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Block 7 Week 1 Colt > Cancer 201 - Barsky > Flashcards

Cancer 201 - Barsky Flashcards

1
Q

T/F: cancer incidence is synonymous with cancer mortality

A

false; highest incidence is prostate and breast for M and F but lung is the highest killer of both

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2
Q

(Carcinoma/sarcoma) causes 99% of all cancers

A

carcinoma

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3
Q

What tissue does carcinoma arise from?

A

epithelial tissue

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4
Q

what tissue does sarcoma arise from?

A

mesenchymal tissue

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5
Q

The increase in smoking in men in women post WWII with mortality increasing from the 70-90s, decades after the increase shows what property of cancer?

A

latency

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6
Q

What has caused the decrease in colorectal and prostate cancer?

A

better screening and regular colonoscopies

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7
Q

What test has reduced the risk of cervical cancer?

A

Pap smear

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8
Q

What four things does a flat line across an age-adjusted mortality chart tell you about that type of cancer?

A
  1. No good Tx for met. disease
  2. No good screening
  3. No decrease in incidence
  4. No good chemo-prevention
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9
Q

What caused the apparent “increase” in prostate and breast cancer in the early 90s?

A

better screening

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10
Q

Define the multi-hit theory of cancer development?

A

It takes numerous mutations over a lifetime to develop cancer

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11
Q

If cancer were dependent solely on rate of cell turnover, where would we see the most cancer? Since we don’t see that, what does it tell us?

A

Neonates and fetuses; that cancer is caused by more than just cell turnover

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12
Q

After a transformation event, what is the classification of a precancer cell?

A

tumorigenic

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13
Q

What takes a tumorigenic cell to an invasive cell?

A

selection pressure

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14
Q

Mutations, rearrangements, or amplifications of (blank) genes leads to tumor progression

A

proto-oncogenes

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15
Q

Reduction of (blank) of tumor suppressor genes caused by deletions or mutations also leads to tumor progression

A

homozygosity

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16
Q

What two types of epigenetic changes within promoters regulate cancer gene expression?

A

methylation and histone deacetylase statuses

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17
Q

Cancer is characterized by a (blank and blank) imablance

A

methylation and histone deacetylation

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18
Q

In terms of prevention, what does the multihit theory promote?

A

early screening and detection

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19
Q

(blank) explains why cancer is a disease of aging

A

multi hit theory

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20
Q

T/F: Cancer is a function of cell division

A

false

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21
Q

What type of cancers are completely curable via surgical resection?

A

carcinoma in situ–no invasion to lymphatics so you cut it out and its alllll gone

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22
Q

What explains the fact that most cancer happens after the age of procreation?

A

Since we’ve already had kids there was no selection pressure to cause us to develop a defense against it

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23
Q

What are the four defining properties of cancer?

A
  1. uncontrolled growth
  2. invasion and metastasis
  3. clonal dominance
  4. loss of differentiation
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24
Q

If tumors are monoclonal, then why can’t we cure cancer with a targeted agent?

A

tumors become heterogeneic via mutant subclones

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25
Q

Mutant subclones in tumors are heterogenous with respect to (blank x 4)

A

invasiveness, metastatic ablility, antigenicity and responsiveness to chemotherapy

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26
Q

What are the four classes of cancer treatment?

A
  1. surgery
  2. chemotherarpy
  3. radiation
  4. immunotherapy
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27
Q

T/F: The monoclonality of cancer means all cancer cells are identical

A

false

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28
Q

The lack of specific antigen, tumor cell heterogeneity, and micrometastais are all (blanks) in treating cancer

A

limitations

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29
Q

T/F: most 1st time diagnoses of cancer are not early enough to prevent micrometastasis

A

true :(

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30
Q

What is the lower limit for detectable cancer cells and what does this mean clinically?

A

fucking 1 million cells! means that even if the test is negative you have more than enough to fucking throw mets everywhere.

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31
Q

What are the etiologies/causes of cancer?

A 
environmental carcinogens
UV radiation
ionizing radiation
viruses
lifestyle, diet, immune status
hereditary factors/genes
unknown
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32
Q

What is the most common etiology of cancer?

A

unknown

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33
Q

Do direct or indirect chemical carcinogens activate the CYP450 system?

A

indirect–activation makes them a carcinogen

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34
Q

Chemical carcinogens are (nucleophiles/electrophiles). What does this mean about how they work?

A

Electrophiles; bind to the positive charge of DNA

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35
Q

When describing chemical carcinogens, (blanks) start the carcinogenic response while (blanks) accelerate it

A

initiators, promoters

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36
Q

Does an initiator or promoter bind directly to DNA and cause a mutation?

A

initiator

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37
Q

Promoters have (genetic/epigenetic) mech of action?

A

epigenetic

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38
Q

What is the result of promoter action?

A

promotes cell division to pass on mutations caused by initiators

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39
Q

What enzymees regulate initiator and promoter carcinogenicity?

A

phase I–CYP450

phase II–conjugation

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40
Q

T/F: carcinogenicity of DNA adducts is location dependent

A

true

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41
Q

Radon is a form of (blank) radiation

A

ionizing

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42
Q

How does ionizing radiation damage DNA?

A

forms DNA adducts

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43
Q

How does ionizing radiation differ in the way it damages DNA from chemical carcinogens?

A

ionizing radiation causes single and double stranded DNA breaks

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44
Q

What damage does ionizing and UV radiation cause?

A

csome breaks, translocations, and point mutations

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45
Q

What type of radiation leads to skin cancer?

A

UV

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46
Q

Pts with xeroderma pigmentosum are at an increased risk of skin cancer from what?

A

UV radiation

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47
Q

9% of children exposed to radiation develop what type of cancer?

A

thyroid

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48
Q

HPV 1,2,4,7 cause what?

A

papillomas or warts

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49
Q

What HPV strains cause cancer?

A

16 and 18

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50
Q

HPV 16 and 18 cause what type of cancer?

A

invasive squamous cell carcinoma

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51
Q

T/F: HPV 6 and 11 have high malignant potential

A

false; low

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52
Q

Early gene products (blank and blank) from HPV inhibit the two suppressor genes (blank and blank)

A

E6 and E7 inhibit TP53 and RB

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53
Q

T/F: full malignant potential of HPV is acheived through viral infection alone

A

false; requires environmental factors

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54
Q

What are the four tumor types associated with EBV?

A
  1. Burkitt’s lymphoma
  2. B cell lymphoma in AIDS
  3. Hodgkin’s disease
  4. Nasopharyngeal cancer in S. China
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55
Q

What cancer is associated with the translocation(8:14) - MYC gene?

A

Burkitt’s lymphoma

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56
Q

In nonendemic areas, what percent of the pop is infected with eBV?

A

20%

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57
Q

What type of cancer has the highest association to a viral infection? What is the virus that causes it?

A

99% of hepatocellular cancer is caused by Hep B

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58
Q

T/F: infection with Hep B is sufficient to reach the full malignant potential

A

false; multifatorial

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59
Q

injury and regeneration of the liver predispose one to mutations caused by (blank)

A

environmental agents; your liver is what detoxes what you take in!

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60
Q

What viral protein disrupts growth control by activating proto-oncogenes and inactivating TP53 in the liver?

A

HBx protein from HBV

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61
Q

Immunodeficient pts have a higher rate of what two classes of cancer?

A

lymphomas and virally induced

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62
Q

What are some of the lifestyle factors that influence cancer dev?

A

Women who are sexually promiscuous have a high rate of cervical cancer
Women who are nulliparous have a high rate of breast cancer
Men who are obese have a higher rate of cancer of the esophagus
Women who eat fatty foods have a higher rate of breast cancer
Men who drink alcohol and smoke have a higher rate of head and neck cancer
People who eat red meat may have a higher incidence of colon cancer.

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63
Q

T/F: Correlation can be causation, you just can be sure about it

A

true

64
Q

Many cancers have a familial component while few cancers have a (blank) component to be inherited

A

germline

65
Q

P53 Li Fraumeni, BRCA1/2, Lynch Syndrome, and Retinoblastoma are all examples of (familial/germline) cancers

A

germline

66
Q

(blank) codes for poducts associated with neoplastic formation

A

oncogenes

67
Q

T/F: oncogenes are regulated by normal growth factors and signals

A

false

68
Q

(blank) are normal genes that affect growth and differentiation

A

proto-oncogenes

69
Q

Retroviral transduction( v-oncs) and changes in situ converting them to c-oncs are (blank)

A

proto-oncogenes

70
Q

RAS mutations are (blank) mutations

A

point

71
Q

chromosomal (blank) is when part of the chromosome is moved near a promoter or chimeric gene product

A

translocation

72
Q

N-MYC neuroblastoma and HER-2 breast carcincoma are examples of gene (blank)

A

amplification

73
Q

What are the five basic categories of oncogenes?

A
  1. growth factors
  2. growth factor receptors
  3. signal transduction proteins
  4. nuclear transcription factors
  5. cyclins and cyclin dependent kinases
74
Q

Active kinases control what part of the cell cycle?

A

G1 to S transition

75
Q

When is cyclin D first phosphorylated?

A

at the beginning of G1

76
Q

When is Rb phosphorylated?

A

G1 to S transition

77
Q

During G2, M, and the beginning of G1, cdk is (active/inactive)

A

inactive

78
Q

Gene products that suppress cell proliferation include:

A

growth inhibitory factors
cell adhesion
signal transduction
nuclear transcription and cell cycle

79
Q

what is the guardian of the genome?

A

TP53

80
Q

What is one of the most commonly mutated genes and is seen in almost all human cancer?

A

TP53

81
Q

What are the two major functions of TP53?

A

antiproliferation and apoptosis

82
Q

TP53 senses DNA damage and halts the cell in what part of the cell cycle to allow for DNA repair?

A

G1

83
Q

increase of CDK1 p21(CDKN1A) prevents phosphorylation of what?

A

Rb

84
Q

Induction of GADD45 by TP53 aids in what?

A

DNA repair

85
Q

If TP53 cannot fix DNA what apoptosis gene is induced?

A

BAX

86
Q

Li Fraumeni is caused by inheriting one mutant of (blank or blank)

A

TP53 or RB

87
Q

T/F: Li Fraumeni puts you at an increased risk of metastasis of a single malignancy

A

false; risk of multiple types of malignancies

88
Q

What viruses can deactivate TP53?

A

HPV, HBV, EBV

89
Q

What gene is associated with childhood retinoblastoma?

A

RB

90
Q

What is the percentage breakdown of the methods of acquiring RB?

A

40% familial, auto DOM

60% sporadic

91
Q

What is the special case of multi-hit theory for RB? How is it different in inherited forms?

A

Needs 2 hits; one to take out each copy of the the gene. In inherited forms, one copy is already bad, so you only need one hit to get it

92
Q

What type of sarcoma do you have an increased risk of getting if you have RB?

A

osteosarcoma

93
Q

Homozygous mutation in both p53 and RB genes causing cancer is an example of (dominant/recessive) action

A

recessive, need both!

94
Q

Failure of only one oncogene allele is sufficient to cause cancer is an example of (recessive/dominant) action

A

dominant

95
Q

What types of collagen are present in the stroma?

A

collagen I and III

96
Q

what type of collegen is found in the basement membrane of the vascular channel?

A

collagen IV

97
Q

The active migration of neoplastic cells out of their tissue origin and across host tissue boundaries is defined as (blank)

A

Cancer invasion

98
Q

What are the two criteria that define a metastasis?

A
  1. secondary tumor colony discontinuous from the primary tumor
  2. must arise from a tumor cell translocated from the primary tumor
99
Q

Cancer must get into the circulation then (blank) to a secondary location to cause metastasis

A

egress

100
Q

T/F: invasion is synonymous with metastasis

A

false!!!

101
Q

what type of vasculature does carcinoma normally spread through?

A

lymphatics

102
Q

what type of vasculature does sarcoma normally spread through?

A

blood vessels

103
Q

What are the three routes by which a neoplasm can metastasize?

A
  1. lymphatic spread
  2. hematogenous spread
  3. transcoelomic seeding
104
Q

What organs are involved in hematogenous spread?

A

lung, liver, brain, bone marrow, and adrenals

105
Q

What organs are affected in transcoelomic seeding?

A

peritoneal, pleural, and pericardial and subarachnoid spaces

106
Q

Grading is the appearance (microscopically/anatomically) while staging is (microscopic/anatomic)

A

grade: microscopic
stage: anatomic

107
Q

What are the four levels of grading>?

A

well, moderately, poorly differentiated and undifferentiated

108
Q

What are the four steps involved in invasion?

A
  1. cell becomes less cohesive
  2. attachment to matrix components
  3. degradation of ECM
  4. migration
109
Q

reduction in E-cadherins facilitates what part of invasion?

A

cell becoming less cohesive

110
Q

laminin and fibronectin are important proteins that invading cells bind in the (blank)

A

ECM

111
Q

Collagenases and plasmin are (blank)proteinases used to break down the ECM

A

metalloproteinases

112
Q

What two factors allow for migration of the invading cells?

A

cytokines and ECM cleavage products

113
Q

When in the vasculature, tumor cells can form (blank) with leukocytes and platelets

A

emboli

114
Q

What determines cancer tissue tropism once it gets into the blood?

A
  1. vascular/lymphatic drainage
  2. tumor adhesion molecules
  3. microenvironment, eg proteases that inhibit binding
115
Q

What does tissue tropism allow us to determine about cancer?

A

Can help figure out what the primary lesion was when you have a met of unknown origin

116
Q

Tissue tropism of cancer is also known was what fancy name?

A

Soil Seed Hypothesis of Paget

117
Q

T/F: Systemic met. is an early event

A

true

118
Q

What clinical importance to CTCs have?

A

you can draw blood and test the cancer for biomarkers, chemo sensitivity and all kinds of shit

119
Q

t/f: oncogenes and suppressor genes are involved in mets. and invasion

A

false; they are only involved in growth disregulation

120
Q

T/F: a DTC is a met by definition

A

true; but a met is an actual grown tumor, a DTC is a single cell that may or may not become a tumore

121
Q

Cancer (blank) cells allows for cancers to repopulate even after a full response to surgery and chemo

A

cancer stem cells

122
Q

what percent of cancer cells are cancer stem cells?

A

0.1%

123
Q

Self-renewal, symmetrical and assymmetrical division and pluripotency are all properties of all (blank) cells

A

stem cells

124
Q

T/F: cancer stem cells are in a dormant state during active cancer

A

true; only involved in relapse or initial growth

125
Q

Cancer stem cells experess what type of stem cell pathway?

A

embryonic stem cell

126
Q 
Hedgehog
Notch
Bmi-1
Wnt
Pten
These are all pathways and proteins involved in what process?
A

stem cell self-renewal; they are also found in the developing fetus!

127
Q

Cancer cells tend to be CD44 (+/-) and CD24 (+/-)

A

CD44 pos and CD24 neg

128
Q

CSC with full malignant potential will lead to mets in what time period?

A

months to years

129
Q

CSC with partial malignant potential will show a period of (blank) followed by mets after many years

A

dormancy

130
Q

What happens during the dormancy period of partially malignant CSCs that reactivate them?

A

secondary hits or changes in the microenvironment

131
Q

Tumor (blank)may be a reflection of destroying the proliferating population of the tumor

A

regression

132
Q

Tumor (blank) may be a reflection of the resistant stem cell fraction repopulating the tumor.

A

recurrence

133
Q

T/F: tumor remission and response rates correlate with overall survival

A

false. :(

134
Q

T/F: any gene or gene product made by cancer is a potential biomarker

A

true, but they must be ALTERED so they are unique

135
Q

T/F: source of tumor biomarkers can be tissue, cytology, fluid, or serum

A

true

136
Q

Small cell lung cancer, SIADH, Eaton-Lambert Syndrome, cerebellar ataxia are all types of (blank) syndromes

A

paraneoplastic

137
Q

Cushing’s syndrome involves the release of what hormone?

A

ACTH

138
Q

small cell CA of the lung, pancreatic CA, and neural tumors that release ACTH are involved in what syndrome?

A

Cushing’s

139
Q

venous thrombosis involved in pancreatic and lung cancer is (blank) phenomena

A

Trousseu’s

140
Q

hypercalcemia associated with breast, renal, and squamous CA involves what hormone and cytokine?

A

PTHrP, TGFa

141
Q

what type of cancer presents with hypertrophic osteoarthropathy and clubbing of the fingers?

A

CA of the lung

142
Q

An increased met. rate despite reduced calorie intake leads to what state?

A

cachexia

143
Q

What cytokine is involved in cachexia?

A

TNFa

144
Q

PSA, CEA, and a-fetoprotein are all (blank) markers

A

tumor

145
Q

T/F: tumor markers definitively diagnose the type of cancer

A

false; used for staging, detecting recurrences and monitoring effectiveness of therapy

146
Q

What type of marker gives us info about prognosis, disease-FREE survival, overall survival, and length of latency?

A

Prognostic markers

147
Q

What is Ki-67?

A

index of cell turnover, used to indicate cancers that divide rapidly

148
Q

ER, Ki-67, p21 and p27 in prostate cancer, p53 in bladder cancer, and microsatellite gene instability products in colon cancer are what types of markers?

A

prognostic markers

149
Q

What do surrogate end point markers tell us?

A

tell us the effectiveness of a Tx strategy before direct tumoral assessments can be made

150
Q

When are surrogate end point markers most important?

A

during clinical trials

151
Q

mTOR pathway in Head/Neck CA and FvG-Actin in bladder CA are (prognostic/SEMs)

A

SEMs

152
Q

T/F: the prognostic biomarker is just as important as the drug

A

true

153
Q

T/F: A survival benefit will not be seen in a randomized trial if benefit is restricted to 10-15% of the study population.

A

true

154
Q

Clinically significant separation of Kaplan Meier curves in a randomized trial requires an effect in at least (blank) % of patients.

A

30-50

155
Q

t/f: patient selection is not important in determining the effectiveness of a chemotherapeutic

A

false

156
Q 
cDNA microarrays
Proteomics
Array CGH
Sequencing
Tissue microarrays (TMAs)
are all high throughput approaches to developing (blank)
A

tumor biomarkers

157
Q

BETTER SCREENING, CHEMOPREVENTION AND TARGETED THERAPY WILL ALL BE PREDICATED ON BETTER (blank)

A

tumor biomarkers

Block 7 Week 1 Colt (9 decks)

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