisation of atoms comprising DNA
• Indirect DNA damage- Radiolysis of H20 and ROS generation, hydroxylysine radical (most reactive but unstable) , H202 (less reactive but stable-time to enter the nucleus and effect DNA, more problematic) ,Superoxide radical
• Risk factors: exposure to X-rays, living at altitude, plane travel

49
Q

What are the types of UV radiation and their wavelength? HOW does it work?

A

UVA- (Wavelength 320-380nm)
UVB- wavelength 290-320nm- most effective carcinogen
UVC (wavelength 200-290nm
Double bonds in DNA absorb UV- mutations cause bends in the DNA which are misread by DNA polymerase

50
Q

What UV is the main cause of skin cancer and why?

A

UVB- - MAIIN CAUSE OF SKIN CANCER
• P53 tumour suppressor commonly affected
• Causes80% of skin cancers- squamous and basal carcinomas - not usually melanoma- mutations in raf (active in driving cell proliferation)
• Risk factors- over exposure to the sun i.e sunburn, sun edges

51
Q

What are direct acting chemical carcinogens?

A

Uncommon
- Reactive electrophiles
- Interact with nitrogen and oxygen atoms in DNA
- Examples include dimethyl sulphate and nitrogen mustards

52
Q

What are indirect acting chemical carcinogens?

A

• Unreactive and water soluble 0 When taken into the body they are processed into the electrophillic carcinogenic form by enzymes in our cells.
Common
• Electrophillic centre produced by enzyme modification e.g via processing by cytochrome p450 enzymes
• Interact with bases in DNA forming addicts
• Examples include polycyclic aromatic hydrocarbons (PAHs) (Cigarette smoke) and aromatic or heterocyclic amines (cooked meats)
Risk: smoking, diet high in cooked or processed meat, preservatives in process food

53
Q

What is the general mechanism of action of chemical carcinogens?

A

• An electrophillic (or electron deficient) form reacts with the nucleophilic sites (sites that can donate electrons) in the purine and pyramiding rings of nucleic acids

54
Q

What are oncogenic viruses?

A

• DNA tumour viruses
• Encode viral proteins that block tumour suppressor action
• Examples HPV- protein promotes degradation of RB protein leading to constitutive activation the cell cycle

55
Q

What are influential factor in human carcinogenicity?

A

Environemnt
• Reproductive life
• Smoking
• Alcohol consuption
• Excerise
• Diet- carnogenic contaminants, dietary deficiencies, obesity nh

56
Q

What are the normal genes implicated in the onset of cancer?

A

Proto-oncogenes
Tumour suppressor genes
Caretaker genes

57
Q

What is the normal role of protooncogenes?

A

Positively promote cell proliferation of celll survival

58
Q

What type of mutation occurs in proto-oncogenes?

A

Gain of function - dominant function

59
Q

What is the normal role of tumour suppressor genes?

A

Inhibit cell survival or negatively regulate cell proliferation

60
Q

What type of mutation happens in tumour suppressor genes?

A

Loss of function and recessive

61
Q

What are the genetic events that can cause loss of function in TS gene?

A

• Loss of entire chromosome
• Chromosomal rearrangements- gene is disrupted or region contains normal gene is deleted
• Mutation in coding sequence which results in non-functional protein
• Gene activity is silenced by epigenetic changes
• Mutations in genes coding for chromatin remodelling complexes e.g SWI/SNF

62
Q

What is the role of a care taker gene

A

Repair or prevent DNA damage

63
Q

What types of mutations are caretaker genes?

A

Loss of function and recessive

64
Q

What repair mechanisms are affected when there are mutations in caretaker genes?

A

DNA mismatch repair, nucleotide excision repair, double stranded DNA break

65
Q

What are the cyclins associated with the cell cycle phases?

A

G1 Cyclins
G1/S cyclins
S phase
M phase

66
Q

What are CDKs influenced by?

A

Cyclin binding
Phosphorylation and Dephosphorylation
Binding to CDK inhibitors e.g p15, p16, -21, -27

67
Q

Where are the cell cycle checkpoints and what are their role?

A

G1 checkpoint- is environment favourable?
G2 checkpoint- is DNA replicated? Is all the DNA damage repaired?
Checkpoint in mitosis- Are all chromosome properly attached to mitotic spindle?

68
Q

What is the p53 gene?

A

TF, binds DNA as a tertamer
Can binds promoter regions in 300 target genes
Multifunctional tumour suppressor

69
Q

What does a mutation in p53 cause?

A

Promote the formation of the malignant phenotype and are seen in tumours

Concepts Of Disease (8 decks)

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