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Foundations of health and disease > cancer > Flashcards

cancer Flashcards

1
Q

what is cancer?

A

A disease caused by normal cells changing so that they grow in an uncontrolled way, invade surrounding tissue and travel to other parts of the body (metastasis)
malignant neoplasm’, ‘malignant tumour’

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2
Q

what is Aetiology

A

the cause, set of causes, or manner of causation of a disease or condition.

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3
Q

why do tumours arise?

A
  • Accumulation of genetic alterations (e.g. mutations, deletions, translocations)
  • Epigenetic changes (e.g. promoter methylation) in cells.
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4
Q

what causes changes in the DNA which cause cancer

A

Inherited
External factors e.g. smoking, diet, UV irradiation, pollutants, viruses
Natural cell process

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5
Q

what is a tumour

A

Swelling, now commonly a synonym for ’neoplasm’

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6
Q

what is neoplasia

A

‘new growth’ of abnormal cells

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7
Q

what are the 2 tumour types and which is cancer

A

Benign- ‘gentle/kind’ - not harmful or non-life threatening
Malignant- ‘evil in nature’ - life threatening- cancer

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8
Q

what is the behavioural classification of neoplasms

A

benign or malignant

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9
Q

what is the histogenic classification of neoplasms

A

cell or tissue of origin

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10
Q

growth rate of benign tumours

A

slow

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11
Q

mitotic figures of benign tumours

A

rare

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12
Q

histological resemblance to normal tissue of benign tumours

A

good

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13
Q

do benign tumours invade tissues

A

no

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14
Q

do benign tumours undergo metastasis

A

never

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15
Q

what are the borders of a benign tumour like

A

well defined or encapsulateed

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16
Q

necrosis of benign tumours

A

rare

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17
Q

the growth rate of malignant tumours

A

relatively rapid

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18
Q

mitotic figures of malignant tumours

A

common

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19
Q

malignant tumours’ histological resemblance to normal tissue

A

variable often poor

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20
Q

do malignant tumours invade tissues

A

yes

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21
Q

do malignant tumours undergo metastasis

A

yes

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22
Q

what are the borders of malignant tumours like?

A

poorly defined or irregular

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23
Q

necrosis of malignant tumours

A

common

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24
Q

what happens when a benign tumour arises in epithelial or mucosal surfaces?

A

the tumour grows away from the surface
a polyp will form which is either
pedunculated (stalked)
sessile (sitting on the surface)
this noninvasive outward direction of growth creates anexophyticlesion (grows outwards)

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25
Q

what are the issues with benign tumours?

A

Pressure on adjacent tissues
Obstruction to the flow of fluid
Production of a hormone
Transformation into a malignant neoplasm
Anxiety

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26
Q

how do malignant tumours form

A

On epithelial or mucosal surfaces may form a protrusion in early stages, eventually invades the underlying tissue; gives rise to an endophytic tumour (grows inwards).

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27
Q

issues with malignant tumours

A

Pressure on and destruction of adjacent tissue
Formation of secondary tumours (metastases)
Blood loss from ulcerated surfaces
Obstruction of flow
Production of a hormone
Other paraneoplastic effects cause weight loss and debility
Anxiety and pain.

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28
Q

what are borderline tumours

A

Show some of the features associated with malignancy but lack the most important criterion of invasion.
Their biological behavior (determined by histology) is intermediate between that of clearly benign and overtly malignant tumours

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29
Q

what is histogenesis

A

Specific cell or tissue of origin of an individual tumour

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30
Q

what is histology

A

Microscopic study of biological tissues
Histology is the microscopic counterpart to gross anatomy, and is sometimes referred to as microanatomy

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31
Q

what is histopathology

A

Microscopic study of diseased tissue

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32
Q

how is the histogenic classification of tumours categorised

A

epithelial cells (forming carcinomas)
connective tissues or mesenchymal tissues (forming sarcomas)
haematopoietic system (forming leukaemias)
the lymphatic system (forming lymphomas)

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33
Q

what do you call epithelial tumours- benign and malignant

A

Benign epithelial tumours - papillomas or adenomas*
Malignant epithelial tumours - carcinomas
papilloma= benign tumour of nonglandular or nonsecretory epithelium
adenoma= benign tumour of glandular or secretory epithelium

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34
Q

what do you call mesenchymal tissue tumours- benign and malignant

A

Benign connective/other mesenchymal tissue tumours - prefix denotes cell of origin
Malignant connective/other mesenchymal tissue tumours – sarcomas

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35
Q

what is tumour grading

A

Describes how closely the tumour resembles its cell or tissue of origin

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36
Q

what is tissue staging?

A

Describes the anatomical extent of spread of the tumour

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37
Q

what are the two grading systems of tumours

A

Numerical: 1/2/3
Description based: Low/medium/high grade or
well/moderately/poorly differentiated

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38
Q

explain the first grade level for tumours

A

1/low grade/well differentiated: Cells generally resemble the normal cells from which they are derived, are well differentiated, with normal tissue organization, growing slowly – mitotic index low

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39
Q

explain the second level of tumours

A

2/medium grade/moderately differentiated: Cells may exhibit some loss of differention, cells exhibit abnormalities - abnormal shape, abnormal nuclei, more rapidly growing

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40
Q

explain the third level of tumours

A

3/high grade/poorly differentiated: Poorly differentiated tissue, abnormal- cell shape, nuclear shape, rapidly growing-mitotic index high

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41
Q

how is tumour staging determined?

A

Histopathological examination of the tumour

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42
Q

what does the TNM system stand for

A

Locally T = Tumour
Lymph nodes N = Nodes
Metastasis M = metastasis

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43
Q

what are the genetic causes of cancer

A
  • Mutations, deletions, translocations
  • Also Epigenetic changes (e.g. promoter methylation) in cells
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44
Q

what is molecular biology

A

Studies the composition, structure and interactions of cellular molecules i.e. nucleic acids and proteins

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45
Q

what is carcinogenesis

A

The process by which normal, healthy cells transform into cancer cells is termed carcinogenesis or oncogenesis

46
Q

multistep nature of carciogenesis

A
47
Q

what are primary cultures used for

A

test of carciongenic/ oncogenic transformation

48
Q

how to do a primary culture

A

The cells from the embryos are enzymatically dissociated.
Seeded as single cells
Treated with radiation or chemicals
Colonies are scored after 8-10 days after staining

49
Q

normal untransformed embryo cells vs radiation-transformed embryo cells

A

normal untransformed embryo cells
show contact inhibition
are orderly
Radiation transformed embryo cells
Densely stained
Piled up cells
Random cell arrangement

50
Q

causes of cancer

A

Smoking
Diet and lack of exercise
Reproductive life
Viruses
Environmental factors/pollutants
Hormones
Ionising radiation/sunlight
Inherited genes
Translocations
Other acquired gene mutations
Natural cell processes

51
Q

oncogenes vs tumour suppressor genes

A
52
Q

what is the pathways for tumour suppressor and oncogenes

A
53
Q

what are proto-goncogenes

A

normal genes that do not lead to cancer development

54
Q

what are oncogenes

A

Proto-oncogenes that have been mutated and lead to cancer development

55
Q

what kind of protein does proto-oncogene c-sis create

A

Platelet derived growth factor (PDGF)
Secreted in wound response

56
Q

what kind of protein does oncogene v-sis create

A

a truncated version of PDGF protein
Located in the cytoplasm, activates pathway at inappropriate times

57
Q

what kind of protein does proto-oncogene c-cerB create

A

epidermal growth factor receptor (EGFR)

58
Q

what kind of protein does oncogene v-erB create

A

truncated form of EGFR
Extracellular domain is deleted

59
Q

what is myc

A

Myc encodes for a transcription factor protein
Promotes proliferation by controlling the expression of target genes
Including N-Ras and p53

60
Q

what is K-ras

A

encodes for a protein expressed in the Ras/MAP kinase pathway
RAS mutations are highly prevalent in lung, colorectal and pancreatic cancers

61
Q

what is immortalisation

A

Cell population obtains the ability to multiply indefinitely

62
Q

how to detect an oncogene in the DNA of cancer cells

A
63
Q

cell cycle of oncogenes

A
64
Q

what are the epigenetic mechanisms in cancer

A

Histone acetylation
Histone methylation
DNA methylation

65
Q

what is DNA methylation

A

alterations are early events in tumorigenesis
Important in regulation of gene expression in cancer cells

66
Q

Why is Angiogenesis so important in tumour progression?

A

Vascular endothelial growth factor (VEGF) is a key growth factor in angiogenesis
VEGFA is secreted from hypoxic cancer cells
This activates VEGF receptor 2 (VEGFR2)
Leads to new blood vessel growth

67
Q

what is a hallmark

A

distinguishing characteristic, trait

68
Q

What are the main hallmarks of cancer

A

resisting cell death
sustaining proliferative signalling
evading growth suppressors
activation invasion and metastasis
inducing angiogenesis
enabling replicative immortality

69
Q

what are the emerging hallmarks of cancer

A

deregulating cellular energetics
avoiding immune destruction

70
Q

what is angiogenesis

A

the formation of new blood vessels.

71
Q

what are the enabling characteristics of cancer

A

genome instability and mutation
tumour promoting inflammation

72
Q

what is the detection of cancer

A

The action or process of identifying the presence of cancer in the absence of signs or symptoms

73
Q

what is the diagnosis of cancer

A

The action or process of identifying cancer from its signs and symptoms

74
Q

how is the diagnosis of cancer done

A

Taking a clinical history - symptoms
Patient (physical) examination - signs
Perform investigations – imaging,
diagnostic tests on patient samples

75
Q

what is metastasis

A

the process whereby malignant tumours spread from their site of origin (theprimary tumour) to form other tumours (secondary tumours) at distant sites

76
Q

what is the haematogenous route of metastasis

A

by the blood stream, to form secondary tumours in organs perfused by blood that has drained from a tumour

77
Q

what is the lymphatic route of metastasis

A

to form secondary tumours in the regional lymph nodes

78
Q

what is the transcoelomic route of metastasis

A

in pleural, pericardial and peritoneal cavities where this invariably results in a neoplastic effusion

79
Q

what is a prognosis

A

the anticipated course of the disease in terms of cure, remission, or fate of the patient

80
Q

how do you predict a cancer prognosis

A

Type of tumour – classification
Grade of the tumour
Stage of tumour
Patient age and general health – ‘Performance status’
How the tumour is predicted to respond to a treatment

81
Q

what is adjuvant therapy

A

treatment given, in the absence of macroscopic evidence of metastases, to patients at risk of recurrence from micrometastases, following treatment given for the primary lesion.

82
Q

what is neoadjuvant therapy

A

is given before primary surgery, both to shrink the tumour in order to improve local excision, and to treat any micrometastases as soon as possible.

83
Q

what is palliative cancer treatment

A

When cure is no longer possible, palliation – relief of tumour symptoms, preservation of quality of life and prolongation of life is possible in many cancers.

84
Q

what are the 3 original pillars of cancer treatment

A

surgery
radiotherapy
chemotherapy

85
Q

what are additional treatment modalities for solid tumours

A

Endocrine therapies
Targeted therapies
Immunotherapy

Other treatments: Stem cell transplant, gene therapy, oncolytic viruses

86
Q

what is a disadvantage of using surgery to treat cancer

A

If cancer has spread to another part of the body, surgery cannot usually cure it

87
Q

what is radical radiotherapy

A

aims to deliver a treatment dose to a well-defined target volume with curative intent, sparing the surrounding normal tissues as much as possible

88
Q

what is adjuvant radiotherapy

A

used to reduce the risk of tumour recurrence after primary surgery. The aim of treatment is to eradicate occult (hidden) micrometastatic disease that cannot be demonstrated on imaging.

89
Q

what is palliative radiotherapy

A

used to alleviate symptoms of local disease (such as haematuria) or distant metastases (such as bone pain)

90
Q

what is electromagnetic radiation

A

X-rays (machine)
Gamma rays (source – radioactive decay)
Particulate radiation
Sub atomic particles including: alpha particles, protons and neutrons

91
Q

how do you deliver external radiation therapy

A

Focused beam of radiation dose often delivered in increments (fractionated) separated by at least 4–6 hours, to try and exploit any advantage in DNA repair between normal and malignant cells.

92
Q

how do you deliver internal radiation therapy

A

Brachytherapyradiation source placed in close contact with the tissue to provide intense exposure over a short distance to a restricted volume.

93
Q

how are radiotherapy doses delivered

A

in fractions

94
Q

what is the radiotherapy treatment based on

A

differing biological properties of cancer versus surrounding normal tissues
Regimes amplify survival advantage of normal tissues over cancer cells
Better repair of sub-lethal radiation damage in normal versus cancer cells
Normal cells proliferate more slowly versus cancer cells - therefore have time to repair damage before replication.

95
Q

what are the types of cancer drugs

A

Biopharmaceuticals (Biologicals, Biologics)
Living organisms or substances derived from living organisms, or laboratory-produced (recombinant) versions of such substances
Antibody
Virus
Vaccine

96
Q

how does chemotherapy operate

A

Operate by interfering with synthesis, structure or function of DNA or mechanics of cell division-often leading to DNA damage
May have narrow therapeutic window due to toxicity towards normal tissue – not cancer specific

97
Q

what is the chemotherapy treatment strategy

A

Often given i.v. over period of a few days
Followed by a rest of a few weeks
Normal tissues more proficient at DNA repair than the cancer cells
Deplete the tumour while normal tissues restore between chemotherapy cycle

98
Q

what are the common side effects of chemotherapy

A

Nausea and vomiting, hair loss, myelosuppression, mucositis and fatigue

99
Q

what is patient stratification

A

The division of a potentialpatientgroup into subgroups, also referred to as ‘strata’ or ‘blocks’

100
Q

what is personalised medicine of cancer

A

Treatment based on the molecular profile of a patient’s tumour

101
Q

what is hormone therapy

A

drugs that block activity or reduce level of hormone in the body

102
Q

which cancers are hormone sensitive

A

breast cancer – tamoxifen
prostate cancer
ovarian cancer
uterine cancer

103
Q

how does targeted therapy differ from standard chemotherapy

A

Deliberately designed to act on specific molecules (targets) involved in growth, progression, spread of cancer
Many standard chemotherapies were identified because they just kill proliferating cells by causing DNA damage
Targeted therapies can be small molecules or biopharmaceuticals

104
Q

what is the most common BRAF mutation

A

V600E

105
Q

which mutations do 50% of malignant melanomas have

A

a point mutation in the BRAF gene

106
Q

what does V600E mutatuons cause

A

causes hyperactivation of BRAF kinase to drive malignant melanoma

107
Q

how does cancer treatment help the immune system fight cancer

A

Immune system detects and destroys abnormal cells
Immune cells are found in and around tumours
Immune cells are a sign the immune system is responding to the tumour

108
Q

how is T-cell induced tumour death caused

A

T- cell receptors can recognize antigens on the tumour

109
Q

what is PD-L1

A

PD-L1 interacts with PD-1 on the T cell and suppresses T cell-induced tumour death – immune checkpoint

110
Q

what is Nivolumab

A

Targets PD-1, Blocks PD-1/PD-L1 interaction

111
Q

what is intrinsic cancer drug resistance

A

Patients show no initial response to a cancer therapy

112
Q

what is acquired cancer drug resistance

A

Patients show an initial response to therapy, but subsequently relapse and progress

Foundations of health and disease (21 decks)

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