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CMD Block 2 > Handorf Cancer > Flashcards

Handorf Cancer Flashcards

1
Q

2 heritable properties defining cancer cells:

A

1) they reproduce in defiance of the normal restraints on cell division
2) they invade and colonize territories normally reserved for other cells

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2
Q

Adenoma

A

neoplastic, benign glandular tissue

fibrous CT capsule

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3
Q

Adenocarcinoma

A

invasive, cancerous gland tissue

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4
Q

Cancers have a ________ origin

A

monoclonal

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5
Q

How does cancer incidence correlate with age?

A

Increased incidence

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6
Q

How does the timing of cancer incidence correlate with carcinogen exposure?

A

“Delayed onset of cancer after exposure to a carcinogen”

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7
Q

T/F: According to Dr. Handorf’s lecture, it’s often one mutation responsible for cancer.

A

F: “multiple mutations in genes associated with cancer” and animal models indiciate that multiple mutations are needed to induce cancer

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8
Q

T/F: Cancer occurs often in certain families, seemingly due to genetic predisposition

A

T

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9
Q

Cancer cells have a shared ______ in their DNA.

A

“abnormality”

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10
Q

What characteristic determines if a cell if malignant?

A

the ability to metastasize

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11
Q

Tumor progression involves successive rounds of:

A

mutation and selection

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12
Q

What is involves in cancer cell success?

A

“immortality”

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13
Q

Indefinite cell growth

A

Immortalization

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14
Q

Independence of growth factors in tumors

A

Transformation

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15
Q

Invasion and growth at distant site

A

Metastasis

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16
Q

Genes the help in cancer avoidance

A

Tumor Suppressor Genes

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17
Q

Genes involved in cancer cell predisposition

A

Oncogenes (Tumor Promoter Genes)

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18
Q

Genes that directly regulate tumor cell growth

A

Gatekeepers

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19
Q

Genes involved in repairing DNA damage or maintaining genomic integrity

A

Caretakers

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20
Q

BRCA is a type of ________ gene

A

Caretaker

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21
Q

Non-hereditary retinoblastoma arises from

A

point mutation

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22
Q

Loss of activity of what genes promote cancer formation?

A

tumor suppressor genes

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23
Q

Condition in which a ton of colon polyps develop by age 20 due to an inherited, inactivated susceptibility gene

A

Familial Polyposis Coli

familial adenomatous polyposis

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24
Q

T/F: Cells usually arise from one cancerous cell.

A

T

25
Q

How do cancers progress (in general terms)?

A

In stages (via clonal expansion)

26
Q

What contributes to the progression of a single cancer cell?

A

Growth advantage over the surrounding cells

27
Q

T/F: As mutant cells proliferate, they continue to accumulate mutations.

A

T (according to one of the pictures in the lecture)

28
Q

What are 5 general characteristics of cancerous cells?

A
  1. Avoidance of apoptosis
  2. Genetic instability
  3. Invasiveness (ability to escape home tissue)
  4. Metastasis (ability to survive/prolif in other sites)
  5. Loss of normal regulation of cell proliferation
29
Q

Gain of function mutations activate:

A

oncogenes

30
Q

Genes that behave in a dominant fashion to stimulate or sustain replication

A

oncogenes

31
Q

Loss of function mutations are associated with:

A

tumor suppressor genes

32
Q

Genes that act in a recessive manner

A

Tumor suppressor genes

33
Q

Loss of function mutations may result what 2 cellular problems?

A
  1. increased/sustained proliferation

2. decreased DNA repair

34
Q

How many inactivating mutations are usually required to eliminate the action of p53 genes?

A

2

p53 = tumor suppressor gene

35
Q

First discovered human oncogene

A

ras

36
Q

Onocgenes’ normal cellular counterpart

A

proto-oncogenes

37
Q

What are the different outcomes for one versus two oncogenes present?

A

1: sporadic tumors
2: MORE sporadic tumors at an earlier age

38
Q

What are 3 ways that proto-oncogenes become oncogenic? What results from each?

A
  1. chromosome rearrangement =
    -nearby regulatory DNA sequence
    results in overproduction of normal
    protein
    -fusion to another (more active) gene
    results in overproduction of normal
    protein or hyperactive protein
  2. gene amplification = normal protein overproduced
  3. mutation in coding sequence = hyperactive protein is made in normal amounts
39
Q

What happens when you fuse normal cells and tumor cells?

A

Your get cells with a normal phenotype (this suggests that there are tumor suppressors in the normal cells

40
Q

APC (adenomatous polyposis coli gene) is an example of what type of tumor suppressor gene?

A

gatekeeper (which directly regulates cell growth)

41
Q

Childhood tumor that arises in neural precursor cells in the immature retina
(What is defective?)

A

Inherited Retinoblastoma

Rb

42
Q

The loss of _____ will drive excessive epithelial proliferation.

A

tumor suppressor gene

43
Q

The loss of __________ drives the excessively proliferating epithelium towards small tumor formation.

A

activation of oncogene (which encourages unrestricted growth)

44
Q

Once a small tumor has formed, what event will result in this tumor becoming larger?

A

loss of a second tumor suppressor gene

the assumption is that loss of the first one led to the tumor

45
Q

Once a tumor has become invasive, what is likely to occur?

A

mutations will begin to accumulate rapidly, resulting in metastasis

46
Q

An inherited (active/inactive) APC gene causes cancer susceptibility.

A

inactivated (it’s a gatekeeper)

47
Q

What type of cellular structure is p53?

A

transcription factor

48
Q

What is the result of p53 inactivation?

A

genome instability

49
Q

3 things that p53 is responsible for in the cell:

A
  1. Induction of cell cycle arrest (G1checkpoint) in response to DNA damage (p21 induction)
  2. Induction of apoptosis (excessive mitogenic stimulation or if damage cannot be repaired)
  3. Induction of genes required for DNA repair
50
Q

What causes cancer by binding and inactivating p53?

A

E6 protein of Human Papillomavirus

51
Q

What causes Li-Fraumeni Syndrome?

A

defective p53

52
Q

Hereditary Nonpolyposis Colorectal Cancer is caused by:

A

mutations in one of five DNA repair genes involved in DNA mismatch repair

53
Q

What is the function of the complex containing BRCA1 and 2?

A

homologous recombination repair

tumor suppression

54
Q

3 Characteristics of Stem cells:

A
  1. Relatively undifferentiated
  2. capacity for unlimited or prolonged self renewal
  3. can produce at least one highly differentiated cell type
55
Q

What abilities do stem cells and cancer cells have in common?

A
  1. extensive ability to proliferate

2. can give rise to abnormal tissues

56
Q

T/F: Most tumors have a clonal origin.

A

T

57
Q

Explain why tumors and stem cells are both considered to be heterogenous.

A

different phenotypic characteristics
different proliferative potentials

(tumor cells have these characteristics because they have a clonal origin)

58
Q

What suggests that tumor and stem cells undergo analogous processes?

A

Because most tumors have a clonal origin, tumorigenic cancer cells must give rise to phenotypically diverse progeny, including cancer cells with different ranges of proliferative potential.

(this needs more clarification)

59
Q

Why are stem cells targets of transformation?

A

already actively proliferating (other cells would have to develop self-renewal potential, in addition to whatever other mutations)

CMD Block 2 (38 decks)

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