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BOD > Cancer > Flashcards

Cancer Flashcards

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

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
Q

Senscense signalling

A

Telomeres get short, signal via p53 to arrest the cell cycle by acting as a TF for p21

26
Q

Li Fraumeni syndrome

A

Mutation in p53

27
Q

Critical step in metastasis

A

Ability to survive in foreign tissue after extravascularisation

28
Q

Are cells in primary tumour able to metastases

A

YES!

So metastasis may just be leakage from the primary tumour

29
Q

Single base pair changes

A

Ras, p53, Raf (B-RAF has mutation from valine-glutamic acid which is positive so acts as if it is always phosphorylated)

30
Q

Indels

A

APC (frameshift causing premature truncation)

PTEN deletion

31
Q

Chromosome rearrangement example

A

Rb

32
Q

Amplification mutations

A

EGFR, HER2

33
Q

Philadelphia chromosome

A

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
Q

TMPRSS2-EGR fusion gene

A

Prostate cancer
EGR gene is linked to the other promoter so expressed at higher levels
- This is involved in cell differentiation

35
Q

Genes silenced by DNA methylation

A

MLH1 in colorectal cancer

CadherinE in lobular breast cancer; involved in cell to cell adherence

36
Q

Driver mutations

A

Give cell a selective advatnage
Adults cancers likely to have 10-20 of these
Colon cancer has 7

37
Q

UV light

A

Causes adjacent thymidine to dimerise

Can cause C to T changes

38
Q

Beta-napthylamine

A

Bladder carcinogen

In bladder, an enzyme removes the glycosyl group to reactivate it

39
Q

Aflatoxin

A

Most potent carcinogen
Causes liver cancer
Activated to reactive epoxide that reacts with DNA via xenobiotic metabolism

40
Q

Aristolochic acid

A

causes kidney and upper urinary tract cancer

Change from A to T in ACTAGG

41
Q

Chemical promoter

A

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
Q

Asbestos

A

Promoter without being mutagenic

Acceleartes mesotheliomas in mesothelial cells lining space via causing chronic wounding and scar tissue

43
Q

Ames test

A

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
Q

Alpha particles (high LET) compared to X rays (low LET)

A

Alpha is more ionising

45
Q

Bacteria that cause cancer

A

Helicobacter pylori causes stomach cancer

Schistosomiasis causes bladder cancer

46
Q

HPV

A

Cervical cancer

47
Q

EBV

A

Nasopharyngeal cancer and Burkitt’s lymphoma

48
Q

HBV

A

Hepatocellular carcinoma

49
Q

HTLV1

A

T cell leukaemia and lymphoma

50
Q

HHV8

A

Kaposi’s sarcoma

51
Q

Vinca alkaloids

A

Binds dimers of tubulin to cause dissociation and prevent polymerisation

52
Q

Taxols

A

Binds tubular microtubules to stabilise

53
Q

DNA damaging drugs

A

Antimetabolites to inhibit DNA synthesis
Topoisomerase inhibitors
Bind covalently via alkylating/cross linking or non-covalently via intercalation

54
Q

Cis-platin

A

alkylating/cross linking

55
Q

PARP inhibitors

A

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
Q

Gleevec

A

Used to block ABL kinase

57
Q

Vemurafenib

A

Targets B-RAF kinase

58
Q

Using viruses to treat cancer

A

oncolytic adenoviruses
E1A to inhibit Rb1
E1B55k to inhibits p53

59
Q

Ipilimumab

A

Anti CTLA-4

BOD (7 decks)

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