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NMSK A Week 4 > 4.15 MolecularBio of Cancer > Flashcards

4.15 MolecularBio of Cancer Flashcards

1
Q

Tumor suppressor genes known as

A

caretaker gene, gatekeeper gene, landscaper gene.

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2
Q

Are cancers genetic?

A

Some are. Some are sporadic.

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3
Q

Viral induced cancer example?

A

HPV

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4
Q

Root cause of all Neoplasms?

A

Damaged DNA

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5
Q

What is p53

A

Potent tumor suppressor implicated in many tumors.

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6
Q

What induces tumors?

A

Carcinogens

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7
Q

If there are multiple locus contributing to a phenotype this is known as

A

Locus heterogeneity

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8
Q

What is the role of proto-oncogenes used for normal cell development?

A

Regulation of cell cycle
Regulation of differentiation
Regulation of senescence

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9
Q

What is transformation?

A

The process by which a cell loses its ability to remain constrained in its growth properties

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10
Q

What do tumor suppressor genes do?

A

They either dampen or repress up-regulation of the cell cycle or promote apoptosis.

  • Repress the continuation of the cell cycle
  • Link entrance of cell cycle to undamaged DNA
  • Link apoptosis to damaged DNA
  • Adhesion/contact inhibition upkeep
  • DNA Repair proteins
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11
Q

Why is getting frequent sunburns related to cancer?

A

When you burn, your cells will apoptosis and creates fresh new layer of cells. When there are repeated burns and constant apoptosis it can lead to mutation and cancer

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12
Q

How can you get retinoblastoma?

A

Inherited- gets one bad copy, then gets a mutation in the other good allele
Sporadic- has two unlucky mutations in both copies
Difference is whether you inherit a bad copy, or get 2 good ones

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13
Q

What gene mutations occurs in Retinoblastoma?

A

Chromosome 13, RB1 gene

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14
Q

What class of cancer causing gene does retinoblastoma fall? Oncogene or tumor supporessor gene?

A

Tumor suppressor because it is knocking out something

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15
Q

Explain the two hit hypothesis?

A

Both alleles for a tumor suppressor must be mutated out as one is haplosufficient for tumor suppression

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16
Q

What suppressor genes do not follow the two- hit rule and why?

A

P53 does not it is a potent tumor suppressor

17
Q

I have a proto-oncogene that is regulating the cell cycle. A mutation in that gene creates a growth hormone receptor that is constitutively “on.” This mutation is a

A

Gain of function mutation

18
Q

I have a tumor suppressor gene that needs a “two-hit” to take out. The mutation that I am creating if I need to hit both alleles to affect the phenotype is a

A

Loss of function mutation

19
Q

If a oncogene can create an oncogenic state by mutating one copy of a proto-oncogene, the oncogene is probably going to be a ____ mutation to the proto-oncogene.

A

Dominant

20
Q

A tumor suppressor that needs a “two-hit” would classify the mutated allele as being a ____ mutation.

A

Recessive

21
Q

Describe the philadelphia Chromosome

A

Translocation mutation. BCR and ABL next to each other prevents cells from accidently being activated. This results in leukemia.

22
Q

What is Senescence?

A

irreversible state of dormancy

Not always a bad thing, some cells are naturally dormant

23
Q

Apoptosis

A

programmed cell death
Not always a bad thing as development requires regulated apoptosis
Can be induced by the immune system

24
Q

How can DNA repair lead to tumors?

A

Rate of DNA damage in cells varies between 10,000 to 1,000,000 molecular lesions per cell per day
- Increase chances of mutation

25
Q

What happens when you have excess Oxygen to the DNA?

A

ENDOGENOUS DNA DAMAGE: Oxidation of DNA- Reactive oxygen species that creates DNA damage. ROS is created by WBC

26
Q

Exogenous DNA Damage

A

Free radicals and ROS can be created by many sources outside of the body
Intercalating agents, viruses and plant toxins
- Aflotoxin- Aspergillus parasiticus and A. flavus

27
Q

How is DNA repaired when there is a single strand break?

A

uses complementary strand

28
Q

How is DNA repaired when there is a double strand

A

Non-homologous end joining (DNA Ligase IV)
Microhomology-mediated end joining
Homologous recombination (like chiasma formation)

29
Q

What does DNA use for repair during the G2 phase if needed?

A

Sister chromatid or homologous chromosome

30
Q

How is a malignant tumor created?

A

DNA injury (Dysplasia)–> Continued DNA injury (Carcinoma in situ)–> Further DNA injury (Early invasive carcinoma through basement membrane)–> Invasion of blood vessels lymphatics with metastasis

31
Q

Cancer grading

A

Grade I Well differentiated
Grade II- Moderately differentiated
Grade III- Poorly differentiated

32
Q

What kills you when you have cancer?Why are tumor cells hot?

A

Cancer cells use up your nutrients. They are hot because they are burning up your sugar and goods.

33
Q

What is the best cancer therapy?

A

Assasinate: Immune system boosters. Your cells, immune system fights the cancer

34
Q

What are other forms of cancer treatment

A

Cut- surgery
Poison- Chemotherapeutics
Burn- radiotherapeutics

35
Q

How can we get cancer?

A

Activation of oncogenes

Destruction of tumor suppressor genes

36
Q

Describe the cell cycle

A

b. G1 Growth phase. Most cells in this phase
c. Cycle Check- “Stop signs”
d. S- Duplicate DNA—Form of aneuoploidy. Cell is turned off and no longer reactive. Only concerned of dividing.
e. G2- DNA finished replicating. Rest of cell gets on board.
f. Cycle Check- Checks to see if all cell components are there (Mitochondria, golgi, etc).
g. M- Mitosis metaphase
h. G0- They step out of the cell phase. Will not go through mitosis again. Can’t easily induce them.

37
Q

How do oncogenes effect the cell cycle

A

they kill the “stop signs”, cycle checks. This activates the system

38
Q

What part of the cell cycle do protooncogenes turn on?

A

G1 phase– same gene involved in gene development

39
Q

How is the cell cycle regulated?

A

CDK

NMSK A Week 4 (11 decks)

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