Ch 7: Neoplasia Flashcards

1
Q

what are the hallmarks of cancer

A

set of properties that produce certain cellular phenotypes that dictate the natural history of cancer and response to therapy

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2
Q

what is neoplasia

A

new tissue growth that is unregulated, irreversible, and monoclonal

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3
Q

what is monoclonal

A

neoplastic cells derived from a single mother cell

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4
Q

what is benign

A

microscopic and gross features are innocent, the humor is localized, and easily removable

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5
Q

what is malignant

A

lesion can invade and destroy nearby structures, can spread, and can cause death

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6
Q

what are the two basic microscopic components of neoplasia

A

parenchyma is made of transformed cells
supporting host stroma contains connective tissue, blood vessels, and inflammatory cells

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7
Q

what is a fibroma

A

benign growth of fibrous tissue

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8
Q

what is a chondroma

A

benign growth of cartilage

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9
Q

what is an adenoma

A

benign lesion that produced gland-like features

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10
Q

what is a papilloma

A

benign lesion on the surface that produces fronds

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11
Q

what is a cystadenoma

A

benign hollow cystic mass
usually in ovary

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12
Q

what is a sarcoma

A

malignant tumor of mesenchymal tissue

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13
Q

what are leukemias and lymphomas

A

malignant tumor of mesenchymal cells in the blood

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14
Q

what is a carcinoma

A

malignant tumor of epithelial cells

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15
Q

what is an adenocarcinoma

A

malignant, epithelial tumor with glandular pattern of growth

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16
Q

what is a squamous cell carcinoma

A

malignant, epithelial tumor that produces squamous cells

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17
Q

what does differentiation mean

A

when new growing parenchymal cells resemble the corresponding normal parenchymal cells
(does the cell still look and function like itself)
if poorly differentiated, suggestive of malignancy

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18
Q

what is divergent differentiation and what are three examples

A

mixed tumors due to the progenitor cell having the ability to differentiate into more than one lineage
ex. pleomorphic adenoma, fibroadenoma, and teratoma

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19
Q

what is a pleomorphic adenoma

A

mixed salivary gland tumor made of a epithelial component and fibromxyoid stroma
example of divergent differentiation

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20
Q

what is a pleomorphic tumor

A

tumor with more than one form; mixed tumors

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21
Q

what is a fibroadenoma

A

proliferating ductal elements and in loose fibrous tissue
example of divergent differentiation

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22
Q

what is a teratoma

A

mixed tumor of mature and immature elements derived from one or more germ layers
example of divergent differentiation

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23
Q

what is a solitary fibrous tumor

A

benign, lung pleural tumor made of solid dense fibrous tissue
not linked to asbestos exposure

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24
Q

what is malignant mesothelioma and what is it caused by

A

malignant lung pleural tumor with disseminated nodules or plaques
spreads
caused by homozygous deletion of chromosome 9p leading to loss of the tumor suppressor gene CDKN2A

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25
Q

what is a hamartoma

A

benign mass of proliferating cartilage outside of the bronchial tree in the lung parenchyma
appear as coin lesions

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26
Q

what is a choristoma

A

a benign congenital anomaly consisting of a heterotropic nest of cells in a place where they shouldn’t be
believed to occur during embryonic development

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27
Q

what is a lingual osseous choristoma

A

benign area of bone found in the tongue due abnormal folding during embryonic development

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28
Q

what is a choristoma of foregut

A

presence of pancreatic tissue in different places of the foregut or mesentery

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29
Q

what is anaplasia

A

lack of differentiation - cells don’t look like they should
indication of malignancy

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30
Q

what is hyperchromatic

A

darkly stained nuclei that is suggestive of malignancy

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31
Q

what is pleomorphism

A

variation in size and shape of tumor cells that is suggestive of malignancy

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32
Q

what is anisonucleosis

A

variation in size and shape of nuclei that is suggestive of malignancy

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33
Q

what is nuclei-cytoplasmic ratio

A

ratio of size of nucleus to cell (normal is 1:4 - 1:6)
can increase 1:1 and be suggestive of malignancy

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34
Q

what are nucleolar changes

A

prominent or lots of changes in the nucleolus which are suggestive of malignancy

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35
Q

what is loss of polarity

A

disrupted orientated of cells (they become crooked) which is suggestive of malignancy

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36
Q

what are mitotic figures

A

numerous mitotic figures which can be suggestive of malignancy
easiest thing to recognize malignancy through

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37
Q

what are tumor giant cells

A

multinucleate tumor giant cells with large bizarre nuclei that are suggestive of malignancy

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38
Q

what are functional changes

A

certain things like glands stop functioning which can be suggestive of malignancy

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39
Q

what are chromosomal abnormalities in relation to malignancy

A

those with certain chromosomal abnormalities are more susceptible to malignancy

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40
Q

what are a few of the main differences between a benign and malignant tumor

A

capsulated vs non-capsulated
slow vs fast growing
metastasis
cell morphology
necrosis vs no necrosis
invasive vs non-invasive

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41
Q

what are the three pathways of malignant dissemination (metastasis)

A

seeding
lymphatic spread
hematogenous spread

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42
Q

what is seeding within the body cavities

A

a metastasis mechanism where seeds of the tumor break off and spread to other areas
typical of ovarian cancers going to peritoneal surfaces

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43
Q

what is lymphatic spread and which cancers use it most

A

tumor travels through lymphatics
typical of carcinomas like breast cancer

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44
Q

what is hematogenous spread and which cancers use it most

A

tumor spreads through vascular supply
typical of sarcomas

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45
Q

what is a sentinel lymph node

A

the first node in a regional lymphatic basin that receives lymph flow from the primary tumor

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46
Q

what are the four steps of metastasis

A

1.) loosening of cell to cell contacts
2.) degradation of the extracellular matrix
3.) attachment to the novel extracellular matrix components
4.) migration of tumor cells

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47
Q

what is loss of cell-to-cell contacts

A

first step of metastasis which is caused by inactivation of E-cadherin by a variety of pathways

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48
Q

what is the breakdown of the extra-cellular matrix

A

second step of metastasis which is mediated by proteolytic enzymes secreted by the tumor and stroma

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49
Q

what is the attachment of extra-cellular matrix components

A

third step of metastasis where proteolytic enzymes release growth factors that cleave fragments from the ECM

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50
Q

what is the migration of tumor cells

A

fourth step of metastasis where tumor moves, usually to a specific site

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51
Q

what is organ tropism

A

when a primary tumor metastasizes to a specific site

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52
Q

where do breast, colon, kidney, and lung cancers like to metastasis to

A

liver and lung

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53
Q

what is skip metastasis

A

cancer reaches blood vessel by thoracic duct

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54
Q

which tumor tends to grow in veins

A

renal cell carcinoma

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55
Q

what is the relationship between age and cancer

A

as you age, you’re more likely to get cancer

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56
Q

cancer accounts for what % of all deaths in children under 15

A

10%

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57
Q

what are three acquired predisposing conditions to cancer

A

chronic inflammation (IBD)
immunodeficiency status (HIV)
precursor lesions (cervical dysplasia)

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58
Q

what are proto-oncogenes

A

genes that are essential for cell growth and differentiation
once mutated, become oncogenes which lead to unregulated cell growth

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59
Q

what is p53

A

protein produced by the tumor suppressor gene TP53 gene
regulates progression of cell cycle from G1 to S phase (guardian of the genome)
induces apoptosis if cells are beyond repair

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60
Q

what is the most frequently mutated gene in human cancers

A

TP53
50% of cancer cases have this gene mutated

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61
Q

what is Li-Fraumeni Syndrome

A

mutation in TP53 gene with one defective copy
gives a 25-fold greater chance of developing a malignant tumor before age of 50
can cause: sarcoma, breast cancer, leukemia, brain cancer, and adrenal cortex cancer

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62
Q

what is RB gene

A

tumor supressor gene that regulates progression of cell cycle from G1 to S phase
called governor of cell cycle
if both alleles are mutated, leads to retinoblastoma

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63
Q

what do tumor suppressor genes do

A

stop cell proliferation

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64
Q

what are some hallmarks of cancer

A

self sufficient in growth signals
insensitive to growth inhibitory signals
altered cell metabolism
won’t go through apoptosis
limitless replicative potential
angiogenesis
metastasis
evasion of immune surveillance

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65
Q

what is a point mutation

A

mutation in single nucleotide that can either activate or deactivate protein products
convert porto-oncogenes to oncogenes
can reduce suppressor genes ability to suppress

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66
Q

what is the most common, point mutated oncogene

A

KRAS (rat sarcoma)
seen in 30% of tumors
higher in pancreatic adenocarcinoma

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67
Q

what are passenger mutations

A

acquired genes that are neutral and do not affect cell behavior
occur randomly throughout genome

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68
Q

what are driver mutations

A

alter function of cancer genes and directly contribute to the development or progression of a given cancer
usually acquired but can be inherited

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69
Q

what are gene rearrangements

A

translocation or inversions
seen commonly in hemopoietic or mesenchymal derived malignancies
can activate proton-oncogenes
occur mostly in lymphoid tumors

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70
Q

what are gene deletions

A

deletion of specific regions of chromosomes can lead to loss of particular tumor suppressor gene

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71
Q

what are gene amplifications

A

porto-oncogenes converted into oncogenes during amplification
leads to over-expression of normal protein

72
Q

what are epigenetic modifications

A

stable and heritable alterations in gene expression and cellular function without changes to original DNA sequence
regulate gene expression

73
Q

what is APC gene

A

adenomatous polypsis coli - gatekeeper of colonic neoplasms
tumor suppressor genes that down regulate growth promoting signal pathways

74
Q

what is von Hipple-Lindau gene

A

targets other proteins to be broken down when not needed
mutation causes von Hipple Syndrome which is associated with renal cell cancers

75
Q

what is HNPCC (hereditary nonpolyposis colon cancer syndrome)

A

Lynch syndrome
mutation that causes deficits in the mismatch repair system leading to carcinomas of the colon

76
Q

what is xeroderma pigmentosum

A

rare genetic syndrome with a defective DNA nucleotide excision repair
presents with extreme sensitivity to UV light and has a high risk of developing skin cancer

77
Q

how is angiogenesis controlled/regulated/treated

A

triggered by hypoxia
regulated by p53 protein, RAS, and MYC
treated using VEGF inhibitors

78
Q

what is VEGF

A

proangiogenic factor released by tumor cells
increases blood vessel expression and movement to tumor

79
Q

what is cancer immunoediting

A

ability for a neoplasm to shape its immunogenic properties to avoid elimination
creates immune tolerance and immune suppression

80
Q

what is the most important class of tumor antigens

A

oncogenic viruses

81
Q

what are three stages of cancer enabling inflammation

A

anemia
fatigue
cachexia

82
Q

how does inflammation effect the tumor microenvironment (TME)

A

causes:
proliferation
unregulated growth
invasion and metastasis
resistance to cell dead
resistance to therapy

83
Q

explain the two steps of chemical carcinogenesis

A

initiation: cells exposed to sufficient dose of carcinogen to cause mutations (cells now initiated)
promotors: promotors cause cell proliferation of initiated (mutated) cells; cells pick up more mutations on the wall until they become cancer

84
Q

what is a direct acting carcinogen

A

chemicals that require no metabolic conversion to become carcinogenic
most are weak as carcinogens
can cure cancers but cause a second form (acute myeloid leukemia)

85
Q

what is an indirect acting carcinogen and give three examples

A

chemicals that require metabolic conversion to become active carcinogens (ultimate carcinogen)
ex. polycyclic hydrocarbons, aromatic amines, and azo dyes

86
Q

what is a “hotspot”

A

clustered mutations in specific sequences or bases

87
Q

what are promotors

A

chemical agents that stimulate cell proliferation and expansion of a clone of mutated cells

88
Q

what is a quiescent tissue

A

one that is not actively dividing

89
Q

what is a mitogenic stimulus

A

small protein that stimulates mitosis

90
Q

what are three types of carcinogenic radiant energy

A

UV rays of sunlight
ionizing electromagnetic
particulate radiation

91
Q

what is human T-cell Leukemia Virus Type 1

A

a type of retrovirus that causes adult T-cell leukemia/lymphoma

92
Q

what is a retrovirus

A

virus that inserts a copy of its RNA genome into DNA of a host cell that it invades, thus changing the genome of that cell

93
Q

which types of HPV cause benign squamous papilloma’s

A

1,2,4, and 7

94
Q

high risk types of HPV, 16 and 18, are known to cause which three types of squamous cell carcinomas

A

cervix
anogenital region
head and neck

95
Q

which strains of HPV are genital warts

A

6 and 11

96
Q

what is Burkitt lymphoma

A

a disease caused by Epstein-Barr virus
causes nasopharyngeal and gastric cancers

97
Q

what percent of hepatocellular carcinomas are caused by infection with Hep B or Hep C

A

70 to 85%

98
Q

what are the oncogenic effects of Hep B and Hep C

A

chronic inflammation and hepatocyte death

99
Q

what is Helicobacter pylori

A

bacteria that causes peptic ulcers, gastric adenocarcinomas, and gastric lymphoma of B cell origin

100
Q

what is thought to be the cause of cachexia in cancer patients

A

TNFalpha (cachectin)

101
Q

what is type 1 hypercoagulability

A

balance of endogenous heparin production and degradation is disturbed with increase degradation of heparin by tumor-secreting heperanse

102
Q

what is type 2 hypercoagulability

A

procoagulant molecules secreted from tumor cells, leading to hypercoagulability

103
Q

what are paraneoplastic syndromes

A

when cancer patients have signs and symptoms that cannot be explained by the tumor
occurs in 10% of patients

104
Q

what types of cancers can cause cushings

A

small cell carcinoma of lung
pancreatic carcinoma
neural tumors

105
Q

what 4 types of cancers can cause hypercalcemia

A

squamous cell carcinoma of lung
breast carcinoma
renal carcinoma
adult T-cell leukemia

106
Q

what are the two processes involved in cancer-associated hypercalacemia

A

osteolysis (breaking down of bone cells)
production of calcemic humoral substances by extra osseous neoplasms

107
Q

what is a tumor marker

A

present in or produced by cancer cells in response to cancer or other condition
provides information about a cancer like how aggressive it is or what kinda of treatment it needs

108
Q

explain grading of a cancer

A

based on degree of differentiation of cells
ex. changing architecture in the cells (nuclei size)
low to high grade

109
Q

explain staging of a cancer

A

based on size/invasion of the primary lesion, its spread, and metastasis
more helpful than grading
uses TNM system

110
Q

what does T0 mean

A

no tumor

111
Q

which staging system is used for prostate

A

Gleason’s grading pattern

112
Q

which staging system is used for breast

A

Nottingham Histology scoring system

113
Q

new tissue growth that is unregulated, irreversible, and monoclonal

A

what is neoplasia

114
Q

neoplastic cells derived from a single mother cell

A

what is monoclonal

115
Q

benign growth of fibrous tissue

A

what is a fibroma

116
Q

benign growth of cartilage

A

what is a chondroma

117
Q

benign lesion that produced gland-like features

A

what is an adenoma

118
Q

benign lesion on the surface that produces fronds

A

what is a papilloma

119
Q

benign hollow cystic mass
usually in ovary

A

what is a cystadenoma

120
Q

malignant tumor of mesenchymal tissue

A

what is a sarcoma

121
Q

malignant tumor of mesenchymal cells in the blood

A

what are leukemias and lymphomas

122
Q

malignant tumor of epithelial cells

A

what is a carcinoma

123
Q

malignant, epithelial tumor with glandular pattern of growth

A

what is an adenocarcinoma

124
Q

malignant, epithelial tumor that produces squamous cells

A

what is a squamous cell carcinoma

125
Q

when new growing parenchymal cells resemble the corresponding normal parenchymal cells
(does the cell still look and function like itself)
if poorly differentiated, suggestive of malignancy

A

what does differentiation mean

126
Q

mixed tumors due to the progenitor cell having the ability to differentiate into more than one lineage
ex. pleomorphic adenoma, fibroadenoma, and teratoma

A

what is divergent differentiation and what are three examples

127
Q

mixed salivary gland tumor made of a epithelial component and fibromxyoid stroma
example of divergent differentiation

A

what is a pleomorphic adenoma

128
Q

tumor with more than one form; mixed tumors

A

what is a pleomorphic tumor

129
Q

proliferating ductal elements and in loose fibrous tissue
example of divergent differentiation

A

what is a fibroadenoma

130
Q

mixed tumor of mature and immature elements derived from one or more germ layers
example of divergent differentiation

A

what is a teratoma

131
Q

benign, lung pleural tumor made of solid dense fibrous tissue
not linked to asbestos exposure

A

what is a solitary fibrous tumor

132
Q

malignant lung pleural tumor with disseminated nodules or plaques
spreads
caused by homozygous deletion of chromosome 9p leading to loss of the tumor suppressor gene CDKN2A

A

what is malignant mesothelioma and what is it caused by

133
Q

benign mass of proliferating cartilage outside of the bronchial tree in the lung parenchyma
appear as coin lesions

A

what is a hamartoma

134
Q

a benign congenital anomaly consisting of a heterotropic nest of cells in a place where they shouldn’t be
believed to occur during embryonic development

A

what is a choristoma

135
Q

benign area of bone found in the tongue due abnormal folding during embryonic development

A

what is a lingual osseous choristoma

136
Q

presence of pancreatic tissue in different places of the foregut or mesentery

A

what is a choristoma of foregut

137
Q

lack of differentiation - cells don’t look like they should
indication of malignancy

A

what is anaplasia

138
Q

darkly stained nuclei that is suggestive of malignancy

A

what is hyperchromatic

139
Q

variation in size and shape of tumor cells that is suggestive of malignancy

A

what is pleomorphism

140
Q

variation in size and shape of nuclei that is suggestive of malignancy

A

what is anisonucleosis

141
Q

prominent or lots of changes in the nucleolus which are suggestive of malignancy

A

what are nucleolar changes

142
Q

disrupted orientated of cells (they become crooked) which is suggestive of malignancy

A

what is loss of polarity

143
Q

certain things like glands stop functioning which can be suggestive of malignancy

A

what are functional changes

144
Q

a metastasis mechanism where seeds of the tumor break off and spread to other areas
typical of ovarian cancers going to peritoneal surfaces

A

what is seeding within the body cavities

145
Q

tumor travels through lymphatics
typical of carcinomas like breast cancer

A

what is lymphatic spread and which cancers use it most

146
Q

tumor spreads through vascular supply
typical of sarcomas

A

what is hematogenous spread and which cancers use it most

147
Q

the first node in a regional lymphatic basin that receives lymph flow from the primary tumor

A

what is a sentinel lymph node

148
Q

when a primary tumor metastasizes to a specific site

A

what is organ tropism

149
Q

cancer reaches blood vessel by thoracic duct

A

what is skip metastasis

150
Q

genes that are essential for cell growth and differentiation
once mutated, become oncogenes which lead to unregulated cell growth

A

what are proto-oncogenes

151
Q

protein produced by the tumor suppressor gene TP53 gene
regulates progression of cell cycle from G1 to S phase (guardian of the genome)
induces apoptosis if cells are beyond repair

A

what is p53

152
Q

mutation in TP53 gene with one defective copy
gives a 25-fold greater chance of developing a malignant tumor before age of 50
can cause: sarcoma, breast cancer, leukemia, brain cancer, and adrenal cortex cancer

A

what is Li-Fraumeni Syndrome

153
Q

tumor supressor gene that regulates progression of cell cycle from G1 to S phase
called governor of cell cycle
if both alleles are mutated, leads to retinoblastoma

A

what is RB gene

154
Q

mutation in single nucleotide that can either activate or deactivate protein products
convert porto-oncogenes to oncogenes
can reduce suppressor genes ability to suppress

A

what is a point mutation

155
Q

acquired genes that are neutral and do not affect cell behavior
occur randomly throughout genome

A

what are passenger mutations

156
Q

alter function of cancer genes and directly contribute to the development or progression of a given cancer
usually acquired but can be inherited

A

what are driver mutations

157
Q

stable and heritable alterations in gene expression and cellular function without changes to original DNA sequence
regulate gene expression

A

what are epigenetic modifications

158
Q

targets other proteins to be broken down when not needed
mutation causes von Hipple Syndrome which is associated with renal cell cancers

A

what is von Hipple-Lindau gene

159
Q

Lynch syndrome
mutation that causes deficits in the mismatch repair system leading to carcinomas of the colon

A

what is HNPCC (hereditary nonpolyposis colon cancer syndrome)

160
Q

rare genetic syndrome with a defective DNA nucleotide excision repair
presents with extreme sensitivity to UV light and has a high risk of developing skin cancer

A

what is xeroderma pigmentosum

161
Q

proangiogenic factor released by tumor cells
increases blood vessel expression and movement to tumor

A

what is VEGF

162
Q

ability for a neoplasm to shape its immunogenic properties to avoid elimination
creates immune tolerance and immune suppression

A

what is cancer immunoediting

163
Q

chemicals that require no metabolic conversion to become carcinogenic
most are weak as carcinogens
can cure cancers but cause a second form (acute myeloid leukemia)

A

what is a direct acting carcinogen

164
Q

chemicals that require metabolic conversion to become active carcinogens (ultimate carcinogen)
ex. polycyclic hydrocarbons, aromatic amines, and azo dyes

A

what is an indirect acting carcinogen and give three examples

165
Q

clustered mutations in specific sequences or bases

A

what is a “hotspot”

166
Q

chemical agents that stimulate cell proliferation and expansion of a clone of mutated cells

A

what are promotors

167
Q

one that is not actively dividing

A

what is a quiescent tissue

168
Q

small protein that stimulates mitosis

A

what is a mitogenic stimulus

169
Q

a type of retrovirus that causes adult T-cell leukemia/lymphoma

A

what is human T-cell Leukemia Virus Type 1

170
Q

virus that inserts a copy of its RNA genome into DNA of a host cell that it invades, thus changing the genome of that cell

A

what is a retrovirus

171
Q

a disease caused by Epstein-Barr virus
causes nasopharyngeal and gastric cancers

A

what is Burkitt lymphoma

172
Q

bacteria that causes peptic ulcers, gastric adenocarcinomas, and gastric lymphoma of B cell origin

A

what is Helicobacter pylori

173
Q

balance of endogenous heparin production and degradation is disturbed with increase degradation of heparin by tumor-secreting heperanse

A

what is type 1 hypercoagulability

174
Q

procoagulant molecules secreted from tumor cells, leading to hypercoagulability

A

what is type 2 hypercoagulability

175
Q

when cancer patients have signs and symptoms that cannot be explained by the tumor
occurs in 10% of patients

A

what are paraneoplastic syndromes

176
Q

present in or produced by cancer cells in response to cancer or other condition
provides information about a cancer like how aggressive it is or what kinda of treatment it needs

A

what is a tumor marker