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Block 7 Week 1 > Cancer-Barsky > Flashcards

Cancer-Barsky Flashcards

1
Q

What does karkinos mean?

A

crab

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2
Q

What are the most common cancers for females and males?

A

females-> breast

males-> prostate

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3
Q

What are the most dangerous cancers for females and males?

A

lung and bronchus for both :(

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4
Q

What cancer has declined dramatically since the 1930s in males?

A

stomach cancer

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5
Q

What is the only cancer that has started to increase recently in males?

A

liver cancer!

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6
Q

What cancer has declined dramatically since the 1930s in females?

A

breast, uterine, stomach and colorectum cancer

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7
Q

Why do people think that some cancer deaths are decreasing?

A

better screaning, antibiotics

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8
Q

If your incidence rate for a cancer is a flat line, what does this mean?

A

we have shit screenings, prevention and treatments

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9
Q

Why was there a huge increase in incidence of prostate cancer and breast cancer?

A

because they got better screenings, they were always there we just didnt have a way to see them. So no cancer epidemic :)

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10
Q

Why would a mammogram be bad in a postmenopausal women?

A

cuz of radiation

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11
Q

WOmen should not get a pap smear until what age?

A

30

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12
Q

Cancer is a (blank) disease

A

genetic and epigenetic

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13
Q

What are the genetic causes of cancer?

A
  • mutations, rearrangments, or amplifications involving proto-oncogenes
  • reduction to homozygosity of tumor suppressor gene deletions or mutations
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14
Q

In addition to genetic alterations, many cancer genes are regulated (blank)

A

epigenetically

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15
Q

(blank) and (Blank) within promoters regulate gene expression of key cancer genes.

A

Methylation status and histone deacytylase status

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16
Q

Cancer is characterized by (blank) and (blank) imbalance

A

methyation and histone deacytylation

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17
Q

How do you go from a normal duct to an invasive ductal cancer?

A

normal duct-> intraductal hyperplasia-> intraductal hyperplasia with atypia-> intraductal carcinoma in situ-> invasive ductal cancer

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18
Q

Most cancers are (blank) events

A

multihit

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19
Q

Why is being a multihit event for cancer good?

A

promotes early detection and screening

explains why cancer is a disease of aging

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20
Q

Pap smears can detect (blank) before any invasion as occured.

A

dysplasia

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21
Q

where do you find blood vessels and lymphatics?

A

Only on the stromal side> NOT epithelial side

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22
Q

Are in situ cancers curable?

A

yes!!! because they havent escaped the epithelium so they havent gotten into the lymphatics and blood vessels. I.e. it hasnt metastasized so it can be surgically resected

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23
Q

Most cancers occur after the age of procreations. What does this mean for us?

A

that there is no evolutionary selection pressure, and that cancer is a disease of our own cells

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24
Q

What are the four properties of cancer?

A

uncontrolled growth
invasion and metastasis
clonal dominance
loss of differentiation

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25
Q

Is microinvasion terrible?

A

no, it can still be removed, but it does pose a risk

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26
Q

What is clonal dominance/ monoclonality?

A

cells of a given cancer have come from a single ancestor cell.

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27
Q

If tumors exhibit monoclonality how come all tumor cells are not the same?

A

because these monoclonal cells produce mutant subclones that are heterogeneous with respect to invasiveness, metastatic ability, antigenicity and responsiveness to chemotherapy

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28
Q

So explain how you can have monoclonality and heterogenity?

A

tumor cells all come from the same ancestor but express differently due to mutations

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29
Q

What are the four types of cancer therapies?

A

surgery
radiotherapy
chemotherapy
immunotherapy

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30
Q

What are limitations in treating cancer?

A

lack of a tumor specific antigen
tumor cell heterogeneity
micrometastasis

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31
Q

What are the causes of human cancer?

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

What makes a chemical carcinogen direct or indirect?

A

cytochrome P450

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33
Q

What are the chemical carcinogens?

A

eletrophiles,

initiatiors and promotors

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34
Q

What is this:

acts by forming DNA adducts which give rise to mutations

A

initiators

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35
Q

initiators tend to be (neutrophiles/electrophiles)?

A

electrophiles

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36
Q

What is a DNA adduct?

A

when carcinogens bind to DNA

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37
Q

What regulates chemical carcinogens?

A

Phase I and Phase II enzymes

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38
Q

How do chemical carcinogens work?

A

acts by forming DNA adducts which give rise to mutations; if mutations occur in hot spots, spots which change gene expression or protein, mutations can be carcinogenic; if mutations occur in introns or junk DNA or in the non-coding strang they can be harmless.

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39
Q

What is the action of UV radiation and other ionizing radiation?

A

formation of DNA adduts but can cause single and double strand DNA breaks

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40
Q

What does ionizing an UV radiation do?

A

causes chromosome breakage, translocations and point mutations

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41
Q

What does UV radiation lead to?

A

skin cancer

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42
Q

Who are at increased risk for skin cancer?

A

xeroderma pigmentosum

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43
Q

What happens to children with radiation exposure?

A

thyroid cancer

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44
Q

How many types of HPV are there?

A

80+

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45
Q

What strains of HPV causes papillomas or warts?

A

1,2,4,7

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46
Q

What strains of HPV are in almost 100% of invasive squamos cell carcinoma and carcinoma in-situ (CIS) of cervix?

A

16 and 18

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47
Q

What strains of HPV have low malignant potential?

A

6 and 11

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48
Q

How does HPV cause malignancy?

A

early gene products E6 and E7 inactivates tumor suppressor genes TP53 and RB, respectively
**full malignant potential requires other environmental factors*

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49
Q

What four tumors is EBV associated with?

A

Burkitt’s lymphoma
B cell lymphomas
Hodgkins disease
Nasopharyngeal cancer

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50
Q

Where is nasopharyngeal cancer endemic?

A

So. China

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51
Q

What is this:
cell proliferation with decreased immunoregulation
all associated with t(8:14) - MYC gene
nonendemic area only 20% have EBV

A

Burkitt’s lymphoma

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52
Q

What is hepatocellular cancer associated with?

A

Hep B virus

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53
Q

What is the greatest association with cancer?

A

Hep B

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54
Q

How does Hep B virus contribute to the incidence of hepatocellular cancer?

A

Injury and regeneration predispose to mutations with environmental agents
AND hepB protein disrupts growth control by activating protooncogenes, may inactivate TP53

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55
Q

Why does immunodeficiency accelerate viral cancers and not other cancers?

A

because viruses cause an antigenicity that the immune system can attack and with immune compromise your viral cancer wil accel. Breast cancer or something does cause an immune response so lack of immunity wont change the tumor.

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56
Q

(blank) hosts have a higher rate of certain cancers like lymphoma and virally-induced cancers.

A

immunodeficient

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57
Q

T or F

women who are nulliparious have a high rate of breast cancer

A

T

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58
Q

Men who are obese have a higher rate of cancer of the (blank)

A

esophagus

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59
Q

Women who eat fatty foods have a higher rate of (blank) cancer

A

breast

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60
Q

Men who drink alcohol and smoke have a higher rate of (blank) and (blank) cancer

A

head and neck

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61
Q

People who eat red meat have a higher incidence of (blank) cancer

A

colon

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62
Q

T or F

Many cancers have a familiar component; fewer cancers have an inherited component

A

T

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63
Q

T or F

some cancers are familial with genes not identified

A

T

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64
Q

T or F

some cancers are inherited (germline) with gene identified

A

T

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65
Q

What is Li-Fraumeni syndrome?

What does it cause and how do you get it?

A

Li-Fraumeni syndrome-1 is caused by heterozygous mutation in the p53 gene
-a hereditary disease that causes many kinds of cancers

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66
Q

What does BRCA1 and BRAC2 do?

A

they are genese associated with breast cancer

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67
Q

(blank), often called hereditary nonpolyposis colorectal cancer (HNPCC), is an inherited disorder that increases the risk of many types of cancer, particularly cancers of the colon (large intestine) and rectum, which are collectively referred to as colorectal cancer.

A

Lynch syndrome

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68
Q

(blank) is the condition of genetic hypermutability that results from impaired DNA Mismatch Repair (MMR)

A

Microsatellite instability (MSI)

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69
Q 
What are these:
P53 (LI-FRAUMENI SYNDROME)
BRCA1 AND BRCA2 IN BREAST CANCER
LYNCH SYNDROME AND MICROSATELLITE INSTABILITY GENES.
INHERITED RB
A

hereditary factors or genes that cause cancer

70
Q

T or F

most cancers are spontaneous and sporadic

A

T

71
Q

What are the 2 key properties of cancers?

A

property of growth in an uncontrolled manner

Property of invasion and metastasis

72
Q

(blank) code for products (oncoprotein) associated with neoplasic transformation

A

oncogenes

73
Q

How are oncogenes regulated?

A

they aren’t

74
Q

(blank) are normal genes that affect growth and differentiation

A

Protooncogenes

75
Q

How do you convert protooncogenes to oncogenes?

A

mutations or through a virus
(retroviral transduction V-oncs)
(changes in situ converting them to c-oncs)

76
Q

What is the most common way to get activation of oncogene?

A

point mutation via RAS

77
Q

What are the three ways to activate oncogenes?

A

point mutations, chromosomal translocations, gene amplifications

78
Q

How can chromosomal translocation cause activation of oncogenes?

A

moving the gene near a promotor or chimeric gene products

79
Q

Give me 2 examples of gene amplification that cause activation of oncogenes?

A

N-Myc neuroblastoma

HER-2 breast carcinoma

80
Q

What are the five basic categories of oncogenes?

A
  • growth factors
  • growth factors receptors
  • signal transducing proteins
  • nuclear transcription factors
  • cyclins and cyclin dependent kinase
81
Q

Cancer may be promoted due to inactivation of genes who’s products suppress cell proliferation. These are called (blank) genes.

A

cancer suppressor genes (antioncogenes)

82
Q

What are the four types of cancer suppressor genes?

A

growth inhibitory factors
molecules that regulate cell adhesion
molecules that regulate signal transduction
molecules that regulate nuclear transciption and cell cycle

83
Q

What is one of the most commonly mutated genes seen in virutally all types of human cancers?

A

TP53 (the guardian of the genome)

84
Q

What does TP53 do?

A

it sense DNA damage and arrests G1 and induces DNA repair
AND
If DNA cannot be repaired it induces BAX (apoptosis gene)

85
Q

how does TP53 sense DNA damage and arrest the cell in GI and induce DNA repair?

A

by increased CDK1 p21 (CSKN1A) preventing phosphorylation of RB and
Induces GADD45 which aids in DNA repair

86
Q

What is this
Inherit one mutant TP53 (or RB)
Marked increased risk of multiple types of malignancies
Requires mutation of second normal allele

A

Li Fraumeni Syndrome

87
Q

TP53 can be inactived by certain DNA viruses. What are they?

A

Oncogenic HPV, HBV, possibly EBV

88
Q

THe RB gene is associated with the childhood tumor (blank)

A

retinoblastoma

89
Q

What percentage of retinoblastoma is familial AND How is it inherited? sporadic?

A

40% (Autosomal dominant)

60%

90
Q

Explain the famous 2 hit retinoblastoma hypothesis.

A

2 normal RB loci requires both genes to be inactivatd by somatic mutation.
BUT
in familial cases with only one normal gene, need only 1 hit.

91
Q

What gives you an increased risk of sarcomas and osteosarcomas?

A

familial RB gene

92
Q

In addition to genetic alterations, many cancer genes are regulated (blank)

A

epigenetically

93
Q

Methylation status and histone deacytylase status within promoters regulate (blank) of key cancer genes

A

gene expression

94
Q

Cancer is characterized by (blank) and (Blank) imbalance

A

methylation and histone deacytylation

95
Q

What is the definition of cancer invasion?

A

active migration of neoplastic cells out of their tissue of origin and across host tissue boundaries

96
Q

What is this an example of:

invasion of carcinoma cells arising in epithelium through basement membrane and into adjacent CT

A

cancer invasion

97
Q

What is this:
A secondary tumor colony discontinuous from the primary tumor. Arising from a tumor cell translocatd from the primary tumor.

A

definition of metastasis

98
Q

Invading cancers must get into the (blank) or (blank) to metastasize

A

circulation

lymphatics

99
Q

Metastasis requires (blank). But (blank) does not mean you have metastasis

A

invasion

invasion

100
Q

What kind of tumor does not need to “invade” (i.e break through the basement membrane to be dangerous)

A

sarcomas because they arise from the mesenchyme so they dont have a surounding basement membrane (makes it difficult to tell if they are malignant or not)

101
Q

(Blank) spread through the lymphatics (usually but can also travel through circulation). (blank) spread through the blood vessels.

A

carcinomas

sarcomas

102
Q

Malignant neoplasms metastasize by three main routes, what are they?

A

lymphatic spread
hematogenous spread
transcoelomic spread (seeding of body cavities)

103
Q

When you have lymphatic spread, what lymph nodes are affected first?

A

regional lymph nodes

104
Q

When you have hematogenous pread, what are often affected first?

A

lung, liver, brain, bone marrow, adrenals

105
Q

When you have transcoelomic spread, what does it affect?

A

periotoneal, pleural, pericardial and subarachnoid spaces

106
Q

How do you grade and stage cancer?

A

Grade via microscope (I-IV)

Stage-anatomic extent of tumor (TNM, AJC)

107
Q

What does TNM stand for?

A

Tumor
Nodes
Metastases

108
Q

Explain the levels of TNM

A

T 0-3
N 0-2
M 0-1-x

109
Q

Grading informs us of (blank) and dictates (blank)

A

prognosis

therapy

110
Q

Is the staging of tumors the same for all cancers?

A

no it is is not

111
Q

T or F

most patients that come in already have micrometastasis

A

T

112
Q

Grading is a measure of the degree of (blank). Staging is a measure of the (blank)

A

differentation/loss of differentiation

invasion and metastasis

113
Q

Can carcinomas metastasize without having nodes?

A

yes

114
Q

What happens to cells during invasion?

A

the cells become less cohesive, you lose expression of adhesion molecules (lose attachment to matrix)

115
Q

What does laminin and fibronectin do?

A

allow for cell attachment to matrix

116
Q

What do tumor cells excrete to get reduce the structrue of the ECM?

A

metalloproteinases (collagenases and plasmin)

117
Q

How do cancer cells get places?

A

they have increased motility because they release cytokine and the cleavage products from teh ECM aid migrations

118
Q

What can tumor cells form with leukocytes and platelets?

A

embolii

119
Q

How do tumor cells disseminate?

A

they can form emboli or can circulate as single cells

120
Q

How does a tumor cell end up where its supposed to end up?

A

organ tropism, it depends on vascular and lymphatic drainage, tumor adhesion moecules, microenvironment

121
Q

What can proteases do to tumor cells?

A

inhibit attachment to organs

122
Q

Do you always know where something has metastasized from?

A

no

123
Q

Is systemic metastasis an early event?

A

yes

124
Q

Whats the evidence that systemic metastasis is an early event?

A

circulating tumor cells (CTS’s) and disseminated tumor cells (DTC’s)

125
Q

What is the difference between a metastasis and a disseminated tumor cell?

A

a metastasis is a disseminated tumor cell that grows while diseminated tumor cells are latent

126
Q

Explain the new cancer stem cell theory

A

There is a small population of cells that have the ability to divide that usually remain dormant and resist chemo and radiation :(

127
Q

What are the 5 different types of stem cells?

A 
embryonic stem cells
induced pluripotent stem cells
adult (somatic) stem cells
stem cells in tissue homeostasis
cancer stem cells
128
Q

What is symmetrical and assymetrical cell division and what can do this?

A

stem cells
symmetrical-same
assymetrical- terminaly different differentiated cell

129
Q

What is pluripotency?

A

the cell can differeniate along all 3 germ cell lines

130
Q

What are the properties of cancer stem cells?

A
  1. exist in a resting or dormant state
  2. resist chemotherapy and radiotherapy
  3. express embryonic stem cell pathways
  4. replenish the dividing cell population of the tumor
131
Q

What are the 5 pathways that are involvd in stem cell self renewal?

A
  • hedgehog
  • notch
  • Bmi-1
  • Wnt
  • Pten
132
Q

Stem cells tend to be cd 44 (blank) and CD 24 (blank)

A

positive

negative

133
Q

How can you get TDC without mets?

A

you have TDC that doesnt contain any CSC (cancer stem cells)

134
Q

What happens if you have TDC where most of the cells are CSC?

A

you have full malignant potential-> mets in a few months to years -> hits up other sites too

135
Q

What happens when you have TDC with some of the cells being CSC?

A

you have partial malignancy potential which can result in dormancy followed by metastases after many years (can occur due to a hit or change in microenvironment)

136
Q

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

A

tumor regression

137
Q

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

A

recurrence

138
Q

Sine recurrence and regression seem to be dependent on the properties of CSC, what does this mean?

A

that remission or response rates may not correlate with overall survival

139
Q

Any gene or gene produt altered in tumor progression is a potential (blank)

A

tumor marker

140
Q

Tumor cells shed or secrete (blank)

A

gene products

141
Q

What are the sources of tumor markers?

A

tissue, cytology, fluid or serum

142
Q

What are the four types of biomarkers?

A

tumor markers (cancer markers)
prognostic markers
surrogate end point markers
predictive markers

143
Q

HOw often do you see paraneoplastic syndromes?

A

10-15% of all cancers

144
Q

What might be the first sign of malignancy?

A

paraneoplastic syndromes

145
Q

What are some examples of paraneoplastic syndromes?

A

cushings syndrome
venous thrombosis
hypercalcemia
hypertrophic osteoarthropathy and clubbing of fingers

146
Q

A (blank) is a disease or symptom that is the consequence of cancer in the body but, unlike mass effect, is not due to the local presence of cancer cells. These phenomena are mediated by humoral factors (by hormones or cytokines) excreted by tumor cells or by an immune response against the tumor.

A

paraneoplastic syndrome

147
Q

What kinds of tumors can result in cushings syndrome?

A

small cell CA of lung, pancreatic CA, neural tumors

148
Q

What kind of tumors can result in venous thrombosis- Trousseu’s phenomenon?

A

pancreatic, lung and other carcinomas

149
Q

What kind of tumors can result in hypercalcemia, PTHrP, TGF alpha?

A

breast, renal, and squamost cell CA

150
Q

What kind of tumors can result in hypertrophic osteoarthropathy and clubbing of fingers?

A

carcinoma of lung

151
Q

What is this:
weakness and wasting of the body due to severe chronic illness.
wt. loss, weakness, anorexia, anemia

A

Cachexia

152
Q

What causes Cachexia?

A

mulifactorial causes, but increased metabolic rate despite reduced calorie intake

153
Q

What is cachexin thought to be due to?

A

TNF-alpha and other cytokines

results in weight loss and muscle breakdown

154
Q

Serum biochemical analysis gives you what?

A

enzymes, hormones and tumor markers

155
Q

What are PSA, CEA and alpha fetoprotein (AFP)?

A

tumor markers

156
Q

What are PSA, CEA and alpha fetoprotein (AFP) can these be used for?

A

May not definitively diagnose, but can used for staging, detecting recurrences and monitoring effectiveness of therapy.

157
Q

(blank) markers give us information about prognosis; disease free survival, overall survival, length of latency

A

prognostic markers

158
Q

What is the prognostic marker for ER and Ki67 for?

A

breast cancer

159
Q

What is the prognostic marker for colon cancer?

A

microsatellite instability gene produts

160
Q

What is the prognostic marker for prostate cancer?

A

p21 and p27

161
Q

What is the prognostic marker for bladder cancer?

A

p53

162
Q

What give us information regarding the effectiveness of a chemopreventive or therapeutic strategy before direct tumoral measurements can be assessed?

A

surrogate end point markers (SEMs)

163
Q

What is anothe rname for a surogate end point marker?

A

intermediate marker

164
Q

What are the mTOR pathway in minimal residual diseases of the head and neck and the F v G actin levels in bladder cancer?

A

surrogate end point markers (SEMs)

165
Q

What do predicitve markers do?

A

guide therapy ( first line generalized treatment, then second line generalized treatment etc)

166
Q

What is personalized medicine?

A

built on premise that lab tests can accurately predict the response of individual patients to a particular treatment

167
Q

What is this:
Built on the premise that laboratory tests can accurately predict the response of individual patients to a particular treatment.
Most drugs are prescribed on the basis of “one size fits all”.
Aims to eliminate the “trial and error” practice of matching the right drugs to the right patients.
Driven by scientific innovation and better understanding of disease heterogeneity.
Patients, doctors, payers, regulators expect it to happen.
The future of Medicine.

A

personalized medicine

168
Q

What was the first FDA approved predictive test for HER2 screening?

A

hercep test

169
Q

THe (blank) is as important as the drug

A

PREDICTIVE BIOMARKER!

170
Q

What are the 5 high throughput approaches to finding tumor biomarkers?

A 
cDNA microarrays
proteomics
array CGH
sequencing
Tissue microarrays (TMAs)
171
Q

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

A

TUMOR BIOMARKERS

Block 7 Week 1 (10 decks)

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