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Pathology > Tumourigenesis and cancer signalling > Flashcards

Tumourigenesis and cancer signalling Flashcards

1
Q

what is tumourigenesis?

A

production or causation of tumours

production of new growth

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2
Q

what is cancer signalling?

A

abnormal cellular/molecular mechanisms that lead to cancer

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3
Q

what is a tumour?

A

“swelling” – any tissue mass: benign or malignant

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4
Q

define neoplasia?

A

New growth: benign or malignant

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5
Q

define cancer?

A

Malignant tumour with potential to metastasize

Synonymous with neoplasia

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6
Q

what is differentiation in terms of tumour?

A

Morphology of tumour cell compared to normal
Well-differentiated
Poorly differentiated

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7
Q

define mutation?

A

Change in one or more DNA bases from normal sequence

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8
Q

define carcinogenesis?

A

Processes involved in the onset/development of cancer

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9
Q

define metaplasia?

A

Reversible replacement of one cell type with another
Frequently associated with development of malignancy in metaplastic tissue
May induce dysplasia

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10
Q

what is dysplasia?

A

Altered cell maturation, orientation & tissue architecture

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11
Q

what is anaplasia?

A

Lack of differentiation

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12
Q

what is the epidemiology of cancer?

A

Predominately a disease of middle-aged & elderly

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13
Q

what can the distribution of cancer indicate?

A

underlying causes

e.g. Hepatocellular carcinoma – SE Asia & Africa, due to high prevalence of hepatitis B & C

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14
Q

what are major predisposing factors of cancer?

A

smoking and diet

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15
Q

what are some environmental factors that contribute to cancer?

A

Chemical carcinogenesis
Radiation
Viruses & cancer

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16
Q

what are some genetic factors that contribute to cancer?

A

Familial cancer syndromes

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17
Q

what are the effects of ionising radiation?

A

Direct DNA damage
Indirect DNA damage
Bystander effects
Adaptive response

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18
Q

what are the effects of UV radiation?

A

Direct DNA damage

Affects protein and lipid function – changes in cell signalling

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19
Q

what is the initation step in carcinogenesis?

A

carcinogen induces non-lethal mutations in cell

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20
Q

what is the promotion step in carcinogenesis?

A

Initiated cell proliferates

(clonal expansion); allows additional mutations to accumulate

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21
Q

what is the progression step in carcinogenesis?

A

Accumulation of multiple mutations results in invasive phenotype

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22
Q

what are examples of carcinogenesis initiators?

A

UV radiation
Cisplatinum
Asbestos
Alkylating drugs

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23
Q

what are some examples of carcinogenesis promoters?

A

Hormones
alcohol
chronic irritation or wounding

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24
Q

what are examples of abnormal proliferation and cellular immortalisation?

A

Uncontrolled proliferation

Prolonged or indefinite life span

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25
Q

what is polyploidy?

A

increased nuclear DNA - nuclear hyperchromasia

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26
Q

what is aneuploidy?

A

inexact multiples of DNA per cell

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27
Q

what are examples of abnormal nuclear DNA in tumour cells?

A
  • polyploidy
  • aneuploidy
  • chromosomal translocations or rearrangements
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28
Q

what happens to mitotic and apoptotic activity in tumour cells?

A
  • Increased mitotic activity in malignant tumours
  • Increased cellular proliferation
  • Deregulation of apoptosis
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29
Q

what are the 2 main groups of teens implicated in cancer?

A

oncogenes

tumour suppressors

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30
Q

how can the implication of oncogenes lead to cancer?

A

the lack of inhibition or gain of function will lead to cancer

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31
Q

how can the implication of tumour suppressors lead to cancer?

A

the increased inhibition or loss of function of which will lead to cancer

32
Q

what are examples of oncogenes?

A
  • cyclins
  • CDKs
  • E2F
  • MYC
  • Mdm2
33
Q

what are examples of tumour suppressors?

A
  • RB
  • p53
  • p21, p27, P57 (CIP/KIP/WAF)
  • p14/ARF
    -p16/INK4a, p17, p18, p19
    TGF-B receptor
    BRCA1, BRCA2
    ATM
34
Q

what are proto-oncogenes?

A

Normal part of genome

Promote cell growth

35
Q

what are oncogenes?

A

Mutated versions of proto-oncogenes

they lead to Uncontrolled growth

36
Q

what is the first step in the process of a proto-oncogene becoming an oncogene?

A

Point mutation of proto-oncogene –>

encodes oncoprotein – differs from normal protein

37
Q

what is the second step in the process of a proto-oncogene becoming an oncogene?

A

Gene amplification of DNA segment that includes a proto-oncogene –>
Over-expression of encoded protein

38
Q

what is the last step in the process of a proto-oncogene becoming an oncogene?

A

Chromosomal translocation so that growth-regulatory gene is under control of different promoter –>
Inappropriate expression of encoded protein

39
Q

what is important about gene amplification and chromosomal translocation in the forming of oncogenes?

A

these mechanisms generate oncogenes that produce proteins identical to normal protein

40
Q

what is the function of tumour suppressor genes?

A

normally act to inhibit cell proliferation

41
Q

what happens to tumour suppressor genes in tumour cells?

A

they are lost/inactivated in tumour cells

42
Q

what are the characteristics of benign tumours?

A
  • Non-invasive, remain localised
  • Slow growth rate
  • Close histological resemblance to parent tissue
43
Q

what are the characteristics of malignant tumours?

A
  • Invasive, capable of metastasis
  • Rapid growth rate
  • Variable histological resemblance to parent tissue
44
Q

how are tumours classified?

A
  • behavioural - benign or malignant

- histogenic - tissue of origin

45
Q

what are the characteristics of an intraepithelial neoplasia?

A

Dysplasia
Carcinoma in situ
Early detection to avoid invasion

46
Q

what are the steps of the metastatic sequence?

A
  • Detachment
  • Invasion
  • Intravasation
  • Evasion
  • Adherence
  • Extravasation
47
Q

what are the possible mediators of detachment in the metastatic sequence?

A

loss of surface adhesion molecules e.g. cadherins

48
Q

what are the consequences of detachment?

A

migration of individual cells enabled

49
Q

what are the possible mediators of invasion the metastatic sequence?

A
  • metalloproteinases
  • up-regulation of integrin expression
  • down-regulation of tissue inhibitors of metalloproteinases
50
Q

what are the consequences of invasion in the metastatic sequence?

A

erosion of tissue boundaries

51
Q

what are the possible mediators of intravasation in the metastatic process?

A
  • metalloproteinases

- down-regulation of tissue inhibitors of metalloproteinases

52
Q

what are the consequences of intravasation in the metastatic process?

A

access to vascular routes of dissemination

53
Q

what are the possible mediators of evasion in the metastatic process?

A
  • reduced expression of MHC class I antigen

- shedding of ICAM-1 blocks T-cell receptor

54
Q

what are the consequences of evasion of host defences?

A

survival against host defences

55
Q

what are the possible mediators of adherence in the metastatic sequence?

A

binding of CD44 to endothelial ligand

56
Q

what are the consequences of adherence in the metastatic sequence?

A

arrest of movement by adhesion to endothelium

57
Q

what are possible mediators of extraversion in the metastatic sequence?

A
  • interns

- Laminin receptor

58
Q

what is the consequence of extravasation in the metastatic process?

A

colonisation of site of metastasis

59
Q

what are the traits of tumours?

A
  • Evasion of apoptosis
  • Self-sufficiency in growth signals
  • Insensitive to growth inhibition signal
  • Sustained angiogenesis
  • Limitless replicative potential
  • Ability to invade and metastasise
60
Q

what are the ways to pathologically diagnose tumours?

A

Biopsies
Cytology
Tumour staging & grading

61
Q

what is an excisions biopsy?

A

entire lesion removed

62
Q

what is an incisional biopsy?

A

fairly large, representative sample taken

63
Q

what is a needle biopsy?

A

thin core of tissue removed

64
Q

what is a disadvantage of needle biopsies?

A

potential for sampling error

65
Q

what is cytology?

A

a sample of body fluids relies on the appearance of individual cells

66
Q

what is grade 1 of tumour grading?

A

well differentiated

67
Q

what is grade 2 of tumour grading?

A

moderately differentiated

68
Q

what is grade 3 of tumour grading?

A

poor differentiated

69
Q

what is stage A in Dukes’ staging?

A

confined to submucosa or muscle layer

70
Q

what is stage B in Dukes’ staging?

A

invasion through muscle layer

71
Q

what is stage C in Dukes’ staging?

A

tumour in lymph nodes

72
Q

what happens in the development of colorectal cancer?

A
  • increasing DNA damage
  • DNA mutations
  • APC gene
  • KRAS oncogene
  • BRAF gene
  • MSI
73
Q

what is the APC gene responsible for in the development of colorectal cancer?

A

chromosome segregation

74
Q

what is the KRAS oncogene responsible for in the development of colorectal cancer?

A

cell growth, differentiation, survival motility

75
Q

what is the BRAF gene responsible for in the development of colorectal cancer?

A

cell growth, apoptosis

76
Q

what is MSI responsible for in the development of colorectal cancer?

A

uneven replication of DNA

Pathology (17 decks)

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