Neoplasia 2 Flashcards

(67 cards)

1
Q

what are the two main factors of carcinogenesis?

A

genetic and environmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the important genes in carcinogenesis?

A

oncogenes, tumour suppressory genes, DNA repair genes, miRNAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does DNA damage lead to?

A

altered gene expression and then altered cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are proto-oncogenes?

A

normal genes which regulate cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the roles of proto-oncogenes?

A

growth factors, growth factor receptors, signal transducers, control of gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do oncogenes produce?

A

oncoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are abnormal variants of proto-oncogenes called?

A

oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

if tight regulation is lost, what can oncogenes do

A

mutations, excess activity of product, enhanced transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do the mutations in the oncogenes cause?

A

increased activity of the product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the cause of excess amounts of the normal product?

A

duplication of the gene, viral product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what occurs in enhanced transcription?

A

translocation or chromosome rearrangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do tumour suppressor genes do?

A

act to inhibit cell division and suppress growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do tumour suppressor genes require?

A

loss of both alleles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

give an example of a tumour suppressor gene

A

retinoblastoma gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the inherited factors of cancer?

A

inherited cancer syndromes, familial cancer, defective DNA repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the inherited cancer syndromes?

A

single mutant genes, often tumour suppressor genes, retinoblastoma, some colon cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the familial cancers?

A

family clusters, genes and pattern of inheritance, breast, ovary and colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what results due to defective DNA repair

A

increased sensitivity to carcinogens and general increased cancer risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

give an example of a defective DNA repair cancer

A

xeroderma pigmentosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is P53?

A

the guardian of the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when does P53 act?

A

just before the restriction point in the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the 2 main functions of P53 in response to damaged DNA

A

stops the cell cycle to allow DNA repair or apoptosis (if repair is not possible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what happens to P53 during cancer?

A

it is often inactivated by mutation or deletion or viral proteins (HPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is affected if P53 is mutated/deleted?

A

other cell division controls, DNA repair mechanisms, apoptosis inhibited, stimulation of blood vessel formation, destructive enzymes activated, cell motility increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the hallmarks of cancer?
insensitivity to anti-growth signals, tissue invasion and metastasis, limitless replicative potential, sustained angiogenesis, evading apoptosis, self-sufficiency in growth signals
26
what is the process of carcinogenesis?
multistep - initiation, promotion, progression
27
what are the modes of spread of malignant tumours?
local spread, lymphatic spread, blood spread (haematogenous), transcoelomic spread, intraepithelial spread
28
what is metastasis?
the spread of malignant cells to distant organ forming secondary tumours
29
how do carcinomas spread?
lymphatic and later blood
30
how do sarcomas spread
blood (lymphatic spread is rare)
31
where do cancers of the lung spread to?
local nodes, liver, bone and brain
32
where do cancers of the tongue spread to?
neck nodes, later lung and spine
33
what are the steps of metastasis?
intravasation, survival in the circulation, arrest in organ, extravasation, survival of cells after extravasation, initial growth of cells after extravasation, persistence of growth
34
what can tumour cells do?
alter adhesion molecules, make poor basement membrane, increase protease production or reduce inhibitors, alter extracellular matrix
35
when talking about grading and staging, what does grade mean?
biological nature of the tumour (histopathology)
36
when talking about grading and staging, what does stage mean?
extent of spread (clinical)
37
what is grading?
a histological assessment of invasion into underlying tissue and cellular atypia
38
what does cellular atypia include?
mitotic activity, nuclear pleomorphism, differentiation, necrosis
39
what are the methods of grading?
numerical, low/intermediate/high, degree of differentiation (SCC)
40
what type of grading is used for squamous cell carcinomas?
degree of differentiation
41
what does pleomorphism cover?
variation in cell shape and size, variation in nuclear shape and size
42
what can be seen in cells of a malignant tumour?
numerous mitoses, abnormal mitoses, variable differentiation
43
what does staging mean?
the extent or severity of a persons cancer
44
what does knowing the staging of the cancer help?
planning treatment and estimating the persons prognosis
45
what is used to determine staging?
physical exams, imaging procedures, laboratory tests, pathology and surgical reports
46
what system is used for staging of oral cancer?
TNM
47
what does T stand for in TNM?
tumour size
48
what does N stand for in TNM?
lymph node involvement
49
what does M stand for in TNM?
presence of metastases
50
what are the clinical effects of lung cancer?
cough, haemoptysis, chest pain, pneumonia
51
what are the systemic effects of cancer often caused by?
cytokines or hormones released by tumour cells or dysfunction of the organ
52
what are the systemic effects of cancer?
fever, anorexia, weight loss/cachexia, neurological problems e.g. neuropathy, endocrine sydromes e.g. Cushings syndrome, metabolic effects e.g. hypercalcaemia
53
how do you treat malignant tumours?
surgery, chemotherapy and radiotherapy
54
what is tumour immunology?
immune surveillance
55
what can tumour immunology do?
suppress or enhance carcinogenesis
56
what is elimination-equilibrium-escape
how does the immune system recognise tumour cells
57
what are the tumour associated antigens?
products of mutated genes, overexpressed proteins, viral proteins, oncofetal antigens
58
what is elimination?
cell mediated immune response
59
what immune cells contribute to elimination?
CD8+, NKC (first line of defence against tumour cells), macrophages
60
what can immunodeficiency lead to?
an increased incidence of malignant tumours
61
what does elimination lead to?
escape
62
what is escape
how do tumour cells evade the immune response
63
how do tumour cells escape?
acquire molecular changes such as alter tumour antigen expression (lack of T cell recognition), activation of immunoregulatory pathways leading to T cell unresponsiveness and apoptosis, immunosuppressive factors e.g. cytokines (inhibit T cell response)
64
what is immunotherapy?
using the patients own immune response to control and destroy malignant cells
65
what are the methods of immunotherapy?
active immunisation, reversal of immunosuppression, adopted cell transfer, strengthening natural immune responses
66
when is immunotherapy used?
in advanced stage of disease
67
when is immunotherapy most successful?
in haematological malignancies