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IMS > AETIOLOGY OF CANCER 2 > Flashcards

AETIOLOGY OF CANCER 2 Flashcards

1
Q

why are cancer cells called selfish cells?

A

they have have a selective advantage over normal, regulated cells – a form of natural selection

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2
Q

why are tumours said to have a ‘life of their own’?

A

Increase in neoplasm size persists whilst the hosts body is wasting (cachexia)
Ultimately kill themselves by killing the host

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3
Q

how do cancer cells and normal cells differ?

A 
Growth control
Contact inhibition
Repair/death mechanisms
Metastatic ability
Appearance
Growth rate
Maturity/differentiation
Immune evasion
Function
Angiogenesis
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4
Q

how can you measure tumour growth?

A

amount of time it takes the cell mass to double in size, and the number of such ‘doublings’

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5
Q

what is carcinogenesis?

A

process of inducing cancer

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6
Q

what kind of process is carcinogenesis?

A

A multistep process

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7
Q

what does carcinogenesis involve?

A

A normal cell evolves progressively to a cancerous state through acquiring a succession of properties
A normal cell acquires a series of molecular changes which result in the cell having new properties

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8
Q

what molecular changes does a cancer cell acquire?

A

changes to its DNA (genetic material) and to the proteins it produces

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9
Q

what is a change to DNA called?

A

mutation

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10
Q

define hallmarks

A

small number of traits

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11
Q

what are hallmarks?

A

traits that are shared by all cancers that govern the transformation of normal cells into cancerous ones

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12
Q

what are the 6 original hallmarks?

A
  • sustaining proliferative signalling
  • evading growth suppressors
  • activating invasion and metastasis
  • enabling replication immortality
  • inducing angiogenesis
  • resisting cell death
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13
Q

what does sustaining proliferative signalling involve?

A

Normal cells need external signals from growth factors to divide
Cancer cells are not dependent on normal growth factor signalling
Acquired mutations `short-circuit’ growth factor pathways leading to unregulated growth

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14
Q

give an example of ustaining proliferative signalling

A

mutation in Ras oncoprotein disrupts the normal -ve feedback mechanisms that dampen a signalling pathway when a mitogenic signal is hyperactivated

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15
Q

what does evading growth suppressors involve?

A

Normal cells respond to inhibitory signals
Cancer cells do not respond to growth inhibitory signals
Acquired mutations interfere with inhibitory pathways

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16
Q

give an example of evading growth suppressors

A

p53 is a common tumour suppressor gene which is inactivated in cancer cells leading to uncontrolled growth and proliferation

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17
Q

what does resisting cell death involve?

A

Apoptosis
Normal cells are removed by apoptosis, often in response to DNA damage
Cancer cells evade apoptotic signals

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18
Q

give an example of resisting cell death

A

dysregulation of anti-apoptotic BCL-2 family members

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19
Q

what does enabling replicative immortality involve?

A

Normal cells have a finite number of cell divisions after which they become senescent
The `cellular counting device’ is the shortening of chromosomal ends (telomeres) that occur after every round of DNA replication

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20
Q

what do cancer cells do in enabling replicative immortality?

A

Cancer cells maintain the length of their telomeres

Altered regulation of telomere maintenance results in unlimited replicative potential

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21
Q

give an example of enabling replicative immortality

A

Overexpression of telomerase allows tumour cells to overcome finite replicative ability

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22
Q

what does inducing angiogenesis involve?

A

Normal cells depend on established BV to supply oxygen and nutrients
Cancer cells induce angiogenesis, the growth of new BV, needed for tumour survival and expansion

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23
Q

give an example of inducing angiogenesis

A

Tumour angiogenesis is a function of multiple signals from a number of cell types residing in the tumour microenvironment

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24
Q

what does activating invasion and metastasis involve?

A

Normal cells maintain their location in the body and generally do not migrate
Cancer cells can move to other parts of the body and start secondary tumours

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25
Q

how does cancer grow?

A

Cells of malignant tumour duplicate rapidly and invade surrounding tissue (break through basement memb)
triggers angiogenesis through production of (TAFs)

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26
Q

how does cancer spread?

A

Cells compete with normal tissue for space and nutrients and eventually kills them
Some cells detach from primary tumour, enter body cavity or blood and establish secondary tumours

27
Q

what are the 4 modes of tumour spread?

A

Local invasion
Lymphatic spread
Vascular spread
Trans-coelomic spread

28
Q

what is the difference between malignant and benign tumours?

A

benign tour cells grow only locally and can’t spread by invasion or metastasis
malignant cells invade neighbouring tissues, enter BV, and metastasise to different sites

29
Q

what are the 4 steps in the metastatic process?

A

Motility and invasion from the primary site – can be as single cells or clumps
Embolism and circulation in blood or lymph system – can also get spread through fluids in a body cavity
Arrest in a distant capillary & adherence to the endothelium
Extravasation into the target organ parenchyma

30
Q

what do tumours need to metastasise?

A

they need an external stimulus through molecular cross-talk with cells in the neoplastic environment

31
Q

what is EMT?

A

Epithelial mesenchymal transition

32
Q

what is EMT involved in?

A

wound repair

metastasis

33
Q

what does genome instability & mutation involve?

A

Cancer cells generally have severechromosomal abnormalities, which worsen as the disease progresses
These genetic alterations drive tumour progression

34
Q

how do cancer cells promote genome instability?

A

they take advantage of mutations in DNA repair pathways

35
Q

what has been found to induce many types of cancer?

A

local chronicinflammation

36
Q

what do inflammatory cytokines promote?

A

tumour growth, proliferation and angiogenesis

37
Q

how does tumour-associated inflammation promote tumour growth?

A

by supplying the microenvironment with growth factors, survival factors, and factors that promote angiogenesis

38
Q

how are cancer cells seen by the body?

A

they appear to be invisible to the body’s immune system

39
Q

how do cancer cells avoid immune destruction?

A

by disabling components of the immune system that have been dispatched to eliminate them
recruitment of inflammatory cells that are actively immunosuppressive

40
Q

how do cancer cells generate energy?

A

use abnormal metabolic pathways

41
Q

how do cancer cells produce energy?

A

by a high rate of glycolysisfollowed by lactic acid fermentation in the cytosol

42
Q

what is the warburg effect?

A

Cancer cells convert available glucose to lactate irrespective of the availability of oxygen

43
Q

what does the warburg effect lead to?

A

they divert glucose metabolites to useful anabolic processes that accelerate cell proliferation

44
Q

what is the tumour stroma?

A

Cells co-opted in to supporting the cancer

45
Q

what does the tumour stroma contain?

A

vascular elements
fibroblasts
macrophages

46
Q

what do vascular elements do?

A

provide growth factors, blood supply (oxygen, nutrients)

47
Q

what do fibroblasts do?

A

contribute MMPs for extracellular matrix degradation during cancer cell migration

48
Q

what do macrophages do?

A

(alternatively activated), may provide defence against immune surveillance

49
Q

what are the causes of cancer?

A

carcinogens
viral infections
oncogenes

50
Q

what are carcinogens?

A

chemical agent or radiation that causes cancer eg. hydrocarbons, UV

51
Q

what are oncogenes?

A

cancer causing cells

52
Q

where are oncogenes derived from?

A

from proto-oncogenes (normal genes)

53
Q

what do porto-oncogenes do?

A

regulate normal growth and development

54
Q

what are carcinogenic agents?

A

chemicals
radiation
microbiologicals

55
Q

what are chemical carcinogenic agents?

A

Some direct acting but most require metabolic conversion (procarcinogens)

56
Q

what are radiation carcinogenic agents?

A

Hard uv light, X-rays, ß, gamma

57
Q

what are microbiologicals carcinogenic agents?

A

RNA viruses-leukaemia
DNA viruses- Kaposi’s sarcoma
Pathogenic species- gastric carcinoma and lymphoma

58
Q

give examples of carcinogens

A

Percival Pott
Soot
Tobacco smoke

59
Q

give examples of cancers

A 
chronic myelogenous leukaemia 
cervical cancer
breast cancer 
melanoma 
retinoblastoma
60
Q

what are the different treatments of cancer?

A

Surgery, chemotherapy, radiotherapy, biological - individually or in combination

61
Q

what are the side effects of radiation therapy?

A

hair loss, nausea and vomiting (destructive effect on hair follicles and lining of stomach and intestine)

62
Q

why does radiation therapy increase susceptibility to infection?

A

due to slow production of WBCs in bone marrow

63
Q

why is treatment of cancer difficult?

A

as cancer contains diverse population of abnormal cells varying in their resistance to drugs

IMS (52 decks)

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