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HSPH/Cancer > Pathology and Cancer therapy > Flashcards

Pathology and Cancer therapy Flashcards

1
Q

6 Hallmarks of Cancer

A 
Evading Apoptosis
Limitless reproductive potential
Growth signals not required for cell survival, growth + differentiation
Insensitivity to anti-growth signals
Increased + sustained angiogenesis
Tissue invasion + metastasis
Defects in DNA repair
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2
Q

H Ras gene

A

Makes protein H Ras
Makes cell either grow or divide
Belongs to class of oncogenes- of mutated, causes cell to become cancerous

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3
Q

Antiproliferative signals

A

Soluble growth inhibitors

Immobilised inhibitors in ECM + surface of nearby cells

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4
Q

Antiproliferative cells MOA

A

Force cells out of active proliferative cycle, into G0

Cells induced to permanently stop proliferation and are induced into post mitotic state

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5
Q

Oncogene

A

A Cancer inducing gene, can transform cells

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6
Q

Tumour suppressor gene

A

Gene whose partial/complete inactivation leads to increased likelihood of cancer developing
Occur either in germ line, or genome of somatic cell
Responsible for constraining cell proliferation
e.g. p53

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7
Q

Limitless reproductive potential

A

Maintain telomeres- aren’t shortened, so can proliferate endlessly

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8
Q

Evading apoptosis

A

Loss of p53 –> thrombospondin-1

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9
Q

Angiogenesis

A

The formation of new blood vessels, including the development of endothelial cells which line the inside wall of blood vessels

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10
Q

Malignant cells + angiogenesis

A

Give off signals to stimulate angiogenesis

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11
Q

Secretion by malignant cells to degrade ECM

A

Collagenases/Proteases

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12
Q

Loss of p53

A

Tumour suppressor gene

Can facilitate both angiogenesis+ resistance to apoptosis

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13
Q

Normal –> hyperplastic epithelium

A

loss of APC

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14
Q

hyperplastic epithelium –> early adenoma

A

DNA hypomethylation

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15
Q

early –> intermediate adenoma

A

K-ras activation

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16
Q

intermediate –> late adenoma

A

loss of 18q TSG 9tumour suppressor gene)

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17
Q

late adenoma –> carcinoma

A

loss of p53

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18
Q

Cancer

A

collection of diseases characterised by uncontrolled growth, caused by changes to DNA

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19
Q

Tumour

A

a mass of tissue formed by an uncontrolled growth of cells, independent of surrounding structures

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20
Q

Neoplasm

A

an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persist in the same excessive manner after cessation of the stimuli which evoked the change

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21
Q

Benign neoplasm

A

neoplasm that grows locally without invading adjacent tissue

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22
Q

Mesenchymal neoplasms

A 
Chondroma= cartilaginous tumour
Fibroma= fibrous tumour
Osteoma= bone tumour
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23
Q

Epithelial neoplasms

A

Adenoma= tumour in glandular tissue
Papilloma= tumour with finger-like projections
Papillary cystadenoma= papillary and cystic tumour in glandular tissue
Polyp- a tumour that projects above a mucosal surface

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24
Q

Chondroma

A

cartilaginous tumour

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25
Q

Fibroma

A

fibrous tumour

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26
Q

Osteoma

A

bone tumours

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27
Q

Adenoma

A

tumour in glandular tissue

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28
Q

Papilloma

A

tumour with finger-like projections

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29
Q

Papillary cystadenoma

A

papillary and cystic tumour in glandular tissue

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30
Q

Polyp

A

a tumour that projects above a mucosal surface

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31
Q

Mesenchymal + epithelial benign neoplasm nomenclature

A

-oma

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32
Q

Malignant neoplasm

A

neoplasm that invades nearby tissue and spawns metastases

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33
Q

Mesenchymal malignant neoplasm nomenclature

A

-sarcoma

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34
Q

Epithelial malignant neoplasm nomenclature

A

-carcinoma

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35
Q

Mesenchymal malignant tumours

A

Chondrosarcoma
Fibrosarcoma
Osteosarcoma

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36
Q

Chondrosarcoma

A

Cartilaginous tumour

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37
Q

Fibrosarcoma

A

Fibrous tumour

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38
Q

Osteosarcoma

A

bone tumour

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39
Q

Epithelial malignant tumours

A

Adenocarcinoma
Squamous cell carcinoma
Undifferentiated carcinoma

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40
Q

Adenocarcinoma

A

Tumour from gland-forming tissue

41
Q

Squamous cell carcinoma

A

squamous differentiation

42
Q

Undifferentiated carcinoma

A

Carcinomas can arise from ectoderm, mesoderm or endoderm

43
Q

Metastasis

A

process by which cells differentiate into specialised tissues and/or organs

44
Q

Histogenesis

A

process by which cells differentiate into specialised tissues and/or organs

45
Q

Well differentiated neoplasm

A

resembles mature cells of tissue of origin

46
Q

Poor differentiated neoplasm

A

composed of primitive cells with little differentiation

47
Q

Most common teratoma

A

Benign cystic teratoma of the ovary

48
Q

Hamartoma

A

disorganised mass of tissue whose cell types are indigenous to the site of lesion

49
Q

Choriostoma

A

Ectopic focus of normal tissue (heterotopia)

50
Q

Malignant tumour MOA

A

Malignant change in the target cell, referred to as transformation
Growth of transformed cells
Local invasion
Distant metastases

51
Q

Anaplasia

A

Structural differentiation loss

52
Q

Pleomorphism

A

Shape + Size

53
Q

Abnormal nuclear morphology

A

Hyperchromasia
High nuclear cytoplasmic ratio
Chromatin clumping
Prominent nucleoli

54
Q

Dysplasia

A

abnormal growth, some but not all hallmarks of malignancy present - may develop into malignancy

55
Q

Local effects of neoplasm on host

A

Destruct vital structure
Obstruct or perforate a hollow organ
Cause haemorrhage, thrombosis or infection
Invade nearby or distant structures

56
Q

Systemic effects of neoplasm on host

A 
Weight loss
Fever
Anaemia
Immunosuppression
Paraneoplastic Syndrome
57
Q

Paraneoplastic Syndrome

A

the set of symptoms caused by non-metastatic malignant disease

58
Q

Cushing’s syndrome

A

Production of ACTH by tumour cells

Prevalent in small-cell lung cancer and pancreatic carcinoma

59
Q

Lambert-Eaton Myasthenic Syndrome (LEMS)

A

Impaired release of acetylcholine causing muscle weakness, drooping of eyelids and double vision
Prevalent in lung cancer
60% of LEMS patients have lung cancer

60
Q

Goals of cancer therapy

A

Cure
Control (stop new growth)
Palliation

61
Q

Low radio-sensitivity cells

A

Nerve cells

Muscle cells

62
Q

Intermediate radio-sensitivity cells

A

Osteoblast
Endothelial cell
Fibroblast
Spermatids

63
Q

High radio-sensitivity

A 
Spermatogonia
Lymphocytes
Stem cells
Intestinal mucosa cells
Erythroblast
64
Q

Types of radiation therapy

A

External beam radiation (gamma photons, neutron beams)
Radioimmunoconjugates (antibody-targeted)
Radioconjugates (isotope tagged to bone-seeking material
Free isotopes (131I, Gallium)

65
Q

First line chemotherapy

A

most effective drug first

66
Q

Adjunctive chemotherapy

A

After the tumour has been controlled by surgery or radiotherapy

67
Q

Neo-adjuvant chemotherapy

A

Before treatment with surgery or radiotherapy

68
Q

Nitrogen mustard gas

A

chemotherapy
causes direct DNA damage by adding methyl onto guanine
most active in resting cells

69
Q

Antimetabolites

A

chemotherapy
interfere with synthesis of purine/pyrimidine bases
mostly active against cells in S phase

70
Q

Antifolates

A

type of antimetabolite

71
Q

Topo i inhbitor

A

chemotherapy

induce single and double strand breaks

72
Q

Topo ii inhibitor

A

insert planar ring between adjacent bases, concentrating drug in nucleus until S phase

73
Q

Drugs interfering with microtubule assembly

A

Vinca alkaloids

Taxols

74
Q

Monoclonal antibodies

A

-mab
target specific antigen
specificity is relative

75
Q

Small molecules (tyrosine kinase inhibitors)

A

-nib
target oncogene production
inhibit signalling at key steps

76
Q

Adjuncts

A

glucocorticoids
biphosphonates
oestrogens/anti-androgens/SERMS

77
Q

Chemotherapy imperfections

A

Lack of selectivity
Toxicity to host- dose levels are well below what is needed to kill effectively
IV- hospitalisation

78
Q

Selective Oestrogen receptor modulators (SERMs)

A

Tamoxifen (Nolvadex)

Toremifene (Fareston)

79
Q

Oestrogen receptor inhibitor and destroyer

A

Fulvestrant (Faslodex)

80
Q

Oestrogen synthesis inhibitors- aromatase inhibitors (Als)

A

Anastrozole (Arimidex)
Letrozole (Femara)
Exemestane (Aromasin)

81
Q

Tyrosine Kinase inhibitors

A 
-nib
Imatinib
Dasatinib
Lapatinib
Gefitinib
82
Q

Monoclonal antibodies MOA

A

Efficient carriers for delivery of anti-tumour agents
Antigen cross-linking- target GFR (antagonise ligand-receptor signalling)
Activation of death receptors

83
Q

Monoclonal antibodies as carriers

A

Accumulate in solid tumours- no lymph drainage so not taken away
Tumour blood vessels leaky so can pass through, compared to normal where can’t

84
Q

Growth factors

A 
EGFR (epidermal)
IGF-1R (insulin-like growth factor-1 receptor)
FGFR (fibroblast)
PDFGR (platelet-derived)
VEGFR (vascular endothelial)
85
Q

Monoclonal antibodies activation of death receptors

A

Cross-link surface antigens on tumour cells + antibody agonists
Activate specific receptors
Intracellular calcium ion increase
Activate caspase 3 + 9 (involved in cell apoptosis)

86
Q

Monoclonal antibodies

A

-mab
Alemtuzumab
Cetuximab
Rituximab

87
Q

CD20

A

Glycosylated phosphoprotein

Expressed on surface of all B cells beginning at pro-B phase

88
Q

Type 1 CD20 antibody

A

Prominent Fc-FcR interaction

Rituximab

89
Q

Type 2 CD20 antibody

A

Strong induction of direct cell death

Tositumomab, Obinutuzumbab

90
Q

Growth factor oncogene

A

EGF

HER2

91
Q

Growth factor receptor oncogene

A

EGF

VEGF

92
Q

Signal-transduction proteins oncogene

A

K-ras

B-raf

93
Q

Transcription factors oncogene

A

c-myc

94
Q

Anti-apoptotic proteins oncogene

A

Bcl-2

95
Q

EGFR overexpression

A

Colorectal cancer (27-77%)
Pancreatic (30-50%)
Lung (40-80%)
Non-small cell lung (14-91%)

96
Q

Ras mutation

A

Pancreatic 90%
Papillary thyroid 60%
Colon 50%
non-small cell lung 30%

97
Q

B-Raf mutation

A

Melanoma 70%
Papillary thyroid 50%
Colon 10%

98
Q

Point mutation within a control element in tumour suppressor gene

A

Bax (pro-apoptotic)

99
Q

Point mutation within the tumour suppressor gene

A

p53 (prevents cells leaving G1)

HSPH/Cancer (8 decks)

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