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Cancer Y2 > Cancer Biology > Flashcards

Cancer Biology Flashcards

1
Q

What are the 6 Hallmarks of Cancer?

A

Activating invasion and metastasis, Sustaining proliferative cell signalling, Resisting cell death, Evading growth suppressors, Enabling replicative immortality, Inducing angiogenesis

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2
Q

What is a proto-oncogene?

A

A gene that is responsible for normal cell growth.

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3
Q

Name some proto-oncogenes.

A

Ras, B-Raf, EGFR, c-MET, tyrosine kinase

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4
Q

What occurs to the Ras proto-oncogene for it to mutate into an oncogene?

A

There is a point mutation from Glycine to Valine.

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5
Q

What happens as a result of a Ras mutation?

A

Constant signalling without growth factor, no ligand binding leads to overexpression of proteins, this is known as sustained proliferative signalling.

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6
Q

Describe the direct mechanism of viral oncogenesis.

A

The virus acts from within the cell to form a tumour. The viral genome can form an episome, or can integrate itself into the genomic DNA. These lead to viral oncogene expression, which leads to rapid cell growth and cancer.

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7
Q

Describe the indirect mechanism of viral oncogenesis.

A

The virus acts from outside the cell to form a tumour. The two ways this can happen are: the virus can trigger chronic inflammation and persistently cause oxidative stress to local tissue, or it can produce immunosuppression which dulls anti-tumour mechanisms.

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8
Q

What viruses can cause oncogenesis?

A

HBV, EBV, HPV, HIV, herpes virus

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9
Q

What common mutations in EGFR signal transduction pathways can cause cancer?

A

EGFR mutation, Ras mutations, B-Raf mutations, EGFR overexpression, EGFR extracellular and intracellular domain mutations, EGFR cytoplasmic domain mutations

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10
Q

How does Trastuzumab work?

A

It binds to HER2 receptors (TRK), which are overexpressed in some breast cancers, which in turn causes an inhibition of the MAPK and PI3K signalling cascade leading to cell cycle arrest. It also attracts immune cells like NK cells to tumour sites.

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11
Q

What is the biomarker for CML?

A

BCR-ABL gene translocation

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12
Q

What is the biomarker for BRCA 1/2 breast cancer?

A

BRCA 1/2 gene mutations

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13
Q

What is the biomarker for HER2 breast cancer?

A

HER2 gene amplification

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14
Q

What is a biomarker for NSCLC?

A

EGFR kinase domain mutation

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15
Q

What is the BCR-ABL oncogene also known as?

A

The Philadelphia chromosome

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16
Q

What does BCR stand for?

A

Break-point cluster region

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17
Q

What does ABL refer to?

A

It is a protein tyrosine kinase that is involved in cell differentiation, adhesion and growth.

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18
Q

Why does the BCR-ABL cause cancer?

A

It mimics growth factors. It will bind to an RTK leading to RAS and PI3K/AKT activation. The phosphorylation of Tyr177 in the BCR section leads to activation of this pathway by interacting with the SH2 domain in GRB2.

19
Q

What drug is indicated to treat BCR-ABL initiated cancer, and how does it work?

A

Imatinib is used for CML caused by BCR-ABL translocation. It binds to intracellular pockets in RTKs and inhibits ATP which prevents phosphorylation, activation of GFR and downstream signalling.

20
Q

Name the important tumour suppressor genes.

A

p53, retinoblastoma, cyclin dependant kinases, cyclin, cyclin dependant kinase inhibitors

21
Q

What are cyclins/cyclin dependant kinases/cyclin dependant kinase inhibitors?

A

They are complexes that control different parts of the cell cycle. A CDK will bind to a cyclin to cause activation. The inhibitors will then in turn switch this off to slow the cell cycle down.

22
Q

What is retinoblastoma?

A

A protein that acts as a ‘brake’ in G1. It inhibits the genes necessary for progression into the S phase. Phosphorylation of this protein will release the E2F transcription factor which activates the transcription of genes that encode proteins for S phase.

23
Q

What is a sporadic cancer?

A

One that has no known cause

24
Q

What is a familial cancer?

A

A cancer that is caused by combination of genetic and environmental factors. There is no particular pattern however.

25
Q

What is a hereditary cancer?

A

A cancer that is caused by a direct parent to child relationship which is triggered by the passing down of an altered gene.

26
Q

What is p53?

A

A tumour suppressor gene that interacts with CDK inhibitor p21. It acts as a ‘brake’ and keeps the cell in G1 if there is DNA damage until repair or apoptosis.

27
Q

How does p53 induce apoptosis?

A

p53 inhibits a pro-survival protein, Bcl-2. It then activates the Bax cell death effector. The activation of Bax causes permeabilisation of the outer membrane of mitochondria which releases cytochrome C into the cytosol. Cytochrome C induces the caspase-3 cascade which initiates apoptosis.

28
Q

How do tumours resist cell death, with respect to p53?

A

Abnormal/mutated p53 means that the apoptosis pathway will not occur causing the cell to live on and differentiate further. Further/more mutations will lead to cancer.

29
Q

What is a telomere?

A

The protective caps on the end of chromosomes, which prevent it from unravelling.

30
Q

What does telomerase do?

A

It is an enzyme that adds a DNA sequence to prevent telomere shortening.

31
Q

How to tumour cells initiate replicative immortality?

A

They upregulate telomerase to keep continually adding more DNA onto the end of chromosomes, hence immortality. They also bypass cell cycle checkpoint genes (p53, p21 and Rb).

32
Q

What is an important factor to consider about the tumour microenvironment?

A

The oxygen concentration

33
Q

What features do ‘normoxic’ tumour cells possess?

A

They are near a blood vessel, have low HIF-1alpha expression and are more susceptible to radio/chemotherapy.

34
Q

What is HIF-1alpha?

A

A transcription factor that helps cells respond to hypoxia. It can increase the flow of oxygen to hypoxic areas.

35
Q

What is neoangiogenesis?

A

A process whereby a tumour cell will form new blood vessels to obtain nutrients required for survival and proliferation.

36
Q

What is the ‘angiogenic switch’?

A

The point where the tumour cell begins to secrete angiogenic factors to further support its growth. This is where the tumour cell begins to grow rapidly and potentially metastasise later on.

37
Q

What occurs in a patient with a Philadelphia chromosome?

A

Chromosome 9 and 22 translocate and create a altered chromosome.

38
Q

How does a tumour cell induce angiogenesis?

A

The tumour cell will release angiogenic (growth) factors (VEGF, FGF, PDGF). The endothelial cells of the local blood supply will begin secreting matrix metalloproteinases (MMPs) which digest and break up the extracellular matrix (ECM) which leads to proliferation and growth towards the tumour. The endothelial cells form new blood vessels which support tumour growth and metastasis.

39
Q

Why is oxygen and nutrient transportation difficult in tumour cells?

A

Because the tumour microvasculature is disorganised and irregular which leads to poor oxygen and nutrient flow throughout. This leads to further difficulty with homogenous drug distribution.

40
Q

What is proteolytic degradation?

A

Macrophages release MMPs which will cleave tumour cell-surface protein E-cadherin and then a tumour cell is released from the bulk of tumour. MMPs will then cleave the extra cellular matrix and the tumour cell migrates using different integrins.

41
Q

What is intravasation/tumour cell migration?

A

Growth factors and chemokines are secreted by macrophages (as well as MMPs) which cause tumour cell migration. As well as this, tumour cells secrete factors that cause macrophage chemotaxis. The pericytes which protect the blood vessels secrete factors (CXCL12) which allow tumour cell migration/intravasation through CXCR4 receptor.

42
Q

What happens in extravasation?

A

The tumour cell exits the blood vessel and either interacts with an active or quiescent stromal cell, or dies from apoptosis via NK cells. If it interacts with an active stromal cell, micrometastasis occurs. If the stromal cell is quiescent, the tumour cell becomes dormant until re-activated by bone marrow dendritic cells.

43
Q

What is Epithelial-Mesenchymal Transition (EMT)?

A

The process whereby a tumour cell changes its shape to navigate and migrate through the extracellular matrix using different integrins.

Cancer Y2 (6 decks)

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