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D1 Fall - Biochem > 10/31: Genetics of Cancer Oncogenes and Tumor Suppressors > Flashcards

10/31: Genetics of Cancer Oncogenes and Tumor Suppressors Flashcards

1
Q

What are the types of genetic diseases?

A

Chromosome disorders
- rearrangements/translocations, deletions, insertions, duplications, aneuploidy
Single gene disorders
- dominant, recessive, codominant
Multifactorial or complex
- multiple genes, gene environment
Sex linked and mitochondrial

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2
Q

What chromosome is associated with chronic myelogenous leukemia (CML)?

A

Philadelphia chromosome

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3
Q

The philadelphia chromosome leads to bone marrow producing excess amounts of

A

Abnormal granulocytes

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4
Q

Is a single mutation enough to cause cancer?

A

No

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5
Q

Tumor growth and progression generally involves what?

A

Multiple genetic changes

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6
Q

Tumors can arise from what 2 things?

A
  1. Increased cell division
  2. Decreased apoptosis
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7
Q

Can tumors arise from genetic or epigenetic changes? (understand this!!!)

A

Yes

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8
Q

Malignant tumors are classified according to what?

A

Tissue or cell they originate from

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9
Q

Carcinomas are cancers that arising from

A

Epithelial cells

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10
Q

Sarcomas arise from what?

A
  1. Connective tissue
  2. Muscle cells
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11
Q

Leukemias are derived from what?

A

White blood cells and their precursors (hematopoietic cells)

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12
Q

Lymphomas are derived from

A

Lymphatic tissue

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13
Q

Gliomas are derived from

A

Glial cells of the CNS

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14
Q

Are benign tumors classified like malignant tumors?

A

Yes

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15
Q

Adenomas are malignant or benign tumors?

A

Benign

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16
Q

Adenomas are what kind of tumors?

A

Benign epithelial tumors

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17
Q

Adenomas have what kind of organization?

A

Glandular organization

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18
Q

Chondromas are benign tumors that arise from

A

cartilage

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19
Q

Many cancers are maintained by a population of

A

Cancer stem cells

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20
Q

Chemotherapy generally target what cells?

A

Rapid dividing cells

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21
Q

Can cancer stem cells survive radiation from chemotherapy?

A

Yes

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22
Q

Are cancer stem cells slow or rapid dividing?

A

Slow dividing

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23
Q

Tumors secrete what kind of signals to promote formation of new blood vessels?

A

Angiogenic

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24
Q

Tumors secrete angiogenic signals which promote the formation of

A

New blood vessels

25
Q

Why do tumors need to form blood vessels?

A
  1. They supply the nutrients so the tumor can grow
  2. Allow ability to metastasis
26
Q

Do cancer cells induce angiogenesis?

A

Yes

27
Q

What do cancer cells produce to stabilize their telomeres?

A

Telomerase

28
Q

What are the classifications of cancer genes?

A
  1. Inhibit cellular proliferation
  2. Activate proliferation
  3. Participate in DNA repair
29
Q

What are the mutated forms of proto-oncogenes?

A

Oncogenes

30
Q

Oncogenes are genes that do what to cell division?

A

Out of control, fast growth

31
Q

Tumor suppressor genes do what to cell division?

A

Inhibit, slow down growth repair

32
Q

What happens when tumor suppressor genes do not work?

A

Cells grow out of control → cancer

33
Q

Gain of function of proto-oncogenes leads to

A

Cancer

34
Q

Loss of function of tumor suppressor genes lead to

A

Cancer

35
Q

Oncogenes result from the _______ of proto-oncogenes

A

Activation

36
Q

Tumor suppressor genes cause cancer when they are

A

Turned off

37
Q

P16 is a

A

CDK inhibitors

38
Q

P53 can induce what 3 things?

A
  1. Cell cycle arrest
  2. Senescence
  3. Apoptosis
39
Q

What is Kudson’s original hypothesis?

A

A person needed to acquire two mutant copies of the Rb gene

40
Q

What is one mutant Rb allele considered?

A

Dominant at the level of the individual, but
recessive at the level of the cell

41
Q

What does the Rb mutation display?

A

reduced penetrance, only about 90% of individuals who inherit the mutant allele experience a second hit and develop a tumor

42
Q

What is a product of the INK4 gene?

A

p16 protein

43
Q

When is the p16 protein produced?

A

When cells are stressed and is an important component of cell cycle arrest

44
Q

Mutations of p16 can also contribute to?

A

Cancer

45
Q

What contributes to stable, active p53?

A

Hyper proliferative signals
DNA damage
telomere shortening
hypoxia

46
Q

What does stable, active p53 lead to?

A

Cell cycle arrest
senescence
apoptosis

47
Q

What are other considerations of breast cancer?

A

Type
Hormone receptor status
Ki-67 proliferation index
Her2/Neu status

48
Q

What are the two consideration types?

A

Noninvasive
Invasive

49
Q

What are examples of noninvasive cancer?

A

Ductal carcinoma in situ
Lobular carcinoma in situ

50
Q

What are examples of invasive cancer?

A

Usually epithelial
Ductal
Lobular
Other

51
Q

What are increased risk genes for breast cancer?

A

BRCA1
BRCA2
CDH1
STK11
TP53

52
Q

Where can virus genomes be found?

A

Form of DNA or RNA

53
Q

What are he two types of viruses?

A

RNA (RNA genome)
DNA (DNA genome)

54
Q

What cells does HIV infect?

A

T-cells
Macrophages
Microglial cells

55
Q

The RNA genome is bound to what key enzymes?

A

Reverse transcriptase
Proteases
Ribonucleases
Integrase

56
Q

How does reverse transcriptase work?

A

Copies the RNA genome into a ss-cDNA and eventually into a ds-cDNA that enters the nucleus and integrates into the host cell genome

57
Q

What does reverse transcriptase high error rate result in?

A

High frequency of mutations in the cDNA copies

58
Q

How does the infleunza virus work?

A

The negative sense RNA is transcribed into a positive sense RNA (cRNA), which serves as a template for protein synthesis and for
negative strands that are incorporated into new viral particles

59
Q

Why doesn’t influenza use a DNA copy?

A

RNA is much less stable than DNA and as such mutates at a faster rate than any other kind of virus

D1 Fall - Biochem (29 decks)

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