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Microbiology BDS1 > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

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1
Q

what are the two main factors of carcinogenesis?

A

genetic and environmental

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2
Q

what are the important genes in carcinogenesis?

A

oncogenes, tumour suppressory genes, DNA repair genes, miRNAs

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3
Q

what does DNA damage lead to?

A

altered gene expression and then altered cell function

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4
Q

what are proto-oncogenes?

A

normal genes which regulate cell division

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5
Q

what are the roles of proto-oncogenes?

A

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

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6
Q

what do oncogenes produce?

A

oncoproteins

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7
Q

what are abnormal variants of proto-oncogenes called?

A

oncogenes

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8
Q

if tight regulation is lost, what can oncogenes do

A

mutations, excess activity of product, enhanced transcription

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9
Q

what do the mutations in the oncogenes cause?

A

increased activity of the product

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10
Q

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

A

duplication of the gene, viral product

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11
Q

what occurs in enhanced transcription?

A

translocation or chromosome rearrangement

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12
Q

what do tumour suppressor genes do?

A

act to inhibit cell division and suppress growth

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13
Q

what do tumour suppressor genes require?

A

loss of both alleles

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14
Q

give an example of a tumour suppressor gene

A

retinoblastoma gene

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15
Q

what are the inherited factors of cancer?

A

inherited cancer syndromes, familial cancer, defective DNA repair

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16
Q

what are the inherited cancer syndromes?

A

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

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17
Q

what are the familial cancers?

A

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

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18
Q

what results due to defective DNA repair

A

increased sensitivity to carcinogens and general increased cancer risk

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19
Q

give an example of a defective DNA repair cancer

A

xeroderma pigmentosum

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20
Q

what is P53?

A

the guardian of the genome

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21
Q

when does P53 act?

A

just before the restriction point in the cell cycle

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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)

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23
Q

what happens to P53 during cancer?

A

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

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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

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25
Q

what are the hallmarks of cancer?

A

insensitivity to anti-growth signals, tissue invasion and metastasis, limitless replicative potential, sustained angiogenesis, evading apoptosis, self-sufficiency in growth signals

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26
Q

what is the process of carcinogenesis?

A

multistep - initiation, promotion, progression

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27
Q

what are the modes of spread of malignant tumours?

A

local spread, lymphatic spread, blood spread (haematogenous), transcoelomic spread, intraepithelial spread

28
Q

what is metastasis?

A

the spread of malignant cells to distant organ forming secondary tumours

29
Q

how do carcinomas spread?

A

lymphatic and later blood

30
Q

how do sarcomas spread

A

blood (lymphatic spread is rare)

31
Q

where do cancers of the lung spread to?

A

local nodes, liver, bone and brain

32
Q

where do cancers of the tongue spread to?

A

neck nodes, later lung and spine

33
Q

what are the steps of metastasis?

A

intravasation, survival in the circulation, arrest in organ, extravasation, survival of cells after extravasation, initial growth of cells after extravasation, persistence of growth

34
Q

what can tumour cells do?

A

alter adhesion molecules, make poor basement membrane, increase protease production or reduce inhibitors, alter extracellular matrix

35
Q

when talking about grading and staging, what does grade mean?

A

biological nature of the tumour (histopathology)

36
Q

when talking about grading and staging, what does stage mean?

A

extent of spread (clinical)

37
Q

what is grading?

A

a histological assessment of invasion into underlying tissue and cellular atypia

38
Q

what does cellular atypia include?

A

mitotic activity, nuclear pleomorphism, differentiation, necrosis

39
Q

what are the methods of grading?

A

numerical, low/intermediate/high, degree of differentiation (SCC)

40
Q

what type of grading is used for squamous cell carcinomas?

A

degree of differentiation

41
Q

what does pleomorphism cover?

A

variation in cell shape and size, variation in nuclear shape and size

42
Q

what can be seen in cells of a malignant tumour?

A

numerous mitoses, abnormal mitoses, variable differentiation

43
Q

what does staging mean?

A

the extent or severity of a persons cancer

44
Q

what does knowing the staging of the cancer help?

A

planning treatment and estimating the persons prognosis

45
Q

what is used to determine staging?

A

physical exams, imaging procedures, laboratory tests, pathology and surgical reports

46
Q

what system is used for staging of oral cancer?

A

TNM

47
Q

what does T stand for in TNM?

A

tumour size

48
Q

what does N stand for in TNM?

A

lymph node involvement

49
Q

what does M stand for in TNM?

A

presence of metastases

50
Q

what are the clinical effects of lung cancer?

A

cough, haemoptysis, chest pain, pneumonia

51
Q

what are the systemic effects of cancer often caused by?

A

cytokines or hormones released by tumour cells or dysfunction of the organ

52
Q

what are the systemic effects of cancer?

A

fever, anorexia, weight loss/cachexia, neurological problems e.g. neuropathy, endocrine sydromes e.g. Cushings syndrome, metabolic effects e.g. hypercalcaemia

53
Q

how do you treat malignant tumours?

A

surgery, chemotherapy and radiotherapy

54
Q

what is tumour immunology?

A

immune surveillance

55
Q

what can tumour immunology do?

A

suppress or enhance carcinogenesis

56
Q

what is elimination-equilibrium-escape

A

how does the immune system recognise tumour cells

57
Q

what are the tumour associated antigens?

A

products of mutated genes, overexpressed proteins, viral proteins, oncofetal antigens

58
Q

what is elimination?

A

cell mediated immune response

59
Q

what immune cells contribute to elimination?

A

CD8+, NKC (first line of defence against tumour cells), macrophages

60
Q

what can immunodeficiency lead to?

A

an increased incidence of malignant tumours

61
Q

what does elimination lead to?

A

escape

62
Q

what is escape

A

how do tumour cells evade the immune response

63
Q

how do tumour cells escape?

A

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
Q

what is immunotherapy?

A

using the patients own immune response to control and destroy malignant cells

65
Q

what are the methods of immunotherapy?

A

active immunisation, reversal of immunosuppression, adopted cell transfer, strengthening natural immune responses

66
Q

when is immunotherapy used?

A

in advanced stage of disease

67
Q

when is immunotherapy most successful?

A

in haematological malignancies

Microbiology BDS1 (20 decks)

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