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Biology of Cancer > Unit 1 Exam Ch 1 2 3 > Flashcards

Unit 1 Exam Ch 1 2 3 Flashcards

1
Q

Cancer

A

Group of diseases, characterized by unregulated growth

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2
Q

Germ Layer

A

a group of cells in an embryo that interact with each

other as the embryo develops and contribute to the formation of all organs and tissues

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3
Q

Ten Hallmarks of most cancers

A 
Sustained Proliferation
Evading growth suppressors
Avoiding immune destruction
Activating invasion and metastasis
Inducing angiogenesis
Genome instability and mutation
Resisting Cell death
Deregulating cellular epigenetics
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4
Q

Evading Growth Suppressors

A

Cancer cells do not respond to growth inhibitory signals and acquire mutations that interfere with inhibition

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5
Q

Avoiding immune suppression

A

Successful cancer cells may be those that do not
stimulate an immune response or can interfere with the
immune response so as to avoid immune destruction

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6
Q

Unlimited replicative potential

A

Normal cells replicate for a certain number of generations and become senescent, after shortening of telomeres (Cancer cells’ telomeres aren’t shortening) and have unlimited replicative potential

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7
Q

Tumor-Promoting inflammation

A

• Inflammation is an immune response that can
facilitate the ability of acquiring the core
hallmarks of cancer.
• In addition, inflammatory cells can release
oxygen species that are mutagenic

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8
Q

Invasion and Metastasis

A

Cancer cells invade other tissues and migrate to other parts of the body, causing multi-system cancers

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9
Q

Invasion and Metastasis

A

Cancer cells invade other tissues and migrate to other parts of the body, causing multi-system cancers

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10
Q

Cancer cells induce angiogenesis, growth of new blood vessels, needed for tumor survival. Altering the balance between angiogenic
inducers and inhibitors can activate the
angiogenic switch

A

Sustained Angiogenesis

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11
Q

Evading Apoptosis

A

Normal cells are able to be destroyed via apoptosis

Cancer cells evade those mechanisms to continue unregulated growth.

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12
Q

Genome instability and mutation

A

Faulty DNA pathways contribute to genome instability

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13
Q

Reprogramming energy metabolism

A

Uncontrolled cell division demands increases in
fuel and biosynthetic precursors that is obtained
by adjusting energy metabolism

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14
Q 
Grows in clusters of cells called foci
Do not exhibit contact inhibition
Can grow in low serum media
Round morphology
Exhibit "anchorange independence"
A

Morphology and characteristics of cancer cells

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15
Q

Anchorage independence

A

Cancer cells Lose contact with the media and won’t die

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16
Q

Benign Tumor

A 
No evidence of cancer
Does not metastasize
Some can be life-threatening
well-defined borders
well differentiated
Lost regulation of the cell cycle
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17
Q

Malignant

A 
Not encapsulated
Invades and metastasized
Large, rapid growth
Poorly differentiated
increased nuclear to cytoplasm ratios
Nuclear hyperchromasia and prominent nuclei (stains brightly)
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18
Q

Neoplasia

A

New growth, not reversible

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19
Q

Dysplasia

A

Disordered growth, often resulting in neoplasia

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20
Q

Tumor

A

Abnormal growth, benign or malignant

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21
Q

Cancer

A

Malignant neoplasm or tumor that invades nearby tissue

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22
Q

benign epithelial tissue

A

adenoma, papilloma

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23
Q

beningn mesenchyme tissue

A

Fibroma, Lipoma

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24
Q

Benign Melanocytes

A

Nevus (Mole)

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25
Q

Benign Lymphocytes

A

Benign lymphoid hyperplasia

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26
Q

Malignant epithelial tissue

A

Adenocarcinoma

Papillary carcinoma

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27
Q

Malignant mesenchyme tissue

A

Sarcoma

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28
Q

Malignant Melanocytes

A

Melanoma

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29
Q

Malignant Lymphocytes

A

Lymphoma

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30
Q

Breast Cancer Main site of metastasis

A

Lungs, liver, bones

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31
Q

Colon Cancer Main site of metastasis

A

Liver, peritoneum, lungs

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32
Q

Lung Cancer main site of metastasis

A

Adrenal gland, liver, lungs

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33
Q

Melanoma main site of metastasis

A

Lungs, Skin, muscle, liver

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34
Q

Why are the liver and lungs common sites for metastasis?

A

Blood flows through both organs frequently (Portal vein, lungs)

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35
Q

Why are malignant tumors so life-threatening?

A

Physical obstruction
Invading other organs and compromising their functions
Competing for nutrients, oxygen, and produce waste product

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36
Q

Mutation

A

Alteration of DNA sequence

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37
Q

Carcinogen

A

Agent that causes cancer

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38
Q

Mutagen

A

Agent that causes mutation

*Not all mutations cause cancer

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39
Q

Translolcation

A

DNA mutations whereby a part of one chromosome is transferred to or exahnged for anohter part of a different chromosome

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40
Q

Proliferation

A

Cell division, cell growth

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41
Q

Apoptosis

A

Programmed cell death

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42
Q

Differentiation

A

cells enter an inactive phase of cell growth and can lead to unregulated cell growth

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43
Q

Leukemia

A

Overproduction of white blood cells or their precursors in the blood or bone marrow

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44
Q

Proto-Oncogenes

A

NOrmal genes that can be activated by mutation to be oncogenic
All normall cells have proto-oncogenes

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45
Q

Oncogenes

A

Mutated genes that produce an increased amount of protein products

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46
Q

Characteristics of Oncogenes

A

Cause increased activity and uncontrolled cell division
Always in “on” state
Platelet dereived growth factor (PDGFR)
Glioblastoma, myeloid leukemia
Acts in a dominant manner to initiate tumor formation (one allele is sufficient for the effect)

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47
Q

Tumor Suppressor Genes

A

Code for proteins that have a role in inhibiting borth growth and tumor formation

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48
Q

Tumor Suppressor Genes mode of function

A

Mutation results in a loss of function of genes that control growth

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49
Q

Tumor suppressor genes mode of inheritance (Dominance vs Recessive)

A

Recessive in nature (both must mutate to lose function)

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50
Q

Knudson’s Two-Hit Hypothesis

A

Explains the methods of tumor suppressor genes
States that both alleles must be mutated to trugger carcinogenesis.
Explains certain individuals have an increased risk for cancer
The have inherited a mutated tumor suppressor allele

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51
Q

Haploinsufficiency

A

only one mutated allele can lead to the cancerous phenotype. One allele (normal) produces half the quantity of protein product produced by normal cells, and this is not enough to suppress tumor formation in these cases

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52
Q

Stem Cells

A

Undifferentiated cells that still have the ability to self-renew and produce differentiated progeny

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53
Q

Self-Renewal

A

A stem celll or other progenitor cell gives rise to a new daughter cell with equivalent developmental potential.

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54
Q

Environmental factors contributing to human carcinogenesis

A

UV radiation, toxins, form pyrimidine dimers and cause mutations

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55
Q

Reproductive life influential factors contributing to human carcinogenesis

A

Age of menstruation, and age of reproduction in women, contraception and fertility treatments alter ovulation, HPV, HIV, Kaposi’s Sarcoma, HSV 8

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56
Q

Diet and Exercise influential factors contirbuting to human carcinogenesis

A

Breast cancer can be reduced by 25%, certain diets from certain regions increase certain cancers

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57
Q

Alcohol influential factors contributing to human carcinogenesis

A

Max intake 28g, accounts for 389,000 cases in the U.S per year (Mouth, Esophageal, breast, and Liver cancer)

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58
Q

Smoking influential factors contributing to human carcinogenesis

A

Causes lung, pancreatic, bladder, kindey, mouth, stomach, and liver cancer. Accounts for 40% of all cancer deaths
Lung cancer is the main cancer worldwide

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59
Q

Number of carcinogens found in cigarette smoke

A

81

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60
Q

Additional Influences contributing to human carcinogenesis

A

LIfespan o the cell, free radicals, disorders related to metabolism

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61
Q

Red meat contributes to cancer development

A

Increases lumenal carcinogens through home, micronbial metabolism of protein rescues and barbequeing heterocyclic amines

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62
Q

How does fat contribute to cancer development?

A

Induces hepatic synthesis of bile acids; clonoc microbes covert Ba to 2YBA= Carcinogenic

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63
Q

Fruit and Vegetables’ affect on cancer development

A

Suppresses colon cancer due to antioxidant and antineoplastic properties (Vitamin C, folate), selenium, calcium, and bioactive phytochemical compounds

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64
Q

Rate of Colon cancer for African People

A

Less than 5 per 100,000

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65
Q

Marijuana’s affects on cancer cells

A

THC and other cannabinoids slow grouth and reduce spread of some forms of cancer

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66
Q

Types of Cancer Therapies

A

Cytostatic and cytotoxic

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67
Q

Cytostatic Cancer therapy

A

Halts proliferation

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68
Q

Cytotoxic Cancer Therapy

A

Kills the cancer cells

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69
Q

How to determine what the best drug or treatment is for cancer

A

THe best drug is the one that can be used in the lowert dose with minimal side effects

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70
Q

Therapeutic index

A

Value between the minimum effective dose and maximum tolerated dose
The larger the value, the better the drug
Many Drugs are given at the MTD (Maximum tolerated dose)

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71
Q

easiest method of cancer treatment

A

Surgery
Works for some cancers, not others
Does not address metastasis

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72
Q

Chemotherapy Methods of treatment

A

Target DNA, RNA, and Protein to disrupt the cell cycle

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73
Q

Main aim of chemotherapy treatments

A

Cause DNA Damage and trigger apoptosis

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74
Q

Side effects of Chemotherapy

A

Alopecia, ulcers, anemia

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75
Q

Interventional Studies (Clinical Trial)

A

Research subjects are assigned to a treatment or intervention and their outcomes are measured (Phase 1-4)

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76
Q

Phase I clinical trial

A

Researchers test an experimental drug or treatment in a small group of people (20-80) for the first time. Evaluates safety, dosage, and range. Identifies side effects

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77
Q

Phase II Clinical trial

A

Larger group (100-300), determines if it’s effective and further evaluates safety

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78
Q

Phase III Clinical Trial

A

1,000 to 3,000 participants to confirm effectivness, monitor side effects, compare to commonly used treatments, and collect information for safety

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79
Q

Phase IV clinical Trial

A

Post-marketing studies delineate additional ifo including drug’s risk, benefits, and optimal use

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80
Q

Gene

A

a specific stretch of DNA that programs the amino acid sequence of a polypeptide

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81
Q

4 parts of a gene

A

Promoter
Terminator
Start codon
Stop Codon

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82
Q

Operon

A

Cluster of genes under the control of the same promoter

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83
Q

True or false: Operons only occur in Eukaryotic organisms

A

FALSE:

Operons only occur in prokaryotes

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84
Q

3 Parts of a nucleotide

A

5-Carbon Sugar
Phosphate group
NItrogenous Base

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85
Q

Purines

A

Adenine

Guanine

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86
Q

Pyrimidines

A

Cytosine
Thymine
Uracil

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87
Q

Which is more stable: DNA or RNA?

A

DNA is more stable, which is why RNA organisms are typically viruses and require a host

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88
Q

Mutations can be

A

Environmental or Endogenous processes during metabolism

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89
Q

Causes of mutation

A

Toxins (Asbestos)
Smoking
UV Light
Radiation

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90
Q

Central Dogma

A

DNA to RNA to Protein

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91
Q

Intron

A

Non-COding DNA Sequence, splicing removes them

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92
Q

Exon

A

Coding region of DNA

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93
Q

Spliceosome

A

a large RNA-protein complex that catalyses the removal of introns from nuclear pre-mRNA.

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94
Q

Translation

A

Synthesis of a protein from an MRNA template

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95
Q

Steps of Translation

A

Initiation (3’ Poly A tail added)
Elongation ( add 1 amino acid down the mrna to grow the polypeptide chain
Termination( Add 5’ Methylated cap)

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96
Q

TRNA

A

Anticodon complimentary to the MRNA

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97
Q

AUG

A

Methionine (Universal Start codon)

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98
Q

What makes the MRNA release from the ribosome TRNA complex

A

STOP CODON

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99
Q

polycistronic

A

two (bicistronic/dicistronic), three (tricistronic), or more separate proteins are encoded on a single molecule of messenger RNA (mRNA). In prokaryotes, polycistronic expression is commo

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100
Q

Which region of DNA is involved in regulating the expression of genes?

A

Promotor Region

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101
Q

The promotor region controls

A

When and where a gene is expressed and interacts with proteins that affect the activity of RNA polymerase

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102
Q

TATA Box CODing Sequence

A

TATAAA

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103
Q

TATA BOX (Definition)

A

An important rgulatory element for most genes
Located neae the start site of transcription
Binding of TATA Box Binding Protein (TBP) is important for initiation of transcription

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104
Q

Response element (RE)

A

Short sequence of DNA within the promoter that is recognized by a specific protein and contributes to the regulation of the gene

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105
Q

Response element can either be

A

Enhancer Element (EE) or Inhibitor Element (IE)

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106
Q

Mutations

A

Alterations in DNA Sequence

Base subsititutions can lead to Amino acid change or may be silent

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107
Q

Silent mutation

A

Does not affect Amino Acid Sequence

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108
Q

Missense Mutation

A

Amino Acid changes, polypeptide changes, structure and function of the protein is affected

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109
Q

Nonsense Mutation

A

Inadvertently causing a stop codon to be produced, stops translation early, and the polypeptide is incomplete

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110
Q

STOP CODONS

A

UAA
UAG
UGA
(DO not code for an Amino Acid)

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111
Q

Start codon

A

Methionine

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112
Q

Frameshift mutation

A

Addition or deletion

changes the reading frame and loss in gene functions

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113
Q

Diseases which cause Frameshift mutations

A

HIV
HTLV
They integrate into the genome and shut down functionality

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114
Q

Transitions

A

Substitution of one purine for another purine or

substitution of one pyrimidine for another pyrimidine

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115
Q

Transversions

A

T to A or G (Pyrimidine to Purine)
C to G or A (Pyrimidine to Purine)
A to T or C (Purine to Pyrimidine)
G to C or T (Purine to Pyrimidine)

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116
Q

Translocation

A

Exchange of part of one chromosome with a part of another chromosome

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117
Q

Burkitt’s Lymphoma Translocation

A

8: 14

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118
Q

Acute Myeloblastic Leukemia Translocation

A

8:21

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119
Q

Gene Amplification

A

Similar to translocation, but only at one gene in the same location

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120
Q

Example of gene amplification

A

Elephants have 20 copies of p53 gene, and have only a 5% cancer rate because the cells kill the cancer quickly

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121
Q

Chromothripsis

A

When fragments of single shattered chromosomes are peiced together

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122
Q

Chromothripsis is common in

A

Bone Cnacers

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123
Q

3 Possible reasons for chromothripsis

A

Ionizing radiation that leads to chromosome breaks
Telomere Defunction which may lead to end-end chromosome fusions
Aborted apoptosis such that cells which have initiated DNA Fragmentation push through and survive

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124
Q

DNAse

A

Enzyme that chops up DNA and those pieces could get picked up and annealed together

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125
Q

Consequence of mutation

A

In a gene is determiend by its location with respect tot to functional parts of the genes

126
Q

Mutations in the promotor or regulatory region

A

Can alter regulation and affect levels of gene product, and halt transcription

127
Q

Driver mutations

A

Located in cancer genes by definition

Confer a growth advantage on cells

128
Q

Passenger Mutations

A

Do not confer a growth advantage

are there for the ride

129
Q

Carcinogenic agents

A

Radiation
Chemicals
INfectious Pathogens
Endogenous Reactions

130
Q

2 forms of radiation energy

A

Waves (Electromagnetic radiation)

Stream of atomic Particles ( alpha and beta) particles

131
Q

Electromagnetic spectrum

A 
Radio Waves
Microwaves
Infared
Visible Light
Ultraviolet LIght
X-Rays
Gmamma Rays
132
Q

EM Spectrum that’s considered ionizing radiation

A

UV Light
X-Rays
Gamma Rays
(Can cause Double-Stranded DNA Breaks)

133
Q

LET (Low-Energy Transfer)

A

Rate at which the energy is released

The amount of energy released by a radiation source as it travels a fixed distance

134
Q

High-LET Radiation (Alpha Particles)

A

Emit more energy than Low-LET radiation (X-Rays) over the same distance

135
Q

Radon Gas is considered

A

A Category 1 Carcinogen

136
Q

Category 1 Carcinogens

A

Radon Gas
Asbestos
Tobacco
Mustard Gas

137
Q

Cancers associated with high-dose radiation exposure

A

Leukemia, Breast, Bladder, liver, lung, esophageal, ovarian, multiple myeloma, and stomach cancers

138
Q

Most common Ionizing Radiation Cancer

A

Leukemia

Children are most often affected

139
Q

Risks of solid tumor increase in linear fashion based on

A

an increased dose of radiation

140
Q

Biological effects of Ionizing Radiation

A

Injured cells repair themselves, no residual damage
Cells die, being replaced through normal biological processes (apoptotic processes)
Cells incorrectly repair themselves, resulting in a biophysical change (and pass on the mutation)

141
Q

Dose of 10,000 mSV

A

Single dose, fatal within weeks

142
Q

Dose of 5,000 mSV

A

1/2 killed within a month

143
Q

Dose of 1,000 mSV

A

Radiation sickness, nausea

144
Q

Dose of 100 mSV

A

Radiation workers every 5 years

145
Q

Dose of 16 mSV

A

CT of the heart

146
Q

Dose of 10 mSV

A

CT of the body

147
Q

Dose of 2 mSV

A

Radiation of most people

148
Q

Dose of .01 mSV

A

Dental X-Ray

149
Q

Ionizing Radiation includes

A

Alpha Particles
Beta Particles
Gamma Rays

150
Q

Characteristics of Ionizing Radiation

A

Convert electrically neutral molecules into ions

Cause radiolysis generating intermediates called reactive oxygen species (ROS)

151
Q

ROS

A

May react with DNA or with other biomolecules and cause damage

152
Q

Free radicals

A

considered potent carcinogens because they can cause oxidation of DNA by oxidizing DNA bases

153
Q

Characteristics of Ultraviolet Radiation

A

SHorter wavelength and higher energy than visible light

Affects human health both positively and negatively

154
Q

What protects the Earth from UV Radiation

A

Stratospheric Ozone Layer

155
Q

UV Radiation that passes through the Ozone layer can cause

A

Skin Cancer
Cataracts
Suppression of the immune system
Premature aging

156
Q

Vitamin D and UV Radiation

A

UV Radiation provides Vitamin D, and a deficiency can result in Ricketts

157
Q

Fluorochlorocarbon (CFCs)

A

Gases that break down Ozone layer
Converts O3 to O2
Depletes the ozone layer in the Earth’s Atmosphere

158
Q

UVA Radiation

A

320-400 nm, not absorbed by ozone layer

penetrates deep into the skin and contributes to premature aging along with smoking

159
Q

UVB Radiation

A 
290-320 nm
MOstly absorbed by the ozone layer
Causes C-T Transition
Causes sunburn
Forms pyrimidine dimers
160
Q

UVC Radiation

A

100-290 nm

Completely absorbed by ozone layer and atmosphere

161
Q

The level of UV Radiation reaching the earth depends on

A 
Cloud coverage,
Time of Day/year
Latitde (Equator has more exposure)
Altitude (higher up, more exposure)
Reflection (Water, Sand, and snow reflect UV light)
162
Q

Skin type scale from FDA

A

1-6
1 and 2 burn rapidly
5&6 have darker skin and do not burn as easily

163
Q

Freckles and skin cancer

A

Studies show that people with freckles and moles have an increased skin cancer risk

164
Q

Darker skin tones and skin cancer

A

These patients tend to have more lethal skin cancer because of access to care and health disparities

165
Q

Sunscreen protects by

A

Absorbing and or reflecting UVA and UVB rays

166
Q

SPF (sun protection Factor)

A

Relative amount of sunburn protection that a sunscreen can provide
15+ is recommended, covers at 90%, 30 SPF covers 97%
Broad spectrum (UVA and UVB) Protection is recommended

167
Q

There is no such thing as

A

a healthy suntan

168
Q

In tanning, a person faces

A

UV radiation as strong or stronger than a midday sun

169
Q

People who tan before age 35

A

have a 60% increased risk for melanoma

170
Q

What countries outlawed skin tanning?

A

Brazil 2011

Austrailia 2015

171
Q

Types of Skin Cancer

A

Basal Cell
Squamous Cell
Melanoma

172
Q

UVA Damage

A

Damages via free radical mediated damage

Water is fragmented generating electron-seeking Reactive Oxygen Species that cause DNA Damage and G-> T Transversion

173
Q

UVB Damage

A

Conjugated double bonds in the rings of nitrogenous bases of DNA absorb UV Radiation
Causes Cylobutane pyrimidine dimers )(Formed more frequently)

174
Q

Pyrimidine-Pyrimidine Photoproducts

A

Mimics abasic site (fills in with nothing there)

175
Q

Cyclobutane pyrimidine dimers cause

A

Bends in the DNA helix and DNA polymerase cannot read the DNA Template
DNA Polymerase skips the misshapen parts and causes a frameshift

176
Q

UV Is carcinogenic to skin because

A

It doesn’t penetrate deeper than skin

177
Q

UV Damaged skin is eliminated by

A

apoptosis

familiar to us as peeling after sunburn

178
Q

Mutations in p53 Gene are important in

A

Squamous cell and basal cell carcinoma and provides an important growth advantage

179
Q

Mutations in what gene are found in 66% of Malignant Melanoma (T->A)

180
Q

Mechanisms of Chemical Carcinogens

A

an electrophilic (Electron-Deficient) form reacts with the nucleophile site in purine and pyrimidine rings of nucleic acids

181
Q

How are Chemical carcinogens activated

A

Some act directly on DNA

Others become activated and cancerous via liver processing

182
Q

10 Groups of Carcinogenic Compounds

A
  • Polycyclic aromatic hydrocarbons
  • Aromatic amines
  • Nitrosamines and Nitrosamides
  • Azo dyes
  • Hyrazo and azoxy compounds
  • Carbamates
  • Halogenated compounds
  • Natural products
  • Inorganic carcinogens
  • Miscellaneous compounds (alkylating agents, aldehydes, phenolics)
183
Q

DMBA (7,12-dimethyl benz(a)anthracene)

A

one of the most potent carcinogens

184
Q

Benzo(a)pyrene (BP)

A

well known carcinogen in cigarette smoke

185
Q

CYP1

A

metabolizes BP in BP diol epoxides

• Cause G → T transversions

186
Q

Aromatic Amines are carcinogenic by

A

cooking meat formed from heated amino acids and proteins

187
Q

Nitrosamines and Nitrosamides (Carcinogenic)

A

Found in tobacco

Formed when preservatives nitrites react with amines in fish and meat during smoking

188
Q

Alkylating agents as a carcinogen

A

Are able to form intra-Chain and inter-chain cross-links on the DNA Directly

189
Q

Alkylating agents as a carcinogen (Examples)

A

Melphalan
Methylchorethamine
Chlorambucil
Cytoxan

190
Q

Asbestos

A

A group of fibrous silicate minerals that were extensively used in building materials
They break down macrophages, bring cytokines and hemokines, causing inflammation (Hallmarks of cancer)

191
Q

Erionite

A

A Fibrous zeolite mineral formed from volcanic rock

192
Q

Asbestos is associated with

A

Several lung diseases and associated cancers, mesothelioma

193
Q

Kaposi’s Sarcoma

A

Associated with Herpesvirus (KSHV or HHV8)

194
Q

Hepatiis B and C as a carcinogen

A

Causes Liver cancer

195
Q

Epstein-Barr Virus as a carcinogen

A

Associated with Nasopharyngeal Cancers

196
Q

Human T-cell lymphotropic virus type 1(HTLV-1) as a carcinogen

A

acute T-cell leukemia (ATL)

197
Q

Helicobacter pylori as a carcinogen

A

stomach ulcers and gastric cancers

198
Q

Salmonella enterica (S. ty) as a carcinogen

A

Hepatobilliary and gallbladder carcinoma

199
Q

Endogenous Carcinogenic Reactions

A

Created during cellular metabolism, causing DNA mutations
Errors in DNA Replication
Deamination of Cytosine to Uracil

200
Q

Oxidative respiration and fat metabolism produce _____ that react with DNA and lipids producing oxidized
products (8-oxoguanine)

A

ROS (Reactive OXygen species)

201
Q

Number of nucleotides in the human genome

202
Q

Error Rate of DNA Polymerase

203
Q

5 Types of DNA Repair systems

A
  • One-step repair
  • Nucleotide excision repair (NER)
  • Base excision repair
  • Mismatch repair
  • Recombinational repair
204
Q

One-Step Repair

A

Direct reversal of DNA Damage

205
Q

Nucleotide Excision Repair

A 
• Specific for helix distorting 
lesions such as pyrimidine dimers 
caused by UVB 
• Cuts out 24-32 bases of one 
strand with the help of 
exonucleases and DNA 
polymerase fills the gap
206
Q

Disease caused by Nucleotide Excision Repair

A

Xeroderma pigmentosum (XP)

207
Q

Two Subpathways of the Nucleotide Excision Repair

A

Global Genome NER

Transcription-Coupled Repair

208
Q

Global Genome Nucleotide Excision Repair

A

surveys genome for helix distortion

209
Q

Transcription- Coupled Repair

A

surveys that damage that interferes with transcription

210
Q

Mismatch Repair

A

Corrects errors that have escaped editing by polymerase and also repairs insertion and deletion mutations

211
Q

Recognition of mismatch is carried out by what proteins

A

hMSH2/3
(hMLH1/hPMS1) and hMLH1/hPMS2 are recruited
• Newly synthesized strand with mutation is identified
• Endonucleases and exonucleases remove bases around and including mismatch
• DNA polymerase synthesizes new strand

212
Q

Hereditary non-polyposis colorectal cancer (HNPCC)

A 
most common cancer syndrome in humans
Lynch Syndrome
Autosomal dominant mutation disease
80% progress to cancer, increased risk for other cancers
Leads to microsatellite instability
213
Q

Recombination Repair

A

Double-Stranded DNA Breaks
2 Types
Homologous Recombination
Non-Homologous End Joining

214
Q

Homogous Recombinaton

A

Depends on presence of sister chromatids

215
Q

Non-Homologous End Joining

A

Does not depend on presence of sister chromatids and can lead to frame shift mutation and chromosomal translocation

216
Q

ATM Kinase

A

ataxia telangiectasis mutated

Activated by a double-stranded break

217
Q

RAD50/MRE11/NBS1 complex uses

A

5’ → 3’

exonuclease activity to create single-stranded 3’ ends

218
Q

BRCA 1/2 aids in the nuclear transport of

219
Q

RAD52 facilitates

A

RAD51 binding to these exposed ends to form a nucleoprotein filament

220
Q

RAD51 can

A

exchange a homologous sequence from a single strand within a double-strand molecule with a singlestranded sequence

221
Q

Resolvace

A

restors the junctions formed as a result of

homologous recombination, called Holliday junctions

222
Q

Holliday Junctions

A

cross-shaped structure that forms during the process of genetic recombination, when two double-stranded DNA molecules become separated into four strands in order to exchange segments of genetic information.

223
Q

Diseases associated with Recombination Repair

A

Burkitt’s Lymphoma

Acute Myeloid Leukemia

224
Q

Ataxia telangiectasis

A

an inherited syndrome where by patients have a mutation in the ATM kinase
• Patients are sensitive to X-rays and have an increased risk of lymphoma

225
Q

Germline Mutations in BRCA 1 and BRCA 2 genes

A

Give rise to an increased risk of breast and ovarian cancer

Those who developed cancer show that they acquired a second mutation later in life

226
Q

BRCA1 and BRCA2 act as

A

Tumor Suppressor Genes

227
Q

Germline Mutations

A

Occur in reproductive cells and pass mutations on to progeny or affect gamete viability

228
Q

Therapeutic Strategies of chemotherapy

A

Apoptosis, killing cells by inducing extensive DNA damage
Inhibiting DNA metabolism by blocking DNA synthesis in rapidly dividing cancer cells
Other drugs interfere with mechanisms of cell division

229
Q

DNA Adduct

A

Form of DNA Damage caused by covalent attachment of a chemical moiety to DNA
A segment of DNA bound to a cancer-causing chemical, can lead to carcinogenesis and can be used as a biomarker of exposure

230
Q

Chlorambucil (DRUG)

A

A member of the nitrogen mustard family of drugs
Targets N7 position of Guanine forming intra strand and inter-strand cross-linking, preventing the separation of DNA strands and interfering with replication

231
Q

Clyclophosphamide (DRUG)

A

Requires metabolic activation within the body

Also used for rheumatoid arthritis

232
Q

Cyclophosphamide method of action

A

Oxidases in the live produce an aldehyde form that decomposes to yield an active form called phosohamide mustard

233
Q

Cisplatin and Carboplatin

A

Platinum-Based drugs that form covalent bonds via platinum atom
Binds to N7 position of Ganine and adenine in its DNA Target
the GG, AG and GXG Adducts comprise over 90% of the total resulting in apoptosis

234
Q

Cisplatin and carboplatin work well on what type of cancer?

A

Ovarian Cancer

235
Q

Cisplatin and Carboplatin side effect

A

Causes irreversible kidney damage

236
Q

Antibmetabolites

A

Structurally simiar to nitrogen bases of DNA and inhibits the role and nucleic acid sequences

237
Q

Fluorideoxyuridylate (Fdump) and Methotraxate

A

F-DUmp competes with DUMP afor the catalytic site of thymidylate synthase, the enxyme that produces thrymidylase (dMTP), inactivating the enzymethrough covalent modification

238
Q

Methotrexate

A

A competetive inhibitor of dihydrofolate reductase (DHFR) required in thymidylate synthase reaction

239
Q

Doxoribucin

A

A fungal anthracycline antibiotic that inhibits topoisomerase II enzyme (Used in colon cancer)

240
Q

Topoisomerase II Enzyme

A

Releases torsional stress during DNA replication, by trapping single-stranded and double-stranded DNA intermediates

241
Q

Doxorubicin Side effects

A

Cardiac damage is the most severe side effect

242
Q

Doxorubicin uses

A

Treating solid tumors (Breast or lung)

243
Q

Vincristine and Vinblastine

A

Madagascar periwinkle plant alkaloids

Binds to tubulin and prevents microtubule assembly and disrupts mitotic spindle formation during cell division

244
Q

Radiation Therapy

A

It is used alone or in combination with other therapies
• Ionizing radiation is usually delivered to the tumor by
electron linear accelerators
• Reacts with water inside the cell generating reactive
oxygen species (ROS) that damage DNA and result in
apoptosis

245
Q

Cells deep within the tumor which are farthest from blood vessels will receive______ doses than cells near the blood vessel

246
Q

Cells within the same tumor can acquire______

mutations and some can become drug resistant

247
Q

Anticancer drugs impose strong _______ ________and can select cells that are drug resistant

A

Selection Pressure

248
Q

________ codes for P-glycoprotein (P-gp) which can bind to drugs such as doxorubicin, vinblastin and taxol and release drug extracellularly

A

The multiple-drug resistance gene (MDR1)

249
Q

Resistance to methotrexate occurs by

A

Mutation of Folate Transporters

250
Q

Some cancer cells ______ ____ ________ that are

responsible for transporting drugs into the cell rendering them non-functional

A

mutate the transporters

251
Q

DHFR (Dihydrofolate reductase) gene

A

is amplified in some cancer cells

252
Q

Increased alkyltransferase activity, can give rise to

A

resistance from alkylating agents

253
Q

Transcription factors

A

proteins that bind to gene promoters and regulate transcription

254
Q

DNA-Binding Domains

A

These domains are characteristic protein
conformations that enable a transcription factor
to bind DNA.
▪ It is the conformation of these protein domains
that facilitates binding to DNA

255
Q

DNA Binding Domains

A

▪ Helix-turn-helix motif
▪ Zinc finger motif
▪ Leucine zipper motif
▪ Helix-loop-helix motif

256
Q

Helix-turn-helix motif

A

The amino acid side-chains of the alpha helix
portions of the helix-turn-helix motif lie in the major
groove of the DNA helix and hydrogen bond to
specific DNA base pairs

257
Q

Zinc finger motif

A

It is approximately 30 amino acids long and is
configured around a zinc atom that links two cysteines
and two histidines or two cysteines and two cysteines.
▪ It consists of a simple ββα fold and side-chains of
specific amino acids recognize a specific DNA
sequence.

258
Q

Transcriptional activation domains

A

function by binding to other components of the transcriptional apparatus in order to inducetranscription by RNA polymerase

259
Q

Dimerization domains

A

Some transcription factors work in pairs (“dimer”) and require a dimerization domain which facilitates protein-protein interactions between the two molecules

260
Q

Ligand-binding domains

A

Some transcription factors
only function upon binding of a ligand and therefore
require a ligand-binding domain

261
Q

The activity of a transcription factor can be

regulated by

A

Several Means

262
Q

EMSA – Electrophoretic Mobility Shift Assay

A

The EMSA s used to study protein: DNA complexes
and interactions
Protein:DNA complexes migrate more slowly than unbound linear DNA on a non-denaturing gel, causing
a “shift.”

263
Q

DNase I Footprinting

A

▪ A method for determining the location of a protein binding site
▪ It involves endonuclease treatment of an end labeled DNA fragment bound to a protein.
▪ Limited digestion yields fragments terminating everywhere except in the footprint region, which is protected from digestion.

264
Q

AP-1 Transcription Factor Family

A

AP-1 is itself activated in response to specific signals such as growth factors, ROS, and radiation
▪ AP-1 binds either to the 12-0-tetradecanoylphorbol13-acetate (TPA) response element or the cAMPresponse element in the promoter region of their
target genes.
▪ That interaction controls the processes of growth, differentiation, and death, and plays a role in carcinogenesis

265
Q

The AP-1 transcription factor is actually composed of ____ components and can be produced by dimers of proteins from the Jun (Jun, Jun B and Jun D) and Fos families (Fos, Fos B, FRAl, and FRA2)

266
Q

Steroid hormones are

A

lipid-soluble signaling molecules that exert their effects by regulating the transcription of sets of genes via specific receptors.
▪ Can result in Self-sufficiency in growth signals

267
Q

The simplest or primary level of organization of chromatin is the wrapping of DNA around a protein “spool” and is referred to as the “____ __ _ _____” array

A

Beads on a string

268
Q

Nucleosome contains

A

147 base pairs (bp) of DNA wrapped 1.7 times around a core of histone proteins

269
Q

The histone core

A

an octomer of histones containing two copies of

histones H2A, H2B, H3, and H4

270
Q

Each histone contains domains for

A

▪ histone-histone
▪ histone-DNA interactions
▪ NH2-terminal lysine-rich
▪ COOH-terminal “tail” domains

271
Q

How do histones attract the DNA to wrap around them?

A

THe net positive charge of the histones attracts the negatively-charged DNA

272
Q

Histone types (5)

A

H1, H2A, H2B, H3, H4

273
Q

Every protein has two ends:

A

C-Terminus (Carboxyl Side)

N-Terminus (Amine Side)

274
Q

HIstone Modification

A

Acetylation
Methylation
Phosphorylation

275
Q

Histone acetyltransferases (HATs)

A

catalyze the transfer of an acetyl group from acetyl coenzyme A (UNWIND DNA)

276
Q 
HDACS
histone deacetylases (HDACs)
A

perform the antagonistic action of removing the acetyl group. Histone acetylation plays an important role in the modulation of chromatin condensation and transcriptional regulation (WIND TIGHTLY)

277
Q

Epigenetic Changes

A

reversible changes in DNA and do not alter the DNA sequence
No Nucleotide changes
They affect gene expression to turn them on and off

278
Q

Epigenetics

A

The study of how your behaviors and environment can cause changes that affect the way your genes work
Heritable information that is encoded by modification of the genome and chromatin components

279
Q

2 Types of Epigenetic Mechanisms

A

Histone modification

DNA Methylation

280
Q

Epigenetic changes are influenced by

A

How DNA gets wrapped around histones making genes readable and unreadable
Instructions on how to differentiate and develop

281
Q

Histone Modification

A

Covalent post-translational modifications (PTM) to histone proteins
These can alter gene expression by altering chromatin structure

282
Q

Histone protein are subject to diverse post-translational modifications including

A

Acetylation
Methylation
Phosphorylation
Ubuquination

283
Q

Histone code hypothesis

A

predicts that the
pattern of these multiple histone modifications
helps to specify the components and activity of the
transcription regulatory molecular machinery

284
Q

Acetylation

A

Addition of an acetyl group to histones from Acetyl Co-A (from the Krebs Cycle)

285
Q

Acetylation plays an important role in the following

A 
Transcription
DNA Replication and Repair
Cell cycle Progression
Differentiation
Gene Silencing
286
Q

EP300

A

Codes for a HAT, and has been found to be mutated with epithelial cancers

287
Q

Acute Promyelotic Leukemia (APL)

A

associated with aberrant recruitment of HDACS (tightening DNA)

288
Q

APL Genetic info

A

Translocation 15:17

289
Q

Methylation or demethylation Can

A

Turn a gene on or off

Causing repression or activation of genes

290
Q

DNA Methyl Transferases (DNMTs)

A

Mediate the covalent addition of a methyl group

291
Q

Hypermethylation of the estrogen receptor

A

a gene promoter was observed in 3/4 of human ovarian cell lines that lacked estrogen receptor protein

292
Q

Retinoblastoma (Rb) gene

A

A tumor suppressor gene that is hypermethylated in several cancers

293
Q

Breast cancer Susceptibility Gene (BRCA1) is mutated in what manner?

294
Q

What type of DNA repair mechanism results in BRCA1 mutation

A

Recombination Repair RAD51

295
Q

Phosphorylation

A

a transient histone modification induced by extracellular signals such as DNA damage

296
Q

DNA Phosphorylation is associated with various biological processes including

A

DNA Damage Repsonse
DAN Repair
Apoptosis
Chromatin Compaction

297
Q

Proteasomes

A

part of a major mechanism by which cells regulate the concentration of particular proteins and degrade misfolded proteins. Proteins are tagged for degradation with a small protein called ubiquitin. The tagging reaction is catalyzed by enzymes called ubiquitin ligases

298
Q

Misregulated epigenetic silencing

Role in cancer

A

Can cause inactivation of large groups of genes

Can result in genome-wide alterations and genomic instability

299
Q

Semiconservative DNA replication

A

two copies of the original DNA molecule are produced, each copy conserving (replicating) the information from one half of the original DNA molecule

300
Q

DNA is copied by DNA polymerase in what direction?

A

In the 5’ → 3’ direction

301
Q

DNA Replication is initiated by

A

an RNA primer

302
Q

The leading strand is synthesized

A

Continuously

303
Q

The lagging strand is synthesized

A

Discontinuously

RNA primers are removed and Okazaki fragments joined by a DNA polymerase and DNA ligase

304
Q

The 3’ end of the parental chromosomal DNA

A

is not replicated and thus chromosomes progressively erode during each round of replication

305
Q

When the chromosomes reach a threshold length, cells enter a stable and irreversible state of growth arrest called

A

cellular senescence

306
Q

If cells bypass the cellular senescense stage because of mutation and telomeres become critically short

A

chromosomal instability results and apoptosis is induced

307
Q

Telomeres are composed of

A

several thousand repeats of the sequence TTAGGG bound by a set of associated proteins called the shelterin complex, which functions to control telomere
length and protect the chromosomal ends

308
Q

Shelterin Complex

A

a six-subunit protein complex (comprising TRF1, TRF2, POT1, TPP1, TIN2 and Rap1) that associates specifically with mammalian telomeres and allows cells to distinguish the natural ends of chromosomes from sites of DNA damage

309
Q

Telomeres shorten by___ ____ with each
round of DNA replication owing to the limits of
DNA polymerases during DNA

A

100-200 bases

310
Q

A ribonucleoprotein containing human telomerase reverse transcriptase activity (hTERT) and a
human telomerase RNA (hTR) maintain telomere length in certain cell types, such as stem cells

A

Telomerase

311
Q

The hTERT contains

A

11 complementary base pairs to the TTAGGG repeats and acts as a template for the reverse transcriptase to add new repeats to telomeric DNA on the 3’ ends of chromosomes

312
Q

Telomere Nucleotide Sequence

Biology of Cancer (4 decks)

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