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INTRGEN > MOD 9: Cancer & Genetics > Flashcards

MOD 9: Cancer & Genetics Flashcards

1
Q

Where are variations observed in the regulation of the cell cycle?

A
  1. Overall length of the cell cycle
  2. Relative length of time spent in the various phases
  3. How closely mitosis and cytokinesis are coupled
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2
Q

This protein kinase plays a role in the signaling network that controls cell size and coordinates with cell cycle progression

A

Target of rapamycin (TOR)

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3
Q

What processes do the target of rapamycin (TOR) promote?

A
  1. Translation
  2. Ribosome biosynthesis
  3. Stability of high affinity amino acid permeases
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4
Q

What processes do the target of rapamycin (TOR) inhibit?

A
  1. Autophagy
  2. Starvation-induced gene transcription
  3. Stability of general amino acid permeases
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5
Q

What conditions must the control of the cell cycle consider?

A
  1. Ensure that events of each phase are carried out in the correct order + at the appropriate time
  2. Ensure that each phase is completed before the next one begins
  3. Respond to external conditions
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6
Q

What factors influence the restriction point (start)?

A
  1. Growth factors
  2. Nutrients
  3. Cell size
  4. DNA damage
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7
Q

What factors influence the G2-M transition point?

A
  1. Cell size
  2. DNA damage
  3. DNA replication
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8
Q

What factor influences the metaphase-anaphase transition point?

A

Chromosome attachments to spindle

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9
Q

Where does the first control point occur?

A

In the late G1: G1 —> S progression

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10
Q

The G1 —> S progression point is called __________ in yeast and __________ in animal cells

A

Start; restriction point

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11
Q

Cells that successfully pass the restriction point are committed to what phase?

A

The S phase

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12
Q

At what transition point is the restriction point observed?

A

G2-M transition

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13
Q

At what transition point is the commitment made to enter mitosis?

A

G2-M transition

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14
Q

This transition point ensures that the DNA replicated is correct

A

G2-M transition point

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15
Q

In most cells, the G1 arrest is the more prevalent type of control. What type of cells consider the G2 arrest to be more important?

A

Frog eggs

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16
Q

At what transition point is the commitment made to move the two sets of chromosomes into the new cells?

A

Metaphase-anaphase transition

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17
Q

What will happen to the cell if a problem occurs in the third transition point — metaphase-anaphase transition?

A

The cells may stay in that state or result to apoptosis

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18
Q

In MEIOSIS, errors in the metaphase-anaphase transition may result to two possible conditions. What are they?

A
  1. Nondisjunction
  2. Aneuploidy
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19
Q

This condition occurs when there are errors in the metaphase-anaphase transition phase in MEIOSIS:

Spindle fibers do not allow sister chromatids to properly segregate

A

Nondisjunction

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20
Q

This condition occurs when there are errors in the metaphase-anaphase transition phase in MEIOSIS:

Different levels of ploidy in the receiving cells

A

Aneuploidy

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21
Q

TRUE OR FALSE: Mutations in genes directly lead to cancer

A

FALSE; It does not

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22
Q

Is cancer caused by a single gene or an accumulation of genes?

A

Cancer is caused by an accumulation of different mutations

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23
Q

What are the three classes of genes that are frequently mutated in cancer?

A
  1. Proto-oncogenes
  2. Tumor suppressor genes
  3. Mutator genes
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24
Q

These are genes that behave normally and have their own function

A

Proto-oncogenes

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25
Q

When these genes are affected by cancer-causing agents, they are the ones that will lead to oncogene

A

Proto-oncogenes

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26
Q

These are genes that may acquire dangerous functions and lead to unregulated cell division

A

Proto-oncogenes

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27
Q

What cellular oncogene is responsible for signaling tyrosine kinase?

A

abl

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28
Q

What cellular oncogene is responsible for receptor tyrosine kinase?

A

erb B-2 (her/neu)

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29
Q

What cellular oncogene is responsible for G protein?

A

ras

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30
Q

What cellular oncogene is responsible for transcription factor?

A

myc

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31
Q

What cellular oncogene is responsible for transcription regulator?

A

jun/fos

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32
Q

What cellular oncogene is responsible for signaling tyrosine kinase?

A

src

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33
Q

What cellular oncogene is responsible for signaling lipid kinase?

A

pi3k

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34
Q

What cellular oncogene potentially leads to chronic myelogenous leukemia?

A

abl

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35
Q

What cellular oncogene potentially leads to carcinoma of breast and ovary; neuroblastoma?

A

erb B-2 (her/neu)

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36
Q

What cellular oncogene potentially leads to carcinoma of colon, lung, and thyroid; melanoma?

A

ras

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37
Q

What cellular oncogene potentially leads to Burkitt’s lymphoma; carcinoma of breast and ovary

A

myc

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38
Q

What cellular oncogene potentially leads to carcinoma of breast and lung?

A

jun/fos

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39
Q

What two cellular oncogenes potentially lead to carcinoma of colon?

A

src and pi3k

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40
Q

What process is prevalent in kinases and can either disrupt, kill, or inactivate a protein?

A

Phosphorylation

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41
Q

What are the genes of interest for colorectal carcinoma?

A
  1. KRAS
  2. BRAF
  3. NRAS
  4. PIK3CA
  5. TP53
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42
Q

What are the genes of interest for breast carcinoma?

A
  1. PIK3CA
  2. TP53
  3. BRAF
  4. PTEN
  5. PTEN LOH by micro-satellite analysis
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43
Q

What are the genes of interest for prostate carcinoma?

A
  1. PTEN
  2. BRAF
  3. TMPRSS2-ERG fusion by FISH
  4. PTEN LOH by micro-satellite analysis
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44
Q

What are the genes of interest for lung carcinoma?

A
  1. EGFR
  2. KRAS
  3. BRAF
  4. ALK rearrangement by FISH
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45
Q

What are the genes of interest for ovarian carcinoma?

A
  1. TP53
  2. PTEN
  3. PIK3CA
  4. BRAF
  5. PTEN LOH by micro-satellite analysis
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46
Q

What are the genes of interest for malignant melanoma?

A
  1. BRAF
  2. KIT
  3. NRAS
  4. PIK3CA
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47
Q

TRUE OR FALSE: Only one gene is involved in order to lead to a particular type of cancer.

A

FALSE; There are many genes involved leading to a particular type of cancer

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48
Q

These are genes that help regulate the growth and division of cells

A

Tumor suppressor genes

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49
Q

These genes ensure that cells do not proliferate uncontrollably and act like a preventive measure

A

Tumor suppressor genes

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50
Q

These are genes that increase the mutation rate of other genes within the gene

A

Mutator genes

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51
Q

When these are altered/defective, they lead to an increase in mutation frequency of the DNA

A

Mutator genes

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52
Q

These monitor the DNA for damage and halt the cell cycle at various points

A

DNA damage checkpoints

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53
Q

How do DNA damage checkpoints halt the cell cycle at various points?

A

By inhibiting different Cdk-cyclin complexes

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54
Q

This is referred to as the guardian of the genome and it plays a central role in these checkpoint pathways

A

p53 protein

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55
Q

This gene is known to be mutated in many cancers

A

P53 gene

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56
Q

What are the 5 brief steps in how p53 works?

A
  1. Cellular stress recognition
  2. Activation of p53
  3. Cell cycle regulation
  4. DNA repair
  5. Apoptosis induction
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57
Q

What activates the p53 gene?

A

Stress, such as DNA damage or hypoxia

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58
Q

What factors trigger the stress that activates the p53 gene?

A

Radiation, chemicals, or DNA replication errors

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59
Q

Once the p53 gene is activated, it acts as a __________, meaning it regulates the expression of specific genes

A

Transcription factor

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60
Q

The p53 gene helps to prevent the damaged cell from dividing by inducing a temporary cell cycle arrest at what phase?

A

Usually at the G1 phase

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61
Q

What is a key protein that is a p53 unregulated modulator of apoptosis?

A

Puma

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62
Q

Puma inactivates __________, an apoptosis inhibitor

A

Bcl-2

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63
Q

What occurs when Bcl-2 is activated?

A

Phosphorylation

64
Q

What occurs when Bcl-2 is deactivated?

A

Cell cycle arrest or apoptosis

65
Q

Who was the first to demonstrate that cancer can be caused by a virus?

A

Peyton Rous (1911)

66
Q

This is the cancer of the connective tissue

67
Q

What was shown to be caused by the Epstein-Barr virus?

A

Burkitt’s lymphoma

68
Q

This virus was not just inherited and can be caused by an enzyme

A

Epstein-Barr virus (EBV)

69
Q

What are the symptoms of Burkitt’s Lymphoma?

A
  1. Abdominal swelling
  2. Distortion of facial bones
  3. Night sweats
  4. Intestinal obstruction
  5. Enlarged thyroid and tonsils
70
Q

What type of cancer does Hepatitis B and C lead to?

A

Liver cancers

71
Q

What type of cancer does Human T-cell Lymphotropic Virus-1 (HTLV-1) lead to?

A

Adult T-cell leukemia

72
Q

What type of cancer does Human papillomavirus (HPV) lead to?

A

Uterine and cervical cancers

73
Q

What oncogenic infectious agent may cause stomach cancer?

A

Bacterium Heliobacter pylori (H. pylori)

74
Q

This antibiotic is associated with stomach ulcers, helping to prevent stomach cancer

75
Q

What oncogenic infectious agent causes bladder and bile duct cancer?

A

Flatworm infections

76
Q

What are the two main classes of DNA mutations?

A

Oncogenes and tumor supressor genes

77
Q

What are the two main classes of DNA mutations?

A

Oncogenes and tumor supressor genes

78
Q

This is referred to as the gene whose presence can trigger cancer

79
Q

What was the first oncogene discovered?

A

Rous sarcoma virus

80
Q

Viruses with defects in the _________ can infect cells but don’t cause cancer

81
Q

This is the uptake of foreign DNA into cells and incorporation into chromosomes

A

Transfection

82
Q

__________ are not sufficient to cancer

A

Single oncogenes

83
Q

__________ are not sufficient to cancer

A

Single oncogenes

84
Q

__________ are converted into oncogenes by several distinct mechanisms

A

Proto-oncogenes

85
Q

When proto-oncogenes’ structure or activity is disrupted by mutation, the mutant form of the gene can cause cancer:

A
  1. Point mutations
  2. Gene amplification
  3. Chromosome translocation
  4. Local DNA rearrangements
  5. Insertional mutagenesis
86
Q

This is the simplest mechanism that converts a proto-oncogene into an oncogene

A

Point mutation

87
Q

This increases the number of proto-oncogene copies, causing the protein product to be produced in-excess

A

Gene amplification

88
Q

This gene encodes growth factor receptors and encodes for the receptor tyrosine-protein kinase erbB-2 and will lead to cancer

A

ERBB2 gene

89
Q

In this process, a part of one chromosome is joined to another chromosome

A

Chromosome translocation

90
Q

What are the chromosomes involved in Burkitt’s lymphoma?

A

Chromosomes 8 and 14

91
Q

Protein formation leads to the expression of the __________

A

Myc protein

92
Q

This is a transcription factor that has target genes which are involved in self-proliferation

A

Myc protein

93
Q

This is a translocation chromosome that involves chromosomes 9 and 22

A

Philadelphia chromosome

94
Q

What are the two chromosomes involved in philadelphia chromosome?

A

Chromosomes 9 and 22

95
Q

This refers to proliferation control failure in blood

A

Chronic myelogenous leukemia (CML)

96
Q

Translocation creates an oncogene called __________

97
Q

Local rearrangements alter base sequences of __________.

A

Proto-oncogenes

98
Q

How are proto-oncogenes’ base sequences altered through local rearrangements?

A
  1. Deletions
  2. Insertions
  3. Ineversions
  4. Transpositions
99
Q

What is the resulting gene that fuses the tyrosine kinase part of the receptor (NTRK1) to a region of the tropomyosin molecule?

A

TRK oncogene

100
Q

TRUE OR FALSE: Retroviruses can sometimes cause cancer by integrating their own genes into a host chromosome in a region where a proto-oncogene is located.

101
Q

What do you call the phenomenon in which the proto-oncogene is converted into an oncogene by causing it to be overexpressed?

A

Insertional mutagenesis

102
Q

TRUE OR FALSE: The loss or inactivation of tumor suppressor does not lead to cancer.

A

FALSE: It may lead to cancer

103
Q

YES OR NO: Is it possible to fuse cells?

104
Q

YES OR NO: Is it possible to fuse cells?

105
Q

How many copies of the tumor suppressor gene is mutated in hereditary cancers?

A

Only one copy

106
Q

If the parent gametes are not mutated, when will the hereditary cancer appear?

A

Only after cell division

107
Q

This is referred to as a rare hereditary eye cancer that develops in young children.

A

Heretidary retinoblastoma

108
Q

Children with hereditary retinoblastoma inherit a deletion in what part of the chromosome?

A

Chromosome 13

109
Q

TRUE OR FALSE: A deletion in chromosome 13 immediately leads to cancer.

A

FALSE: A deletion alone does not cause cancer

110
Q

What phase progression does the Rb protein control?

A

The G1 to S phase progression

111
Q

TRUE OR FALSE: Mutations in the Rb gene are only detected in hereditary cancers.

A

FALSE: They are also detected in nonhereditary cancers

112
Q

This is referred to as one of the most important tumor suppressor genes in humans.

A

p53 gene (TP53 in humans)

113
Q

What happens when p53 is inactivated?

A

Apoptosis, allowing defective cells to divide continuously

114
Q

This is referred to as an inherited condition caused by a defective copy of the p53 gene.

A

Li-Fraumeni syndrome

115
Q

This syndrome is characterized by the development of various types of cancers by early adulthood.

A

Li-Fraumeni syndrome

116
Q

The Li-Fraumeni syndrome is caused by mutations in what copy of the p53 gene?

A

The second copy of the p53 gene

117
Q

This refers to the fact that mutation rates in cancer cells are thousands of times higher than normal

A

Genetic instability

118
Q

Most hereditary forms of breast cancer arise in women who inherit a mutant copy of either __________ or __________

A

BRCA1 or BRCA2 (breast cancer gene 1 and 2)

119
Q

BRCA1 has a mutation in what chromosome number?

A

Chromosome 17

120
Q

BRCA2 has a mutation in what chromosome number?

A

Chromosome 13

121
Q

Both of these genes code for proteins involved in repair of double-strand DNA breaks

A

BRCA1 and BRCA2

122
Q

Both of these genes code for proteins involved in repair of double-strand DNA breaks

A

BRCA1 and BRCA2

123
Q

Breast and ovarian cells with these mutations exhibit chromosomal __________

A

Rearrangements

124
Q

Women inheriting BRCA mutations exhibit a __________ lifetime risk for breast cancer and a __________ risk for ovarian cancer

A

40-80%; 15-65%

125
Q

Genetic instability can be traced to mutations in __________

A

DNA repair genes

126
Q

What pathway is defective in most cancer cells? This removes an important protective mechanism against genetic instability

A

p53 pathway

127
Q

At which checkpoint can defects be found in cancer cells?

A

Mitotic spindle checkpoint

128
Q

Loss of the mitotic spindle checkpoint due to mutations in the genes that regulate it can lead to __________

A

Chromosome mis-segregation

129
Q

What are the genes and proteins involved in the mitotic spindle checkpoint?

A

Mad and Bub

130
Q

These genes and proteins are involved in making sure that the spindle fibers are attached to the centromeres

A

Mad and Bub

131
Q

The loss of these genes directly opens gates to excessive proliferation and formation of tumors

A

Gatekeepers

132
Q

What are examples of gatekeepers?

A

Tumor suppressor genes, such as APC, RB, and p53 genes

133
Q

These are genes involved in DNA repair and chromosome sorting because they maintain genetic stability. They are not, however, directly involved in controlling proliferation.

A

Caretakers

134
Q

What will happen if the caretaker cannot repair, but the gatekeeper does not let it proceed?

A

Nothing…

135
Q

Enumerate the 7 examples of gatekeeper genes.

A
  1. APC
  2. CDKN2A
  3. PTEN
  4. RB
  5. SMAD4
  6. TGFB receptor
  7. p53
136
Q

Enumerate examples of caretaker genes.

A
  1. BRCA1, BRCA2
  2. MSH2, MSH3, MSH4, MSH5, MSH6, PMS1, PMS2, MLH1
  3. XPA, XPB, XPC, XPD, XPE, XPF, XPG
  4. XPV (POLn)
137
Q

This tumor suppressor gene affects the Wnt signaling pathway. Is it a gatekeeper or caretaker?

A

APC gene; gatekeeper

138
Q

This tumor suppressor gene affects the Rb and p53 signaling pathways. Is it a gatekeeper or caretaker?

A

CDKN2A gene; gatekeeper

139
Q

This tumor suppressor gene affects the PI3K-Akt signaling pathway. Is it a gatekeeper or caretaker?

A

PTEN gene; gatekeeper

140
Q

This tumor suppressor gene affects the restriction point control pathway. Is it a gatekeeper or caretaker?

A

RB gene; gatekeeper

141
Q

These tumor suppressor genes affect the TGFB-Smad signal pathway. Are they gatekeepers or caretakers?

A

SMAD4 gene and TGFB receptor gene; gatekeeper

142
Q

This tumor suppressor gene affects the DNA damage response pathway. Is it a gatekeeper or caretaker?

A

p53 gene; gatekeeper

143
Q

What tumor suppressor genes affect DNA double-strand break repair? Are they gatekeeper or caretaker genes?

A

BRCA1 and BRCA2; caretaker

144
Q

What tumor suppressor genes affect DNA mismatch repair? Are they gatekeeper or caretaker genes?

A

MSH2, MSH3, MSH4, MSH5, MSH6, PMS1, PMS2, MLH1; caretaker

145
Q

What tumor suppressor genes affect DNA excision repair? Are they gatekeeper or caretaker genes?

A

XPA, XPB, XPC, XPD, XPE, XPF, XPG; caretaker

146
Q

What tumor suppressor genes affect DNA translesion synthesis? Are they gatekeeper or caretaker genes?

A

XPV (POLn) gene; caretaker

147
Q

What tumor suppressor genes affect DNA translesion synthesis? Are they gatekeeper or caretaker genes?

A

XPV (POLn) gene; caretaker

148
Q

The common mutations in cancers involve the inactivation of __________ genes and the conversion of __________ to __________

A

Tumor suppressor genes; proto-oncogenes; oncogenes

149
Q

What is the most common pattern detected in colon cancer?

A
  1. Active KRAS oncogene
  2. Mutation in tumor suppressor genes APC, SMAD4, and p53
150
Q

In what manner does colon cancer occur?

A

Stepwise manner involving a lot of genes

151
Q

Mutations in KRAS and SMAD4 are seen when __________ grow larger

152
Q

TRUE OR FALSE: Mutations in p53 accompany the development of cancer

153
Q

This pathway is frequently disrupted in colon cancer, inhibiting epithelial cell proliferation

A

TGFB-SMAD Pathway

154
Q

TRUE OR FALSE: Epigenetic changes alter both a gene’s expression and its sequence

A

FALSE; They alter a gene’s expression only, not its sequence

155
Q

What is the function of MLH1 gene-on chromosome 3?

A

DNA mismatch repair

156
Q

What are the 6 hallmarks of carciogenesis?

A
  1. Self-sufficiency in growth signals
  2. Insensitivity to antigrowth signals
  3. Evasion of apoptosis
  4. Limitless replicative potential
  5. Sustained angiogenesis
  6. Tissue invasion and metastasis
157
Q

This is referred to as the formation of blood vessels.

A

Angiogenesis

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