Exam 3 Part 2 Flashcards
(214 cards)
1
Q
Scientific investigation into the “distribution an determinants of health-related states or events in specified populations”
Study of death or disease in groups of people (populations)
A
Epidemiology
2
Q
Common cancer(s) in the US
A
Breast Cancer
Colorectal Cancer
Esophageal Cancer
3
Q
Common cancer(s) in Africa
A
Liver Cancer
4
Q
Common cancer(s) in Japan
A
Stomach Cancer
5
Q
________ exposures appear to have a dominant role in the formation of many common cancers.
A
Environmental
6
Q
_____ plays a major role in carcinogenesis, restricting it may increase life expectancy.
A
Diet
7
Q
What are the environmental risk facts for cancer?
A
Ultraviolet (UV) Light Ionizing Radiation Asbestos Arsenic Various Viral Infections Chemical Agents
8
Q
What age group is most likely to suffer the highest rates of cancer-related deaths?
A
55-75
9
Q
Cancers that develop in the absence of a family history of such a cancer and are thought to be primarily, the result of harmful environmental exposures and the resulting damage to individual’s genetic material.
A
Sporadic Cancer
10
Q
_______ and inherited risk factors frequently interact to create an individuals unique cancer risk.
A
Environmental
11
Q
Cellular ______ and ______ are characteristic preneoplastic lesions.
A
Metaplasia
Dysplasia
12
Q
Removal of preneoplastic lesions ______ the cancer risk
A
Lowers
13
Q
Bronchial epithelia resulting form habitual cigarette smoking is unable to be removed and is known as cellular _____
A
Dysplasia
14
Q
Gastroesophageal reflux disease (GERD) known as Barrett’s Esophagus is unable to be removed and is known as cellular ______
A
Metaplasia
15
Q
T/F. In most cases of preneoplastic lesions, they develop into cancer.
A
False (most cases do not develop into cancer)
16
Q
The one exception of benign tumors having a high rate of malignant transformation (roughly 30%) is a(an)
A
Adenoma
17
Q
Cancers develop following
A
Genetic alterations
18
Q
When cellular growth becomes severely dysregulated, ______ forms.
A
Cancer
19
Q
Gene alterations may be inherited down the _____ ____
A
Germ Line (germ line mutations)
20
Q
Normal genes that promote cellular growth
A
Proto-Oncogenes
21
Q
When _______ are altered (mutated or over-expressed), it promotes excessive cellular growth.
A
Proto-Oncogenes
22
Q
When a proto-oncogene is altered it is then referred to as a
A
Cancer-Promoting Oncogene
23
Q
___ allele(s) need to be altered to cause a proto-oncongene to change its phenotype and behave as an oncogene.
A
1
24
Q
When a single allele alters a proto-oncogene which changes its phenotype, this is referred to as a ______ change of gene expression
A
Dominant
25
Normal genes that slow down cellular growth (defense mechanism)
Tumor Suppressor Genes
26
If TSG's become altered (mutated or over-expressed), they _____ the ability to slow down growth.
Lose
27
___ allele(s) need to be altered to cause TSG's to change its phenotype and lose normal ability to suppress tumor growth
2
28
When two alleles alter TSG's which changes its phenotype is referred to as a _______ change of gene expression
Recessive
29
Kill off cells that are detected as having genetic alterations.
Apoptosis
30
If the body loses the ability to rid of dangerous cancer-promoting mutations, they will survive and contribute to
Carcinogenesis
31
What are the two types of genetic alterations causing cancer?
1. Mutations
| 2. Epigenetic Modifications
32
There are two types of mutations:
1. Driver Mutations
| 2. Passenger Mutations
33
Mutation that directly contributes to progression of a specific cancer. Acquired from an environmental carcinogen
Driver Mutations
34
Mutation more randomly throughout the genome, producing genetic variants (subclones)
Passenger Mutations
35
May give a tumor or selective advance against various forms of therapy
Subclones
36
Affect the entire body and may be inherited
Germline mutations
37
Affected somatic cells, more localized
Acquired Mutatiosn
38
RB gene
Retinoblastoma
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39
TP53 gene
Li-Fraumeni Syndrome
40
APC Gene
Colorectal Cancer
41
NF1 Gene
Neurofibromatosis
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42
BRCA1 Gene
| BRCA2 Gene
Breast Cancers and Ovarian Cancers
43
May activate/deactivate proteins, but are most well-known for activating proto-oncogenes
Point Mutations
44
This single mutations is associated with dominant gain-of-function change in gene expression
Point Mutations
45
Single point mutations are known to activate the ____ gene
RAS
46
____ _______ may deactivate one of the TP53 genes
Point Mutations
47
Occur on the level of the chromosome and included balanced translocations
Gene Rearrangements
48
__ ___ cancers are frequently associated with very specific balanced translocations between two chromosomes
B cell (leukemia and lymphomas)
49
Chronic Myelongenous Leukemia (CML) involve a specific balanced translocation between genetic material on chromosome __ and ___, which is termed a Philadelphia chromosome
9 and 22
50
Most cases of Burkitt Lymphoma have a balanced translocation between chromosome ___ and ____.
8 and 14
51
Involve the loss of a section of genetic material
Genetic Deletions
52
Deletions may contribute to carcinogenesis by altering one (of the two) alleles that must be altered to deactivate a _____________
Tumor Suppressor Gene
53
Segment of genetic material is multiplied many times, and may over-express a proto-oncogene and effectively activate an oncogene
Gene Amplifications
54
Gene amplification that occurs in about 20% of all cases of breast cancer
HER2 Gene (HER2/neu)
55
Amplification of HER2 gene allows breast cancer cells to become much more sensitive to low levels of
Growth Factors
56
Gene amplifications may also produce ______ ______, which are extrachromosomal DNA fragments that are evident within an involved cell.
Double Minutes
57
Reversible changes to gene expression
Epigenetic Modifications
58
What are the two mechanisms of gene modification?
DNA Methylation
| Histone Modification
59
May contribute to carcinogenesis if TSG's or DNA repair genes are deactivated
Epigenetic Modification
60
Multistep process that involves the accumulation of multiple genetic alterations, over time.
Carcinogenesis
61
Over time, cancers evolve and become
1. More aggressive
| 2. Less responsive to Therapy
62
Cancers accumulate greater gene alterations, which develop
Subclones
63
Even though cancers develop from a single transformed cell, in time these clonal cells will acquire _______ gene alterations.
Different
64
As _____ _______ occurs, cancer will develop greater invasive and malignant potential
Tumor Progression
65
Unique characteristics that contribute to the dysregulated cellular growth of cancer cells
Hallmarks of Cancer
66
Self-Sufficiency in Growth Signaling
Evasion of Immune Detection (Surveillance)
Insensitivity to Anti-Growth (inhibitory) Signaling
Cellular Immortality (limitless growth potential)
Altered Cellular Metabolism
Increased (sustained) Angiogenesis
Evasion of Apoptosis
Invasion and Metastasis
Hallmarks of Cancer
67
Hallmarks of Cancer
Self-Sufficiency in Growth Signaling
Evasion of Immune Detection (Surveillance)
Insensitivity to Anti-Growth (inhibitory) Signaling
Cellular Immortality (limitless growth potential)
Altered Cellular Metabolism
Increased (sustained) Angiogenesis
Evasion of Apoptosis
Invasion and Metastasis
68
Cancers may also involve tumor-promoting inflammation and genomic instability, which is referred to as
Enabling Hallmarks of cancer
69
Evading growth suppression and evading anti-growth signals =
Tumor has become insensitive to normal inhibitory signals of the body
70
Group of genes that encode for inhibitory proteins that enact the function of limiting and controlling cellular growth
Tumor Suppressor Genes
71
Their protein products "apply the brakes to cell proliferation", servicing to suppress tumor growth
Tumor Suppressor Genes
72
The two-mutation loss-of-function change in TSG expression is known as the
Two-Hit Hypothesis (Knudson Hypothesis)
73
TSG located on chromosome 13 and is an important mediator of the cell cycle
RB Gene (Retinoblastoma Gene)
74
First discovered in childhood eye cancer, but can be found in nearly all cells of the body
RB Gene
75
RB gene produces the ___ protein which regulates the G1-to-S phase of the cell cycle
Rb
76
Common oncovirus that deactivates the RB gene's regulatory control of the cell cycle
Human Papillomavirus (HPV)
77
A virus that may cause cancer
Oncovirus
78
Classic TSG that produces protein product p53 and is known as the "Guardian of the Genome"
TP53 Gene (P53)
79
Three stimuli that activate a p53 response
1. Cellular Anoxia
2. Inappropriate pro-growth signaling (activation of oncogene)
3. Genetic Damage
80
p53 will attempt to control harmful situations by initiating control mechansims:
1. Quiescence
2. Senescence
3. Apoptosis
81
p53 control mechanism that is a temporary pause affected cells cell cycle activity
Quiescence
82
p53 control mechanism that is a permanent arresting of affected cells cell cycle activity
Senescence
83
p53 control mechanisms that is a controlled/programmed cellular death
Apoptosis
84
TP53 will regulate the cell cycle and attempt to fix genetic damage while a cell is in ______ via activation of DNA repair genes.
Quinescence
85
If DNA repair occurs, TP53 will release the affected cell back into normal cell cycle activity; if not, it will initiate _________ or ________.
Senescence
| Apoptosis
86
TP53 gene mutations are present in at least ____ of all human cancers
70%
87
T{53 gene alterations are present in lethal cancers such as
Lung
Colorectal
Breast
88
When the protein produce (p53) of TP53 is deactivated it is known as a
Functional Mutation
89
When an altered TP53 gene is inherited this is known as
Li-Fraumeni Syndrome
90
Involves affected individuals developing multiple primary tumors at a younger age
Li-Fraumeni Syndrome
91
Li-Fraumeni Syndrome increases the risk of developing a cancer by about ___-fold
25
92
Cancers of Li-Fraumeni Syndrome
```
Sarcomas
Breast Cancers
Brain Tumors
Leukemias
Adrenal Cortex Adenocarcinomas
(SBLA)
```
93
Cancer cells shirt their metabolism to a unique form of metabolism known as
Aerobic Glycolysis
94
When cancer cells shift their metabolism to Aerobic Glycolysis
Warburg Effect
95
T/F. Cancer cells do not shift their metabolism if there is a presence of adequate oxygen levels.
False
---Cancer cells shift to Aerobic Glycolysis EVEN in the presence of adequate oxygen levels---
96
What are the normal periods of rapid growth that will utilize aerobic glycolysis
Embryogenesis
| Immune Response
97
Normal cells have a limited number of cellular divisions, known as its
Hayflick Limit
98
T/F. Cancer cells do not have a Hayflick Limit
True
99
When a normal cell's telomeres become critically shortened following prolonged cellular growth, it initiates cellular
Senescence
100
If a normal cell with shortening telomeres doesn't enter cellular senescence the cell will enter
Non-Homologous End Joining
101
Once the shortened telomere cell enters Non-Homologous End Joining this will result in the creation of
Dicentric Chromosomes (irregular chromosome with two centromeres)
102
Dicentric Chromosomes will enter the cell cycle where they will be pulled apart (during Anaphase), and __________ chromosomal breaks are formed.
Double-Stranded
103
Once double-stranded chromosomal breaks occur, this will produce mutations which will activate the enzyme
Telomerase
104
Telomerase will ______ the telomeres of the haphazard chromosomes, giving immortality to these tumor cells
Lengthen
105
Reactivation of telomerase is observed in about ____ of all cancers
90%
106
A tumor must stimulate ______ in order to grow larger.
Angiogenesis
107
Angiogenesis may allow sites of tumor metastasis to enter the _________ ________ and metastasize to distant sites.
Systemic Circulation
108
What are the characteristics of new blood vessels formed form neoangiogenesis:
1. Dilated
2. Haphazardly Formed (Tortuous)
3. Leaky
109
Angiogensis is a common mechanism for
Edema
110
Invasion and metastasis are classic features of more _______ cancers
Aggressive
111
What are the steps of Invasion-Metastasis Cascade
Step 1: Invasion into the surrounding ECM
Step 2: Spreading into the Vasculature (intravasation)
Step 3: Spreading out of the circulation and invading a distant tissue (extravasation)
112
Tumor cells must first loosen their surrounding intercellular connections, performed by cancer cells deactivating ________ genes.
E-Cadherin
113
After E-Cadherin Genes are deactivated _____ enzymes degrade the local ECM
Proteolytic
114
Once a carcinoma penetrates its surrounding ______ _____, it is no longer consdiered an "in situ" or Stage 0 Cancer.
Basement Membrane
115
Once a carcinoma penetrates its surrounding basement membrane it is considered to be at least a Stage __ or _____ cancer.
1
| "Invasive"
116
Once a cancer cell has navigated into a _______ or ________ vessel it has the ability to spread throughout the body.
Lymphatic
| Hematopoietic (blood)
117
Cancer cells that are within circulation are referred to as
Cancer Embolus
118
Cancer Embolus is vulnerable to the host's immune destruction via
Natural Killer Cells
CD8+ T Cells
---Both kill detected cancer cells---
119
If a cancer embolus avoids death by the immune system, it may travel to sites that will support survival, these sites are predicted by:
1. Anatomical Location
2. Vascular Drainage
3. First Capillary Bed Encountered (in circulation)
120
Sites that tend to be favorable for metastatic spread of cancer cells are equipped wtih:
1. Area of Stasis
2. Abundant Capillaries
3. Physical protection/Protection from the Immune System
121
Sites that fit the criteria of favorable sites for metastatic spread:
1. Lungs
2. Liver
3. Bone Marrow
122
T/F. Cancer is predicatable
False
| ---Cancer is unpredictable by its very nature---
123
High frequency of mutations that occur in cancer cells
Genomic Instability
124
The result of gene alterations to cancer genes, such as TSG's or genes that control genetic repair.
Genomic Instability
125
Three inherited DNA repair defects that result in unique cancer presentations:
1. DNA Mismatch Repair
2. Nucleotide Excision Repair
3. Homologous Recombination
126
Without fully functional _________, nucleotide mismatches go uncorrected
DNA Mismatch Repair
127
Hereditary Nonpolyposis Colon Cancer (HNPCC or Lynch Syndrome) is the prototypical cancer syndrome that is associated with an inherited defect in
DNA Mismatch Repair
128
Individuals with HNPCC inherit ___ altered allele(s) and acquire the second alteration from an environmental carcinogen.
1
129
Xeroderma Pigmentosunm (XP) is the prototypical condition that develops following an altered
Nucleotide Excision Repair (NER)
130
Repairs damage from Ultraviolet (UV) Light, specifically correcting the cross-linking of pyrimidine residues.
Nucleotide Excision Repair (NER)
131
Children with XP are sometimes referred to as
"Moon Children"
132
Familial breast cancer that is positive for the BRAC1 and 2 gene mutations are classically associated with altered
Homologous Recombination Repair
133
Active in repairing damage associated with chromosomal breaks
Homologous Recombination Repair
134
When an individual has abnormal homologous recombination, they are ____ sensitive to environmental carcinogens
More
135
Individuals with BRAC1 or BRAC2 mutations have an increased risk of developing:
```
Breast Cancer
Ovarian Cancer
Fallopian Tube Cancer
Prostate Cancer
Pancreatic Cancer
Stomach Cancer
Melanoma
```
136
Known to assist in the reparative process that occurs at an area of inflammation
Growth Factors
137
Various cells at the area of inflammation will release growth factors that promote _______ at the area of inflammation and repair.
Angiogenesis
138
Sustained angiogenesis is a hallmark of tumor growth and is needed for tumors of growth beyond
1-2 mm in diameter
139
Macrophages that are present at the site of inflammation will release proteases in
Local Invasion
140
_____ may assist in a cancer's ability to invade locally and metastasize to distant sites by breaking down the ECM that surrounds a mass of cancer cells
Proteases
141
The three primary environmental carcinogens:
1. Carcinogenic Chemicals
2. Ionizing Radiation
3. Microbial Infections
142
Involve waves on the upper-end of the UV light spectrum, X-rays, and Gamma Rays
Ionizing Radiation
143
Various elements in the environment may contain high levels of Ionizing Radiation:
Uranium
UV Light
Potassium (from a Banana)
144
Most common forms of skin cancer:
Basal Cell Carcinoma
| Squamous Cell Carinoma
145
T/F. The most common forms of skin cancer are associated with intense UV exposure.
False
---The most common forms of skin caner (Basal and Squamous Cell Carcinoma) are associated with a total lifetime exposure to UV light---
146
The most deadly form of skin cancer
Melanoma
147
Melanoma is more likely to be associated with an
Intense UV exposure
148
T/F. The risk of contracting skin cancer does not change if you have had multiple intense sunburns early in life.
False
| ---The risk of contracting skin cancer is amplified if you have had multiple intense sunburns early in life ---
149
Unprotected miners have about a ___-fold increased risk of developing lung cancer, due to their exposure to radioactive elements.
10
150
Individuals surviving the atomic blasts at the end of WWII saw a spike in:
```
Leukemia
Thyroid Cancer
Breast Cancer
Colorectal Caner
Lung Cancer
```
151
How long was the latency period for most individuals exposed to the radiation from the atomic bombs?
7-year latency period
152
Ionizing Radiation is known to cause
Chromosomal Breaks
153
Microbial agents most likely to be associated with Carcinogenesis:
```
HTLV-1
HPV
EBV
HBV and HCV
H. Pylori
```
154
Oncogenic RNA virus that increases the risk of developing T Cell Leukemia or Lymphoma.
Human T-Cell Lymphotropic Virus Type 1 (HTLV-1)
155
Where is HTLV-1 most commonl?
Japan, Caribbean, Africa and South America
156
HTLV-1 tends to infect
CD4+ T Cells
157
HTLV-1 can spread via
Sexual Contact
Direct contact with blood
Breastfeeding
158
HTLV-1 injects its RNA genes, particularly ____ Genes, into infected cells.
Tax
159
The Tax Gene will activate _____, which accelerates cellular growth.
Cyclins (Cyclin D)
160
Name given to a group of viruses that are likely to produce warts
Human Papillomavirus (HPV)
161
HPV's producing warts
HPV-6 HPV-11
162
Aggressive HPV's that increase the risk of cancerous transformation
HPV-16 HPV-18
163
HPV infections are most commonly associated with _______________ of the cervix or anogenital region.
Squamous Cell Carcinoma
164
HPV infections cause _______ ______ in two classic TGS's
Functional Mutations
165
Responsible for causing infectious mononucleosis ("mono") and the 1st virus detected to have an association with cancer.
Epstein-Barr Virus (EBV)
166
Known to increase the risk of various B cell lymphomas, such as Burkitt Lymphoma
EBV
167
_____ infections increase the risk of developing nasopharyngeal carcinomas
EBV
168
Cause chronic inflammation in the liver (hepatitis)
Hepatitis B Vrius (HBV)
| Hepatitis C Virus (HCV)
169
70-85% of all cases of liver cancer worldwide, are the result of chronic
HBV or HCV infections
170
Patients of hepatitis viral infection-related liver cancer are most likely to occur in areas of
Africa
| Asia
171
Bacterial infection that involve the distal stomach or proximal small intestine
Helicobacter Pylori (H. Pylori)
172
Infections that involve gastric adenocarcinomas or mucosa associated lymphoid tymors (MALT Lymphomas).
H. Pylori
173
H. Pylori causes chronic inflammation in the area of involvement, contributing to increased ______ exposure and ______ supply.
Reactive Oxygen Species
| Growth Factor
174
Impact of tumor growth depends upon:
1. Location of the tumor
2. Functional Activity
3. Destruction Caused from growth/invasion
175
Wasting away of body fat and lean muscle mass is known as
Cachexia
176
When Cachexia occurs because of advanced cancer, it is known as
Cancer Cachexia
177
Widespread cancer having a hypermetabolic state on the body
Cancer Cachexia
178
____ is a cytokine that is commonly increased in the presence of advanced cancer or in states when cancer cachexia is present
Tumor Necreosis Factor (TNF)
179
Present in about half of all patients with advanced (metastatic) cancer
Cancer Cachexia
180
Collection of signs or symptoms that occur in someone with a neoplasia, most commonly an advanced cancer.
Paraneopalstic Syndrome
181
Paraneoplastic syndromes are most likely to manifest following ________ ________ or ______ _____
Hormonal Abnormalities
| Immune Dysregulation
182
Paraneoplastic syndromes occur in up to ____ of all cases of cancer representing the earliest manifestation of an occult
15%
183
Examples of Paraneoplastic Syndromes:
```
Cushing Syndrome
Hypercalcemia
Polycythemia
Acanthosis Nigricans
Hypertrophic Osteoarthropathy
```
184
What cancers are associated with Cushing Syndrome?
Lung Cancer (Small Cell Lung Cancer)
185
What cancers are associated with Hypercalcemia?
Lung Cancer, Breast Cancer, Renal Cancer, or Leukemia/Lymphoma
186
What cancers are associated with Polycythemia?
Renal Cancer, Liver Cancer
187
What cancers are associated with Acanthosis Nigricans?
Stomach Cancer, Lung Cancer, Uterine Cancer
188
What cancers are associated with Hypertrophic Osteoarthropathy?
Lung Cancer
189
An endocrine disorder involving elevated glucocorticoid levels (Hypercortisolism).
Cushing Syndrome
190
The most common reason for elevated glucocorticoids is receiving
Exogenous Glucocorticoid Medications (Steroids)
191
When Hypercortisolism results from a pituitary adenoma
Cushing Disease
192
Clinical features of Cushing Syndrome:
```
Weight Gain (moon face, buffalo hump)
Purple Striae (stretch marks)
Hypertension
Muscle Atrophy/Weakness
Osteoporosis
Hirsutism
Menstrual Abnormalities
Psychological Irregularities
```
193
Quantifies the tumor's level of cellular differentiation
Grading of Cancer
194
The higher the grade, the more ______ the cells of the tumor are and the worse the cancer's prognosis.
Anaplastic
195
Method for quantifying the tumor's extent of spread
Staging of Cancer
196
The higher the stage, the greater the extent of _____ and worse the prognosis.
Spread
197
T/F, Grading cancer has been shown to be of greater clinical value than staging cancer.
False
| ---Staging caner has been shown to be of greater clinical value than grading cancer---
198
Information for establishing a cancer's stage incorporates:
1. Size of primary tumor
2. Whether cancer has spread to the lymph nodes
3. Presence of hematopoietic metastasis
4. Information obtained during clinical examinations
5. Imaging Studies
199
The four histological (cellular) evaluations to examine a neoplasm:
1. Excision
2. Biopsy
3. Fine-Needle Aspiration
4. Cytological (Papanicolaou) Smear
200
Partial removal of an organ or tissue from the body
Excision
201
Removal of a smaller sample of cells
Biopsy
202
Imaging procedure used to view an illuminated and magnified image of the cervix
Colposcopy
203
Removal of cells via aspiration with a needle
Fine-Needle Aspiration
204
Most likely to be used with superficial tumors and easily palpated
Fine-Needle Aspiration
205
Examples of organs that can have fine-needle aspiration:
1. Breast
2. Thyroid
3. Lymph Nodes
4. Salivary Glands
5. Liver
6. Pancreas
206
a.k.a. "Pap smear", sampling of shed cells of the cervix
Cytological (Papanicolaou) Smear
207
Examples of organs that can have cytological smears:
1. Cervix
2. Endometrium
3. Meninges (CSF)
4. Bronchi
5. Urinary Bladder
6. Prostate
7. Stomach
208
Body's fluids may be sampled for biochemical abnormalities or irregular enzyme levels, which may indicate the presence of cancers, these types of techniques are known as
Tumor Markers
209
Tumor markers are best used for _______ purposes.
Screening
210
T/F. Tumor markers are diagnostic and can indicate the presence of cancer.
False
| ---Tumor markers are non-diagnostic and cannot indicate the presence of cancer, alone---
211
Evaluates for a specific prostate enzyme
Prostate-Specific Antigen Test (PSA Test)
212
PSA is secreted by the prostate gland and increased levels of PSA indicates _______ levels of prostate activity.
Elevated
213
May increase activity levels of the prostate gland:
1. Benign Prostatic Hyperplasia (BPH)
2. Recent ejaculation
3. Prostate Cancer
214
PSA Tests may be useful when _______ for suspected prostate cancer.
Screening
