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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

19
Q

Why should we screen for cancer

A

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

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

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

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

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

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

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

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

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

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

Concepts Of Disease (5 decks)

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