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Unit 2 > Cancer Cell Biology > Flashcards

Cancer Cell Biology Flashcards

1
Q

Most cancers arise from…

A

Epithelial tissues

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2
Q

What are cancers arising in epithelia called?

A

Carcinomas

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3
Q

What do epithelial cells act together to form?

A

Glands

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4
Q

What are the cancers of glands called?

A

Adenocarcinomas

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5
Q

What are cancers of supporting tissues (connective, fat and muscle) called?

A

Sarcomas

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6
Q

How do you name cancers of the nervous system?

A

named after originating tissue

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7
Q

What are the cancers of glial tissue called?

A

Glioblastomas

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8
Q

What are cancers of WBCs called?

A

Lymphomas and Leukaemias

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9
Q

Hyperplastic tissue (2)

A
  • highly proliferative
  • appear normal
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10
Q

Dysplastic tissue (2)

A
  • highly proliferative
  • appear abnormal
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11
Q

Metaplastic tissue

A

original cells are displaced by cells of another type

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12
Q

What is Anaplasia? (3)

A
  • lack of differentiation in cells
  • as tumour cells become more abnormal
  • so the identity of tissue from which cells have arise cannot be determined
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13
Q

Differentiation is used to grade tumours (3)

A

Grade 1 - well differentiated
Grade 2 - moderately differentiated
Grade 3 - poorly differentiated

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14
Q

Colorectal cancer originates from… (2)

A
  • Polyps
  • Small Adenomas
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15
Q

What are Adenomas?

A

abnormal outgrowth of the colonic epithelium

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16
Q

Adenomas eventually grow into…

A

Adenocarcinomas

17
Q

Colonic epithelium is formed from (1) which is produced by (2)

A

1) Enterocytes
2) Stem cells

18
Q

What are the 3 continuous stages that enterocytes go through?

A

1) Proliferation
2) Upward Migration
3) Apoptosis

19
Q

When do intestinal stem cells proliferate?

A

When they receive a WNT signal

20
Q

What does APC stand for?

A

Adenomatous Polyposis Coli

21
Q

What is APC?

A

A protein that forms a complex to turn off WNT signalling

22
Q

Mutation of APC (4)

A
  • makes APC non-functional
  • hence WNT signalling remains on
  • allowing cells to continuously proliferate
  • blocking their ability to differentiate and migrate
23
Q

What releases WNT signals?

A

Stromal cells

24
Q

What is WNT?

A

A ligand (signalling protein) that triggers intestinal stem cells to undergo proliferation

25
Q

Activation of WNT signalling (5)

(in the presence of wnt)

A

1) wnt ligands bind to stem cell receptors

2) to inactivate degradation complex which contains APC

3) hence the degradation complex won’t target beta-catenin

4) hence beta-catenin levels remain high

5) beta-catenin binds to TFs to induce cell proliferation

26
Q

Deactivation of WNT signalling (5)

(in the absence of wnt)

A

1) degradation complex becomes active

2) it acts as a ligase

3) to phosphorylate and ubiquinate the beta-catenin

4) causing to be shipped to proteasome to be degraded

5) hence beta-catenin can no longer activate gene expression

27
Q

Name 4 things that contribute to Colorectal cancer

A
  • APC mutation
  • FAP
  • Loss of TSG
  • K-Ras mutation
28
Q

How does APC mutation contribute to colorectal cancer? (5)

A

1) beta-catenin levels remain high

2) gene expression remains active

3) stem cell proliferation continues

4) failure to migrate upwards and remain undifferentiated

5) polyp/small adenoma formation

29
Q

What does FAP stand for?

A

Familial Adenomatous Polyposis

30
Q

Features of FAP (3)

A
  • increases risk of colorectal cancer
  • due to APC mutation
  • hundreds to thousands of polyps develop due to FAP
31
Q

How does loss of Tumour Suppressor Genes contribute to colorectal cancer? (4)

A
  • loss of p53 and TGF-beta tumour suppressors
  • results in failure to arrest cell cycle
  • results in failure to induce apoptosis
  • hence unrestrained cell proliferation
32
Q

How does Ras mutation contribute to colorectal cancer? (4)

A
  • further mutations involving K-Ras
  • subtype of Ras G-protein
  • cells gain advantage to proliferate independently
  • hence growth of adenoma
33
Q

Hallmarks of cancer (6)

A

1) Sustaining Proliferative Signalling

2) Evading Growth Suppressors

3) Resisting Cell Death

4) Enabling Replicative Immortality

5) Inducing Angiogenesis

6) Activating Invasion and Metastasis

34
Q

Hallmarks of Cancer:

Sustaining Proliferative Signalling (4)

A
  • receptor overexpression
  • hyper-responsive to mitogens
  • activate ligand independent mitogenic signalling (caused by mutations)
  • develop autocrine signalling
35
Q

Hallmarks of Cancer:

Evading Growth Suppressors (2)

A
  • TSGs arrest cell cycle or trigger apoptosis
  • TSG inactivation
36
Q

Hallmarks of Cancer:

Resisting Cell Death (4)

A

Cancer cells:
- activate pro-survival factors (Bcl2)
- inhibit death factors (Bax and Bak)
- block activation of capsases
- resulting in blockade of apoptosis

37
Q

Hallmarks of Cancer:

Enabling Replicative Immortality (4)

A
  • senescence and apoptosis prevent cells becoming immortal
  • telomere shortening induces apoptosis in normal cells
  • cancer cells activate telomerase to extend telomeres
  • acquiring immortality
38
Q

Hallmarks of Cancer:

Inducing Angiogenesis (4)

A
  • growth of tumour requires O2 and nutrients
  • cancer cells activate pro-angiogenic signalling (VEGF, PDGF) in endothelial cells
  • they also suppress the function of angiogenic inhibitors e.g. thrombospondin-1 (TSP-1)
  • net result is proliferation of endothelial cells and activation of angiogenesis
39
Q

Hallmarks of Cancer:

Activating invasion and metastasis (6)

A
  • cancer cells undergo cellular transformation: epithelial-mesenchymal transition (EMT)
  • they induce down regulation of cell adhesion molecules (CAMs)
  • normally CAMs establish adherens junction
  • loss of CAMs = destabilisation of adherens junction
  • cancer cells become motile
  • resulting in activation of invasion

Unit 2 (7 decks)

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