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AETIOLOGY OF CANCER 1 Flashcards

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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
what are the tumour-specific classification systems?
Bloom and Richardson- breast carcinoma Dukes’ - colorectal carcinoma Ann Arbour - lymphoma Breslow/Clarke’s- melanoma
26
Why do we need new anticancer treatments?
majority don’t respond well – treatment is palliative (symptom relief) rather than curative
27
what is a neoplasm?
A mass formed by the autonomous proliferation of cells that persists after cessation of the stimulus that provoked the change or “new growth”
28
what causes neoplasm or tumour?
Abnormal proliferation of cells
29
are all neoplasms malignant?
no
30
how do normal cells transform to neoplastic cells?
via a series of changes
31
what does cell transformation result in?
results in a cell population capable of proliferating independently of both internal and external signals that normally regulate their growth
32
what are the 2 controls on cell division?
external | internal
33
what does external cell division include?
population density cytokines (growth factors) substratum signals
34
what does internal cell division include?
activity of proliferation genes | activity of anti-proliferation genes
35
what is cell division dependent on?
on signals and sensors
36
what happens if signals and sensors become damaged?
cell division is unregulated
37
what do unregulated dividing cells form?
Unless they die, | they will form a tumour (swelling)
38
what is tumourigenesis?
carcinogenesis
39
what are the 3 types of cells that body cells can resolve into?
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
what is the cell cycle?
the orderly sequence of events required for the duplication of an eukaryotic cell
41
what are the phases of the cell cycle?
Gap phase 1 synthesis of a duplicate genome Gap phase 2 mitosis, splitting of the genome
42
what is the G1 phase?
``` High rate of metabolism Protein synthesis Vigorous growth Duplicates most of its organelles Centriole replication begins ```
43
what is the S phase?
DNA replicates. Synthesis of new histones Assembly of new chromatin
44
what is the G2 phase?
Synthesis of enzymes and proteins essential for cell division Their transport to final site Replication of centrioles complete
45
what is the M phase?
Mitosis | Splitting of the genome
46
what are the 2 critical points for dividing cells?
G1/S boundary when the cell is committed to DNA synthesis | G2/M boundary when the cell is committed to mitosis
47
what is the G1/S control point?
Most critical phase in the cell cycle
48
what happens at the G1/S control point?
Once S phase begins, DNA is replicated. | Failure to undergo mitosis - apoptosis
49
what controls the advance into the next phase?
factors in the cytoplasm
50
what factors regulate entry into the S phase?
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
what is G2/M control point?
Cyclin dependent protein kinase 1 (Cdk1) in presence of cyclin B (maturation/mitosis-promoting factor, MPF)
52
what is the cell switch?
modifies proteins associated with the chromosomes, nuclear envelope, nucleolus, centrosomes
53
what happens at the G2/M control point?
Sets in motion a sequence of changes that culminates in mitosis
54
what does activation at G2/M boundary ensure?
ensures cell does not to undergo multiple rounds of mitosis
55
what is post mitosis?
p
56
what does DNA replication require?
special proteins not used by non-dividing cells
57
what is E2F-1?
transcription factor that activates transcription of genes coding for these proteins
58
what is the effect of E2F-1 in non-dividing cells?
E2F-1 is inhibited as it is bound to protein pRb
59
what is protein pRb?
the product of a gene that is mutated in the cancer, retinoblastoma
60
what is the extra level of regulation that G1 Cdk1 has?
CDKs inhibited by Cyclin dependent kinase inhibitor proteins (CKI) There are a number of CKI mediating a number of pathways. Prevent cell division
61
what are the 3 signals which lead to the arrest of cell growth?
Mitogen withdrawal Loss of adhesion Contact inhibition
62
what is contact inhibition?
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
what does the production of p16 INK4a and p27 KIP1 cause?
They inhibit G1 CDKs and prevent DNA synthesis
64
what does the loss of contact inhibition show?
it's one of the first changes seen in the transformation of normal cells into cancer
65
what is p53?
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
what is produced in response to the transcription factor p53?
CKI called p21CIP1 is produced
67
what happens when DNA damage occurs?
the destruction of p53 is stopped
68
what do increased p53 conc activate?
multiple processes including DNA repair
69
what does p21CIP1 inhibit?
inhibits G1 CDKs preventing replication of defective DNA
70
what happens if DNA can't be repaired in time?
the cell is triggered to self destruct by apoptosis
71
what is apoptosis?
Programmed cell death
72
what is apoptosis characterised by?
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
what 3 events can cells activate apoptosis?
Extrinsic pathway Intrinsic pathways Stress activated apoptosis
74
what is the extrinsic pathway?
``` Instructed death (Death domain receptors) e.g. during viral infection ```
75
what is the intrinsic pathway?
Default death (absence of growth factors) (Activation of BAD promoter due to non functioning of phosphate kinase B)
76
what is Stress activated apoptosis?
Direct activation of mitochondria p53 which activates a bcl2 protein called BAX Through protein kinase p38 (p38 MAPK).
77
what is senescence?
irreversible cell cycle arrest driven by a variety of mechanisms, including telomere shortening, other forms of genotoxic stress, or mitogens or inflammatory cytokines
78
give examples of cell senescence
``` Replicative Stress-induced premature Oncogene-induced Replicative stress-induced Developmental Cell-cell fusion ```
79
what are telomeres?
Chromosome capping function - protects against homologous recombination and non-homologous end joining
80
what do telomeres prevent?
prevents ends of chromosomes from being seen as double stranded breaks
81
what is the end replication problem?
DNA polymerases cannot lengthen terminal section of lagging strand (primer site)
82
what is telomerase?
enzyme that repairs telomeres
83
what does reverse transcriptase (TERT) do?
synthesises (maintains) telomere length in germ cells, some stem cells (e.g. embryonic stem cells), some WBC
84
what does telomerase do?
Lengthens lagging strand (5’-3’), DNA polymerase-alpha completes complementary strand
85
when is telomerase activated?
in cancers
86
what is the Alternative Lengthening of Telomeres (ALT) pathway?
recombination mediated lengthening of telomeres
87
what is angiogenesis?
development of new BV
88
what would happen without blood supply?
hyperplasia/cancer growth is reduced - tumour remains as carcinoma in situ

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