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PathoPhys > Tutorial 4 - Cancer & cell death > Flashcards

Tutorial 4 - Cancer & cell death Flashcards

1
Q

2 types of hallmarks of cancer?

A

Emerging (newly discovered) and underlying

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2
Q

Emerging hallmarks of cancer?

A
  • reprogramming of energy metabolism

- evasion of destruction by immune system

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3
Q

Underlying hallmarks of cancer?

A
  • genetic instability

- inflammation

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4
Q

how are cancer cells involved with sustaining proliferative signalling?

A
  • produce own growth factors
  • induce surrouding normal cells to produce growth factors
  • signaling can be deregulated (by cancer cells, intentionally) by increased expression of growth receptors (ie. HER2 overexpression)
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5
Q

how are cancer cells involved with evading growth suppressors?

A
  • inactivation tumor suppressor genes (RB and tp53)

- disables body ability to induce normal senescence and apoptosis

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6
Q

how are cancer cells involved with resisting cell death?

A
  • loss of tp53 (which induces apoptosis)
  • increased expression of anti-apoptotic factors
  • down regulate pro-apoptotic factors (Bax, Bim)
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7
Q

how are cancer cells involved with enabling replicative immortality?

A
  • overexpression of telomerase enzyme to lengthen telomeres, thereby avoiding senescence or apoptosis
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8
Q

how are cancer cells involved with inducing angiogenesis?

A
  • VEGF-a (its expression being upregulated by hypoxia and oncogene signalling)
  • peri-tumoral inflammatory cells help induce angiogenesis
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9
Q

how are cancer cells involved with activating invasion and metastasis?

A
  1. Local invasion by cancer cells, breakdown of ECM
  2. Intravasation (BV and lymphatics)
  3. Extravasation (into distant tissues)
  4. Micro-metastases (small nodule formation)
  5. Colonization (growth of micro-metastatic lesions into tumors)
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10
Q

Cancer cells undergo invasion and metastasis. What is EMT, and how does it relate to this?

A

Epithelial-Mesenchymal transition:

  • process by which epithelial cells lose polarity, gain migratory and invasive properties, become mesenchymal stem cells (multipotent)
  • cancer cells undergo EMT(?), this augments their ability to invade/ resist apoptosis/ disseminate
  • basically makes cells become much more motile
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11
Q

what orchestrates EMT?

A

transcription factors (Snail, slug, twist)

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12
Q

to go from epithelial to mesenchymal state, what process is required?

A

EMT!

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13
Q

how are cancer cells involved with deregulating cellular metabolism?

A
  • use glycolysis instead of oxidative phos.

- 18 fold less efficient, but provides intermediates (nucleoslides, amino acids) needed for rapidly dividing cells

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14
Q

normal cell:

a. ) what % oxidative phos.?
b. ) what % glycolysis?

A

a. ) 90%

b. ) 10%

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15
Q

cancer cell:

a. ) what % oxidative phos.?
b. ) what % glycolysis?

A

a. ) 40%

b. ) 60%

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16
Q

how are cancer cells involved with avoiding immune destruction?

A
  • highly immunogenic cancer cells destroyed (immuno-editing)
  • lowly immunogenic cancer cells survive, these variants grow and generate tumors
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17
Q

how are cancer cells involved with genome instability and mutation?

A
  • tp53 mutation
  • DNA mismatch repair defects
  • this disables detection DNA damage, activation repair machinery etc.
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18
Q

how do inflammatory cells contribute to hallmark capabilities of cancer?

A

By releasing…
• growth factors that sustain proliferative signalling
• survival factors that limit cell death
• pro-angiogenic factors
• matrix-modifying enzymes that facilitate invasion, and metastasis
• inductive signals that lead to activation of EMT
• reactive oxygen species that are actively mutagenic for cancer cells

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19
Q

state the therapeutic means of targeting the following cancer hallmark: sustaining proliferative signalling

A

EGFR inhibitors

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20
Q

state the therapeutic means of targeting the following cancer hallmark: evading growth suppressors

A

Cyclin dependent kinase inhibitors

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21
Q

state the therapeutic means of targeting the following cancer hallmark: avoiding immune destruction

A

immune-activating anti-CTLA4 mAb

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22
Q

state the therapeutic means of targeting the following cancer hallmark: enabling replicative immortality

A

telomerase inhibitors

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23
Q

state the therapeutic means of targeting the following cancer hallmark: tumor promiting inflammation

A

anti-inflammatory drugs

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24
Q

state the therapeutic means of targeting the following cancer hallmark: invasion and metastasis

A

inhibitors of MET

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25
Q

state the therapeutic means of targeting the following cancer hallmark: inducing angiogenesis

A

VEGF inhibitors

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26
Q

state the therapeutic means of targeting the following cancer hallmark: genome instability

A

PARP inhibitors

27
Q

state the therapeutic means of targeting the following cancer hallmark: deregulating cell metabolism

A

aerobic glycolysis inhibitors

28
Q

whats meant by cell adaptation?

A

cell physiological response to stress or pathologic stimuli used to achieve new steady state; preserving cell viability but modifying function

29
Q

whats meant by cell injury?

A

adaptive means exceeded, reversible but can lead to cell death

30
Q

whats meant by cell death?

A

via necrosis or apoptosis

31
Q

State main causes of cell injury?

A
  1. Hypoxia (impinging on respiration)
  2. Physical agents
  3. Chemical agents
  4. Infectious agents
  5. Immunologic reactions
  6. genetic derangements (congenital)
  7. nutritional imbalance (under or over)
32
Q

state the mechanisms of cell injury?

A
  1. O2 & O2 derived free radicals
  2. Intracellular Ca+2, loss Ca+2 homeostasis
  3. ATP depletion
  4. Defected membrane permeability
33
Q

Injured cell morphology may be reversible - state some types of reversible injure

A
  1. Ultrastructural change (plasma membrane, microvilli)
  2. Mitochondrial change (swelling, densities)
  3. Dilation of ER
  4. Nucleolar alteration
34
Q

State an irreversible cell injury(s)?

A

necrosis & apoptosis

35
Q

how do necrotic cells look under light microscopy?

A
  • increased eosinophilia (loss RNA)
  • glassy, homogenous
  • vacuolated look to cytoplasm
  • various nuclear changes
  • calcification
36
Q

necrotic cells have various nuclear changes when viewed under light microscope - state these?

A
  • Karyolysis–basophilia of chromatin fades
  • Pyknosis–nuclear shrinkage, increased basophilia
  • Karyorhexis–pyknotic nucleus undergoing fragmentation
  • Disappears with time
37
Q

how do necrotic cells look under electron microscopy?

A
  • membrane discontinuities
  • dilation mitochondria, densities
  • myelin figures
  • amorphous debris; aggregrates of denatured protein
  • nuclear changes (same as in LM)
38
Q

State the types of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. caseous
  5. enzymatic fat necrosis
39
Q

Types of necrosis - coagulative:

a. ) hows it look?
b. ) characteristic of what?

A
  • basic outline of cell preserved

- characteristic of hypoxic injury

40
Q

Types of necrosis - liquefactive:

a. ) Due to?
c. ) Be found where?

A
  • due to bactertial infection

- hypoxic cells in CNS

41
Q

Types of necrosis - gangrenous

A

not a real distinctive type but often used in clinical practice

  • loss of blood supply to limb (really coagulative)
  • superimposed bacterial infection (“wet gangrene”, really liquefactive)
42
Q

Types of necrosis - caseous - seen in what?

A
  • seen in Tb; coagulative

- granuloma formation

43
Q

Types of necrosis - enzymatic fat necrosis

A

???

44
Q

how do apoptotic cells look under light microscope?

A
  • single cells or small clusters
  • cell shrinks
  • cytoplasmic blebs
  • eosinophillic cytoplasm, dense nuclear chromatin fragments
  • always quickly cleared (phagocytosis), so must be considerable amount of apoptosis in order for it to be seen under light microscope
45
Q

Cell adaptation is the “state in between normal and injured cell”. State some ways the cell can adapt?

A
  1. Up/ down regulation of surface receptors
  2. New protein synthesis
  3. Switch from producing one type of protein to another
  4. Cell growth/ differentiation
46
Q

what is the difference between cell hypertrophy and cell hyperplasia?

A

hypertrophy - cells enlarge

hyperplasia - increased cell number

47
Q

define cell atrophy?

A

cell shrinkage due to loss of cell substance; entire organ may diminish in size. Fewer mitochondria, smaller ER etc.

48
Q

describe some causes of cell atrophy?

A
  1. decreased workload
  2. loss innervation
  3. decreased blood supply/ nutrition
  4. loss endocrine stimulation
  5. aging

basically - loss of need for the cell (less stimulation for it to function)

49
Q

what is the purpose of cell atrophy?

A

allows cell to still survive, although at smaller size - cells form a new equilibrium with environment

50
Q

Define metaplasia?

A

transformation of one differentiated cell type into another differentiated cell type

51
Q

is metaplasia reversible?

A

yes

52
Q

purpose of metaplasia?

A

allows substitution of cell more sensitive to type of stress experienced in that area

53
Q

example of metaplasia?

A

smoker –> columnar epithelial becomes stratified squamous

54
Q

t/f: most of the time, metaplasia comes with desirbale consequences

A

false - undesirable, like excessive mucus secretion

55
Q

link between metaplasia and cancer?

A

persistence of stimulus for metastasis may cause cancer - ie. squamous cell carcinoma in lung, adenocarcinoma in oesophagus

56
Q

how is metaplasia thought to arise?

A

genetic reprogramming of stem cells

57
Q

define infarction

A

cellular response to obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue.

58
Q

types of infarcts?

A

White (anaemic) - arterial occlusion in solid organ, heart/ kidney/ spleen
Red (haemorrhagic) venous occulusion in loose tissue, lung/ bowel/ brain

Septic (bacterial infection caused) or bland (non infection caused

59
Q

explain cell morphology in infarction?

A
  • ischaemic coagulative necrosis
  • inflammatory exudate at borders
  • fibroblastic response (scar)
60
Q

how long does it take for cell morphology changes in infarction?

A

12-18 hrs, then haemorrhage and swelling

61
Q

4 major types of shock?

A
  1. Cardiogenic - pump failure
  2. Hypovolaemic - inadequate plasma volume
  3. Septic - severe infection
  4. Neurogenic - SC injure, anaesthetic complication
62
Q

what is shock categorised by physiologically?

A
  • widespread hypo-perfusion of tissue
  • inadequate circulating volume
  • insufficient nutrient/ waste movt.
  • switch to anaerobic respiration, increased lactic acid
63
Q

is shock reversible?

A

initially yes, but with persistence comes cell death

64
Q

difference between tp53 and p53?

A

tp53 is the gene, p53 is the protein

PathoPhys (25 decks)

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