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BIO 102 FINAL > Cancer > Flashcards

Cancer Flashcards

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Biology 101 flashcards
1
Q

What causes Cancer

A

multistep mutation of genes that encode for regulatory proteins

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2
Q

What are the different cell cycle regulators

A

Inhibiting regulators and activation regulators

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3
Q

What occurs when cell cycle regulators mutate

A

Inhibiting regulators can be mutated to decrease in activity or lose all function
Activation regulators: increase in activity

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4
Q

What characterizes a normal cell

A
  1. Contact Inhibition- Contact with other cells stop cell growth
  2. Limited lifespan-mortal
  3. Anchorage-Dependent Growth- Needs to be attached to some type of surface.
  4. Growth Factor Dependent Growth- Need receive growth factors in order to grow.
  5. Can perform Apoptosis
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5
Q

What protein in the cell induces apoptosis?

A

p53

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6
Q

What activates p53?

A

DNA damage activates sensory proteins (Kinases), sensory proteins activates p53, p53 stops cell cycle (activates cell cycle inhibitors) and binds to DNA.

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7
Q

What is the role of p53?

A

p53 can bind to DNA, stop the cell cycle, and does a 3 step process

  1. Stops cell at G1 checkpoint
  2. Activates DNA enzyme repairs
  3. If DNA is not repaired, signals cell to induce APOPTOSIS
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8
Q

What are the two types of proteins affected by cancer mutations?

A

Proto-oncogenes, and tumor supressors

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9
Q

How are proto-oncogenes affected by mutations?

A

Proto-oncogenes are Dominant genes that turn into oncogenes when one of their alleles are mutated. Oncogenes increase cell division.

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10
Q

Example of proto-oncogene affected by mutation?

A

RAS protein. When RAS receptor is mutated. It does not need growth factor to stimulate cell division. It remains in an active state (RAS + GTP).

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11
Q

What are various ways in which proto-oncogenes can be mutated?

A

Amplification–Copies of more genes leads to copies of more proteins.
Change in amino acid—-> point mutation (leaves genes in an ON state.

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12
Q

What are Tumor Supressors?

A

Tumor Suppressors- proteins that are responsible for detecting and preventing any potential cancer like characteristics or behaviors. Negative Regulators

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13
Q

What are some examples of Tumor Suppressors

A

p53 and Rb protein. p53 monitors the stages between G1 and S phase. It will bind to DNA and stop it from proceeding to the next phase of the cell cycle, it will activate repair systems in efforts to repair the cell. If the efforts to repair are not met, then it will induce APOPTOSIS.

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14
Q

What is the Rb protein

A 
The Rb proteins binds to proliferating factors to STOP it from activating genes that will produce proteins responsible for the proliferation of cell division. 
RB proteins (non-phosphorylated), will bind to transcription, to bring cell division to a halt. When phosphorylated, it releases the transcription factors and the cell progresses from G1 to the S phase.
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15
Q

What is the difference between p53 and Rb protein

A

Rb protein is a tumor suppressor that is not activated or deactivated based on the damage that is done. It is like a traffic light. While p53, job is to stop the cell cycle to fix the damage.

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16
Q

What happens to the tumor suppressors in presence of the virus

A

The Virus will integrate itself into the genome of the cell. this will produce the proteins E6 and E7. E6 binds to p53 and inactivates it while E7, binds to pRb and inactivates it.

17
Q

True of false: the presence of a virus mutates the tumor suppressors p53 and pRb.

A

False: the virus just inactivates the tumors. However, the tumor suppressors can be mutated if both alleles are mutated (TUMOR SUPPRESSORS HAVE RECESSIVE GENES)

18
Q

When can a cell be considered tumorous?

A

When multiple facets that enable controlled cell cycle proliferation are mutated. Example: Mutation in both proto-oncogenes and tumor suppressors, mutation to DNA repair enzymes and etc.

19
Q

True or false: Cancer cells have many characteristics that make them distinct form normal cells. They do not make their own signals, but BULLY other cells to produce signals for their benefit. They adhere to external signals but change the normal metabolic process found in cells.

A

False: Cancer cells do make their own signals. An example of this would be growth factor pathways. They manipulate or bully other cells to produce signals for their benefit. They can also proliferate without growth factor signals. They do not adhere to external signals such as contact inhibition. They do change their normal metabolic systems.

20
Q

What is the importance of cyclins and cyclin dependent kinases?

A

Cyclin and CDK complexes are important for phosphorylating the proteins that are involved in the proliferation of the cell cycle.

21
Q

What is an example of Cyclin and CDK importance.

A

Cyclin and CDK complex phosphorylates the Rb proteins in order for it to release the E2F transcription factors which produce proteins that allow the cell to continue in the cell cycle.

22
Q

What can occur to proto-oncogenes when mutated

A

a mutation in an proto-oncogene will turn it into an oncogene. One of two things can occur:

  1. the change in gene sequence can cause a different protein to be produced
  2. an increase in the making of the protein made by the proto-oncogene
23
Q

True or false: Mutations in wither Proto-oncogenes or tumor suppressors can either leave the protein the same or make more of the same protein

A

Mutations to both can lead to a CHANGE in the PROTEIN, or an INCREASED amount of protein made.

24
Q

What are the two ways in which tumors can behave

A
  1. Normal Cell division, decreased apoptosis (Not killing off or getting rid of bad cells.)
  2. Increased Cell division, and normal apoptosis (Too many cells are being made)
25
Q

What are the role of each check point in the cell cycle

A

G1, make sure there is no DNA damage or mutation.
S phase: makes sure DNA replication was successful
M phase: to make sure the chromosome binds to the mitotic spindle.

26
Q

How many mutations must occur for a cell to be considered cancerous?

A

10 mutations

27
Q

Growth factors

A

Growth factors are responsible for increasing the size of the cell

28
Q

Mitogens

A

signals the cell to perform cell division

29
Q

True or False: Cancer cells of the same tissue have the same mutation set up

A

False: As the cells continue to mutate, they become more different from one another. Each cell becomes adapted to different environments or behaviors.

30
Q

True or False: Cancer cells do not die off. They are immortal due to the telomerase they have acquired. This prevents their telomeres from shortening and killing the cell

A

False: although cancer cells have acquired telomerase to keep their telemoeres from shortening, cancer cells do not have a guaranteed promise of immortality. They must have the right mutations that enable them to adapt to their environment as well.

31
Q

What is the relationship between VEGF and cancer

A

Cancers that are able to live longer, will being to acquire vascular epithelial growth factors. These allow for blood vessels to be formed in order for the cancer cells to receive the required nutrients and oxygen it needs to survive. It can express these growth factors themselves or it can bully other cells to produce it for them.

32
Q

TRUE or FALSE: Tumor cells secrete VEGF

A

FALSE: they do not secrete VEGF, but they do turn on the gene which allows for it to bring in blood.

33
Q

TRUE or FALSE: STEM cells are CANCEROUS

A

False: Stem cells are not cancerous, they have telomerase, but their cell division is controlled. They share many characteristics with cancer cells.

34
Q

What are the two receptors of the T-cell that are responsible for shutting down the immune system

A

PD-1 and CTLA-4

35
Q

How does cancer take advantage of this

A

When the T- cell/immune system recognizes a strange cancer cell, it binds to the PD-1 and CTLA-4 receptors in order to shut it up. The immune system will not be able to attack the cancer cell

36
Q

What is the solution to this mechanism

A

the two drugs by Bristol Meyer Smith are antibodies that bind to these receptors on the T-cell without shutting it down. So it can still detect cancer cells without being manipulated or shut down

37
Q

What is the downside of this medication

A

The T-cell will not be able to shut off, Immune system will always be on. This can lead to autoimmune disease

38
Q

what are the key things that make cells cancerous

A
  1. Ignoring external and internal signaling
  2. Avoiding APOPTOSIS
  3. By passing cell cycle regulation
  4. Uncontrolled cell replication
  5. Avoiding cell death of old age (senescence)
  6. Having the ability to metastasis
  7. Angiogenesis
  8. Avoid cell differentiation

BIO 102 FINAL (2 decks)

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