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Cancer Flashcards

(59 cards)

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1
Q

Metaplasia

A

Transformation from one differentiated cell type to another

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2
Q

Hyperplasia

A

Increased proliferation of cells

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3
Q

Dysplasia

A

Abnormal development of cells within tissues

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4
Q

Neoplasia

A

Uncontrolled abnormal growth of cells

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5
Q

Malignant tumour of mesenchyme

A
  • Sarcoma
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6
Q

Malignant tumour of epithelium

A
  • Carcinoma
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7
Q

Benign tumour

A

tissue name - Oma

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8
Q

Liquid/solid lymph related tumours

A 
Leukaeima = liquid neoplasms
Lymphoma = solid lymphatic neoplasms
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9
Q

Tumour suppressors in the cell cycle

A

Rb

p21, p16aka

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10
Q

Oncogene in cell cycle

A

CyclinD1

CDK4

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11
Q

p53 mutations

A

Tumour suppressor but binds as a tetramer so lots affected even by one alley loss
Stress signalling hub
Activates BAX to inactivate anti-apoptotic BCl2
Acts as a promoter for p21 to arrest cell cycle

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12
Q

Sequence level instability

A

For failure at DNA repair: MLH1 (mismatch repair) e.g Lynch syndrome
For replication: polymerase epsilon mutation

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13
Q

Chromosome level instability

A

For failure at DNA repair: BRCA1/2 mutations for homologous repair in breast cnacer
For replicatioN: lagging chromosomes

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14
Q

Familial adenomatous polyposis

A

Inherit mutation in APC (controls cell cycle)
Rapidly get lots of polyps
Eventually one will lose the other gene and become malignant

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15
Q

Retinoblastomas

A

Inherit mutation in Rb gene that normally inhibits the cell cycle

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16
Q

Is genetic instability needed to kill

A

No!
BRCA2 double mutant tumour treated with cis-platen to select for frameshift to recover ability to make BRCA2 and do HR
BUT: tumour still kills even if no longer malignant

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17
Q

RTK signalling pathway

A

Growth factor binds to RTK

  • Activates RAS via adaptor -> RAF -> MAPK
  • Activates P13Ka -> PIP3 -> AKT

Second pathway has PTEN as a tumour suppressor that reverses this

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18
Q

Wnt signalling pathway

A

Wnt binds to Wnt receptor
This inhibits APC complex which usually inhibits beta-catenin

Beta-catenin now free to cause proliferation

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19
Q

TGFbeta signalling pathway

A

TGFbeta binds to receptors which activates Smads

These inhibit proliferation

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20
Q

Chronic myeloid leukaemia

A

Myeloid precursor cell mutates so can do unlimited proliferation
Still differentiates so blood fills with PMNs, monocytes, , RBC, megakaryocytes

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21
Q

Acute myeloid leukaemia

A

Myeloid progenitor cell mutates for unlimited proliferation but there is differentiation block on progenitor so blood fills with precursor stem cells

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22
Q

Chronic lymphocytic leukaemia

A

Mutation in lymphocyte precursor means unlimited differentiation, blood fills with mature B and T cells

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23
Q

Acute lymphocytic leukaemia

A

Mutation in lymphocyte precursor means unlimited differentiation but differentiation block means circulation fills with precursors

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24
Q

Hayflick’s limit

Study These Flashcards
A

Limit on the humber of times a cell can replicate (50-70)

Telomerase activity due to mutation in promoter or swap with another promoter means this can be bypassed

25
Senscense signalling
Telomeres get short, signal via p53 to arrest the cell cycle by acting as a TF for p21
26
Li Fraumeni syndrome
Mutation in p53
27
Critical step in metastasis
Ability to survive in foreign tissue after extravascularisation
28
Are cells in primary tumour able to metastases
YES! | So metastasis may just be leakage from the primary tumour
29
Single base pair changes
Ras, p53, Raf (B-RAF has mutation from valine-glutamic acid which is positive so acts as if it is always phosphorylated)
30
Indels
APC (frameshift causing premature truncation) | PTEN deletion
31
Chromosome rearrangement example
Rb
32
Amplification mutations
EGFR, HER2
33
Philadelphia chromosome
Chromosome translocation between Chr9 and Chr22 Fusion of Bcr gene with Abl (kinase) gene Means inhibitory terminus of Abl is lost Tyrosine kinase gets activated by dimerisation of the Bcr Bcr promoter controls both and is more active
34
TMPRSS2-EGR fusion gene
Prostate cancer EGR gene is linked to the other promoter so expressed at higher levels - This is involved in cell differentiation
35
Genes silenced by DNA methylation
MLH1 in colorectal cancer | CadherinE in lobular breast cancer; involved in cell to cell adherence
36
Driver mutations
Give cell a selective advatnage Adults cancers likely to have 10-20 of these Colon cancer has 7
37
UV light
Causes adjacent thymidine to dimerise | Can cause C to T changes
38
Beta-napthylamine
Bladder carcinogen | In bladder, an enzyme removes the glycosyl group to reactivate it
39
Aflatoxin
Most potent carcinogen Causes liver cancer Activated to reactive epoxide that reacts with DNA via xenobiotic metabolism
40
Aristolochic acid
causes kidney and upper urinary tract cancer | Change from A to T in ACTAGG
41
Chemical promoter
Enhances the emerge of mutant cells as tumours Doesn't directly cause mutations May cause inflammation, increased cell turnover, increased division TPA = most powerful promoter (mimics DAG which is a PKC agonist
42
Asbestos
Promoter without being mutagenic | Acceleartes mesotheliomas in mesothelial cells lining space via causing chronic wounding and scar tissue
43
Ames test
Used on mutant bacteria which can't synthesis histidine Rat liver extract is included incase the chemicals need xenobiotic metabolism Look for colony growth
44
Alpha particles (high LET) compared to X rays (low LET)
Alpha is more ionising
45
Bacteria that cause cancer
Helicobacter pylori causes stomach cancer | Schistosomiasis causes bladder cancer
46
HPV
Cervical cancer
47
EBV
Nasopharyngeal cancer and Burkitt's lymphoma
48
HBV
Hepatocellular carcinoma
49
HTLV1
T cell leukaemia and lymphoma
50
HHV8
Kaposi's sarcoma
51
Vinca alkaloids
Binds dimers of tubulin to cause dissociation and prevent polymerisation
52
Taxols
Binds tubular microtubules to stabilise
53
DNA damaging drugs
Antimetabolites to inhibit DNA synthesis Topoisomerase inhibitors Bind covalently via alkylating/cross linking or non-covalently via intercalation
54
Cis-platin
alkylating/cross linking
55
PARP inhibitors
PARP is part of single strand repair So PARP inhibitors cause single strand breaks to be converted to double strand breaks SO if cell lacks BRCA2 then will have to apoptosis
56
Gleevec
Used to block ABL kinase
57
Vemurafenib
Targets B-RAF kinase
58
Using viruses to treat cancer
oncolytic adenoviruses E1A to inhibit Rb1 E1B55k to inhibits p53
59
Ipilimumab
Anti CTLA-4

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