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Foundations of Medicine > TBL 4 Carcinogenesis > Flashcards

TBL 4 Carcinogenesis Flashcards

1
Q

____ is regulated cell death that is not associated with inflammatory response, whereas ____ is unregulated cell death that is associated with inflammation.

A

Apoptosis is regulated cell death that is not associated with inflammatory response, whereas Necrosis is unregulated cell death that is associated with inflammation.

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2
Q

What are the two phases in apoptosis?

A

Latent phase: Death pathways are activated, but cell remains the same.

Execution phase: Apoptotic morphological structures begin to occur.

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3
Q

_____ is the enzyme used to tag DNA with an extra fluorescently-tagged base at the __ ends.
It is used to detect apoptotic cell death.

A

TUNEL is the enzyme used to tag DNA with an extra fluorescently-tagged base at the 3’ ends.

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4
Q

______ are enzymes which execute the apoptotic mechanisms directly.

A

Caspases

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5
Q

What is the amino acid on the catalytic site of Caspases?

A

Cysteine

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6
Q

_____ caspases trigger the cell death programmes and contain additional domains at their N-terminals.

A

Initiator

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7
Q

Caspase 2 and 9 contain _____ whereas Caspase 8 and 10 contain _____ domains.

A

2 and 9 – CARD

8 and 10 – DED

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8
Q

What cleaves and activates the effector caspases?

A

Initiator caspases

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9
Q

Effector caspases can activate enzymes known as _______ which breaks down DNA into regular fragments for apoptosis.

A

Caspase-activated DNase (CAD)

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10
Q

Fas is a death receptor found on many cells. It is (upregulated/downregulated) on infected cells. It is activated by its ligand, ____.

A

upregulated, FasL

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11
Q

FADD is an adaptor protein that recruits _____ to form the death-inducing signalling complex (DISC).

A

Proscaspase 8

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12
Q

The FLIP protein inhibites the death receptor activation of ______, by competitively binding to FADD on the trimerised receptor.

A

Caspase 8

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13
Q

Death by default refers to programmed cell death initiated by endogenous signals that are dependent on (organelle).

A

Mitochondria

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14
Q

The apoptosome is a large complex which contains Apaf-1, ATP, cyt-c and initiator procaspase __.

A

9

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15
Q

In the apoptosome, the Apaf-1 contains CARD which binds to _____; ATPase domain which binds to ____; WD-40 repeats which bind to ____.

A

Caspase 9; ATP; cyt-c

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16
Q

The binding of cytochrome-c to the ____ repeats on the Apaf-1 cause it to assemble into a wheel-like heptamer.

A

WD40

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17
Q

Seven procaspase 9 molecules are brought together to the centre of the wheel, binding to CARD domains on the Apaf-1, and this allows for _____ to occur.

A

transcleavage

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18
Q

Caspase 8, which is involved in the (extrinsic/intrinsic) pathway and Caspase 9, which is involved in the (extrinsic/intrinsic) pathway both activate Caspase _.

A

extrinsic; intrinsic; 3

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19
Q

Caspase 8 also cleaves ____ protein, which enhances the release of mitochondrial proteins.
(costimulation between both pathways)

A

Bid

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20
Q

The Bcl-2 family of proteins help to modulate the (organelle) intrinsic pathway of apoptosis.

A

mitochondrial

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21
Q

The domain that all Bcl-2 proteins have in common is ___, and they therefore use this as a protein-protein interaction domain between different members of the family.

A

BH3

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22
Q

(Anti/pro-apoptotic) Bcl-2 proteins include the Bcl-2, Bcl-xL.

(Anti/pro-apoptotic) Bcl-2 proteins include the Bid, Bax, Bad.

A

Anti; Pro

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23
Q

The PI3’-kinase pathway promotes cell survival and proliferation. It is therefore (anti/pro-apoptotic.)

A

Anti

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24
Q

Phosphatidylinositol 3’-kinase is a ___ kinase. It converts PIP2 to ___.

A

lipid; PIP3

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25
Q

PIP3 is recognised by the PH domain of the protein kinase ___/___, which is (anti/pro-apoptotic).

A

PFB/Akt, anti

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26
Q

PKB protein kinase phosphorylates Bad, which is then (activated/inactivated).

Bad is a (anti/pro-apoptotic) protein, hence inactivated Bad causes the cyt-c to (leave/remain) in the mitochondrial membrane.

A

Inactivated; pro; remain

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27
Q

PTEN is a ____ phosphatase, which dephosphorylates PIP3 back to ___, to counteract the effects of PI3-K signalling pathway.

A

lipid; PIP2

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28
Q

___ gene is a tumor suppressor gene, but unlike normal TS genes, it requires only ONE copy of the mutated gene to cause an effect. i.e. it acts in a dominant manner. This term is called haploinsufficiency.

A

p53

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29
Q

Inherited breast cancer is caused by inherited mutation in the ____ genes.

A

BRCA1/BRCA2

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30
Q

Chromosomal __________ occurs between chromosomes 9 and 22 in Chronic Myeloid Leukemia (CML).

This leads to a new fusion gene BCR-ABL1 on chromosome ___. This gene codes for a continually active ___________ (protein), leading to constant activation of downstream signalling cascades and overproduction of _______ (cells).

A

Chromosomal TRANSLOCATION occurs between chromosomes 9 and 22 in Chronic Myeloid Leukemia (CML).

This leads to a new fusion gene BCR-ABL1 on chromosome 22. This gene codes for a continually active TYROSINE KINASE RECEPTOR (protein), leading to constant activation of downstream signalling cascades and overproduction of GRANULOCYTES (cells).

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31
Q

Imatinib (Glivec) is a ___________ inhibitor, which is therefore used in the treatment of CML to prevent the overproduction of granulocytes.

A

Tyrosine Kinase

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32
Q

There are three methods to monitor disease progression of Leukemia:
1) Cytogenics; 2) FISH; 3) RT-PCR.

Amongst the three, _______ is the most accurate and sensitive, and is therefore used when the number of gene transcripts is greatly reduced.

A

RT-PCR

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33
Q

Chromosomal __________ occurs between chromosomes 15 and 17 in Acute Promyelocytic Leukemia (APML).

This leads to a new fusion gene PML-RARA. This gene codes for a protein which binds too (strongly/loosely) to DNA via enhanced interaction with co-repressors, (blocking/activating) transcription.

A

translocation; strongly; blocking

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34
Q

____ responds to all trans-retinoic acid (ATRA) therapy, which dissociates co-repressors, allowing for normal transcription and cell differentiation.

A

APML

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35
Q

Patients with K-ras mutation will lower the likelihood of response to _____ (drug) for colorectal cancer.

A

Cetuximab

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36
Q

Patients with EGFR mutation has a (greater/lower) likelihood of response to Geftinib for _______ (cancer).

A

greater; non-small cell lung cancer

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37
Q

Patients with _____ (gene) mutation is unlikely to respond to Dasatinib in CML.

A

BCR-ABL1

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38
Q

______ is the most vulnerable period of the cell cycle as cells are more easily killed, DNA damage cannot be repaired and gene transcription is silenced. (reduced metabolism)

A

Mitosis

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39
Q

___ phase occurs when the cell leaves the cell cycle and stops dividing.

A

G0

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40
Q

___ phase (10h) occurs after mitosis, and serves as a decision point whether the cell is to continue in the cell cycle.

A

G1

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41
Q

_ phase involves ______ ensuring that in the following mitotic division, the daughter cells possess the same amount of DNA as the parent cell originally had.

A

S; DNA Replication

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42
Q

In S phase, besides DNA replication, _____ synthesis is also increased. There is also replication of ______. In the case of mitochondria, the process needs to be coordinated with the replication of ____.

A

protein; organelles; mtDNA

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43
Q

___ phase (4h) occurs after DNA replication, and serves as a decision point.

A

G2

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44
Q

The centrosome consists of two ______ at right angles to each other. Each of them are made up of _______ microtubules.

A

centrioles; 9 triplets

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45
Q

The mother centriole and the daughter centriole are held together by ____________.

A

Interconnecting fibres

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46
Q

In the G1 phase, the mother and daughter centrioles ______, and ________ in the S phase, generating complete and new sets of centrioles by the time of mitosis.

A

separate; duplicate

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47
Q

The centrioles form a cloud of protein structures providing ________ sites for microtubules.

A

nucleation

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48
Q

In prophase, the ______ condenses to prevent DNA entanglement during segregation.
The duplicated ______ migrate to opposite poles of the nucleus and organise the assembly of ________.

A

chromatin; centrosomes; spindle microtubules

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49
Q

The DNA double helix first wraps around _____-charged _____ octamers with the presence of linker DNA.

A

positively; histone

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50
Q

The 10nm chromatin fibre further condenses around ___ histones and ______ DNA to form 30nm chromatin fiber.

A

H1; Linker

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51
Q

The 30nm chromatin fibre associates with ____ proteins and non-histone proteins to form ______ domains, which coil and condense further to form metaphase chromosomes.

A

scaffold; looped

52
Q

____ are radial microtubule arrays which form around each centrosome, followed by meeting of radial arrays in prophase.

A

ASTERS

53
Q

At _______ (stage), the nuclear membrane breaks down and the chromosomes attach to the mitotic spindle via _______ protein at the centromere region.

A

(Early) Prometaphase; kinetochore

54
Q

At (early/late) Prometaphase, microtubule from opposite poles are captured by sister kinetochores. Chromosomes migrate to the equator of the cell.

A

Late

55
Q

_______ senses when the kinetochore is bound to the microtubules.

A

CENP-E

56
Q

At _______(stage), chromosomes are aligned singly at the equator of the spindle along the metaphase plate.

A

Metaphase

57
Q

______ holds the sister chromatids together before segregation.

A

Cohesin

58
Q

At Anaphase A, _____ is broken down, as kinetochore microtubules shorten, pulling the daughter chromosomes towards the opposite spindle poles.

A

Cohesin

59
Q

At Anaphase B, daughter chromosomes migrate towards opposite poles, and the ________ migrate apart as the cell (elongates/shortens) due to the sliding of polar microtubules.

A

centrosomes; elongates

60
Q

At ______ (stage), contractile ring of _____ and _____ filaments is assembled at the equator of the cell.

A

Telophase; actin and myosin

61
Q

The M phase checkpoint occurs at _____ (stage), and checks for completion of chromosome alignment and spindle assembly.

A

Metaphase

62
Q

The M phase checkpoint requires _____ and ____ protein kinases, which dissociate from kinetochore when chromosomes are properly attached to the spindle.

A

CENP-E and BUB

63
Q

When all ____ kinases dissociate from the kinetochore, the cell is driven through the M checkpoint and anaphase proceeds.

A

BUB

64
Q

Amphelic (normal) attachment of kinetochore to microtubules occurs when the kinetochore is attached to ___ microtubule from each centrosome.

A

one

65
Q

Merotelic attachment occurs when one/both kinetochores are attached to _____ centrosomes.

A

both

66
Q

Syntelic attachment occurs when BOTH kinetochores are attached to the ____ centrosome.

A

same

67
Q

Monotelic attachment occurs when only ____ kinetochore is attached to a centrosome.

A

one

68
Q

Taxanes and vinca alkaloids is a type of anti-cancer therapy that alter microtubule dynamics and produces unattached _______, causing long-term mitotic arrest.

A

kinetochores

69
Q

Exit from G0 phase to enter mitosis and cell division is highly regulated, requiring ________ and ________ signalling cascades.

A

growth factors; intracellular

70
Q

Some growth factors include _____ growth factor (EGF) and ______ growth factor (PDGF), which bind to and activate receptors.

A

epidermal; platelet-derived

71
Q

Tyrosine phosphorylation on the RTK provide docking sites for ______ proteins which leads to protein-protein interactions.

A

adaptor

72
Q

The transcription factor _____ plays a key role in the entry of quiescent cells into the cell cycle by stimulating the expression of cell cycle genes, and it peaks when _____ are present.

A

c-Myc; growth factors

73
Q

Mitogenic growth factors bind to the transmembrane receptor _____. this leads to receptor activation by cross-________, activating ____ proteins.

A

RTK (Tyrosine Kinases); phosphorylation; adaptor

74
Q

Anti-HER2 antibody (Herceptin) is a drug which targets the early stage of cellular signalling, by blocking the _______. (implicated in many breast cancers)

A

HER2 Receptor Tyrosine Kinase

75
Q

Mitogenic growth factor pathway to stimulate mitosis:

_____ (ligand) binds to ______ (receptor), causing receptor to be cross-phosphorylated and activated. Adaptor protein ____ then binds to receptor and gets activated, associating itself with ____ (exchange factor), which can activate ____ (G protein).

A

Growth factors bind to RTK, causing receptor to be cross-phosphorylated and activated. Adaptor protein Grb2 then binds to receptor and gets activated, associating itself with SoS, which can activate Ras protein.

76
Q

Ras protein must be bound to the ________ (organelle) to be activated. Many anti-cancer therapies are targeted at preventing Ras binding to _____.

A

plasma membrane

77
Q

Ras is a _ protein. It is activated when bound to ____ and inactivated when bound to ____. It contains an internal _____ (enzyme) to hydrolyse the molecules.

A

GTP; GDP; GTPase

78
Q

Internal GTPase of Ras might be a very slow process, hence the cell makes use of _____ proteins to promote the hydrolysis.

A

GTPase activating proteins (GAPs)

79
Q

Ras mutations:

Mutation of glycine to _____ can result in steric hinderance preventing ____ binding.

A

valine; GAP

80
Q

Ras mutations:

Mutation of ______ to leucine, which inhibits the GTPase activity and thus GTP hydrolysis.

A

glutamine-61

81
Q

For growth-factor activated Ras transduction, the ____ cascade is used.

A

ERK (Extracellular signal-regulated kinase) cascade

82
Q

Kinases specific to the ERK cascade (hence activated by Ras protein):

Kinase 1 - _____
Kinase 2 - _____
Kinase 3 - _____

A

Kinase 1 - Raf
Kinase 2 - MEK
Kinase 3 - ERK

83
Q

The activated ___ protein may result in changes in gene expression of the ___ gene, resulting in cell proliferation.

A

ERK; Myc

84
Q

The cyclin-Cdk complex (known as MPF) involved in the M phase is:

A

Mitotic cyclins A and B and Cdk1

85
Q

To form active MPF,

  1. Cyclin A and B must activate Cdk_ to form (inactive/active) MPF.
  2. Requires activating phosphorylation by ___________.
  3. Removal of inactivating phosphorylation ____ by phosphatase Cdc25.
A

To form active MPF,

  1. Cyclin A and B must activate Cdk1 to form INACTIVE MPF.
  2. Requires activating phosphorylation by Cdk-activating kinase (CAK)
  3. Removal of inactivating phosphorylation (Wee1) by phosphatase Cdc25.
86
Q

Phosphatase Cdc25 (which removes inactivating phosphorylation for MPF) is itself activated by phosphorylation by ____. (This is known as positive feedback.)

A

MPF

87
Q

Cyclins activate Cdks and also alter _____.

A

substrate specificity

88
Q

Cyclin D activates Cdk _ and _ to stimulate the synthesis of cyclin _.

A

Cyclin D activates Cdk 4 and 6 to stimulate the synthesis of cyclin E.

89
Q

Rb gene is a _________ gene, and pRb is active in the (phosphorylated/unphosphorylated) state during G0, binding the inactive transcription factor ___, so that the target geen cannot be upregulated. (brake in the cell cycle)

A

tumor suppressor; unphosphorylated; E2F transcription factor

90
Q

In proliferating cells, Cdk4/6-cyclinD / Cdk2-cyclinE (Start kinases) phosphorylates pRb and (activate/inactivate) it, (releasing/binding) E2F, allowing for the upregulation of target genes.

A

inactivate; releasing

91
Q

______ act on active Cdk-cyclin complexes to inactivate them.

There are two families of inhibitors: ____ and ____.

A

CDK Inhibitors (CKI)

INK and KIP

92
Q

INK family of CKIs are expressed during the __ phase of the cell cycle, act by competing for cyclin binding sites on Cdk____. This essentially displaces Cyclin D from the complex.

A

G1; Cdk4/6

93
Q

CIP/KIP family of CKIs are expressed during the __ phase, and act by binding to the Cdk-cyclin complexes to inactivate the complex.

A

S

94
Q

Cell-ECM adhesion will (increase/decrease) the chance of the cell entering S phase.

A

increase

(This is because cells require binding to the ECM to be fully competent to responding to soluble growth factors. This is known as ANCHORAGE DEPENDENCE.)

95
Q

_____ (receptors) are heterodimer complexes of a and B subunits. They are the most important ECM receptors.

A

Integrins

96
Q

Integrins recognise short specific peptide sequences.

E.g.: Fibronectin (glycoprotein) receptor binds the ____ motif.

A

RGD (arg-gly-asp)

97
Q

Most integrins are linked via ____-binding proteins to the ____ cytoskeleton.

A

actin

Exception: a6B4 integrin complex is found in epithelial hemidesmosomes linked to the intermediate filament network instead.

98
Q

Integrins cluster to form ________ involved in signal transduction.

A

focal adhesions

99
Q

(Outside-in/Inside-out) signalling involves signal transduction using ECM receptors. Cells may receive information about its surroundings via its adhesion to the ECM.

A

Outside-in

100
Q

(Outside-in/Inside-out) signalling involves signal generated inside the cell as the result of receptor-ligand binding can act on integrin complexes to alter their affinity for ECM binding.

A

Inside-out

101
Q

The _____ (type/part) of the ECM is the most ideal for cellular differentiation.

A

Basal lamina/basement membrane

102
Q

Both sets of signals - ________ dependence and _______ dependence must be present before the cell undergoes division.
There is cross-talk between the ECM and the growth factor signalling.

A

density (GFs) and anchorage (ECM) dependence

103
Q

Long-term cell-cell contacts involve forming _______ between cells. These are specific to some cell types such as ______.

A

cell junctions; epithelial and endothelial cells

104
Q

Cell-cell junctions are usually arrange either as _________ (zonula) or ________ (macula).

A

zonula - continuous belts

macula - discrete spots

105
Q

The presence of cell-cell junctions (inhibits/activates) cell proliferation and division.

A

inhibits

106
Q

Cell-cell junctions are affected by ___ (ion) concentration.

At high ___ (ion) concentration, cell-cell junctions are stable and there is (high/low) cell proliferation.

A

Ca2+; low

Cell-cell junctions are also affected by the presence of adhesion-blocking antibodies.

107
Q

_____ junctions are cell-cell junctions which have cytoplasmic links to the actin cytoskeleton.

There are a few components:
E-cadherin; B-catenin and a-catenin.

A

Adherens

108
Q

______ is an important junction-associated molecule which is regulated primarily by the Wnt signalling pathway.

A

B-catenin

109
Q

The APC gene product (tumor suppressor) is a protein involved in the degradation of the ______.

A

B-catenin

110
Q

Loss of APC function results in the accumulation of ______, which translocates into the nucleus and activates the ______ transcription factor complex, upregulating a large number of cell cycle control genes.

A

B-catenin; Tcf/Lef-1

111
Q

Most human cancers are _______ (epithelial origins).

A

carcinomas

112
Q

__ checkpoint checks for the presence of growth factors, DNA damage, cell size, sufficient nutrients.

A

G1

113
Q

__ checkpoint checks if DNA is successfully replicated without damage.

A

G2

114
Q

__ checkpoint that occurs at ____ checks if there is successful formation of spindle fibres and attachment of spindle fibres to the chromosome kinetochores. (BUB proteins)

A

M; metaphase

115
Q

_______ genes code for essential proteins involved in the maintenance of cell growth, division and differentiation.

A

Proto-oncogenes

116
Q

__________ mutation convert proto-oncogenes to oncogenes.

A

Gain-of-function

117
Q

Oncogenes act in a _______ manner.

A

dominant

118
Q

Philadelphia chromosome involves a chromosomal translocation between chromosomes __ and __.
This produces a fusion protein ______, which causes RTK to be continually turned on.
Commonly found in ____ (Cancer).

A

9 (ABL) and 22 (BCR); BCR-ABL1; CML

119
Q

________ genes typically encode proteins regulating cellular proliferation and maintaining cell integrity.

A

Tumor suppressor

120
Q

Tumor suppressor genes usually act in a ________ manner.

Exception: ____ protein

A

recessive; p53

121
Q

_______ mutations occur in tumor suppressor genes, causing it to lose its original function

A

loss-of-function

122
Q

Retinoblastoma is the malignant cancer of developing retinal cells due to mutation of both copies of ____________.

A

RB1 tumor suppressor gene

encodes a nuclear protein that is involved in the regulation of the cell cycle

123
Q

p53 protein is usually kept in check by ____, which inhibits the activity of p53 via negative feedback.
(p53 transcriptionally upregulates this protein.)

A

MDM2

124
Q

The ___ gene is an important tumor suppressor gene implicated in colorectal carcinoma.

A

APC

125
Q

APC participates in the ___ signalling pathway, helping to regulate the activity of ______, thereby preventing uncontrolled growth.

A

WNT; B-catenin

(recall: gene product of APC will degrade B-catenin in the cytoplasm, preventing it from forming Tcf/Lef-1 complex which will upregulate transcription of cell cycle genes.)

126
Q

In colorectal cancer, at least three ________ genes and one ______ gene must be mutated for an epithelial cell to become metastatic.

A

3 tumor suppressor genes and 1 proto-oncogene

  1. APC gene
  2. K-ras gene
  3. DCC gene
  4. p53 gene
127
Q

Mutations may be inherited for (tumor suppressor/onco) genes.

A

tumor suppressor

Foundations of Medicine (21 decks)

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