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IMS > AETIOLOGY OF CANCER 1 > Flashcards

AETIOLOGY OF CANCER 1 Flashcards

1
Q

what is cancer?

A

a generic term for a large group of diseases that can affect any part of the body

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2
Q

what is one defining feature of cancer?

A

the rapid creation of abnormal cells that grow beyond their usual boundaries,

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3
Q

what is metastasis?

A

cells invade adjoining parts of the body and spread to other organs

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4
Q

what is the major cause of death from cancer?

A

Metastases

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5
Q

what is oncology?

A

study of tumours

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6
Q

what are tumours?

A

may be cancerous (malignant) and often fatal or they may be harmless

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7
Q

what are malignant neoplasms?

A

carcinoma in situ and cancer

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8
Q

what are malignant tumours capable of undergoing?

A

metastasis - break through the basement membrane and migrate to additional sites

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9
Q

what are benign tumours?

A

don’t metastasize - remain encapsulated by connective tissue fibrous sheath

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10
Q

what are the 5 main groups of cancer?

A 
Carcinoma (epithelial) 
Lymphoma (lymphatic system) 
Leukaemia (blood cells) 
Sarcomas (connective tissue) 
CNS tumours (brain & spinal chord)
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11
Q

what are the characteristics of benign tumours?

A

Microscopic appearance considered innocent implying the tumour will remain localised
Tumour remains encapsulated in CT (fibrous) sheath (basement memb)

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12
Q

how are benign tumours treated?

A

Amenable to surgical removal

or patient survives in they’re encapsulated

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13
Q

what are malignant tumours?

A

Malignant neoplasms can invade and destroy adjacent structures
Tumour cells breach encapsulated CT (fibrous) sheath (basement memb)

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14
Q

what happens if malignant tumours metastasise?

A

Can lead to patient death

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15
Q

how can benign epithelial tumours vary?

A

according to appearance

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16
Q

what are the different classes of benign epithelial neoplasms?

A

Glands – adenoma
Surfaces – papilloma
Mucous surfaces – polyp
Hollow masses - cysadenoma

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17
Q

what are cells derived from mesenchyme called?

A

sarcoma

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18
Q

what are cells derived from epithelia called?

A

carcinoma

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19
Q

what are the exceptions in malignant tumour terminology?

A

melanoma, lymphoma are malignant

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20
Q

why are tumours bad for us?

A

Local tissue destruction
Obstruction/compression
Hormonal malregulation

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21
Q

what is tumour prognosis based on?

A

Based on a diagnostic assessment of
grade
stage

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22
Q

what is grade?

A

how closely the tumour histology resembles the tissue of origin

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23
Q

what is stage?

A

how far the tumour cells have spread from the nidus (place where something is formed/deposited)

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24
Q

what does TMN stand for?

A

Tumour, size Node, local number involved Metastasis occurrence

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25
Q

what are the tumour-specific classification systems?

A

Bloom and Richardson- breast carcinoma
Dukes’ - colorectal carcinoma
Ann Arbour - lymphoma
Breslow/Clarke’s- melanoma

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26
Q

Why do we need new anticancer treatments?

A

majority don’t respond well – treatment is palliative (symptom relief) rather than curative

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27
Q

what is a neoplasm?

A

A mass formed by the autonomous proliferation of cells that persists after cessation of the stimulus that provoked the change
or “new growth”

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28
Q

what causes neoplasm or tumour?

A

Abnormal proliferation of cells

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29
Q

are all neoplasms malignant?

A

no

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30
Q

how do normal cells transform to neoplastic cells?

A

via a series of changes

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31
Q

what does cell transformation result in?

A

results in a cell population capable of proliferating independently of both internal and external signals that normally regulate their growth

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32
Q

what are the 2 controls on cell division?

A

external

internal

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33
Q

what does external cell division include?

A

population density
cytokines (growth factors)
substratum signals

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34
Q

what does internal cell division include?

A

activity of proliferation genes

activity of anti-proliferation genes

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35
Q

what is cell division dependent on?

A

on signals and sensors

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36
Q

what happens if signals and sensors become damaged?

A

cell division is unregulated

37
Q

what do unregulated dividing cells form?

A

Unless they die,

they will form a tumour (swelling)

38
Q

what is tumourigenesis?

A

carcinogenesis

39
Q

what are the 3 types of cells that body cells can resolve into?

A

Cells that never divide during the lifetime of an organism (terminally differentiated)
Cells that retain the ability to divide but ordinarily do not (in G0 phase)
Cells that routinely divide and can alter the rate of division (stem cells)

40
Q

what is the cell cycle?

A

the orderly sequence of events required for the duplication of an eukaryotic cell

41
Q

what are the phases of the cell cycle?

A

Gap phase 1
synthesis of a duplicate genome
Gap phase 2
mitosis, splitting of the genome

42
Q

what is the G1 phase?

A 
High rate of metabolism
Protein synthesis
Vigorous growth
Duplicates most of its organelles
Centriole replication begins
43
Q

what is the S phase?

A

DNA replicates.
Synthesis of new histones
Assembly of new chromatin

44
Q

what is the G2 phase?

A

Synthesis of enzymes and proteins essential for cell division
Their transport to final site
Replication of centrioles complete

45
Q

what is the M phase?

A

Mitosis

Splitting of the genome

46
Q

what are the 2 critical points for dividing cells?

A

G1/S boundary when the cell is committed to DNA synthesis

G2/M boundary when the cell is committed to mitosis

47
Q

what is the G1/S control point?

A

Most critical phase in the cell cycle

48
Q

what happens at the G1/S control point?

A

Once S phase begins, DNA is replicated.

Failure to undergo mitosis - apoptosis

49
Q

what controls the advance into the next phase?

A

factors in the cytoplasm

50
Q

what factors regulate entry into the S phase?

A

Cdk 2, Cdk 4 and Cdk 6
Cyclin E for the proper functioning of Cdk 2
Cyclin D for the proper functioning of Cdk 4 and Cdk 6

51
Q

what is G2/M control point?

A

Cyclin dependent protein kinase 1 (Cdk1) in presence of cyclin B (maturation/mitosis-promoting factor, MPF)

52
Q

what is the cell switch?

A

modifies proteins associated with the chromosomes, nuclear envelope, nucleolus, centrosomes

53
Q

what happens at the G2/M control point?

A

Sets in motion a sequence of changes that culminates in mitosis

54
Q

what does activation at G2/M boundary ensure?

A

ensures cell does not to undergo multiple rounds of mitosis

55
Q

what is post mitosis?

A

p

56
Q

what does DNA replication require?

A

special proteins not used by non-dividing cells

57
Q

what is E2F-1?

A

transcription factor that activates transcription of genes coding for these proteins

58
Q

what is the effect of E2F-1 in non-dividing cells?

A

E2F-1 is inhibited as it is bound to protein pRb

59
Q

what is protein pRb?

A

the product of a gene that is mutated in the cancer, retinoblastoma

60
Q

what is the extra level of regulation that G1 Cdk1 has?

A

CDKs inhibited by Cyclin dependent kinase inhibitor proteins (CKI)
There are a number of CKI mediating a number of pathways. Prevent cell division

61
Q

what are the 3 signals which lead to the arrest of cell growth?

A

Mitogen withdrawal
Loss of adhesion
Contact inhibition

62
Q

what is contact inhibition?

A

Dividing cells growing in a culture dish or edge of a wound come in to contact with neighbouring cells, stop dividing because contact (e.g. cadherins) causes production of 2 CKIs called p16 INK4a and p27 KIP1

63
Q

what does the production of p16 INK4a and p27 KIP1 cause?

A

They inhibit G1 CDKs and prevent DNA synthesis

64
Q

what does the loss of contact inhibition show?

A

it’s one of the first changes seen in the transformation of normal cells into cancer

65
Q

what is p53?

A

tumor suppressor gene found on chromosome 17 that is involved in DNA repair, cell cycle arrest, and apoptosis, and its overexpression is a feature of many human cancers

66
Q

what is produced in response to the transcription factor p53?

A

CKI called p21CIP1 is produced

67
Q

what happens when DNA damage occurs?

A

the destruction of p53 is stopped

68
Q

what do increased p53 conc activate?

A

multiple processes including DNA repair

69
Q

what does p21CIP1 inhibit?

A

inhibits G1 CDKs preventing replication of defective DNA

70
Q

what happens if DNA can’t be repaired in time?

A

the cell is triggered to self destruct by apoptosis

71
Q

what is apoptosis?

A

Programmed cell death

72
Q

what is apoptosis characterised by?

A

Cell shrinkage
Cell contents being packaged into blebs
Chopping up of DNA and its enclosure in fragments of nuclear memb
Secretion of cytokines to inhibit inflammation

73
Q

what 3 events can cells activate apoptosis?

A

Extrinsic pathway
Intrinsic pathways
Stress activated apoptosis

74
Q

what is the extrinsic pathway?

A 
Instructed death (Death domain receptors)
e.g. during viral infection
75
Q

what is the intrinsic pathway?

A

Default death (absence of growth factors) (Activation of BAD promoter due to non functioning of phosphate kinase B)

76
Q

what is Stress activated apoptosis?

A

Direct activation of mitochondria
p53 which activates a bcl2 protein called BAX
Through protein kinase p38 (p38 MAPK).

77
Q

what is senescence?

A

irreversible cell cycle arrest driven by a variety of mechanisms, including telomere shortening, other forms of genotoxic stress, or mitogens or inflammatory cytokines

78
Q

give examples of cell senescence

A 
Replicative
Stress-induced premature 
Oncogene-induced 
Replicative stress-induced 
Developmental 
Cell-cell fusion
79
Q

what are telomeres?

A

Chromosome capping function - protects against homologous recombination and non-homologous end joining

80
Q

what do telomeres prevent?

A

prevents ends of chromosomes from being seen as double stranded breaks

81
Q

what is the end replication problem?

A

DNA polymerases cannot lengthen terminal section of lagging strand (primer site)

82
Q

what is telomerase?

A

enzyme that repairs telomeres

83
Q

what does reverse transcriptase (TERT) do?

A

synthesises (maintains) telomere length in germ cells, some stem cells (e.g. embryonic stem cells), some WBC

84
Q

what does telomerase do?

A

Lengthens lagging strand (5’-3’), DNA polymerase-alpha completes complementary strand

85
Q

when is telomerase activated?

A

in cancers

86
Q

what is the Alternative Lengthening of Telomeres (ALT) pathway?

A

recombination mediated lengthening of telomeres

87
Q

what is angiogenesis?

A

development of new BV

88
Q

what would happen without blood supply?

A

hyperplasia/cancer growth is reduced - tumour remains as carcinoma in situ

IMS (52 decks)

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