Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIO207 > Genetics of Cancer > Flashcards

Genetics of Cancer Flashcards

1
Q

What are the common features of cancer?

A

Somatic cells accumulate mutations in a variety of genes
Normal function of these genes is to act as accelerators or brakes for cell division
Mutations cause cancer cells to divide rapidly and uncontrollably

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three ways cancer cells evade normal controls on cell growth?

A

Produce cell division signals (autocrine stimulation?
Lose contact inhibition
Avoid programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How many divisions do normal cells undergo before death?

A

20-50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the length of chromosome ends maintained in cancer cells?

A

Expression of telomerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is angiogenesis?

A

Production of substances that encourage blood vessel growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is metastasis?

A

Blood vessels provide nutrients to tumor, allow movement to other locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why do cancer cells have a higher rate of mutation than normal cells?

A

Enzymatic systems that repair DNA damage or mistakes during replication are often defective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is cancer correlated with old age? What does this support?

A

INcidence of cancer rises dramatically with age
Supports idea that cancer involves the accumulation of mutations in the clonal descendants of a somatic cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does inheritance of some mutations predispose a person to cancer?

A

They have to accumulate fewer mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are passenger mutations?

A

Occur due to increased mutation rate of cancer cells
Do not contribute to disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are driver mutations?

A

Cause cancer phenotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which is more common in cancer genomes, passenger or driver mutations?

A

Passenger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What needs to happen in order for cancer to appear?

A

Accumulation of several driver mutations in different genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does feedback result in tumor progression?

A

Mutation result in more cancer-like properties
Cells with more cancer-like properties accumulate more mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are mitogens?

A

Growth factors that stimulate cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are receptors?

A

Found on surface of cell
Bind growth factors
Initiate signal transductioncascade
Ultimately activates synthesis of transcription factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are transcription factors?

A

Regulate genes whose protein products cause cells to divide or stop dividing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two basic types of signals that initiate cell division?

A

Extracellular and cell-bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are extra-cellular signals?

A

Act over long or short distances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are extracellular signals collectively known as?

A

Hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are cell-bound signals?

A

Require direct contact between cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give an example of an extracellular signal that acts over large distances

A

Thyroid-stimulating hormone (TSH) produced in pituitary gland
Moves through blood to thyroid gland, which expresses throxine, which influences metabolic rate

23
Q

How do growth factors transmit signals into cells?

A

Through transmembrane receptors

24
Q

What relays a signal transmitted into a cell?

A

Signal transducers

25
Q

What are oncoproteins?

A

Receptors that normally bind growth factors and do not require growth factor to be active. Retain their functionality but no longer respond to normal regulatory cell signals

26
Q

What are CDKs?

A

Family of kinases that regulate the transition through stages of the cell cycle

27
Q

When do CDKs function?

A

When associated with Cyclins

28
Q

What does phosphorylation by CDKs do?

A

Activate or inactivate proein

29
Q

What activates the G1 to S checkpoint?

A

DNA damage

30
Q

how is p53 related to apoptosis?

A

If DNA damage is great enough, cells producing p53 not only arrest in G1, but commit apoptosis

31
Q

Outline apoptosis

A

DNA is degraded, nucleus condenses, phagocytic cells devour and destroy dying cell

32
Q

What are checkpoints need?

A

They are not essential for cell division but cells with defective checkpoints are more vulnerable to DNA damage

33
Q

What are the three types of genomic instability checkpoints helps prevent transmission of?

A

Point mutations
Translocations
Gene amplification

34
Q

What is a proto-oncogene?

A

Nonmutant allele

35
Q

What proteins do proto-oncogenes often encode?

A

Those needed for cell cycle progression

36
Q

When are oncogenes produced?

A

When mutations cause improper activation in a gene

37
Q

What are two approached to identifying oncogenes?

A

Tumor-causing viruses
Tumor DNA

38
Q

Outline how oncogenes can be identified through association with tumor viruses

A

After infection, retroviral genome integrates into host genome and may activate a proto-oncogene
Genes near viral integration sites in cancer cells may be oncogenes
Host proto-oncogenes may be packaged into RNA virus particles

39
Q

How can oncogenes be identified through cell transformation assays?

A

Human gene that is oncogenic can be identified and clone from transformed mouse cells

40
Q

Give examples of oncogenes

A

Ras, c-ABL, Her2

41
Q

Describe Ras

A

Usually active when bound to growth factor
Onocgenic point mutation makes constitutively active protein

42
Q

Describe c-Abl

A

Chromosomal translocation fuses the c-abl and bcr genes
hybrid protein encodes a constitutively active tyorsine kinase

43
Q

Describe Her2

A

FOund in 20% of breast cancers
Ocerexpressed growth factor receptor

44
Q

Give an example of an ancient cancer treatment

A

Egpytian physicians treated it with surgery or sticking hot pokers into tumors

45
Q

What is chemotherapy

A

Drugs that may kill cancer cells that are unreachable or missed by surgery

46
Q

What does chemotherapy do?

A

Directed against pathways needed for cell proliferation

47
Q

What is an issue with chemotherapy?

A

Our bodies require cell renewal
Normal proliferating cells are killed by chemotherapy

48
Q

Explain how Gleevec works

A

ATP required for Bcr/c-Abl enzyme to phosphorylate target proteins
Gleevec binds to the ATP binding site, inactivating enzyme
Leukemic blood cells disappeard in 98% of patients

49
Q

Explain Herceptin

A

Antibody that binds to the Her2 receptor
Prevents activation
Results in destruction of cancer cells

50
Q

What are some challenges with counteracting mutations in tumor suppressor genes?

A

Cancer cells lack both functional copies of tumor suppressor genes - nothing to tatger

51
Q

What are two cancer therapies that increase the ability of T cells to destroy cancer cells?

A

Blocking T-cell inhibitoris
CAR T-cell therapy

52
Q

Explain blocking T-cell inhibitors

A

Some cancer cells avoid immmune system by using immune checkpoints
PD-1 protein off switch on T cells prevents T cells from attacking normal body cells when bound by the PDL-1 protein on normal body cells
Some cancer cells also express PDL-1, switching the PD-1 protein to off
Antibodies against PD-1 or PDL-1 can act as cancer drugs, allowing T cells to attack cancer cells, but can have sever side effects

53
Q

Explain CAR T-cell therapy

A

A gene encoding a synthetic chimeric antigen receptor (CAR) is added to a pateint’s T cells
Receptor is designed to bind antigens on cancer cells but not normal cells
Allows CAR T cells to destroy tumor cells

BIO207 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions