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Cancer > Cancer Biology > Flashcards

Cancer Biology Flashcards

1
Q

What is a carcinoma?

A

Type of cancer that arise from the external and internal body surfaces.

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2
Q

What is a Sarcoma?

A

Originate from cells found in supporting tissues of the body.

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3
Q

What is lymphoma?

A

Cancer that arise in the lymph nodes and tissues of the body’s immune system.

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4
Q

What is Leukaemia?

A

Cancer of the immature white blood cells that proliferate in the bone marrow and accumulate in the blood stream.

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5
Q

What DNA viruses cause cancer?

A

HHV, HPV, EBV, HBV

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6
Q

How does DNA virsues cause cancer?

A

Viral genome can persist in the infected cells as a episome and promote the expression of proteins that promote proliferation or that inhbit tumour suppressor genes.

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7
Q

Name RNA viruses that cause cancer?

A

HCV, HTLV1

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8
Q

How do RNA viruses cause cancer?

A

Providing a gene that alters growth. RNA viruses contain an extra gene additonal to the sequence needed for viral replication.
Virus intergrates into the host genome close to a host gene that regulates growth.

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9
Q

What is atrophy?

A

Degeneration of muscle tissue.

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10
Q

What is hypertrophy?

A

Enlargement of an organ/tissue from the increase in the size of its cells.

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11
Q

What is hyperplasia?

A

Enlargment of cells due to increase reproduction rate.

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12
Q

What is dysplasia?

A

Presence of abnormal cells.

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13
Q

What is Neoplasia?

A

Growth is rapid and results in a tumour, metastais and acusition of more mutations.

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14
Q

Name Growth factors.

A

Epidermal growth factor, FGF, VEGF, KGF

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15
Q

EGFR signalling

A

EGFR forms homodimers.
Specific adaptor molecules (Sch, Sos, Grb2) permit Ras, Raf, MAPK, PIP3 pathway -> activaton of target genes.
Activated receptors undergo endocytosis
Lysosomal degredation / importin mediated nuclear translocation, act as a trasncription factor (Cyclin D1 up-reg) or as co-reg of transcription factors.
Results in nuclear activation of genes related with cell proliferation, survival, invasion & metastasis.

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16
Q

Name some proto-oncogene?

A

Ras, Raf, ERK, MET, EGFR, Tyrosine kinase.

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17
Q

What are proto-oncogenes?

A

Are genes that regulate normal cell growth.

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18
Q

What mutation occurs at the Ras Proto-oncogene

A

1 point mutation leads to a change in function.

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19
Q

What happens when there a mutation at the Ras proto-oncogene?

A

G-protein always stuck on.
Constitutive signalling -> over expression of a protein.
Sustained proliferation.

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20
Q

What is gene amplification?

A

Too many copies of a gene so too much of a product.

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21
Q

What is gene rearrangements?

A

Promotor in the wrong place so normally a weakly expressed gene can be expressed at high lvls.

22
Q

What is large structual deletions?

A

Deletion in receptors sequences.

23
Q

What are the common mutations in Signal pathways?

A

EGFR extra/intra cellular domain mutations
EGFR overexpression
Ras Mutation
B-Raf mutation
EGFR cytoplasmic domain mutations
EGFR mutation

24
Q

What drugs block EGFR activity?

A

Cetuximab & Panitumumab

25
Q

What causes Chronic myeloid leukaemia?

A

BCR-Abl Mutation (Philadelphia Chromosome)

26
Q

What does BCR stand for?

A

Break point cluster region

27
Q

What is Abl?

A

Protein kinase invloved in cell differentiation, adhesion and growth.

28
Q

How is the philadelphia chromosome made?

A

The end of chromosome 9 & 22 break and translocate (swap) with each other and the the ends fuse to the wrong chromosome

29
Q

How does BCR-Abl Cause growth factor activation?

A

Activation of RTK which activate Ras & PI3K.
Phosphorylation of Tyr177 within the BCR leads to activation of the pathway by interacting with SH2 in the Grb2.

30
Q

What drugs are used to treat CML?

A

Imatinib binds to an intracellular pocket located within tyrosin kinases, inhibit ATP preveting phosphorylation and activation of GFR and down stream signallign pathways.

31
Q

Name tumour gene supressor genes?

A

Cyclin, Cylcin dependent kinases
Retinoblastoma
p53

32
Q

Where does retinoblastoma act in the cell cycle?

A

Acts as a brake keeping the cell in G1
Inhibits genes nescessary for progression into S

33
Q

How does of Rb cause constitiutive activation of the cell?

A

Active G1-Cdk phosphorylates and inactivates Rb
Rb releases E2F transcription factor
E2F activates transcription of genes that encode proteins required for S phase
Cell enters S phase.

34
Q

How can Rb as a resseive gene cause cancer?

A

Offspring must inherit one mutated gene.
They requuire 2 hits or mutational events.

35
Q

What is sporadic cancer?

A

No known cause.

36
Q

What is familial cancer?

A

combination of genetic and environmental factors with releatives shwoting the same type of cancer.

37
Q

What does p53 interact with in the cell cycle?

A

Interacts with CDK inhibitor p21
Acts as a brake keeping the cell in G1 if there is DNA dmg until there is either repair or apoptosis.

38
Q

How does p53 work?

A

If theres DNA dmg p53 is phosphorylated which causes the transcription of p21 whitch then causes the deactivation of the CDK complex which theb causes the cell to arrest or undergo DNA repair

39
Q

What is a tumour supressor gene?

A

Genes that normally block mitosis and must be knocked out for cancer to occur.

40
Q

How does P53 induce cell apoptosis?

A

Inhibits Bcl-2 (Pro-survival protein)
Activates Baxa cell death effector.
Activation of Bax causes mitochondrial outer membrane permeabilisation and release of cytochrome c into the cytosol.
Cytochrome C triggeres caspase-3 activation through formation of the cytochrome c containing apoptosome complex that dismantles the cell.

41
Q

What is temoleres?

A

Protective caps at the end of repetitive DNA at the end of chromosomes, keep chromosomes from unravelling

42
Q

What is temolerase?

A

Cellular reverse transcriptse that adds DNA sequences onto telomeres to prevent shortenning.

43
Q

What are normoxic cells?

A

Near blood vessels
Low HIF-1alpha expression
More scusceptible to chemo and radiation therapy.

44
Q

What are hypoxic cells?

A

Increased genetic instability
Poor immune response
Influence on ECM remodelling
HIF-1alpha expression results
Less susceptibility to chemo and radiation therapy.

45
Q

What can lack of oxgen do to tumours?

A

Cause impaired waste removal causes necrosis
Necrosis results in spilling of cellular contents causing inflammation and injury to nearby cells.

46
Q

What is neoangiogenesis?

A

Promotion to form new blood vessels to supply the tumour.

47
Q

What the steps of angiogensis?

A

Tumour starts to release agniogenic factors (VEGF, FGF, PDGF). Diffuse into epithelial cells, cause area to be hypoxic to increase HIF-1alpha.
Endothelial cells secrete MMP, digest extracellular matrix of the endothelial cells -> allow for proliferation and growth towards the tumour.
Endothelial cells form new aberrant blood vessels which allow for metastasis and growth.

48
Q

What does the messed up vasculature in tumours mean for chemo delivery?

A

Doesnt allow for even distrubution of the chemo drug which means some some tumour cells will survive.

49
Q

How does the mesastatis of cancer occur?

A

Macrophages come along & produce MMP which cleaves E-cadherin
Causes the release of the tumour cell (Called cell-epithelial to mesenchymal transition)
Tumour cells secrete factors that affect macrophage function / chemotaxis
Pericytes secrete factors that cause cell migration.

50
Q

How does the new cancer cell become a tumour?

A

Activated stomal cells bind which allow for the cancercell to slightly replicate.
Then BMDC come along and allow for angiogenesis of the new cancer cell to form a tumour.

Cancer (4 decks)

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