Cancer II Flashcards

1
Q

What are Hanahan and Weinberg’s (2000) original hallmarks of cancer?

A

1) Evading growth suppressors
2) Activating invasion and metastasis
3) Sustaining proliferative signalling
4) Inducing angiogenesis
5) Enabling replicative immortality
6) Resisting cell death

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2
Q

What were Hanahan and Weinberg’s (2011) emerging hallmarks of cancer?

A

1) Deregulating cellular energetics
2) Avoiding immune destruction

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3
Q

What were Hanahan and Weinberg’s (2011) enabling characteristics of cancer?

A

1) Tumour promoting inflammation
2) Genome instability and mutation

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4
Q

What may be used to slow the inducing of angiogenesis in cancer?

A

Inhibitors of VEGF signalling can slow angiogenesis

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5
Q

What original hallmark of cancer do telomerase inhibitors work to prevent?

A

Telomerase inhibitors work to disenable replicative immortality.

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6
Q

What does the original hallmark “evading growth suppressors” describe?

A

The failure of signals which stop proliferation in cancer.

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7
Q

What does p53 sense?

A

p53 senses DNA damage, cell cycle abnormalities and hypoxia.

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8
Q

What does normal p53 do in response to cellular damage?

A

p53 will arrest the cell cycle until damage is repaired. If the damage cannot be repaired, it will trigger apoptosis.

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9
Q

What does mutated p53 do in response to cellular damage?

A

Mutated p53 does not arrest the cell cycle therefore the damaged cell continues to divide. This may result in cancer.

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10
Q

What enzyme shows increased activity in cancer cells?

A

Telomerase shows increased activity in cancer cells.
In normal cells, telomeres progressively shorten with each cell division. In most cancer cells there is an increase in telomerase activity, allowing cancer cells to acquire unlimited replicative potential. This process is described by the hallmark “enabling replicative immortality”.

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11
Q

Angiogenesis is a normal process in growth and development, as well as in wound healing. Why is it switched on in cancer cells?

A

Cancer cells require new blood vessels to be formed in order to survive and grow. They do this through angiogenesis.

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12
Q

Name the system which regulates hundreds of genes which induce angiogenesis.

A

Hypoxia-inducible transcription factor (HIF) system regulates hundreds of genes (including VEGF) which induce angiogenesis.

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13
Q

What steps follow tumour cells leaving the primary tumour?

A

Tumour cells invade the ECM. Intravasation occurs then the tumour cells enter the circulatory system where they pick up platelets. The next step is extravasation followed by pre-metastatic niche, micrometastasis and colonisation.

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14
Q

As well as alternations to their shape, which other alterations do carcinomas develop?

A

Carcinomas develop alterations to their attachment to other cells, as well as to their shape.

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15
Q

Name three types of conventional cancer treatments.

A

1) Surgery
2) Radiation therapy
3) Chemotherapy

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16
Q

Name three types of alternative cancer treatments.

A

1) Gene therapy
2) Antiangiogenesis
3) Targeted chemotherapy

17
Q

Describe the mechanism by which Tamoxifen treats breast cancer.

A

Oestrogen can induce proliferation of existing mutant cells. The oestrogen receptor triggers gene activation. Tamoxifen is similar in shape to oestrogen and can bind to the oestrogen receptor without changing its shape, meaning the receptor cannot bind to its coactivators to be activated.

18
Q

Which gene is amplified or receptor overexpressed in ~25% of metastatic breast cancers?

A

HER2

19
Q

What are HER2-positive tumours associated with?

A

HER2-positive tumours are associated with poor prognosis and shortened survival.

20
Q

How may the HER2 receptor help in cancer treatment?

A

HER2 receptor provides an extracellular target for novel and specific anticancer treatments using monoclonal antibodies.

21
Q

What is Herceptin?

A

Herceptin is an anti-HER2 antibody which has a high affinity and specifity.

22
Q

What is the mechanism of action of Anastrozole?

A

Anastrozole blocks oestrogen production by inhibiting the aromatase enzyme.