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HSPH/Cancer > Pathology and Cancer therapy > Flashcards

Pathology and Cancer therapy Flashcards

(99 cards)

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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
Fibroma
fibrous tumour
26
Osteoma
bone tumours
27
Adenoma
tumour in glandular tissue
28
Papilloma
tumour with finger-like projections
29
Papillary cystadenoma
papillary and cystic tumour in glandular tissue
30
Polyp
a tumour that projects above a mucosal surface
31
Mesenchymal + epithelial benign neoplasm nomenclature
-oma
32
Malignant neoplasm
neoplasm that invades nearby tissue and spawns metastases
33
Mesenchymal malignant neoplasm nomenclature
-sarcoma
34
Epithelial malignant neoplasm nomenclature
-carcinoma
35
Mesenchymal malignant tumours
Chondrosarcoma Fibrosarcoma Osteosarcoma
36
Chondrosarcoma
Cartilaginous tumour
37
Fibrosarcoma
Fibrous tumour
38
Osteosarcoma
bone tumour
39
Epithelial malignant tumours
Adenocarcinoma Squamous cell carcinoma Undifferentiated carcinoma
40
Adenocarcinoma
Tumour from gland-forming tissue
41
Squamous cell carcinoma
squamous differentiation
42
Undifferentiated carcinoma
Carcinomas can arise from ectoderm, mesoderm or endoderm
43
Metastasis
process by which cells differentiate into specialised tissues and/or organs
44
Histogenesis
process by which cells differentiate into specialised tissues and/or organs
45
Well differentiated neoplasm
resembles mature cells of tissue of origin
46
Poor differentiated neoplasm
composed of primitive cells with little differentiation
47
Most common teratoma
Benign cystic teratoma of the ovary
48
Hamartoma
disorganised mass of tissue whose cell types are indigenous to the site of lesion
49
Choriostoma
Ectopic focus of normal tissue (heterotopia)
50
Malignant tumour MOA
Malignant change in the target cell, referred to as transformation Growth of transformed cells Local invasion Distant metastases
51
Anaplasia
Structural differentiation loss
52
Pleomorphism
Shape + Size
53
Abnormal nuclear morphology
Hyperchromasia High nuclear cytoplasmic ratio Chromatin clumping Prominent nucleoli
54
Dysplasia
abnormal growth, some but not all hallmarks of malignancy present - may develop into malignancy
55
Local effects of neoplasm on host
Destruct vital structure Obstruct or perforate a hollow organ Cause haemorrhage, thrombosis or infection Invade nearby or distant structures
56
Systemic effects of neoplasm on host
``` Weight loss Fever Anaemia Immunosuppression Paraneoplastic Syndrome ```
57
Paraneoplastic Syndrome
the set of symptoms caused by non-metastatic malignant disease
58
Cushing's syndrome
Production of ACTH by tumour cells | Prevalent in small-cell lung cancer and pancreatic carcinoma
59
Lambert-Eaton Myasthenic Syndrome (LEMS)
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
Goals of cancer therapy
Cure Control (stop new growth) Palliation
61
Low radio-sensitivity cells
Nerve cells | Muscle cells
62
Intermediate radio-sensitivity cells
Osteoblast Endothelial cell Fibroblast Spermatids
63
High radio-sensitivity
``` Spermatogonia Lymphocytes Stem cells Intestinal mucosa cells Erythroblast ```
64
Types of radiation therapy
External beam radiation (gamma photons, neutron beams) Radioimmunoconjugates (antibody-targeted) Radioconjugates (isotope tagged to bone-seeking material Free isotopes (131I, Gallium)
65
First line chemotherapy
most effective drug first
66
Adjunctive chemotherapy
After the tumour has been controlled by surgery or radiotherapy
67
Neo-adjuvant chemotherapy
Before treatment with surgery or radiotherapy
68
Nitrogen mustard gas
chemotherapy causes direct DNA damage by adding methyl onto guanine most active in resting cells
69
Antimetabolites
chemotherapy interfere with synthesis of purine/pyrimidine bases mostly active against cells in S phase
70
Antifolates
type of antimetabolite
71
Topo i inhbitor
chemotherapy | induce single and double strand breaks
72
Topo ii inhibitor
insert planar ring between adjacent bases, concentrating drug in nucleus until S phase
73
Drugs interfering with microtubule assembly
Vinca alkaloids | Taxols
74
Monoclonal antibodies
-mab target specific antigen specificity is relative
75
Small molecules (tyrosine kinase inhibitors)
-nib target oncogene production inhibit signalling at key steps
76
Adjuncts
glucocorticoids biphosphonates oestrogens/anti-androgens/SERMS
77
Chemotherapy imperfections
Lack of selectivity Toxicity to host- dose levels are well below what is needed to kill effectively IV- hospitalisation
78
Selective Oestrogen receptor modulators (SERMs)
Tamoxifen (Nolvadex) | Toremifene (Fareston)
79
Oestrogen receptor inhibitor and destroyer
Fulvestrant (Faslodex)
80
Oestrogen synthesis inhibitors- aromatase inhibitors (Als)
Anastrozole (Arimidex) Letrozole (Femara) Exemestane (Aromasin)
81
Tyrosine Kinase inhibitors
``` -nib Imatinib Dasatinib Lapatinib Gefitinib ```
82
Monoclonal antibodies MOA
Efficient carriers for delivery of anti-tumour agents Antigen cross-linking- target GFR (antagonise ligand-receptor signalling) Activation of death receptors
83
Monoclonal antibodies as carriers
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
Growth factors
``` EGFR (epidermal) IGF-1R (insulin-like growth factor-1 receptor) FGFR (fibroblast) PDFGR (platelet-derived) VEGFR (vascular endothelial) ```
85
Monoclonal antibodies activation of death receptors
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
Monoclonal antibodies
-mab Alemtuzumab Cetuximab Rituximab
87
CD20
Glycosylated phosphoprotein | Expressed on surface of all B cells beginning at pro-B phase
88
Type 1 CD20 antibody
Prominent Fc-FcR interaction | Rituximab
89
Type 2 CD20 antibody
Strong induction of direct cell death | Tositumomab, Obinutuzumbab
90
Growth factor oncogene
EGF | HER2
91
Growth factor receptor oncogene
EGF | VEGF
92
Signal-transduction proteins oncogene
K-ras | B-raf
93
Transcription factors oncogene
c-myc
94
Anti-apoptotic proteins oncogene
Bcl-2
95
EGFR overexpression
Colorectal cancer (27-77%) Pancreatic (30-50%) Lung (40-80%) Non-small cell lung (14-91%)
96
Ras mutation
Pancreatic 90% Papillary thyroid 60% Colon 50% non-small cell lung 30%
97
B-Raf mutation
Melanoma 70% Papillary thyroid 50% Colon 10%
98
Point mutation within a control element in tumour suppressor gene
Bax (pro-apoptotic)
99
Point mutation within the tumour suppressor gene
p53 (prevents cells leaving G1)

HSPH/Cancer (8 decks)

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