Exam I Flashcards
(95 cards)
1
Q
What is Cancer?
A
1) Uncontrolled cell proliferation
2) Ability to spread
2
Q
Hypertrophy
A
Increase in cell sized
Normal organization
Ex: uterine growth in pregnancy and muscle growth with weightlifting
3
Q
Hyperplasia
A
Increase in cell #
Normal organization
Hormonal
Compensatory - injury
Pathologic - skin warts
4
Q
Dysplasia
A
Disorganized growth
Warning sign
5
Q
Neoplasia
A
Disorganized growth
Net increase in # of dividing cells
Neoplasm - Cancer
6
Q
Cell Differentiation
A
cells acquire specialized properties that distinguish different types of cells from one another
7
Q
Road to Cancer
A
Shift in balance between proliferation and differentiation
8
Q
Metaplasia
A
Conversion of one cell type to another
Reversible
Pathological always
9
Q
Benign
A
local growth pattern rarely life threatening growth rate usually slow well differentiated Oma
10
Q
Malignant
A
Spreads by invasion and metastasis often life threatening growth rate may be rapid differentiation variable carcinoma/sarcoma
11
Q
Carcinoma
A
malignant neoplasm of skin and organ cells (85%)
12
Q
Sarcoma
A
malignant neoplasm of muscle, bone or connective tissue
13
Q
Leukemia/Lymphoma
A
cancers of the blood forming organs leading to proliferation of WBC
14
Q
Epithelium (Parenchyma)
A
- Protective covering on all surfaces
2. secretions (function)
15
Q
Stroma (Connective)
A
provides blood vessels, lymph for the epithelial (support)
16
Q
Tumor Grading
A
cancers of the same type are assigned different numerical grades based on their microscopic appearance
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
18
Q
Tumor Staging
A
Tumor (X, 0, is, 1,2,3,4)
Lymph Nodes (X, 0, 1,2,3)
Metastasis (X, 0, 1)
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
20
Q
Cachexia
A
Life-threatening condition characterized by extensive weight loss, weakness and malnutrition
21
Q
Normal Cells v. Cancer cells
A
- Anchorage Independent
- Decreased Density-Dependent Inhibition of Growth
- Limitless Replicative Potential (Activated Gene for Telomerase)
- Tumorigenicity when injected in lab animals
22
Q
Functions of ECM
A
Support
Adhesion
Movement
Regulation
23
Q
Anoikis
A
Apoptotic death triggered by lack of ECM contact
24
Q
Growth Factor Independence
A
- make their own GF
- mutant receptors that are permanently activated (no longer require ligand)
- Hyperactive proteins involved in relaying signal
25
Cell Cycle Clock
master governor operates in the cell nucleus that decides the cell's fate from outside input
26
DNA synthesis
only in S phase
27
Cell growth vs. Cell proliferation
increase in size vs. cell division
28
Checkpoints
RP in G1
DNA damage cp in G1, S, G2
Spindle cp in M
29
Cyclins
group of proteins that activate CDKs that are involved in regulating progression through cell cycle
Regulatory component
30
Cyclin Dependent Kinase
Inactive as monomers; active only after binding to cyclin partner
Catalytic component
31
Cyclin circulation
D in G1
E after RP
A in S and G2
B in M
32
CDK Inhibitors
D - p15, p16, p18, p19
| E, A, B - p57, p27, p21
33
Retinoblastoma
Phosphoprotein that functions as a dimer with transcription factor E2F
Phosphorylated Rb allows G1 to proceed to S; releases E2F transcription factor
34
Extrinsic Apoptosis
External signal to death receptors turns Procaspase into active Caspase
Death ligands > FADD protein > Caspase 8 or 10
35
Intrinsic Apoptosis
Often in response to DNA damage > p53 > death-promoting proteins > removal of Bcl2 from mitochondria surface which releases Cytochrome C
Caspase 9
36
Caspases
proteases that activate signaling cascade to induce apoptosis
37
Most common types of spontaneous mutations are cause by...
Interactions between DNA and water molecules
Depurination
Deamination
38
DNA Repair Mechanisms
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
39
Cell surface alterations that affect adhesiveness and cell-cell communication
1. Loss of E-Cadherin
2. Enhanced tendency to clump together
3. Decrease in gap junctions
40
Steps in Metastatic Cascade
1. Local Invasion of primary tumor
2. Intravasation - travel through CS
3. Extravasation
4. Survival in new site and colonization
41
Angiogenesis
New blood vessels form by sprouting off existing vessels
Required for tumors to grow beyond a few millimeters in diameter
42
VEGF and FGF
Angiogenesis Activators
> production of MMPs
43
Matrix Metalloproteinases (MMPs)
Edward Scissor Hands
| protein degrading enzymes that breaks down ECM and BM
44
Angiostatin
Endostatin
Thrombospondin
Interferon
Angiogenesis Inhibitors
Normally predominate
45
What causes cancer?
Identifiable group of environmental and lifestyle factors
46
Epidemiology
investigates the frequency and distribution of diseases in human population
47
Power - Statistically Significant
Statistical power - enough evidence to draw a conclusion from data
48
Confounding Factor
prevents you from finding the true link
49
Bias
1. Experimenter Bias
2. Detection Bias
3. Recall Bias
4. Selection Bias
50
Retrospective
Look at past (case-control)
51
Prospective
Look at future (cohort)
52
Post Hoc Fallacy
Draw the wrong conclusion
53
Greatest Risk Factor
Age
54
Tobacco
Dose-Response Relationship between tobacco smoke and cancer risk
cigarettes per day
age started smoking
depth of inhalation
55
General Causes of Cancer
```
Age
Chemicals
Radiation
Viruses
Nutrition and Diet
```
56
Multistage Carcinogenesis
1. Initiation
2. Promotion - most variable phase
3. Progression - NOT reversible
57
Role of Increased Cell Proliferation in Carcinogenesis
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
Carcinogen
agent that increases the probability of developing cancer
59
Complete Carcinogen
has BOTH initiating and promoting activity
60
Incomplete Carcinogen
agent that can function in the initiation OR promotion stage
61
Initiator
initiates genetic change in cell
62
Promoter
promotes proliferation of initiated cell - not a carcinogen by itself
63
Categories of Chemical Carcinogens
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
Liver Metabolism
Cytochrome P450
tries to make toxin soluble for excretion
65
Indirect Carcinogen
requires metabolism to become active
66
Direct Carcinogen
metabolism is NOT required
67
Phorbol Ester
Bypasses normal signaling pathways for cell proliferation
68
Genotoxic
```
Actual DNA damage
DNA adducts
Chromosome breakage
Chromosome fusion
Chromosome deletion
```
69
Non-Genotoxic
```
Inflammation
Immunosuppression
Free Radicals
Receptor Activation
Epigenetic silencing
```
70
UVA
Not filtered by ozone
Causes aging
Stimulates proliferation
71
UVB
Partially filtered by ozone
| Causes sunburn, tanning and skin cancer
72
Favorite mutation of UV
Pyrimidine Dimer
73
Ionizing Radiation
X-rays and Nuclear
removes electrons from biological molecules which damage DNA
74
Alpha particles
most damaging form of nuclear radiation but cannot penetrate the skin
Can be inhaled or ingested
75
BERT
Background Equivalent Radiation Time
76
Koch's Postulates
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
3. pathogen isolated from new host must be identical to original pathogen
77
Burkitt's Lymphoma
linked to Epstein-Barr Virus (EBV) after immune response depleted
Chromosomal Translocation
78
EBV
also linked to Hodgkin's Disease and mononucleosis
79
HPV
sexually transmitted virus responsible for cervical cancer and cancer of the penis
High risk: HPV16, HPV18, HPV45, HPV31
80
HBV or HCV
responsible for most cases of liver cancer
81
HTLV-I
retrovirus associated with adult T cell Leukemia and Lymphoma
82
HIV
infection increases risk for Karposi's sarcoma
83
SV40
monkey virus that contaminated early batches of polio vaccine
84
H. pylori
associated with stomach cancers
85
Flatworms infections involving blood flukes or liver flukes
associated with bladder or bile duct cancers respectively
86
Infections
1. can cause cancer directly or indirectly
2. Indirect - IS depression, chronic inflammation
3. Direct - viral alteration of genes
87
Acutely Transforming Retroviruses
cause animals to develop tumors rapidly (oncogenes)
88
Slow-Acting Retroviruses
require months or years to induce cancer (NO oncogenes)
| rely on insertional mutagenesis
89
Insertional Mutagenesis
Inserting viral genes into host chromosomal site where viral DNA can activate the transcription of a nearby cellular proto-oncogene
90
Oncogenes
code for oncoproteins that bind and interfere with Rb and p53
91
Ultrasound-Guided Core Biopsy
Palpable masses
| Other masses seen on mammogram
92
Stereotactic Core Biopsy
Calcifications
93
MRI-Guided Core Biopsy
very detailed
94
H&E Staining
Hematoxylin (+)
| Eosin (-)
95
Cancer Immunoediting Hypothesis
dual host-protective and tumor-promoting actions of immunity on developing tumors and predicts that cancer immunoediting proceeds through 3 phases of variable length
