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Mol Basis of Cancer (1) Flashcards

1
Q

A metazoan organism possesses …

A

more genetic information than it requires

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2
Q

Stored information (in cell of metazoan organism) can be …

A

altered and corrupted … or misused = cancer

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3
Q

Over 80% of cancer occur in epithelial tissues, they are called …

A

Carcinomas

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4
Q

Cancer of mesenchymal tissues …

A

Sarcomas, (~1%), e.g. fibrosarcoma

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5
Q

Mesenchymal stem cells eg. what do they differentiate into

A

Fibroblasts, develop into connective tissue, blood vessels & lymphatic tissue

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6
Q

Cancer of Hematopoietic Tissues …

A

Lymphoma/Leukemia (~10%)

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7
Q

Cancer of Neuroectoderm Tissues …

A

= Blastoma/Melanoma

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8
Q

Example of cancer of Neuroectoderm tissues

A

Glioblastoma (aggressive cancer of brain and spinal cord)

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9
Q

Level of malignancy is determined through what staging

A

TNM staging (characteristics of a tumour)

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10
Q

Grading of cells in a tumour = low

A

cells in tumour are similar to normal tissue

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11
Q

Grading of cells in a tumour = high

A

cells in tumour look very different, poorly differentiated (don’t resemble normal tissue anymore, due being less differentiated)

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12
Q

T1 & T2

A

Mild hyperplasia,
Advanced hyperplasia
& Carcinoma in situ

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13
Q

T3

A

Invasive carcinoma

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14
Q

N & M stage

A

Metastatic carcinoma
(N = indicates lymph node metastasis)
(M = distant metastasis)

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15
Q

T stage

A

Indicates size & how invasive the tumour is

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16
Q

Familial cancer

A

mutation isn’t known yet !
cancer can run in family, and skip generations,

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17
Q

In more advanced hyperplasia what happens to the lumen

A

lumen is almost gone

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18
Q

ductal carcinoma in situ

A

Duct is much bigger
Necrotic cells in duct - pushing to get cancerous cells out - but cannot break basement membrane

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19
Q

Invasive ductal carcinoma

A

cells break basal membrane and get out

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20
Q

One true hallmark of cancer

A

Tissue invasion & metastasis
(achieved by mutations)

(only tissue invasion is due to misused mutations!
bc there are no genes associated with metastasis)

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21
Q

Carcinogenesis is a multistep process of ….

A

Clonal selection
…selective pressures cause clonal expansion of cells after beneficial mutations

22
Q

5 steps of carcinogenesis of Colon Cancer

A
  1. Loss of APC gene (=increased cell division -> hyperplastic epithelium
  2. DNA hypomethylation (= early adenomas)
  3. Activation of K-ras (= intermediate adenomas)
  4. Loss of 18q TSG (=late adenoma)
  5. loss of p53 (=carcinoma)

Then no mutation involved with carcinoma metastasising !

23
Q

Oncogene

A

Potential to cause cancer, when mutated or overexpressed

24
Q

Activating oncogenes in 3 ways …

A
  1. Activating mutations (e.g. Ras, CDK4)
  2. Gene amplification (e.g. myc, mdm2, Her2, Cyclin D1)
  3. Translocation (myc/IgH, bcr/abl)
25
Identifying oncogenes experiment
- isolate + shear DNA - put on normal fibroblasts (and some will become cancerous) - DNA precipitates with Ca phosphate (cells take it up) - cells express the genes they've acquired - cells grow on top of each other (formation of focus of morphologically transformed cells) - inject into mouse = tumour grows - remove tumour -> compare these tumour cells with normal mouse DNA to identify the oncogenes
26
Ras bottleneck, main 5 steps of ERK (main) pathway ...
signal transduction pathways from outside cell, through RTKS (receptor tyrosine kinases) like GPCRs 1. pro-survival signals go to Ras 2. = Ras is activated 3. Ras activates RAF, MEK and ERK 4. ERK activates TFs (e.g. JUN, FOS, MYC) 5. = activation of cyclin D1 -> makes cells divide
27
Ras cycle
- Bound to GDP = inactive - +GEF (upstream signalling molecule) - removes GDP - GTP binds Ras (=active) - can activate downstream signalling pathways - GTP dissociates and is hydrolysed --> cycle continues
28
What can block the Ras cycle?
Oncogenic mutations in Ras, block GTP hydrolysis, (GTP remains bound to Ras, so Ras is always active
29
Ras makes proteins which control ...(4)
1. Oncogenic transcription 2. Cell survival 3. Cell growth + metabolism 4. Cell motility + migration
30
Hot spot
Where a mutation generally occurs (mutations are generally clustered)
31
Whats mutated in Ras that gives rise to human cancer ?
Gly(cine) is converted to Val(anine) at codon 12 proto-oncogene --> oncogene
32
Gly (at codon 12) in Ras function
- Gives binding site loop its flexibility, so GTP can unbind & be hydrolysed Ras binds gamma-phosphate on GDP which crated a flexible area (opposed by other hot spot Gln61)
33
what mutation is found in almost all cancers?
Ras mutation
34
Oncogene activation through amplification eg.?
EGFR2 (HER2)
35
EGRF2 is
a growth factor which binds to 2 receptors, allowing their RTK domains to cross phosphorylate with each other (Ligand dependant firing)
36
Ligand dependant firing causes ? ...
activation of downstream cascade
37
mutation of EGFR2 which causes cancer
- extracellular domain lost/ or structure changed the domains can come together in the absence of GF - or extracellular domain is over expressed, so close they can phosphorylate each other = and activate down stream cascades
38
Oncogene activated through translocation e.g.?
Myc
39
Myc translocation in cancer
Chr8 with tip of Chr14 & Chr14 with tip of Chr8 (contains Myc gene) -leads to over expression of Myc gene (instead of IgH - if this translocation occurs in cells where a lot of IgH is expressed this causes a problem ...
40
Tumour suppressor genes ...
regulate cell division and replication
41
2 classes of tmuour suppressor gene ...
1. Gatekeepers 2. Caretakers
42
Gatekeeper TS genes, e.g.'s and role;
- (Rb, p53, APC, p16) - Encode system of checks and balances that monitor cell division and death
43
Caretaker TS genes, e.g.s and role;
- (MLH1, MSH2, BRCA1, BRCA2) - Responsible for genomic integrity
44
what enzyme phosphorylates retinoblastoma ?
Cdk4
45
How Cdk4 causes retinoblastoma
Cdk4 binds Cyclin D in G1 phase causes RB protein to be phosphorylated RB+P... releases E2F to nucleus and activates cyclins E and A cell progresses into S phase + certain genes are activated
46
Retinoblastoma (Rb) is ...
Canonical tumour supressor gene
47
How many oncogenes create hereditary cancers?
5
48
TP53
Transcription factor which controls cell division, apoptosis & DNA fidelity -stress response protein
49
what activates P53?
Stress signals e.g. DNA damage
50
Acitvation of P53 =
Cell cycle arrest
51
How P53 functions
4 bind together = tetramer = binds DNA = activates genes for cell cycle arrest and DNA repair etc. .. can return to proliferation - If damage is too great it ca cause apoptosis

Cell+Mol Pathology (8 decks)

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