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Cancer Biology > Exam I > Flashcards

Exam I Flashcards

1
Q

What is Cancer?

A

1) Uncontrolled cell proliferation

2) Ability to spread

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2
Q

Hypertrophy

A

Increase in cell sized
Normal organization

Ex: uterine growth in pregnancy and muscle growth with weightlifting

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3
Q

Hyperplasia

A

Increase in cell #
Normal organization

Hormonal
Compensatory - injury
Pathologic - skin warts

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4
Q

Dysplasia

A

Disorganized growth

Warning sign

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5
Q

Neoplasia

A

Disorganized growth
Net increase in # of dividing cells

Neoplasm - Cancer

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6
Q

Cell Differentiation

A

cells acquire specialized properties that distinguish different types of cells from one another

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7
Q

Road to Cancer

A

Shift in balance between proliferation and differentiation

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8
Q

Metaplasia

A

Conversion of one cell type to another

Reversible

Pathological always

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9
Q

Benign

A 
local growth pattern
rarely life threatening
growth rate usually slow
well differentiated
Oma
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10
Q

Malignant

A 
Spreads by invasion and metastasis
often life threatening
growth rate may be rapid
differentiation variable
carcinoma/sarcoma
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11
Q

Carcinoma

A

malignant neoplasm of skin and organ cells (85%)

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12
Q

Sarcoma

A

malignant neoplasm of muscle, bone or connective tissue

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13
Q

Leukemia/Lymphoma

A

cancers of the blood forming organs leading to proliferation of WBC

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14
Q

Epithelium (Parenchyma)

A
  1. Protective covering on all surfaces

2. secretions (function)

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15
Q

Stroma (Connective)

A

provides blood vessels, lymph for the epithelial (support)

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16
Q

Tumor Grading

A

cancers of the same type are assigned different numerical grades based on their microscopic appearance

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17
Q

Anaplastic

A

so poorly differentiated and abnormal in appearance and organization that it bears little resemblance to the cells of the tissue in which the tumor arose

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18
Q

Tumor Staging

A

Tumor (X, 0, is, 1,2,3,4)

Lymph Nodes (X, 0, 1,2,3)

Metastasis (X, 0, 1)

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19
Q

DNA Microarray Analysis

A

technique that allows the activity of thousands of genes to be measured simultaneously; looks at tumors that appear to be identical and subdivides them into groups based on differing patterns of gene expression

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20
Q

Cachexia

A

Life-threatening condition characterized by extensive weight loss, weakness and malnutrition

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21
Q

Normal Cells v. Cancer cells

A
  1. Anchorage Independent
  2. Decreased Density-Dependent Inhibition of Growth
  3. Limitless Replicative Potential (Activated Gene for Telomerase)
  4. Tumorigenicity when injected in lab animals
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22
Q

Functions of ECM

A

Support
Adhesion
Movement
Regulation

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23
Q

Anoikis

A

Apoptotic death triggered by lack of ECM contact

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24
Q

Growth Factor Independence

A
  1. make their own GF
  2. mutant receptors that are permanently activated (no longer require ligand)
  3. Hyperactive proteins involved in relaying signal
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25
Q

Cell Cycle Clock

A

master governor operates in the cell nucleus that decides the cell’s fate from outside input

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26
Q

DNA synthesis

A

only in S phase

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27
Q

Cell growth vs. Cell proliferation

A

increase in size vs. cell division

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28
Q

Checkpoints

A

RP in G1
DNA damage cp in G1, S, G2
Spindle cp in M

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29
Q

Cyclins

A

group of proteins that activate CDKs that are involved in regulating progression through cell cycle
Regulatory component

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30
Q

Cyclin Dependent Kinase

A

Inactive as monomers; active only after binding to cyclin partner
Catalytic component

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31
Q

Cyclin circulation

A

D in G1
E after RP
A in S and G2
B in M

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32
Q

CDK Inhibitors

A

D - p15, p16, p18, p19

E, A, B - p57, p27, p21

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33
Q

Retinoblastoma

A

Phosphoprotein that functions as a dimer with transcription factor E2F

Phosphorylated Rb allows G1 to proceed to S; releases E2F transcription factor

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34
Q

Extrinsic Apoptosis

A

External signal to death receptors turns Procaspase into active Caspase

Death ligands > FADD protein > Caspase 8 or 10

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35
Q

Intrinsic Apoptosis

A

Often in response to DNA damage > p53 > death-promoting proteins > removal of Bcl2 from mitochondria surface which releases Cytochrome C

Caspase 9

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36
Q

Caspases

A

proteases that activate signaling cascade to induce apoptosis

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37
Q

Most common types of spontaneous mutations are cause by…

A

Interactions between DNA and water molecules
Depurination
Deamination

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38
Q

DNA Repair Mechanisms

A
  1. Translesion Synthesis and Excision Repair: abnormal bases
  2. Mismatch Repair: mismatched bases
  3. Non-Homologus End-Joining and Homologous Recombination: double stranded DNA breaks
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39
Q

Cell surface alterations that affect adhesiveness and cell-cell communication

A
  1. Loss of E-Cadherin
  2. Enhanced tendency to clump together
  3. Decrease in gap junctions
40
Q

Steps in Metastatic Cascade

A
  1. Local Invasion of primary tumor
  2. Intravasation - travel through CS
  3. Extravasation
  4. Survival in new site and colonization
41
Q

Angiogenesis

A

New blood vessels form by sprouting off existing vessels

Required for tumors to grow beyond a few millimeters in diameter

42
Q

VEGF and FGF

A

Angiogenesis Activators

> production of MMPs

43
Q

Matrix Metalloproteinases (MMPs)

A

Edward Scissor Hands

protein degrading enzymes that breaks down ECM and BM

44
Q

Angiostatin
Endostatin
Thrombospondin
Interferon

A

Angiogenesis Inhibitors

Normally predominate

45
Q

What causes cancer?

A

Identifiable group of environmental and lifestyle factors

46
Q

Epidemiology

A

investigates the frequency and distribution of diseases in human population

47
Q

Power - Statistically Significant

A

Statistical power - enough evidence to draw a conclusion from data

48
Q

Confounding Factor

A

prevents you from finding the true link

49
Q

Bias

A
  1. Experimenter Bias
  2. Detection Bias
  3. Recall Bias
  4. Selection Bias
50
Q

Retrospective

A

Look at past (case-control)

51
Q

Prospective

A

Look at future (cohort)

52
Q

Post Hoc Fallacy

A

Draw the wrong conclusion

53
Q

Greatest Risk Factor

54
Q

Tobacco

A

Dose-Response Relationship between tobacco smoke and cancer risk
cigarettes per day
age started smoking
depth of inhalation

55
Q

General Causes of Cancer

A 
Age
Chemicals
Radiation
Viruses
Nutrition and Diet
56
Q

Multistage Carcinogenesis

A
  1. Initiation
  2. Promotion - most variable phase
  3. Progression - NOT reversible
57
Q

Role of Increased Cell Proliferation in Carcinogenesis

A
  1. decreases time available for DNA repair
  2. converts repairable DNA damage into non repairable mutations
  3. necessary for chromosomal aberrations, insertions, deletions and gene amplification
  4. clonallly expands existing cell populations with mutations
58
Q

Carcinogen

A

agent that increases the probability of developing cancer

59
Q

Complete Carcinogen

A

has BOTH initiating and promoting activity

60
Q

Incomplete Carcinogen

A

agent that can function in the initiation OR promotion stage

61
Q

Initiator

A

initiates genetic change in cell

62
Q

Promoter

A

promotes proliferation of initiated cell - not a carcinogen by itself

63
Q

Categories of Chemical Carcinogens

A
  1. Polycyclic Aromatic Hydrocarbons
  2. Aromatic Amines and Aminoazo compounds - (-NH2 or N=N)
  3. N-Nitroso Compounds - (N=O)
  4. Alkylating Agents - readily attach C to other molecule
  5. Natural Products - produced by biological organisms
  6. Inorganic Substances - metals
64
Q

Liver Metabolism

A

Cytochrome P450

tries to make toxin soluble for excretion

65
Q

Indirect Carcinogen

A

requires metabolism to become active

66
Q

Direct Carcinogen

A

metabolism is NOT required

67
Q

Phorbol Ester

A

Bypasses normal signaling pathways for cell proliferation

68
Q

Genotoxic

A 
Actual DNA damage
DNA adducts
Chromosome breakage
Chromosome fusion
Chromosome deletion
69
Q

Non-Genotoxic

A 
Inflammation
Immunosuppression
Free Radicals
Receptor Activation
Epigenetic silencing
70
Q

UVA

A

Not filtered by ozone
Causes aging
Stimulates proliferation

71
Q

UVB

A

Partially filtered by ozone

Causes sunburn, tanning and skin cancer

72
Q

Favorite mutation of UV

A

Pyrimidine Dimer

73
Q

Ionizing Radiation

A

X-rays and Nuclear

removes electrons from biological molecules which damage DNA

74
Q

Alpha particles

A

most damaging form of nuclear radiation but cannot penetrate the skin
Can be inhaled or ingested

75
Q

BERT

A

Background Equivalent Radiation Time

76
Q

Koch’s Postulates

A
  1. suspected pathogen must be detected in diseased tissue
  2. suspected pathogen must be isolated from diseased host and grown in lab
  3. lab grown pathogen must cause disease when administered to healthy host
  4. pathogen isolated from new host must be identical to original pathogen
77
Q

Burkitt’s Lymphoma

A

linked to Epstein-Barr Virus (EBV) after immune response depleted
Chromosomal Translocation

78
Q

EBV

A

also linked to Hodgkin’s Disease and mononucleosis

79
Q

HPV

A

sexually transmitted virus responsible for cervical cancer and cancer of the penis

High risk: HPV16, HPV18, HPV45, HPV31

80
Q

HBV or HCV

A

responsible for most cases of liver cancer

81
Q

HTLV-I

A

retrovirus associated with adult T cell Leukemia and Lymphoma

82
Q

HIV

A

infection increases risk for Karposi’s sarcoma

83
Q

SV40

A

monkey virus that contaminated early batches of polio vaccine

84
Q

H. pylori

A

associated with stomach cancers

85
Q

Flatworms infections involving blood flukes or liver flukes

A

associated with bladder or bile duct cancers respectively

86
Q

Infections

A
  1. can cause cancer directly or indirectly
  2. Indirect - IS depression, chronic inflammation
  3. Direct - viral alteration of genes
87
Q

Acutely Transforming Retroviruses

A

cause animals to develop tumors rapidly (oncogenes)

88
Q

Slow-Acting Retroviruses

A

require months or years to induce cancer (NO oncogenes)

rely on insertional mutagenesis

89
Q

Insertional Mutagenesis

A

Inserting viral genes into host chromosomal site where viral DNA can activate the transcription of a nearby cellular proto-oncogene

90
Q

Oncogenes

A

code for oncoproteins that bind and interfere with Rb and p53

91
Q

Ultrasound-Guided Core Biopsy

A

Palpable masses

Other masses seen on mammogram

92
Q

Stereotactic Core Biopsy

A

Calcifications

93
Q

MRI-Guided Core Biopsy

A

very detailed

94
Q

H&E Staining

A

Hematoxylin (+)

Eosin (-)

95
Q

Cancer Immunoediting Hypothesis

A

dual host-protective and tumor-promoting actions of immunity on developing tumors and predicts that cancer immunoediting proceeds through 3 phases of variable length

Cancer Biology (1 decks)

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