Smith Flashcards

1
Q

A protooncogene is one which?

a) generally shows a recessive phenotype when mutated.
b) will cause cells to proliferate when it is mutated.
c) regulates normal cell growth and division.
d) is an antiproliferative gene.
e) is activated during mitosis.

A

b) will cause cells to proliferate when it is mutated.

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2
Q

When a growth factor binds to its receptor molecule, a common sequence of event is?

a) Activation of the receptor—oligomerization of the receptor—creation of docking sites—recruitment and activation of signaling enzymes.
b) Oligomerization of the receptor—activation of the receptor—creation of docking sites—recruitment and activation of signaling enzymes.

A

Oligomerization of the receptor—activation of the receptor—creation of docking sites—recruitment and activation of signaling enzymes.

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3
Q

Which of the following is critical to the formation of a docking site?

An intrinsic protein tyrosine kinase

Retinoblastoma

GAP

Grb2

An intrinsic phosphotyrosine phosphatase

A

An intrinsic protein tyrosine kinase

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4
Q

It has been found in some breast cancer patients that Cyclin D1 expression is increased. How would this affect the retinoblastoma protein?

It would be hyperphosphorylated and thus inactive.

It would be hyperphosphorylated and thus constitutively active.

It would be degraded by caspases.

It would bind to transcription factors of the E2F family.

It would bind to Ras.

A

It would be hyperphosphorylated and thus inactive.

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5
Q

p53 may activate apoptosis, at least in part, by downregulating the expression of ______ and upregulating the expression of _____.

Bcl-2, Bax

Bax, Bcl-2

Caspases, Bax

Caspases, Bcl-2

A

Bcl-2, Bax

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6
Q

While viruses can gain control of the expression of a protooncogene, leading to cellular transformation, 85% of human tumors are simply caused by

Point mutations or deletions in tumor suppressor genes.

Routine intron splicing that leads to activation of a protooncogene.

Ras mutations.

Point mutations or deletions in oncogenes.

p53 mutations.

A

Point mutations or deletions in oncogenes.

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7
Q

HPV E7 can inhibit the association of Retinoblastoma (Rb) with _______, thereby leading to cell immortalization.

Epidermal growth factor (EGF)

Platelet derived growth factor (PDGF)

Transcription factor E2F

p53

Cyclins

A

Transcription factor E2F

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8
Q

As part of a cytokine-dependent pathway to cell growth, ______ can phosphorylate ______, leading to the transcription of GAS elements.

Retinoblastoma, itself

JAKs, STAT

PDGF, itself

Retinoblastoma, E2F

Sos, Ras

A

JAKs, STAT

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9
Q

In the PDGF-mediated pathway of cell growth, _________ acts as a guanine nucleotide exchange factor that will _________ Ras.

Grb2, activate

GAP, activate

GAP, inactivate

Sos, activate

Sos, inactivate

A

Sos, activate

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10
Q

As smoking has declined in the U.S., __________ has taken over as the most commonly encountered risk factor associated with oral cancers.

Alcohol consumption

Use of mouthwash

Poor hygiene

Betel quid use

HPV infection

A

HPV infection

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11
Q

Protooncogene is a normal cellular gene that functions in cell proliferation. These _______ signaling molecules, etc. that keep telling the cell to ________.

A

encode; cell to divide

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12
Q

Oncogenes are

A

mutated protooncogenes

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13
Q

What are antiproliferative genes?

A

tumor suppressor genes

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14
Q

The mutant phenotype of a protooncogene is _____ and occurs with a mutation in _____ allele(s).

A

dominant; one allele

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15
Q

The mutant phenotype of a tumor supressor gene is _____ and occurs with a mutation in _____ allele(s).

A

recessive; both alleles which leads to uncontrolled cell division!

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16
Q

Cell division limitations of:

1) unicellular organisms
2) multicellular organisms

A

1) primary limitation s availability of nutrients and energy

2) usually stop dividing when they bump up against another cell (regardless of availability of nutrition)

17
Q

In multi-cellular organisms, even _______ is controlled.

A

apoptosis (cell death0

18
Q

In unicellular organisms, the more divisions, the more______.

A

mutations = faster evolution

19
Q

Timing of the cell cycle:
S through M:
M:
G0

A

S through M: 12-24 hr
M: ~1 hour
G0: vast majority of the cell cycle period

20
Q

Environmental signalling molecules at G1 and G2 checkpoints:

A

hormones, cytokines, and growth factors; also PTK (protein tyrosine kinases) are often involved in checkpoint signaling

21
Q

enzymes that transfer the gamma phosphate from ATP to a tyrosine on a target (substrate) protein. Targets can be intrinsic or extrinsic.

A

PTK (protein tyrosine kinases)

22
Q

On a general transmembrane PTK, there are 3 domains:

A

external (receptor for tyrosine kinase), transmembrane, and internal domain (tyrosine kinase domain)

23
Q

What binds to the external domain of an transmembrane receptor?

A

external signaling factor (dimer)

24
Q

Growth factors are signals for________.

A

proliferation

some can induce cell growth, but not division!

25
Q

Breast cancer: cyclin D1 expression increased causing…

A

hyperphosphorylation and inactivation of RB = deregulated malignant cell proliferation

26
Q

Retinoblastomas: mutational inactivation of Rb genes causing…

A

deregulated malignant cell proliferation

27
Q

Cervical cancer: sequestration of Rb by HPV E7 protein causing….

A

loss of Rb control of the cell cycle

28
Q

When there is a deletion of the CDK1 gene causing….

A

loss of inhibition of cyclin-D- CDK4/6 complexes, resulting in loss of Rb control of the cell cycle

29
Q

Bcl-2 is __________, which promotes the survival of the cell.

A

antiaoptotic

30
Q

Survival factors activate ________ proteins, which lead to the survival of the cell.

A

Bcl-2

31
Q

P21 is a CDK inhibitor, thus inhibits _______ which doesn’t allow for the _____ checkpoint.

A

Rb; G1 checkpoint

32
Q

When Rb is phosphorylated, it goes or doesn’t go past the G1 checkpoint?

A

doens’t go past G1 checkpoint

33
Q

Cyclins interact with ____ which leads to the phosphorylation of Rb

A

CDK’s

34
Q

p53 is a …

A

tumor supressor gene

35
Q

CDKIs =

A

cyclin dependent kinase inhibitors

36
Q
  1. Cytokines bind to receptor causing_______ to occur
  2. JAKs is ______.
  3. JAKs phosphorylates _____.
  4. STAT _____.
  5. and thus migrates to the nucleus to activate transcription factors!
A
  1. oligomerization
  2. JAKs is recruited.
  3. phosphorylates STAT
  4. STAT dimerizes