Brainscape's Knowledge GenomeTM

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


See full index

Cancer Biology T1 > Transformation (1 and 2) > Flashcards

Transformation (1 and 2) Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

anchorage dependence

A
  • normal cells need physical matrix to grow on
  • cells normally anchor (epithelial and endothelial cells will perform apoptosis if not)
  • haemopoietic cells and early stem cells can grow in suspension
  • cancer cells LOSE this
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

life span of cells

A

normal cells have limitied life-span
- cells stop growing (growth arrest)

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

senescence

A
  • cell not in cycle but still growing
  • happens in normal cells
  • cancer cells avoid this, making them immortal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the consequence of the body’s attempts to eliminate foreign, lipophilic substances from the body?
a. Generation of active carcinogens
b. Inactivation of carcinogens
c. Formation of stable conjugates
d. None of the above

A

a

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

Which phase of metabolism involves oxidation by the cytochrome P450 system of the ER?
a. Phase I
b. Phase II
c. Phase III
d. Phase IV

A

a

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

bWhat is the significance of the lag period between carcinogen exposure and tumor appearance?
a. It indicates a direct correlation between dose and lag duration.
b. It suggests multiple independent steps or “genetic hits” for tumor formation.
c. It is inversely proportional to the dose of carcinogen.
d. It indicates a lack of association between carcinogen exposure and tumor formation.

A

b

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

What is the role of promoters in the process of initiation and promotion in carcinogenesis?
a. Promoters initiate the formation of tumors.
b. Promoters are substances that cause tumors on their own.
c. Promoters stabilize the effects of initiators.
d. Promoters are responsible for the lag period between carcinogen exposure and tumor appearance.

A

c

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

Which of the following statements is true about the order of exposure to initiator and promoter?
a. Exposure to promoter before initiator results in tumor formation.
b. Exposure to initiator before promoter results in tumor formation.
c. Exposure to both initiator and promoter simultaneously results in tumor formation.
d. Exposure to initiator and promoter in any order results in tumor formation.

A

b

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

Can the effects of promoters on tumor formation be reversed?
a. Yes, the effects of promoters are stable and irreversible.
b. Yes, the effects of promoters are unstable and reversible.
c. No, the effects of promoters are always irreversible.
d. No, the effects of promoters are always stable and irreversible.

A

b

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

What type of plot is typically used to represent the relationship between tumor incidence and exposure time for chemical carcinogens?
a. Linear plot
b. Logarithmic plot
c. Bar plot
d. Scatter plot

A

b

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

What does a slope greater than 1 in a log-log plot of tumor incidence vs exposure time suggest?
a. The relationship between tumor incidence and exposure time is linear.
b. The relationship between tumor incidence and exposure time is exponential.
c. The presence of multiple independent steps or “genetic hits” in tumor formation.
d. The presence of a single step or “genetic hit” in tumor formation.

A

c

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

How can exposure to initiator and promoter be separated by a long interval and still result in tumor formation?
a. Initiation is a stable state that persists over time.
b. Exposure to initiator and promoter simultaneously results in tumor formation.
c. Exposure to promoter has a delayed effect on tumor formation.
d. Exposure to promoter stabilizes the effects of initiator over time.

A

a

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

What is the role of repeated exposure to promoter with gaps between doses in tumor formation?
a. It promotes the formation of stable conjugates.
b. It stabilizes the effects of initiator.
c. It has no effect on tumor formation.
d. It reverses the effects of initiator.

A

b

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

What are the signal transduction pathways involved in promoting cell growth regulated by?
a. Tumor suppressor genes
b. Proto-oncogenes
c. Oncogenes
d. DNA repair genes

A

b

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

What is the role of proto-oncogenes in the regulation of apoptosis?
a. Proto-oncogenes promote apoptosis
b. Proto-oncogenes inhibit apoptosis
c. Proto-oncogenes have no effect on apoptosis
d. Proto-oncogenes regulate apoptosis indirectly through other pathways

A

b

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

What is the function of proto-oncogenes in the regulation of differentiation?
a. Proto-oncogenes promote cellular differentiation
b. Proto-oncogenes inhibit cellular differentiation
c. Proto-oncogenes have no effect on cellular differentiation
d. Proto-oncogenes regulate differentiation indirectly through other pathways

A

a

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

How do proto-oncogenes regulate cellular lifespan?
a. Proto-oncogenes promote cellular senescence
b. Proto-oncogenes inhibit cellular senescence
c. Proto-oncogenes have no effect on cellular lifespan
d. Proto-oncogenes regulate cellular lifespan indirectly through other pathways

A

b

18
Q

Which of the following is NOT a function of proto-oncogenes?
a. Signal transduction pathways involved in promoting cell growth
b. Regulation of apoptosis
c. Regulation of differentiation
d. Promotion of tumor growth

A

d

19
Q

What is the normal state of proto-oncogenes in healthy cells?
a. Activated oncogenes
b. Inactive tumor suppressor genes
c. Inactive proto-oncogenes
d. Active DNA repair genes

A

c

20
Q

How do proto-oncogenes differ from oncogenes?
a. Proto-oncogenes are normal genes, while oncogenes are mutated forms of proto-oncogenes
b. Proto-oncogenes promote tumor growth, while oncogenes inhibit tumor growth
c. Proto-oncogenes are inactive, while oncogenes are active genes
d. Proto-oncogenes have no effect on cellular processes, while oncogenes regulate cellular processes

A

a

21
Q

What happens when proto-oncogenes are mutated and become oncogenes?
a. They lose their normal cellular functions
b. They become inactive and are unable to regulate cellular processes
c. They gain new cellular functions that promote tumor growth
d. They become tumor suppressor genes

A

c

22
Q

How are proto-oncogenes typically activated to become oncogenes?
a. Environmental factors
b. Inherited mutations
c. Spontaneous mutations
d. DNA repair mechanisms

A

c

23
Q

Which of the following is NOT a characteristic of proto-oncogenes?
a. They regulate normal cellular processes
b. They are important for cell growth and development
c. They are prone to mutation and can become oncogenes
d. They always promote tumor growth

A

d

24
Q

What is Fibroblast Growth Factor (FGF)?
a. A type of tumor suppressor gene
b. A type of oncogene
c. A protein that regulates cell growth and development
d. A type of chemotherapy drug

A

c

25
Q

What is the primary role of FGF in cellular processes?
a. Promotion of cell division
b. Inhibition of cell differentiation
c. Promotion of cell differentiation
d. Regulation of cell death

A

c

26
Q

How many types of Fibroblast Growth Factors (FGFs) are there in humans?
a. 5
b. 10
c. 23
d. 50

A

c

27
Q

Which of the following is NOT a known function of FGFs?
a. Promotion of cell migration
b. Regulation of tissue repair
c. Induction of angiogenesis
d. Inhibition of cell division

A

d

28
Q

How do FGFs transmit signals into cells?
a. By binding to cell membrane receptors
b. By entering the cell nucleus
c. By interacting with cytoplasmic enzymes
d. By binding to extracellular matrix proteins

A

a

29
Q

What type of receptor do FGFs typically bind to on the cell membrane?
a. G-protein coupled receptor
b. Ion channel receptor
c. Receptor tyrosine kinase
d. Nuclear receptor

A

c

30
Q

What is the significance of FGFs in embryonic development?
a. FGFs play a role in organogenesis and tissue patterning
b. FGFs regulate blood sugar levels
c. FGFs promote bone growth
d. FGFs inhibit muscle development

A

a

31
Q

Which of the following is a well-known example of FGF?
a. Epidermal Growth Factor (EGF)
b. Insulin-like Growth Factor (IGF)
c. Platelet-derived Growth Factor (PDGF)
d. Transforming Growth Factor Beta (TGF-β)

A

a

32
Q

How are FGFs involved in cancer development?
a. FGFs inhibit tumor growth
b. FGFs promote angiogenesis, which can facilitate tumor growth
c. FGFs induce apoptosis in cancer cells
d. FGFs inhibit cell proliferation in cancer cells

A

b

33
Q

What are the potential therapeutic applications of FGFs?
a. Treatment of cancer
b. Promotion of wound healing
c. Stimulation of tissue regeneration
d. All of the above

A

d

34
Q

How can cytokines contribute to cancer development?
a. By promoting cell differentiation
b. By inhibiting cell proliferation
c. By inducing inflammation and immune response
d. By promoting angiogenesis and tumor growth

A

d

35
Q

How does dysregulation of signal transduction pathways contribute to cancer?
a. It increases apoptosis and cell death
b. It promotes cellular differentiation
c. It disrupts the normal balance between cell proliferation and cell death, leading to uncontrolled cell growth and tumor formation

A

c

36
Q

How are Receptor Tyrosine Kinases (RTKs) implicated in cancer development?
a. Mutations in RTK genes can lead to aberrant RTK signaling, resulting in uncontrolled cell growth and tumor formation*
b. RTKs are not involved in cancer development
c. RTKs promote apoptosis and inhibit tumor growth
d. RTKs regulate cell differentiation and inhibit angiogenesis

A

a

37
Q

Which RTK family is commonly associated with cancer?
a. Insulin-like Growth Factor (IGF) family
b. Epidermal Growth Factor (EGF) family
c. Platelet-derived Growth Factor (PDGF) family
d. All of the above

A

d

38
Q

How can aberrant EGF family receptor signaling contribute to cancer development?
a. By inhibiting cell proliferation
b. By promoting apoptosis
c. By inducing differentiation
d. By promoting cell growth and proliferation, angiogenesis, and metastasis

A

d

39
Q

What is the significance of Receptor Tyrosine Kinases (RTKs) as targets for cancer therapy?
a. RTKs are not targeted in cancer therapy
b. Inhibitors of RTKs can block aberrant signaling and suppress tumor growth
c. RTKs are only targeted in viral infections
d. RTKs are not involved in cancer development

A

b

40
Q

How does understanding signal transduction pathways and RTK signaling help in cancer research?
a. It helps in developing targeted therapies that specifically inhibit cancer cells without affecting normal cells
b. It does not have any relevance in cancer research
c. It promotes cell proliferation and tumor growth
d. It inhibits apoptosis and promotes angiogenesis

A

a

Cancer Biology T1 (2 decks)

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