lecture 18 Flashcards

1
Q

what are cancer cells within a tissue

A

Cancer cells are cells within a tissue that no longer respond to many of the signals that control cellular growth and death.

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2
Q

cancer is a result of what?

A

Cancer is the result of an accumilation of mutations. Most of these mutations being associated with DNA replication.

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3
Q

tumour supressor genes normally do what function

A

Encode proteins that normally prevent cell growth. For example they might code for proteins that inhibit cell division. May also code for DNA repair proteins which prevent other mutations.

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4
Q

what does a lack of tumour suppressor genes mean for the cell

A

A lack of these genes means that cell growth is unregulated.

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5
Q

mutations to tumour suppressor genes is normally recessive, what does this mean

A

These mutations are normally recessive as both sets of genes need to be deactivated so that cell growth can be unregulated and thus over proliferate.

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6
Q

what are proto-oncogenes

A

Proto-oncogene (a normal gene that when mutated can promote uncontrolled cell growth)

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7
Q

what do oncogenes encode for

A

Encode for proteins that promote cell growth. For example proteins that stimulate cell division.
Cancerous mutations increase the activity of these genes.

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8
Q

what is E2F and whats its relation to RB

A

E2F is a key protein for cell division. E2F is a transcription factor which acts on DNA replication and cell division genes. E2F is prevented from causing cell division by RB proteins in the cytoplasm.

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9
Q

what does an activation signal do for tumour suppressor genes

A

Signal for cell division results in P16 releasing a kinase. The kinase phosphorylates E2F which allows E2F to travel into the nucleus where it acts as a transcription factor for cell division and thus
Cell division genes can then be expressed.

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10
Q

loss of RB means

A

Loss of function mutation in the RB gene causes over proliferation of E2F transcription factor and thus too much cell division.
this loss of function coming from a recessive mutation

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11
Q

why is loss of RB or P16 recessive and only seen when recessive homozygous

A

as the dominant still functioning copies of the gene are still able to do their job, masking the lack of activity. thereby with one dominant we can still regulate the cell division

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12
Q

what two onco-genes mutations can we see

A

Mutations that increase protein activity
Mutations that increase transcription

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13
Q

explain mutations that increase protein activity

A

There can be mutations in the protein itself, these are rare and create a protein that is always active or doesn’t get degraded. This type of protein will exist for longer than it needs to thus further promoting cell division.

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14
Q

explain mutations that increase protein transciption

A

Oncogenes may also see a mutation in the repressor secgment of the promotor. This will lead to excessive transcription of cell division proteins and thus increased cell grwoth.

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15
Q

how is a translocation an oncogene

A

A translocation is an example of oncogene. As the translocated part may not regulate the newly translocated gene segment. Thus proteins will be under new promotor region and will then be overproduced.

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16
Q

translocation examples

A

ABL gene is a kinase. It responds to receptor signals and goes on to activate transcription factors.
When translocated with BCR, BCR-ABL can activate transcription factors without outside signal. The BCR-ABL will phosphorylate transcription factors helping them over produce cell division and DNA replication genes.

17
Q

what are 3 possible cancer treatments and explain them

A

In early stages cancer isnt a large issue as we can remove the cancer tumor.
Radiation therapy – targeted radiation treatment to kill cancer cells
Chemotherapy uses an adenine DNA base analog to target dividing cells. Cancer cells are always dividing, so chemotherapy targets these. But chemo does also kill non cancerous dividing cells.

18
Q

whats a 4th possible cancer therapy

A

Targetted therapy:
drugs that target changes in cancer cell that allow them grow and divided
For example targetting BCR-ABL. This BCR-ABL protein is only present in cancerous cells, so they made a drug to bind to only this mutated protein.