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Cancer Biology > Exam 2 > Flashcards

Exam 2 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Most of these are proteins

A

Secondary messengers

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2
Q

Proteins on the cell membrane that receive signals and transduce it to the inside of the cell

A

Receptors

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3
Q

This is what controls the relative numbers and positions of each cell types which is necessary to create normal tissue structure and function. This is done between the same cell types and different cell types.

A

Cell signaling

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4
Q

All the decisions made by an individual cell must represent some sort of decision that is shared between the cells that resides in its neighborhood

A

Consensus

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5
Q

This is what Src proteins are and they work in signaling programming and can transform cells

A

Tyrosine kinase

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6
Q

EGF R and this consists of 3 functional domains in which part of the cytoplasmic domain shows homology with src

A

Epidermal growth factor receptor

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7
Q

621 AA domain of EGF R and where the ligands bind

A

Ectodomain

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8
Q

23 AA domain of EGF R and where the ligand binds

A

Transmembrane domain

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9
Q

542 AA domain of EGF R and is where the src region of homology is

A

Cytoplasmic domain

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10
Q

This is another receptor type with 3 functional domains; EGF receptor, tyrosine kinase domain (intracellular), and cysteine rich domain (extracellular).

A

Tyrosine kinase receptor

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11
Q

This is formed on the EGF R following ligand addition

A

Phosphotyrosine

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12
Q

This can occur when tyrosine kinase receptors dimerize and bind to an EGF molecule which will phosphorylate itself.

A

Transphosphorylation

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13
Q

The two critical changes of tyrosine kinase receptors following ligand binding

A

Dimerization and phosphorylation

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14
Q

Deletion of the ectodomain of EGF R results in this happening to the receptor

A

Activation

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15
Q

An oncoprotein in avian erythroblastosis virus

A

V ErbB

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16
Q

Some cancer cells will have deregulation of receptor firing that comes from receptor mutation/over-expression and this phenomenon

A

Ligand independent firing

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17
Q

These are what can generate ligand independent firing.

A

Mutation or overexpression

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18
Q

This causes constitutively dimerized receptors with a fusion protein and dimerization

A

Gene fusion

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19
Q

These normally do not produce their own ligands and exhibit paracrine signaling, Ex: a mesenchymal cell will produce the ligand for an epithelial cell receptor

A

Normal cells

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20
Q

What many cancer cells do and it is a form of signaling in which a cell manufactures its own mitogens. Ex: a cell has activation of a GF gene, secretes a ligand that binds to a receptor on the same cell.

A

Autocrine signaling

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21
Q

This carries an oncogene (v sis) which is similar to PDGF (growth factor) which means that this virus can produce an autocrine signaling growth factor

A

Simian sarcoma virus

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22
Q

The two major structures of a tyrosine kinase receptor.

A

EGF R and PDGF R

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23
Q

The number of different proteins with EGF R and PDGF R structures in the human genome

A

59

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24
Q

This is caused by abnormal dimerization of RTKs (tyrosine kinase receptors) which can occur via over-expression, mutation, truncation, and fusion of RTKs to other proteins.

A

Deregulated activation

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25
Q

Ordered sequences of biochemical reactions inside the cell with high specificity and speed. Mostly consists of proteins.

A

Signaling cascades

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26
Q

This encodes a homolog of the FGF R gene in fruit fly ommatidia

A

Sevenless gene

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27
Q

This is an upstream stimulator of Ras which functions downstream of the seven less gene.

A

Son of Sevenless (Sos)

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28
Q

This is a GEF (guanine nucleotide exchange factors). Turns GDP to GTP

A

Sos in fly

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29
Q

Tyrosine kinase receptor to Grb2 to Sos to Ras or to Shc before Grb2. Middle proteins are mainly connector proteins.

A

Signaling cascade of Ras

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30
Q

RTKs affect the physical location downstream components without necessarily changing their intrinsic activity

A

Localization model

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31
Q

RTKs

A

Tyrosine kinase receptors

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32
Q

This contains the SH1, SH2, and SH3 domains

A

Src protein

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33
Q

This is the catalytic domain of Src (kinase domain)

A

SH1 domain

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34
Q

This is the domain that binds to pY containing peptide. Composed of 100 amino acid residues and assembled from a pair of anti parallel beta pleated sheets surrounded by a pair of alpha helices

A

SH2 domain

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35
Q

This is the domain that binds to the proline rich sequence of the peptide

A

SH3 domain

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36
Q

This is what the SH2 domain works like since it recognizes both a phosphotyrosine and the side chain of amino acids (3 to 6 AA) that flank this phosphotyrosine on its C terminal side. The amino acid sequence determines the specificity for the substrates.

A

Modular plug

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37
Q

The number of distinct SH2 groups in the human genome

A

120

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38
Q

Bridging proteins that create intermolecular links in activating Ras

A

Grb2 and Shc

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39
Q

the type of protein that Ras is and is located on the inner membrane surface, active when bound to GTP

A

G protein

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40
Q

Guanine nucleotide exchange factor, converts Ras into its active form by replacing GDP with GTP

A

GEF

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41
Q

Ras intrinsic activity that hydrolyzes GTP to GDP

A

GTPase

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42
Q

GTPase activating protein that inactivates RAS by hydrolyzing GTP. An oncogenic mutation can inactivate this which leaves RAS continuously active

A

GAP

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43
Q

This interacts with at least three of the downstream effectors of Ras

A

Effector loop

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44
Q

MAPK, a downstream pathway of Ras.

A

Mitogen activated protein kinase pathway

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45
Q

MAPK pathway, PI3K pathway, and Real GEFs pathway

A

Ras downstream pathways

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46
Q

This is attracted from the cytosol by Ras and binds to Ras which causes a conformational change and activation of MEK

A

Raf

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47
Q

With the Raf conformational change, this phosphorylates both Try and Ser/Thr kinase which activates Erk

A

MEK

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48
Q

Extracellular signal regulated kinases that phosphorylate and activate transcription factors and other proteins

A

Erk 1 and 2

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49
Q

This can lead to certain cancers phenotypes like loss of contact inhibition, anchorage independence etc and can contribute to some cancers

A

MAPK deregulation

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50
Q

Phosphatidylinositol 3 kinase that synthesizes phosphatidylinositol triphosphate (PIP3) which attracts Akt/PKB and Rho GEFS.

A

PI3 pathway

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51
Q

Bad inhibition of apoptosis, mTOR stimulation of protein synthesis, and GSK 3B stimulation of cell proliferation

A

Result of PI3 pathway

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52
Q

This is activated by Ras and can convert PIP2 to PIP3

A

PI3K

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53
Q

These are located in a small minority of the head groups in the phospholipid bilayer

A

Inositol sugars

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54
Q

This is composed of two fatty acids with a long hydrocarbon tail, a glycerol, and a phosphate with an inositol

A

Phosphatidylinositol

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55
Q

These are tethered to plasma membrane

A

PI, PIP2, and PIP3

56
Q

This cleaves PIP2 to yield diacylglycerol which activates protein kinase C (PKC)

A

Phospholipase C

57
Q

This attracts and activates Akt/PKB and Rho GEFs by serving as a docking site for these three molecules in which once they are bound they are phosphorylated and activated

A

PIP3

58
Q

This can inhibit apoptosis, stimulate cell division, and promote cell growth

A

Akt/PKB

59
Q

This along with PI3K control the formation of PIP3

A

PTEN

60
Q

The anti growth genes which are just as important as oncogenes

A

Turmor suppressor gene

61
Q

1 in 20,000 children are diagnosed with this from birth to 8 years old

A

Retinoblastoma

62
Q

This affects only a single eye, the sporadic form, less diagnosed, this requires two hits for tumor formation

A

Unilateral retinoblastomas

63
Q

This affects both eyes, the familial form. This is more common to form a tumor. This requires one hit for tumor formation since there is one copy already inactivated by mutation

A

Bilateral retinoblastomas

64
Q

Recombination that occurs during cell proliferation, this occurs more frequently than sporadic mutation in which a mutant allele can get on two chromatids, can lead to loss of heterozygosity

A

Mitotic recombination

65
Q

Aka allelic deletion, a genetic alteration that converts a chromosome region from heterozygous to homozygous. Two chromosomes with a mutation or two chromosomes without a mutation. This happens the most frequent in cancer growth

A

Loss of heterozygosity

66
Q

Happens more frequent than mitotic recombination and this is when a DNA polymerase will jump to a homologous chromosome during replication the jump back to the main template strand.

A

Gene conversion

67
Q

This leads to a loss of a chromosome which can also cause a loss of heterozygosity

A

Chromosomal nondisjunction

68
Q

This is what usually causes the first mutation and then loss of heterozygosity can amplify it

A

Sporadic mutation

69
Q

There is a deletion of the 2nd and 4th bands of the 1st region in this chromosome in a retinoblastoma patient

A

Chromosome 13

70
Q

There are mutations in this gene in retinoblastomas which plays an important role in cell division by being the molecular governor of the R point transition in cell cycling

A

Rb gene

71
Q

This is what an unphosphorylated Rb binds to which prevents this from activating the transcription of genes coding for proteins required for DNA replication in S phase

A

E2F

72
Q

This phosphorylates the Rb protein in cells stimulated by growth factors which prevents Rb to bind to E2F

A

CDK cyclin

73
Q

Covalent attachment of a methyl group to a cytosine base which is an important mechanism to shut down genes. This is heritable and reversible and when this occurs in the vicinity of a gene promoter the expression of the gene can be repressed

A

DNA methylation

74
Q

Methylation is found only when cytosines are located in a position that is 5’ to guanosine

A

MeCpG

75
Q

An important mechanism in deactivating tumor suppressor genes in tumors. Over half of the tumor suppressor genes that are involved in familial cancer syndromes are silenced by this.

A

Promoter methylation

76
Q

The study of heritable changes in gene function that occur without a change in the DNA sequence

A

Epigenetics

77
Q

These work together to shut down suppressor genes, one copy can be hit with the first and the second can be lost by the other.

A

DNA methylation and loss of heterozygosity

78
Q

Form of colon cancer that is hereditary and it consists of the colon carpeted with hundreds of small polyps

A

Familial adenomatous polyposis

79
Q

The pathway that controls colon cancer formation as well as other type of cancer formations by contributing to cell proliferation

A

Wnt B catenin

80
Q

Bind of this substrate to the frizzled receptors causes inhibition of GSK 3B via disheveled and axon binding which prevents phosphorylation and degradation of B catenin. This leads to B catenin being present and promoting cell proliferation.

A

Wnt

81
Q

In this condition, glycogen synthase kinase 3B (GSK 3B) phosphorylates B catenin which leads to the degradation of B catenin and cell proliferation halting.

A

Absence of Wnt

82
Q

This associates with TF Tcf/Lef in the nucleus and drives cell proliferation

A

B catenin

83
Q

The epithelial projections in the colon where colonic polyps form.

A

Villus

84
Q

This can also lead to proliferation and colon cancer as it also works with B catenin

A

Apc mutation

85
Q

The stem cells receive the Wnt signal from the stroma, B catenin interacts with Tcf/lef to promote stem cell proliferation, as stem cells move up the villus stimulation by Wnts decreases which leads to increased degradation of B catenin and cells enter apoptosis after 3 or 4 days.

A

Normal colon cell

86
Q

Apc protein defects and B catenin levels remain high even in the absence of a Wnt signal, cells will stop migrating upward and accumulate within crypts to generate an adenomatous polyp.

A

Tumor colon cells

87
Q

This contains multiple protein binding domains and the gene encoding this protein is frequently mutated which can lead to tumor growth. Key function is to bind to B catenin and down regulate its function in promoting proliferation

A

Apc protein

88
Q

Gatekeepers and caretakers

A

Anti growth genes

89
Q

Genes that directly control the biology of cells by affecting how they proliferate, differentiate, or die. Ex: tumor suppressor genes

A

Gatekeepers

90
Q

Genes that control the biology of cells through maintenance of cellular genomes

A

Caretakers

91
Q

How cells communicate with their surroundings

A

ErbB signaling network

92
Q

The central governor of growth and proliferation located in the nucleus. Can send cells to G0 or the active cell cycle in which it can program the cell cycle phases. It is a network of interacting proteins that receives signals from various sources and integrates them to decide the cell’s fate

A

Cell cycle clock

93
Q

4 Phases of mitosis; prophase, metaphase, anaphase, and telophase. And 3 phases of interphase; G1, S and G2

A

Mammalian cell cycle

94
Q

During this stage DNA is not visible with a light microscope

A

Interphase

95
Q

Control mechanisms that ensure the fidelity of cell division in eukaryotic cells. These are essentially quality control systems. If requisites are met, cells are allowed to advance to the next phase.

A

Checkpoints

96
Q

If genome is damaged after G1 entrance into S is blocked

A

G1, S checkpoint

97
Q

DNA replication is stopped if genome is damaged

A

S checkpoint

98
Q

Entrance into M is blocked if replication is not completed

A

G2, M checkpoint

99
Q

Cell does not go into anaphase if the chromatids are not properly assembled on the mitotic spindle

A

Metaphase checkpoint

100
Q

The point in time when the cell must make the commitment to advance through the reminder of the cell cycle through the M phase, remain in G1, or retreat into G0. This is close to the end of G1.

A

Restriction point

101
Q

This is the period during which cells are responsive to mitogenic GFs and to TGF B

A

G1 phase

102
Q

The regulatory subunits of the heterodimeric protein kinases that control cell cycle events

A

Cyclin

103
Q

Aka CDKs, and are a group of serine/threonine kinases that are involved in the regulation of the cell cycle. The association of cyclins with these activates them.

A

Cyclin dependent kinases

104
Q

These make up the engine of the cell cycle clock. The association increases the catalytic activity 400,00 fold.

A

Cyclin CDK complexes.

105
Q

The four types of cyclin

A

A, B, D, E

106
Q

The three types of cyclin dependent kinases

A

CDK 4/6, CDK2, and CDC2

107
Q

This pairs with cyclins A and B

A

CDC2

108
Q

This pairs with cyclins A and E

A

CDK2

109
Q

This pairs with cyclin D

A

CDK 4/6

110
Q

The cell cycle progression depends on the changes in this during the phases of the cell cycle

A

Level and availability of cyclin

111
Q

This is relatively stable through the cell cycle

A

CDK level

112
Q

During this cyclin B is high

A

Mitosis

113
Q

During this nuclear D1 is high

A

G1

114
Q

During this cyclin E is high and nuclear D1 drops

A

Beginning of S

115
Q

During this cyclin A is high while cyclin E drops

A

End of S

116
Q

Cyclin B rises during this through mitosis

A

G2

117
Q

These strongly influence the levels of D type Cyclins

A

Mitogenic growth factors

118
Q

These serve to convey signals from extracellular environment to the cell cycle clock in the nucleus during G1. Levels of this are influenced by extracellular signals, these can be growth factor signals, Wnts, cytokine, hedgehog, or other various ligands

A

D type cyclins

119
Q

Where the cell cycle can be influenced the extracellular signals

A

80 to 90 percent of G1

120
Q

During this, the cyclin cdk complexes in one phase of the cycle are responsible for activating those in the subsequent phase and for shutting down those that were active in the previous phase.

A

After R point

121
Q

These are a group of proteins that affect the activities of cyclin CDK complexes

A

CDK inhibitors

122
Q

4 INK4s that affect only CDK4/6 and three others that affect CDK2 and CDC2

A

Types of CDKIs

123
Q

p16, p15, p18, and p19

A

4 INK4s

124
Q

p57(kip2), p27(kip1), and p21(cip2)

A

The three others

125
Q

This can strongly increase the expression of p15 INK4B, and slightly increase expression of p21(cip1)

A

The three others

126
Q

This can strongly increase the expression of p15 INK4B, and slightly increase expression of p21(Cip1)

A

TGF B

127
Q

This causes rapid increases in p21(Cip1)

A

DNA damage

128
Q

The molecular governor of the R point transition. Contains 14 amino acids that can be phosphorylated. Dephosphorylation occurs at M by PP1 and through G1 it becomes phosphorylated unless it enters G0 which means it is not phosphorylated at the R point it is hyperphosphorylated.

A

pRb

129
Q

These control the restriction point transition

A

Mitogens

130
Q

At this point levels of cyclin E increased dramatically

A

R point

131
Q

These complexes drive pRb hyperphosphorylation

A

E CDK 2

132
Q

This is the inactive form

A

Hyperphosphorylation

133
Q

When this binds to E2Fa it blocks their transcription activating domain. After hyperphosphorylation this will release E2Fs and allow them to work as transcription factors. As a cell enters into S phase the E2Fs are inactivated/degraded

A

pRb

134
Q

This is what a phosphorylated pRb will bind to to repress transcription

A

Histone deacetylase

135
Q

Control of this perturbed in most, if not all, human cancers.

A

pRb

136
Q

The binding of E2Fs by pRb is prevented by some of these. Examples include Adenovirus E1A, SV40 large T, and human papilomavirus E7.

A

DNA tumor virus oncoproteins

137
Q

Low expression of this has been linked to increased survival of breast cancer.

A

Cyclin E

Cancer Biology (2 decks)

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