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Cell+Mol Pathology > Mol Basis of Cancer (1) > Flashcards

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
Q

Identifying oncogenes experiment

A
  • 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
Q

Ras bottleneck, main 5 steps of ERK (main) pathway …

A

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
Q

Ras cycle

A
  • 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
Q

What can block the Ras cycle?

A

Oncogenic mutations in Ras, block GTP hydrolysis,
(GTP remains bound to Ras, so Ras is always active

29
Q

Ras makes proteins which control …(4)

A
  1. Oncogenic transcription
  2. Cell survival
  3. Cell growth + metabolism
  4. Cell motility + migration
30
Q

Hot spot

A

Where a mutation generally occurs
(mutations are generally clustered)

31
Q

Whats mutated in Ras that gives rise to human cancer ?

A

Gly(cine) is converted to Val(anine) at codon 12
proto-oncogene –> oncogene

32
Q

Gly (at codon 12) in Ras function

A
  • 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
Q

what mutation is found in almost all cancers?

A

Ras mutation

34
Q

Oncogene activation through amplification eg.?

A

EGFR2 (HER2)

35
Q

EGRF2 is

A

a growth factor which binds to 2 receptors, allowing their RTK domains to cross phosphorylate with each other (Ligand dependant firing)

36
Q

Ligand dependant firing causes ? …

A

activation of downstream cascade

37
Q

mutation of EGFR2 which causes cancer

A
  • 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
Q

Oncogene activated through translocation e.g.?

A

Myc

39
Q

Myc translocation in cancer

A

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
Q

Tumour suppressor genes …

A

regulate cell division and replication

41
Q

2 classes of tmuour suppressor gene …

A
  1. Gatekeepers
  2. Caretakers
42
Q

Gatekeeper TS genes, e.g.’s and role;

A
  • (Rb, p53, APC, p16)
  • Encode system of checks and balances that monitor cell division and death
43
Q

Caretaker TS genes, e.g.s and role;

A
  • (MLH1, MSH2, BRCA1, BRCA2)
  • Responsible for genomic integrity
44
Q

what enzyme phosphorylates retinoblastoma ?

A

Cdk4

45
Q

How Cdk4 causes retinoblastoma

A

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
Q

Retinoblastoma (Rb) is …

A

Canonical tumour supressor gene

47
Q

How many oncogenes create hereditary cancers?

A

5

48
Q

TP53

A

Transcription factor which controls cell division, apoptosis & DNA fidelity
-stress response protein

49
Q

what activates P53?

A

Stress signals e.g. DNA damage

50
Q

Acitvation of P53 =

A

Cell cycle arrest

51
Q

How P53 functions

A

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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