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Pathology and Immunity > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

what are some important genes in carcinogenesis

A
  • oncogenes
  • tumour suppressor genes
  • dna repair genes
  • miRNAs
  • chromosomal aberrations
  • epigenetic mutations
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2
Q

what are oncogenes also known as

A

accelerators

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3
Q

what are accelerators of carcinogenesis

A

oncogenes

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4
Q

what are brakers of carcinogenesis

A

tumour suppressor genes

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5
Q
A
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6
Q
A
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7
Q

what can oncogenes be abnormal variants of

A
  • growth factors
  • growth factor receptors
  • signal transducers
  • control of gene expression
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7
Q

what are proto oncogenes

A

normal genes which regulate cell division

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7
Q

what do oncogenes produce

A

oncoproteins

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8
Q

which type of tissue is more sensitive to radiation

A

those where the cells are rapidly renewed

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9
Q

how do miRNA act as carcinogens

A

they have a controlling function over the rest of the genes
thousands are the target for drug development to control the development of carcinogenesis

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10
Q

what are epigenetic mutations

A

changes to dna that regulate whether genes are switched on or off
caused by behaviour and environment
do not change dna sequence
reversible

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11
Q

what is the most important carcinogen group

A

oncogenes

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12
Q

what is the normal version of oncogenes called

A

proto oncogenes

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13
Q

what forms can proto oncogenes come in

A
  • growth factors
  • growth factor receptors
  • signal transducers
  • control of gene expression
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14
Q

what is the important function for proto oncogenes

A

regulation of cell division

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15
Q

what happens if tight regulation of cell division is lost

A

increase in growth factor production and acting on specific cells which will divide and grow at a fast rate
often occurs if the gene is mutated

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16
Q

what is the activity of oncogenes held in check by

A

tumour suppressor proteins

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17
Q

what are the three mechanisms by which tight regulation of cell division is lost

A
  • mutation
  • excess normal product
  • enhanced transcription
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18
Q

what does a mutation of oncogenes lead to

A

increased activity of the product

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19
Q

what can cause an excess production of normal product

A
  • duplication of the gene
  • viral product
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20
Q

what can cause enhanced transcription of the normal product

A

translocation
chromosome rearrangement

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21
Q

describe chronic myeloid leukaemia

A
  • translocation can cause formation of a hybrid gene
  • hybrid genes are nicknamed the philadelphia chromosome for this condition
  • production of tyrosine kinase which is a growth factor that stimulates lots of pathways
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22
Q

what is burketts lymphoma associated with

A

epstein barr virus

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23
Q

what is the function of tumour suppressor genes

A

act to inhibit cell division and suppress growth
act as anti oncogenes
requires loss of both alleles

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24
Q

what is the knudson two hit hypothesis

A

idea that most tumour suppressor genes require both alleles to be inactivated, either through mutations or epigenetic silencing to cause a phenotypic change

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24
Q

describe the retinoblastoma gene and how it links to the knudson two hit hypothesis

A

person inherits defective gene from parents and passes this to children who has both genes mutated to form a malignancy

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25
Q

describe the function of TP53

A
  • acts just before the restriction point
  • two main functions in response to damaged DNA which are to stop the cell cycle and allow dna repair
  • trigger apoptosis if repair is not possible
  • often inactivated in cancer through mutation or deletion or due to viral proteins
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26
Q

in how many cases of head and neck cancer are there mutations in the tp53 gene

A

50%

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27
Q

what is included in genetic susceptibility to cancer

A
  • inherited cancer syndromes
  • familial cancer
  • defective dna repair
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28
Q

describe inherited cancer syndromes

A
  • single mutated genes that are often tumour suppressors
  • retinoblastoma and some colon cancers
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29
Q

what is an example of an inherited cancer

A

retinoblastoma

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30
Q

what is an example of familial cancer

A

breast ovary and colon

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31
Q

describe the cause of familial cancer

A

family clusters, genes and pattern of inheritance are not clear

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32
Q

describe defective dna repair

A

increased sensivity to carcinogens and general increased cancer risk if a person inherits a defective dna repair system

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33
Q

what is an example of a cancer resulting from a defective dna repair system

A

xeroderma pigmentosum

34
Q

what is xeroderma pigmentosum

A

this is when people do not go out in the sunlight because mutations will occur and will not be repaired so they can develop many skin malignancies

35
Q

what are some other systems affected by malignancies

A
  • cell division control
  • dna repair mechanisms
  • apoptosis inhibition
  • stimulation of blood vessel formation
  • destructive enzymes activated
  • cell motility increased
36
Q

main differences between a cancer cell and a healthy cell

A
  • proliferate faster
  • live longer
  • not fully differentiated
  • invade and destroy surrounding tissues
  • avoid apoptosis
  • produce its own food
37
Q

how do cancer cells proliferate

A

they are not dependent on growth signals coming from other areas of the body and develop their own growth signals and formation

38
Q

what are the six basic hallmarks of a cancer

A
  • evading apoptosis
  • self sufficiency in growth signals
  • insensitivity to anti growth signals
  • tissue invasion and metastasis
  • limitless replicative potential
  • sustained angiogenesis
39
Q

what are the modes of spread of malignant tumours

A
  • local and then systemic
  • lymphatic spread
  • blood spread
  • transcoelomic spread
  • intraepithelial spread
40
Q

what is haemotegenous spread

A

spread of maligancies through the blood

41
Q

what is an example of a disease that spreads intraepithelially

A

pagets disease of the breast

42
Q

what is metastasis

A

the spread of the malignant cells to distant organs forming secondary tumours

43
Q

what is transcoelomic spread

A

route of tumour metastasis across a body cavity, when a malignancy penetrates the surface of the cavity

44
Q

describe the metastatic behaviour of carcinomas

A

they spread in the lymph first and later in the disease they spread in the blood

45
Q

describe the metastatic behaviour of sarcomas

A

spread in the blood first and then in the lymphatics

46
Q

describe the metastatic behaviours of lung cancer

A

lung to lymph node to liver bone and brain

47
Q

describe the metastatic pathway of tongue cancer

A

tongue to neck nodes to lung and spine

48
Q

what are the stages to cancer spreading through the blood into other organs and tissues

A
  • direct spread and invasiveness
  • angiogenesis
  • vascular invasion and spread
  • establishment of new colony
49
Q

what happens in step one of blood spread of cancer

A

reduced cell to cell adhesion and invasion of the basement membrane and stroma

50
Q

what happens in step two of cancer spreading in the blood

A

increased cell motility due to factors produced by tumour cells

51
Q

what happens in step three of cancer spreading in the blood

A

walls of new vessels are thin and more easily invaded
cancer cells move in circulation and are packed in the capillary bed and will break out the capillaries

52
Q

what happens in the final stage of blood spread of cancer

A

cells invade the surrounding tissues and proliferate and stimulate angiogenesis and spread further

53
Q

what is tumour grading looking at

A

biological nature of the tumout

54
Q

what is tumour staging looking at

A

the extent of the spread

55
Q

how is the grade of a tumour studied

A

through histopathology

56
Q

how is the stage of the tumour determined

A

clinical investigation

57
Q

describe the process of grading tumours

A

histological assessment of the following factors:
- invasion into underlying tissue
- cellular atypia

58
Q

what are some examples of cellular atypia that are looked for in histological assessment of a tumour

A

abnormal mitotic activity
nuclear pleomorphism
differentiation
necrosis

59
Q

what are some methods of histological assessment when grading tumours

A

numerical grades
low, intermediate or high
degree of differentiation

60
Q

what does cancer staging describe

A

the extent or severity of a persons cancer
knowing the stage of the disease helps when planning treatment and estimating the persons prognosis

61
Q

what are the assessments that determine the stage of a cancer

A
  • physical examinations
  • imaging procedures
  • lab tests
  • pathology
  • surgical reports
62
Q

how do the staging systems of cancer differentiate

A

according to the organs involved

63
Q

what is the clinical staging system for oral cancer

A

TNM system

64
Q

describe the TNM staging system

A

T is tumour size
N is lymph node involvement
M is presence of metastasis

65
Q

if there is metastasis, what number is used in TNM staging

A

M1

66
Q

if there is no metastasis, what number is used in TNM staging

A

M0

67
Q

what is the staging classification used for haemopoeitic malignancies

A

the ann arbor staging classification

68
Q

what are the three stages to tumour immunology

A

elimination
equilibrium
escape

69
Q

how does the immune system recognise tumour cells

A

tumour associated antigens

70
Q

what are TAAs

A

tumour associated antigens

71
Q

what can neoantigens also be known as

A

tumour associated antigens

72
Q

what can neoantigens be made from

A
  • products of mutated genes
  • overexpressed proteins like tyrosinase
  • viral proteins
  • oncofetal antigens like carcinoembryonic antigens
73
Q

why can the immune system not recognise tumour cells

A

because they change their antigens continuously to evade the immune system

74
Q

what brings about the elimination stage of tumour immunology

A

recognition of tumour cells by immune cells, some will elicit a poor immune response and will not be destroyed
over time the malignant cells will increase the number of cells that do not cause a reaction to escape the immune system

75
Q

elevated levels of what molecule in patient serum indicates a malignancy

A

carcinoembryonic antigen

76
Q

what kind of response is elimination

A

cell mediated

77
Q

what are the cells involved in the elimination stage of immune response to tumour antigens

A
  • cytotoxic lymphocytes
  • natural killer cells
  • macrophages
78
Q

what is the first line of defence against tumour cells

A

natural killer cells

79
Q

describe the mechanism of action of macrophages

A

mechanisms similar to anti microbial killing

80
Q

how can tumour cells evade the immune response

A

cells may acquire molecular changes such as
- altered tumour antigen expression, lack of t cell recognition
- activation of immunoregulatory pathways leading to t cell unresponsiveness and apoptosis
- immunosupppressive factors like cytokines which inhibit t cells

81
Q

what is a cytokine that inhibits t cells

A

transforming growth factor beta

82
Q

how does immunotherapy treat cancer

A

through the use of the patients own immune response to control and destroy malignant cells

83
Q

list the types of immunotherapy

A
  • active immunisation
  • reversal of immunosuppression
  • adopted cell transfer
  • tumour infiltrating lymphocytes
  • CAR t cell therapy
  • strengthening the natural immune response
84
Q

what is CAR T cell therapy used for

A

haemotological malignancies

85
Q

summarise the haematogenous spread of cancer

A

step 1 - direct spread and invasiveness
- reduced cell to cell adhesion
- invasion of basement membrane and stroma

step 2 - angiogenesis
- increased cell motility
- due to factors produced by tumour cells

step 3 - vascular invasion and spread
- walls of new vessels are thin and more easily invaded
- cells move into the circulation
- cells are packed in the capillary bed and then break out of the capillaries

step 4 - establishment of a new colony
- cells invade surrounding tissues
- cells proliferate
- cells stimulate angiogenesis

Pathology and Immunity (16 decks)

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