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CANCER BIOLOGY > LECTURE 1 > Flashcards

LECTURE 1 Flashcards

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1
Q

What are the characteristics of Benign tumours?

A
  • Cells remain clustered together
  • Do not metastasise (spread)
  • Non-cancerous
  • Just like normal cells
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2
Q

What are the characteristics of Malignant tumours?

A
  • Spread wider distances
  • Go all the way to tissues and to the bloodstream
  • Metastasise uncontrollably & are cancerous
  • Abnormal shape and darker & larger nucleus
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3
Q

What are the major classes of cancer?

A
  • CARCINOMA = arises in epithelium
  • SARCOMA = starts in supporting or connective tissues of body
  • LEUKEMIA = begins in blood-forming tissues
  • LYMPHOMA = forms in lymph cells
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4
Q

What are the hallmarks of cancer?

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Avoiding immune destruction
  • Enabling replicative immortality
  • Activating invasion & metastasis
  • Inducing angiogenesis
  • Resisting cell death
  • Deregulating cellular energetics
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5
Q

What is the most prominent of the signalling channels that accelerate growth?

A

Growth promoting signals transmitted through the RAS_RAF-MEK-MAPK pathway

[1/3 of human tumours express an active mutant form of RAS]

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6
Q

What are the main members of the RAS gene family?

A
  • KRAS
  • HRAS
  • NRAS
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7
Q

What does a mutant form of RAS cause?

A

Uncontrolled growth, proliferation and migration

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8
Q

What is TP53?

A

It sense the need to halt cell cycle progression and can trigger apoptosis -> 50% of tumours have mutation -> LI-FRAUMENI SYNDROME (5% chance of developing cancer by 30)

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9
Q

What is RB?

A

Gatekeeper of cell cycle progression

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10
Q

What happens in Necrosis?

A

1) Chromatin clumping, swollen organelles & fluorescent mitochondria
2) Disintegration
3) Release of intracellular contents
4) Inflammation

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11
Q

What happens in Apoptosis?

A

1) Mild convolution, chromatin compaction and segregation and condensation of cytoplasm
2) Nuclear fragmentation, Blebbing and apoptotic bodies
3) Phagocytosis

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12
Q

What are the immune programs that cancer cells avoid?

A
  • APOPTOSIS (maintains homeostasis)
  • NECROSIS (activated by oxygen and energy deprivation)
  • AUTOPHAGY (degrading cellular organelles, autophagy generates the metabolites and nutrients that cells are unable to acquire from their surroundings)
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13
Q

Describe ‘Enabling replicative immortality’

A

The cellular timekeeper “TELOMERE” is destroyed -> cells acquire the unlimited replicative potential (CELLULAR IMMORTALITY) that is required to spawn large tumour masses

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14
Q

Describe the loss of telomeric repeats leads to growth arrest

A

1) DNA POLYMERASE is unable to replicate the tips of chromosomes -> loss of DNA at the specialised ends of chromosomes with each replication cycle
2) Loss of TELOMERIC REPEATS with each cell division cycle -> gradual telomere shortening
3) GROWTH ARREST when one or more critically short telomeres trigger P53-REGULATED DNA-DAMAGE CHECKPOINT RESPONSE

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15
Q

How do all cancer cells maintain their telomeres?

A

Increase the production of TELOMERASE ENZYME (telomerase functions by adding TELOMERIC DNA to the ends of chromosomes)

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16
Q

What is Angiogenesis?

A

Turning on new blood vessel growth to feed and nurture the growing mass of cancer cells

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17
Q

What do tumours require?

A

A steady supply of oxygen, glucose and other nutrients to evacuate metabolic waste and sustain CELL VIABILITY and PROLIFERATION

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18
Q

What is the function of the Hypoxia-Inducible Transcription Factor (HIF) system?

A

Regulates hundreds of genes, including ones that directly or indirectly induce angiogenesis and other stress-adaptive capabilities

19
Q

What are the three major features of tissue invasion?

A
  • Cell adhesion to the basement membrane
  • Local proteolysis of the membrane
  • Movement of the cell through the ECM
20
Q

What is the difference in energy pathways for cancer cells and normal cells?

A

CANCER CELLS = utilise anaerobic glycolysis -> increased lactic acid production

NORMAL CELLS = utilise oxidative phosphorylation

21
Q

Describe the Warburg effect

A

Cancer cells produce energy through a less efficient process of AEROBIC GLYCOLYSIS consisting of high levels of glucose uptake and glycolysis followed by LACTIC ACID FERMENTATION taking place in the CYTOSOL, not mitochondria, despite abundant oxygen

22
Q

What drugs inhibit ‘Evading growth suppressors’?

A

Cyclin-dependent kinase inhibitors

23
Q

What drugs inhibit ‘Avoiding immune destruction’?

A

Immune activating anti-CTLA4 MAb

24
Q

What drugs inhibit ‘Enabling replicative immortality’?

A

Telomerase inhibitors

25
Q

What drugs inhibit ‘Tumour-promiting inflammation’?

A

Selective anti-inflammatory drugs

26
Q

What drugs inhibit ‘Activating invasion and metastasis’?

A

Inhibitors of HGF/c-Met

27
Q

What drugs inhibit the inducing of angiogenesis?

A

Inhibitors of VEGF signalling

28
Q

What drugs inhibit ‘Genome instability and mutation’?

A

PARP inhibitors

29
Q

What drugs inhibit ‘Resisting cell death’?

A

Pro-apoptotic BH3 mimetics

30
Q

What drugs inhibit ‘Deregulating cellular energetics’?

A

Aerobic glycolysis inhibitors

31
Q

What drugs inhibit ‘Sustaining proliferative signalling’?

A

EGFR inhibitors

32
Q

What is the difference between Somatic DNA changes and Germline DNA changes?

A

SOMATIC DNA CHANGES
- acquired over a person’s lifetime in single cells
- can lead to cancer
- can not be inherited

GERMLINE DNA CHANGES
- present in every cell of the body including egg and sperm
- can increase cancer susceptibility
- can be inherited

33
Q

What are the progressive steps of cancer?

A

1) HYPERPLASIA = cell divides more rapidly than normal
2) DYSPLASIA = cells change form
3) CARCINOMA IN SITU = cells stay in one place
4) MALIGNANT TUMOUR = cancer cells invade normal tissue & enter blood and lymph -> tumours form at distant sites

34
Q

What does the p53 gene produce?

A

A protein that turns “off” the cell cycle and helps to control cell growth

35
Q

Describe Proto-oncogenes

A

NORMAL FUNCTION: promote cell survival or proliferation

EFFECT OF MUTATION: Gain-of-function mutations allow unregulated cell proliferation and survival (usually dominant)

ORIGINS: Point mutation, chromosomal translocation & amplification

36
Q

Describe Tumour-suppressor genes

A

NORMAL FUNCTION: inhibit cell survival or proliferation

EFFECT OF MUTATION: Loss-of-function mutations allow unregulated cell proliferation and survival (usually recessive)

ORIGINS: deletion, point mutation & methylation

37
Q

Describe Caretaker genes

A

NORMAL FUNCTION: Repair or prevent DNA damage

EFFECT OF MUTATION: Loss-of-function mutations allow mutations to accumulate

ORIGINS: deletion, point mutation & methylation

38
Q

Describe the clonal origin theory of cancer

A

A tumour arises initially from 1 specific cell which then develops a growth advantage over other cells

39
Q

Describe the multistep nature of cancer

A

1) Loss of normal tumour-suppressor gene APC and a POLYP (small growth forms)
2) A benign, precancerous tumour grows
3) Activation of oncogene RAD and an ADENOMA (benign tumour) grows
4) Loss of tumour-suppressor gene p53 and a CARCINOMA (malignant tumour) develops
5) Cancer metastises

40
Q

What are the non-modifiable risk factors for cancer?

A
  • Age
  • Genetics/Family history
41
Q

What are the modifiable risk factors for cancer?

A
  • Diet
  • Physical activity levels
  • Toxic exposures
  • Immune health
  • Stress levels
42
Q

Describe Xeroderma Pigmentosum

A

A condition in which thymine dimerisation from exposure to UV is not repaired; exposure to sunlight results in SKIN LESIONS.

It is an AUTOSOMAL RECESSIVE DISORDER in which there is a decreased ability to repair DNA damage. Mutations in repair genes have been known to cause cancer.

[signs appear in infancy or early childhood & affects the eyes and areas of skin exposed to the sun]

SIGNS AND SYMPTOMS:
- severe sunburn after a few minutes in the sun
- redness & blistering
- freckling
- dry skin (XERODERMA)
- skin colouring (PIGMENTATION)
- multiple skin cancers

43
Q
A

CANCER BIOLOGY (7 decks)

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