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PathoPhys > Tutorial 4 - Cancer & cell death > Flashcards

Tutorial 4 - Cancer & cell death Flashcards

(64 cards)

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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
state the therapeutic means of targeting the following cancer hallmark: inducing angiogenesis
VEGF inhibitors
26
state the therapeutic means of targeting the following cancer hallmark: genome instability
PARP inhibitors
27
state the therapeutic means of targeting the following cancer hallmark: deregulating cell metabolism
aerobic glycolysis inhibitors
28
whats meant by cell adaptation?
cell physiological response to stress or pathologic stimuli used to achieve new steady state; preserving cell viability but modifying function
29
whats meant by cell injury?
adaptive means exceeded, reversible but can lead to cell death
30
whats meant by cell death?
via necrosis or apoptosis
31
State main causes of cell injury?
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
state the mechanisms of cell injury?
1. O2 & O2 derived free radicals 2. Intracellular Ca+2, loss Ca+2 homeostasis 3. ATP depletion 4. Defected membrane permeability
33
Injured cell morphology may be reversible - state some types of reversible injure
1. Ultrastructural change (plasma membrane, microvilli) 2. Mitochondrial change (swelling, densities) 3. Dilation of ER 4. Nucleolar alteration
34
State an irreversible cell injury(s)?
necrosis & apoptosis
35
how do necrotic cells look under light microscopy?
- increased eosinophilia (loss RNA) - glassy, homogenous - vacuolated look to cytoplasm - various nuclear changes - calcification
36
necrotic cells have various nuclear changes when viewed under light microscope - state these?
* Karyolysis–basophilia of chromatin fades * Pyknosis–nuclear shrinkage, increased basophilia * Karyorhexis–pyknotic nucleus undergoing fragmentation * Disappears with time
37
how do necrotic cells look under electron microscopy?
- membrane discontinuities - dilation mitochondria, densities - myelin figures - amorphous debris; aggregrates of denatured protein - nuclear changes (same as in LM)
38
State the types of necrosis?
1. Coagulative 2. Liquefactive 3. Gangrenous 4. caseous 5. enzymatic fat necrosis
39
Types of necrosis - coagulative: a. ) hows it look? b. ) characteristic of what?
- basic outline of cell preserved | - characteristic of hypoxic injury
40
Types of necrosis - liquefactive: a. ) Due to? c. ) Be found where?
- due to bactertial infection | - hypoxic cells in CNS
41
Types of necrosis - gangrenous
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
Types of necrosis - caseous - seen in what?
- seen in Tb; coagulative | - granuloma formation
43
Types of necrosis - enzymatic fat necrosis
???
44
how do apoptotic cells look under light microscope?
- 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
Cell adaptation is the "state in between normal and injured cell". State some ways the cell can adapt?
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
what is the difference between cell hypertrophy and cell hyperplasia?
hypertrophy - cells enlarge | hyperplasia - increased cell number
47
define cell atrophy?
cell shrinkage due to loss of cell substance; entire organ may diminish in size. Fewer mitochondria, smaller ER etc.
48
describe some causes of cell atrophy?
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
what is the purpose of cell atrophy?
allows cell to still survive, although at smaller size - cells form a new equilibrium with environment
50
Define metaplasia?
transformation of one differentiated cell type into another differentiated cell type
51
is metaplasia reversible?
yes
52
purpose of metaplasia?
allows substitution of cell more sensitive to type of stress experienced in that area
53
example of metaplasia?
smoker --> columnar epithelial becomes stratified squamous
54
t/f: most of the time, metaplasia comes with desirbale consequences
false - undesirable, like excessive mucus secretion
55
link between metaplasia and cancer?
persistence of stimulus for metastasis may cause cancer - ie. squamous cell carcinoma in lung, adenocarcinoma in oesophagus
56
how is metaplasia thought to arise?
genetic reprogramming of stem cells
57
define infarction
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
types of infarcts?
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
explain cell morphology in infarction?
- ischaemic coagulative necrosis - inflammatory exudate at borders - fibroblastic response (scar)
60
how long does it take for cell morphology changes in infarction?
12-18 hrs, then haemorrhage and swelling
61
4 major types of shock?
1. Cardiogenic - pump failure 2. Hypovolaemic - inadequate plasma volume 3. Septic - severe infection 4. Neurogenic - SC injure, anaesthetic complication
62
what is shock categorised by physiologically?
- widespread hypo-perfusion of tissue - inadequate circulating volume - insufficient nutrient/ waste movt. - switch to anaerobic respiration, increased lactic acid
63
is shock reversible?
initially yes, but with persistence comes cell death
64
difference between tp53 and p53?
tp53 is the gene, p53 is the protein

PathoPhys (25 decks)

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