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Final Exam

Total questions: 75

Worksheet time: 4hrs 45mins

Name
Class
Date
1.

Stem cells are

a)

cell that grow uncontrollably

b)

undifferentiated and can be any type of cell

c)

never go through cell division

d)

only found in embryos

2.

Stem cells can be obtained from

a)

embryos

b)

some adult tissues

c)

umbilical cord blood

d)

all of the above

3.

What does “pluripotent” mean?

a)

able to divide and make many different types of cells

b)

not able to divide

c)

can only divide and make one cell type

d)

if it divides, it will make a cancerous tumor

4.

Which is true about embryonic stem cells?

a)

they no longer divide, their cell type is set and cannot change

b)

they develop into only one type of cell

c)

they can become any cell type in the body

d)

they are bound in adults

5.

How do stem cells know what type of cells to differentiate into?

a)

the nucleus has instructions to turn some genes on and some genes off

b)

signals from chemicals in the organism or from the environment determine which genes will be turned on and off

c)

genes turn on and off randomly

d)

the cell has unique DNA that determines what the cell will become

6.

Which type of cell is unspecialized?

a)

keratinocyte

b)

hepatocyte

c)

stem cell

d)

muscle cell

7.

Which is true about Adult Stem Cells?

a)

They no longer undergo mitosis, their cell type is set and cannot change

b)

They can become any cell type in the body

c)

They are limited to the type of cell they can become

d)

They are found in embryos

8.

What is the role of stem cells in the body?

a)

fight against infections

b)

provide specialized roles in the body

c)

used for fertility treatment

d)

they produce new specialized cells in the body to replace old cells that are use up

9.

Adult stem cells are

a)

multipotent

b)

pluripotent

c)

totipotent

d)

fully differentiated

10.

As cells become more specialized

a)

cells have access to more genes

b)

some gene segments get lost

c)

some genes are turned off

d)

proliferate faster

11.

Which of the following external stimuli dictate a stem cell’s self-renewal vs differentiation programing?

a)

Matrix Molecules

b)

Soluble Factors

c)

Cell-Cell Interactions

d)

All of the above

12.

What process best explains how muscle cells and nerve cells develop from the same fertilized egg?

a)

genetic engineering

b)

survival of the fittest

c)

differentiation

d)

selective breeding

13.

Protein molecules around which DNA is tightly coiled in chromatin

a)

histones

b)

whey

c)

casein

d)

hemoglobin

14.

The difference between DNA code and the epigenome is that the DNA code is

a)

flexible, which the epigenome is fixed for life

b)

fixed for life, while the epigenome is flexible

c)

determined by the environment, while the epigenome is not

d)

determined by one’s stress level, while the epigenome is not

15.

Epigenetics regulation include (s)

a)

Post-translational histone modifications

b)

DNA methylation

c)

Expression of non-coding RNAs

d)

Incorporation of histone variants

e)

all of the above

16.

Histone modifications contribute to gene regulation

a)

histone lysine acetylation is associated with gene activation (H3-K9, K14, K18, K27, K56; H4-K5, K8, K12, K16)

b)

histone lysine methylation is associated with gene repression (H3-K9, K27)

c)

histone lysine methylation is associated with gene activation (H3-K4, K36, K79)

d)

all of the above

17.

Activated signaling cascade, e.g., kinase cascades, can alter the epigenetic landscape either directly by phosphorylating histone proteins or indirectly by modifying chromatin modifiers, such as

a)

histone modifying enzymes

b)

chromatin remodelers

c)

histone chaperone proteins

d)

all of the above

18.

1. Estrogen signaling is mediated by epigenetic mechanisms, e.g.,

a)

DNA methylation-mediated silencing of estrogen receptor gene

b)

Histone deacetylation-mediated down-regulation of estrogen receptor gene

c)

Interaction between ER and co-activators such as AT (acetyltransferase e.g. p300) in the promoter of ER-target genes

d)

all of the above

19.

Cytosine methylation at the 5 position on the pyrimidine ring generates 5-methyl Cytosine (5-mC). When 5-mC undergoes deamination, you get

a)

Cytosine

b)

Adenosine

c)

Thymine

d)

none of the above

20.

While the majority of CpGs (~60-80%) are methylated, CpG-rich regions termed CpG islands are generally unmethylated (~50% of CpG are located in gene promoter regions)

a)

True

b)

False

21.

What are major types of histone modifications?

a)

H3.1

b)

H3.2

c)

H3.3

d)

H3t

e)

H3.X

22.

What is the relationship between estrogen levels (E2) and ferritin levels during menopausal transition?

a)

an inverse relationship in which E2 decreases and ferritin increases

b)

a positive relationship in which they both increase with age

c)

a positive relationship in which they both decrease with age

d)

there is no relationship between estrogen and ferritin but rather progesterone and ferritin, and it is concurrent but inverse

23.

Which of the following enzymes play a role in synthesis of estrogen (E2) from cholesterol?

a)

CYP21

b)

CYP11

c)

P-450 aromatase

d)

CYP1a1

24.

Which is/are pathways of ER action?

a)

ER dimers directly bind to EREs following ligand activation

b)

upon ligand binding, ERs interact with other transcription factors such as AP-1 and Sp-1 through a process referred to as transcription factor cross-talk

c)

estrogen may elicit effects through nongenomic mechanisms via ERα or GPR30 in the cell membrane, involving interactions with cytoplasmic signal transduction proteins

d)

ER activity can be regulated through a ligand-independent pathway in which ERs are phosphorylated by activated kinases

25.

How does 17β-estradiol (E2) affect iron absorption from the liver?

a)

suppressed expression of hepcidin

b)

increase expression of hepcidin

c)

induce hepcidin degradation

d)

bind to hepcidin to increase iron uptake

26.

What role does BMP6 play in hepatic iron regulation?

a)

iron carrier, presents extracellular iron to hepatocytes for sensing

b)

binds to TfR1 and TfR2

c)

binds to hemojuvelin

d)

iron-specific ligand of the BMP receptor, increased by hepatic iron

27.

What tissues are affected by estrogen and estrogen signaling?

a)

brain, skin, heart, breast, liver, uterus, bone

b)

brain, skin, lung, breast, pancreas, uterus, bone

c)

brain, spleen, breast, uterus, small intestine

d)

skin, breast, heart, uterus, colon

28.

Which of the following is not true?

a)

iron is required for electron transport in mitochondrian, DNA replication, and numerous other biological functions

b)

excess iron can lead to free radicals formation and damage to cellular proteins, membranes, and DNA

c)

iron deficiency can lead to anemic conditions

d)

there is more iron in the bone marrow than in the liver parenchyma

29.

Addition of iron to osteoprogenitor cells in the presence of BMP-2 (a bone morphogenic protein that stimulates osteogenic differentiation)

a)

increased the number of progenitor cells that matured into osteoblasts but increasing Runx2 and ALP

b)

blocked differentiation of progenitor cells to osteoblasts and suppressed BMP-2-mediated increased Runx2 and ALP expression

c)

promoted proliferation of the osteoprogenitor cells

d)

induced osteoprogenitor cells to differentiate into red blood cells

30.

Increased efflux of drugs has been considered to be the major reason for chemotherapy resistance.

a)

True

b)

False

31.

Tumor heterogeneity is one of mechanisms that cause drug resistance. There are several levels of heterogeneity, including

a)

Genetic heterogeneity

b)

Cell type heterogeneity

c)

Metabolic heterogeneity

d)

Temporal heterogeneity in dynamic tumor progression

e)

all of the above

32.

Resistance to chemotherapy continues to be a major problem in cancer therapies. Chemoresistance is generated only after the therapy which is responsible for most relapses of cancer.

a)

True

b)

False

33.

Mechanisms of drug resistance do not include

a)

Alteration of drug target

b)

Epigenetic alterations

c)

Tumor heterogeneity

d)

Decreased efflux of drugs

34.

Epigenetic alterations play important roles in drug resistance, e.g., hypomethylation of transporter ABCB1 promoter

a)

Decreases expression of ABCB1, resulting in decreased efflux of drugs from cancer cells

b)

Decreases expression of ABCB1, resulting in increased efflux of drugs from cancer cells

c)

Increases expression of ABCB1, resulting in decreased efflux of drugs from cancer cells

d)

Increases expression of ABCB1, resulting in increased efflux of drugs from cancer cells

35.

Arsenic induces resistance to tamoxifen in breast cancer cells by

a)

Downregulation of both ERalpha and BRAC1

b)

Upregulation of both ERalpha and BRAC1

c)

Downregulation of ERalpha but upregulation of BRAC1

d)

Upregulation of ERalpha but downregulation of BRAC1

36.

Heavy metal exposures may ­ the sensitivity of cancer cells to chemotherapy.

a)

increase

b)

decrease

c)

both increase or decrease

d)

neither increase or decrease

37.

Cancer cells exhibit resistance to RTK therapy due to

a)

Disruption of interaction between drug and receptor

b)

Activation of alternate RTK signaling

c)

Both

d)

Neither

38.

A dysfunctional PI3K/AKT pathway serves as a hub to regulate drug resistance by

a)

triggering XIAP to suppress the activity of caspase-3, inhibiting apoptosis

b)

affecting tumor proliferation through regulating mTOR, GSK-3β, and NF-κB

c)

altering drug efflux through effective expression of ABC transporter

d)

all of the above

39.

The cause of acquired drug resistance include

a)

mutations or altered expression levels of the drug targets

b)

inactivation of second proto-oncogene that becomes the newly emerged driver gene

c)

changes in tumor microenvironment (TME) after treatment

d)

all of the above

40.

Oxidation is the ______ of electrons

a)

loss

b)

gain

c)

sharing

d)

destruction

41.

Reduction is the _____of electrons.

a)

loss

b)

gain

c)

sharing

d)

destruction

42.

Reactive sites of lipids for oxidation:

a)

ester bond between glycerol and fatty acid

b)

polyunsaturated fatty acids that contain two or more double bonds

c)

unsaturated fatty acids

d)

phytosterols

43.

The presence of one or more unpaired electron in the outer orbit make free radicals highly reactive

a)

True

b)

False

44.

Which is a reactive oxygen species but not a radical?

a)

Hydroxyl

b)

Peroxyl

c)

Ozone

d)

Hydroperoxyl

45.

Which is a reactive nitrogen species and a radical?

a)

Peroxynitrite

b)

Nitrous Acid

c)

Nitroxyl Anion

d)

Nitric Oxide

46.

Redox signaling is a process in which small redox molecules under physiological conditions modulate signal transduction, gene expression, and cellular response.

a)

True

b)

False

47.

Superoxide anion O2- is only generated enzymatically by NADPH oxidase

a)

True

b)

False

48.

Hydrogen Peroxide

a)

a non-radical potent oxidizing agent primarily enzymatically generated from superoxide anion by superoxide dismutase and removed by catalase or glutathione peroxidase

b)

a radical potent oxidizing agent that easily diffuses across biological membranes non-enzymatically generated by the intervention of redox components, such as the electron transport chain in the mitochondria

c)

a non-radical potent oxidizing agent that cannot diffuse across biological membranes and is enzymatically generated from superoxide anion by superoxide dismutase and removed by catalase or glutathione peroxidase

d)

none of the above

49.

What are extracellular sources of free radicals?

a)

virus

b)

tobacco

c)

chemotherapy

d)

diet

e)

all of the above

50.

Which is not a consequence of lipid peroxidation following increased ROS?

a)

structural changes in the plasma membrane

b)

lipid peroxidation products form adducts/crosslinks with non-lipids, such as proteins and DNA

c)

disruptions in membrane-dependent signaling

d)

increased plasma membrane rigidity

51.

How can oxidative damage affect DNA?

a)

DNA base damage

b)

DNA sugar damage

c)

single and double-strand breaks

d)

DNA-protein cross-links

e)

all of the above

52.

How can ROS/RNS affect cancer development and cancer progression?

a)

induce DNA damage resulting in mutations and thus cancer initiating cells

b)

increase cell proliferation

c)

alter cell apoptosis response

d)

promote angiogenesis

e)

all of the above

53.

HIF is a ________transcription factor composed of ________ alpha subunit and __________ beta subunit.

a)

homodimeric, an oxygen-sensitive, a constitutively expressed

b)

heterodimeric, an oxygen-sensitive, a constitutively expressed

c)

heterodimeric, a constitutively expressed, an oxygen-sensitive

d)

homodimeric, a constitutively expressed, an oxygen-sensitive

54.

The HIF bHLH domain is essential for _______ and the PAS domain is essential for ________.

a)

DNA-binding, dimerization

b)

dimerization, DNA-binding

c)

transphosphorylation, dimerization

d)

DNA-binding, transphosphorylation

55.

HIF1alpha and HIF2alpha each have _____ transactivation domain(s) (TAD).

a)

3

b)

2

c)

4

d)

1

56.

The C-terminal transactivation domain of HIF1alpha and HIF2alpha interacts with ________ to _______ gene transcription under _________.

a)

p300/CREB-binding protein co-activators, modulate, normoxia

b)

p300/CREB-binding protein co-activators, modulate, hypoxia

c)

VHL protein repressor, suppress, hypoxia

d)

VHL protein repressor, suppress, normoxia

57.

The von Hippel-Lindau (VHL) tumor suppressor protein binding to the ________ of HIF1alpha results in _______ of HIF1alpha and ____________________.

a)

ODD domain, sumoylation, lysosomal degradation

b)

ODD domain, ubiquitination, lysosomal degradation

c)

ODD domain, sumoylation, proteasomal degradation

d)

ODD domain, ubiquitination, proteasomal degradation

58.

The von Hippel-Lindau (VHL) protein acts as _____ of a ubiquitin E3 ligase complex.

a)

a ubiquitin-conjugating enzyme (E2)

b)

a ubiquitin-activating enzyme (E1)

c)

a specificity factor (E3) that function in substrate recognition

d)

a substrate

59.

How does the E3 ligase complex with von Hippel-Lindau (VHL) recognize HIF1alpha?

a)

Proline residues 402 and 564 can be hydroxylated by prolyl hydroxylase, which binds VHL to the ODD domain

b)

Proline residues 402 and 564 can be hydroxylated by prolyl hydroxylase, which binds VHL to the C-TAD domain

c)

Asparagine residue 803 can be hydroxylated by prolyl hydroxylase, which binds VHL to the C-TAD domain

d)

Asparagine residue 803 can be hydroxylated by prolyl hydroxylase, which binds VHL to the ODD domain

60.

Which of the following statements is FALSE?

a)

Hydroxylation by prolyl hydroxylase does not require O2 as a co-factor.

b)

Under hypoxia, prolyl hydroxylase cannot be activated.

c)

HIF1alpha accumulates and translocates into the nucleus.

d)

HIF1 binds to co-activators CBP/p300 and transactivates downstream target genes

e)

Prolyl hydroxylases are involved in HIF1alpha degradation

61.

CBP/p300 cannot bind when_______ on HIF1alpha, therefore HIF1alpha ___________ and _________.

a)

Proline 402 is hydroxylated, binds to another protein, transcription of different genes occurs

b)

Asparagine 803 is hydroxylated, no transcription occurs, HIF1alpha is degraded.

c)

Proline 402 is phosphorylated, no transcription occurs, HIF1alpha is degraded.

d)

Asparagine 803 is phosphorylated, no transcription occurs, HIF1alpha is degraded.

62.

Under _______ O2, HIF1alpha Proline 402, Proline 584 and Asparagine 803 are not ______, HIF1alpha binds to _________ and ________.

a)

high, hydroxylated, CBP/p300, transcription occurs

b)

low, hydroxylated, CBP/p300, transcription occurs

c)

high, ubiquitinated, CBP/p300, transcription occurs

d)

low, ubiquitination, CBP/p300, transcription occurs

63.

Initiation of carcinogenesis

a)

reversible epigenetic alteration

b)

irreversible epigenetic alteration

c)

irreversible genetic alteration

d)

none of the above

64.

End result of carcinogenesis progression:

a)

changes in rate of growth

b)

adoption of migration and invasion

c)

anchorage independent growth

d)

aneuploidy

65.

What may explain cancer cell heterogeneity?

a)

genetic/epigenetic clonal evolution

b)

environmentally determined effects on cancer cell properties

c)

cancer stem cell renewal and differentiation

d)

combination of all mentioned

66.

There are no immune cells in a tumor

a)

True

b)

False

67.

Cancer cells can evade being killed by the immune system by

a)

downregulate type I interferon signaling to reduce T-cell infiltration into the tumor and inducing T-cell exhaustion

b)

generating hypoxic and inflammatory microenvironment to impair antigen-presenting cells (APCs) and natural killer (NK) cells

c)

cancer cells express inhibitory cell surface proteins

d)

cancer cells create a hypoxic environment to avoid phagocytosis by macrophages

68.

Extracellular matrix molecules play no role in cancer progression

a)

True

b)

False

69.

Loss of type I interferon signaling in stromal cells within the tumor (fibroblasts and endothelial cells)

a)

increases tumor growth

b)

changes ECM deposition within the tumor microenvironment

c)

promotes angiogenesis

d)

has no effect

70.

Cancer cells release the following to promote tumor growth

a)

Growth factors

b)

Cytokines

c)

Chemokines

d)

Extracellular Vesicles

71.

Intravasation

a)

following accumulation of mutations, migrating cancer cells follow a chemokine gradient through the endothelial barrier and into circulation

b)

cancer cells and apoptotic cancer cells are pushed into nearby vasculature

c)

both

d)

neither

72.

How can macrophages help tumor cells survive in circulation?

a)

Integrin molecules on macrophages bind to V-CAM1 on the circulating tumor cell to activate survival signaling (phosphorylation of Ezrin results in activation of PI3K/AKT pathway)

b)

macrophages secrete fibrin to protect tumor cells

c)

macrophages do not help circulating tumor cells

73.

Cancer metastatic lesions

a)

are difficult to treat and comprise of cancer cells that are different to those in the primary tumor

b)

flourish in tissue pre-education by tumor-derived factors from the primary tumor

c)

have altered ECM composition compared to nearby normal tissue

74.

What are major types of histone modifications?

a)

phosphorylation

b)

acetylation

c)

methylation (arginine)

d)

Ubiquitylation

e)

Sumoylation

75.

The pre-metastatic niche

a)

is created by soluble factors released by the tumor

b)

is comprised of different cellularity and ECM deposition compared to surrounding tissue

c)

facilitates colonization when circulating tumor cells arrive

d)

does not affect cancer progression

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