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Patho I > Chapter 7 > Flashcards

Chapter 7 Flashcards

1
Q

what is a mixed tumor

A

single neoplastic clone along 2 lineages

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2
Q

what is a mixed tumor of salivary gland

A

epithelial parts in mixed stroma

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3
Q

what is a pleomorphic adenoma

A

different size and shapes

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4
Q

what is a teratoma

A

mature or immature cells of tissues from more than 1 germ line

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5
Q

what are cystic teratomas

A

differentiate along extodermal line to make cystic tumor lined by skin with hair, teeth etc

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6
Q

what is desmoplasia

A

a lot of collagen stroma in tumor

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7
Q

what are 2 main parts of any tumor

A

stroma and parenchyma

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8
Q

what is a scirrhous tumor

A

stony hard

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9
Q

what is a hamartoma

A

benign appearing masses made of cells indigenous to a site

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10
Q

what does -oma mean

A

of msenchymal origin

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11
Q

what is an adenoma

A

benign epithliela neoplasm from glands

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12
Q

what are papillomas

A

benign epithelial neoplasms with finger like progections from surfaces

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13
Q

what are polyps

A

when neoplasm makes macroscopically visible projection

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14
Q

what are sarcomas

A

arise in mesenchymal tissue and have a fleshy look with little stroma

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15
Q

what is a carcinoma

A

malignant neoplasm of epithelial origin from any germ layer

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16
Q

what is the most common carcinoma

A

squamous cell

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17
Q

where do squamous cell carcinomas arise in lung “bronchogenic”

A

hilar regions centrally

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18
Q

what is a sign of leukoplakia and what should you order

A

white patches in oral cavity

order biopsy immediatelt

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19
Q

what is anaplasia

A

lack of differentiation

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20
Q

mitoses of undifferentiated tumors reflects what

A

increase in proliferative activity or parenchymal cells

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21
Q

what is dysplasia

A

loss in uniformity of cells and architectural orientation

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22
Q

What is carcinoma in situ

A

dysplasia changes involving thickeness of epithelium but NOT invading BM

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23
Q

what factors determine rate of growth for a tumor

A

doubling time of tumore cells
fraction of cells in replicative pool
rate at which cells are shed or die

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24
Q

how do cancer stem cells have high R to conventioinal therapies

A

low rate cell division and expression of factors like MDR1

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25
Q

What is CML from

A

malignant counterpart of normal hematopoietic cells

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26
Q

what is AML from

A

more differentiated myeloid precurors that gain abnormal capacity for self renewal

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27
Q

what cancers do not metastasize

A

glial cells in CNS gliomas

basal cell carcinoma in skin

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28
Q

what are the pathways of spreading cancer

A

seeding, lymph , blood

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29
Q

what is pseudomyxomaperitoneal

A

mucus secreting appendicieal carcinomas filling peritoneal cavity with a gelatinous neoplastic mass

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30
Q

what do you do when detect undifferentiate small cell carcinoma in lungs

A

close becasue metastasizes and responds well to chemo

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31
Q

where does cancer enter lymph node

A

subcapsular sinus

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32
Q

where do carcinomas of thyroid and prostate metastasize to

A

vertebral column

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33
Q

where do renal cell carcinomas metastasize to

A

renal v, IVC then R heart

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34
Q

where do adenocarcinomas metastasize to

A

liver, see central necrosis

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35
Q

hispanics are at high risk for what cancers

A

stomach, liver, uterine cervix and gallbladder

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36
Q

what cause increase cancer

A

accumulations mutations, decline in immune competence

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37
Q

Describe characteristics autosomal dominant cancer

A

early onset with increase risk. Usually point mutaiton in TSG

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38
Q

What is retinoblastoma and what kind of cancer is it

A

autosomal dominant

carry mutant RB allele

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39
Q

what causes familial adenomatous polyposis

A

mutation of APC TSG

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40
Q

what causes Li-Fraumeni syndrome

A

mutations in p53

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41
Q

What causes Multiple endocrine neoplasia type 1/2

A

MEN 1 2

mutations in TF for RET tyrosine kinase

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42
Q

what is HNPCC from

A

inactivation DNA mistmatch repair gene

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43
Q

What type of pattern are defective DNA repair syndromes

A

autosomal recessive

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44
Q

examples of defective DNA repair syndrome

A

xenodermapigmentosum, ataxia-telangiectasia and Bloom syndrome

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45
Q

what is an autosomal dominant form of defective DNA repair

A

HNPCC

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46
Q

what are the most common familial cancers

A

carcinomas of colon, breast, ovary and brain

usually b/l

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47
Q

What cancers are common with AIDs

A

non-hodgkin lymphoma, squamous cell carcinoma, cervical neoplasia, kaposi sarcoma

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48
Q

how can chronic inflammation lead to cancer

A

immune response becomes maladaptive

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49
Q

what are some precancerous conditions

A

chronic atrophic gastritis or pernicious anemia, solar keratosis of skin, chronic ulcerative colitis, leukoplakia of oral caivity vulva and penis

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50
Q

what are the 4 classes of normal reg genes

A

growth promoting proto-oncogenes, growth inhibiting TSG, genes that regulate programmed cell death, genes involved in DNA repair

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51
Q

what type of mutation in a single allel is enough (dominant) to cause cancer

A

in proto-oncogenes.

TSG you need both alleles

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52
Q

what is haploinsufficiency

A

loss of genetic function caused by damage to single allele

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53
Q

What is a FLT3 mutation assoc with

A

constitutive signaling in meyloid leukemia

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54
Q

what type of tumors have active c-kit tyrosine kinase

A

GI stromal tumors

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55
Q

What R gene is overexpressed in majority cell carcinomas of lung

A

EGF R ERBB1

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56
Q

What is ERRB2 overexpressed in

A

breast cancers and human adenocarcinomas in ovary, lung, stomach and salivary glands

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57
Q

What is the single most common abnormalibyt of pro to-oncogenes in human tumors

A

point mutations in RAS oncogene H K N

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58
Q

mutations in KRAS are what

A

carcinomas

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59
Q

mutations in hRAS are what

A

bladder tumors

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60
Q

mutations in nRAS are what

A

blood tumors

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61
Q

In inactive state what is RAS bound to

A

GDP

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62
Q

what is the downstrem regulator of RAS

A

MAP kinase

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63
Q

What does the mutation in RAS cause

A

GTPase activity, uncontrolled RAS

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64
Q

What is the 9-22 translocation

A

BCR-Abl fusion cuasing CML and acute lymphoblastic leukemias

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65
Q

polycythemia vera and primary myelofibrosis have point mutations in what

A

JAK2

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66
Q

What is MYC activation do

A

apoptosis without survival signals

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67
Q

what causes Burkitt lymphoma

A

dysregulated c-MYC

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68
Q

what cancers are n-MYC and L-MYC amplified in

A

neuroblastoma and small cell cancers of lung

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69
Q

activation of cyclin D causes what cancers

A

breast, esophagus, liver, lymphomas

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70
Q

activation of CDK4s cause what cancers

A

melanomas, sarcomas and glioblastomas

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71
Q

what is responsible for G1/S checkpoint

A

p53 via p21 to arrest cell cycle if DNA damage detected

72
Q

Where is the RB allele

A

13q14

73
Q

familial vs spradic RB

A

familial inherit mutant allele which them mutates other allele
sporadic aqcuire somatic mutation son both alleles

74
Q

What cancers have genes on short arm CS11

A

Wilms tumor, hepatoblastoma and rhabdomyosarcoma

75
Q

What is VHL

A

TSG that causes familial clear cell renal carcinoma

76
Q

when is RB active

A

in hypoPi state

77
Q

What is RB dependent on to get out of G1

A

E cyclin

78
Q

where is the p53 gene

A

17p13.1

79
Q

what are the most common tumors from p53 mutations

A

sarcomas, breast, leukemias, brain, carcinomas of adrenal Cx

80
Q

What viruses can promote degradation p53

A

E6 and HPV

81
Q

what genes regulate p53

A

MDM2 and MDMX

82
Q

what does MDM2 do

A

activates mir34 which binds mRNA preventing translation

83
Q

ATM and RAD3 (ATR) influence p53 how

A

Pi it to active so that there is a puase in cell cycle

84
Q

when DNA repair is successful wha tis role of p53

A

upregulate MDM2 to destruct and release cell cycle block

85
Q

what is p63 related to

A

differentiations of stratified squamous epithelium

86
Q

what is p73 assoc with

A

pro-apoptotic effects after DNA damage from chemo

87
Q

What does the APC gene control

A

down regulation growth promoting signals

88
Q

defect in APC gene results in

A

familial adenomatous polyposis (adenomatous polyps in colon)

89
Q

describe B catenin- APC pathway

A

B catenin binds E cadherin resultin gin cell adhesion

90
Q

loss of contact inhibition by mutation of E cadherin/b catenin are key in what cancers

A

carcinomas

91
Q

What type of mutation occur in colon cancer with bcatenin APC zxis

A

APC fine but mutations in b catenin that prevent destruction APC and accumulation in cytoplasm

92
Q

What is the role of INK4/ARF

A

blocks Pi of RB and activates p53 pathway bu inhibiting MDM2

93
Q

describe TGFb pathway in cell cycle arrest

A

binds serine-threonine kinase complex dimerization causing Pi SMADs activation p15 and dec Pi RB

94
Q

what is common mutaion in pancreatic cancer

A

SMAD4

95
Q

all pancreatic cancers have a mutation where

A

in TGFb pathway

96
Q

What is mutated in cowden syndrome

A

PTEN

acts as TSG for the pro-apoptotic PI3K/AKT pathway

97
Q

What happens in NF1 mutation

A

benign neuroblastomas and optic n gliomas

conversion of RAS from active to inactive

98
Q

what happens in NF2 mutation

A

neurofibromin or merlin deficiency
lack of cell cell junctions and insensitivity to normal growth arrest
parth of SWH TSpathway

99
Q

what type of cancers form with VHL

A

hereditary renal cell cancers, pheochromocytomas, hemangioblastomas of CNS, retinal angioma and renal cysts

100
Q

What factor does VHL need

A

HIF1a do cause degradation

except in hypoxia causes angiogenic GF proliferation

101
Q

What is from a mutation in WT1

A 
Wilms tumor (kidney)
TSG
102
Q

where is WT1 overexpressed

A

leukemias and breast cancers

103
Q

What is PAtched PTCH

A

TSG of hedgehog

104
Q

what is syndrome from mutation in PTCH

A

gorlin syndrome (nevoid basal cell carcinoma)

105
Q

how do cancers evade apoptosis

A

inactivate p53 or activate anti-apoptotic genes

106
Q

pro-apoptotic genes

A

BAX BAK

107
Q

what regulate pro and anti apoptotic B proteins

A

BAD BID PUMA

108
Q

What is the main antiapoptotic protein

A

BCL2

109
Q

hwo do cancer cells accomplish limitless replicative potential

A

don’t deplete telomerase

110
Q

What is main cause of epithelial tumors

A

down regulation E cadherin expression or mutation in catenin

111
Q

How do tumors degrade BM and interstitial CT

A

proteolytic enzymes, MMPs, cathepsin D, urokinase plasminogen activator

112
Q

what direct mobility of tumors

A

the cytokines (autocrine)

113
Q

how do tumor cells migrate to selective sites in lymph

A

CD44

114
Q

What chemokines for breast cancer are markers for metastasis

A

CXCR4 and CCR7

115
Q

what mir promote or suppress metastasis of breast

A

mir335 and 126 suppress while 10b promotes

116
Q

What oncogenes promote epithliela to mesenchymal transition

A

SNAIL and TWIST which encode the TFs needed

117
Q

Xeroderma Pigmentosum is at increased risk for what

A

development of cancers of skin follwing UV light because cross linking pyrimidine residues

118
Q

What are the main metabolic alterations in tumore cells. warburg effect

A

switch to aerobic glycolysis

119
Q

what are the advantages of hypoxic conditions for tumors

A

HIF1a

allows carbons to be shunted to anabolic pathways

120
Q

what genes cause metabolic changes in tumor cells

A

RAS, p53 and PTEN

121
Q

What TSG are mutated in TB

A

TSC 1 and 2

122
Q

what type of translocations occur in lymphoid tumors

A

overexpression of pro to-oncogenes by changing regular elements with another gene

123
Q

what type of cancers arise from fusion of translocated CCS

A

hematopoietic, sarcomas, certain carcinomas

124
Q

What is the translocation if Burkitt lymphoma

A

8q24 where MYC gene is and replaced with IGH locus with B cell precursor gene

125
Q

what occcurs from cyclin D1 gene overexpressed on 11q13 by juxtaposition to chrom 14

A

mantel cell lymphoma

126
Q

what is the most common translocation of lymphoid malignancies

A

follicular lymphomas from activation of BCL2 gene

127
Q

what is the philedelphia chrom

A

BCR ABL 9-22 translocation

target for leukemia therapy

128
Q

What causes prostatic adenocarcinoma

A

translocation in androgen regulate gene and one E family TFs

129
Q

What type of tumors occur from deletions

A

nonblood assoc solid tumors

130
Q

What mutation causes small cell lung carcinoma

A

3p

131
Q

what deletions can cause colorectal cancers

A

17p, 5q and 18q

132
Q

What cancer is EzH2 overexpressed in

A

breast and prostate carcinoma repressing TSG p21

133
Q

leukemias and lymphomas have increased expression of what

A

BCL2

134
Q

what are direct acting agents for carcinogenesis

A

do not need a metabolic conversion and are weak

135
Q

what are indirect acting agents for carcinogenesis

A

require metabolic conversion
polycyclic hydrocarbons
benzopyrene
p450 dependent mono oxygenases

136
Q

people with CYP1A1 genotype are at higher risk for what

A

lung cancer

137
Q

What are the molecular targets from carcinogens

A

RAS, p53

138
Q

what does aflatoxin B1 do

A

mutations in p53

139
Q

What form of UV ray cause cutaneous cancers

A

UVB 280-320, and the nucleotide excision repair pathway is overwhelmed

140
Q

what are the most common cancers from ionizing radiation

A

AML and CML

141
Q

Describe integration HPV

A

interupts viral DNA within E1/2 reading farm so lose E2 viral repressor and then overexpression E6 and 7

142
Q

What is the role of HPV E6 and 7

A

interact with growth regulatin proteins

143
Q

E7 HPV has higher affinity for what gene

A

RB, inactivates CDKIs p21 and 27 then activates cyclin E and A

144
Q

E6 HPV does what

A

degrades p53 and BAX

145
Q

what tumors are more likely in EBV

A

herpes, burkit lymphoma, B cell lymphoma, gastric carcinomas NK lymphomas

146
Q

how does EBV get into cells

A

infects B cells via CD21 C’ R

147
Q

What proteins does EBV to evade death

A

MLP1 to actvate BCL2
EBNA2 activates NOTCH
IL10

148
Q

what is most common child tumor in central africa and new guinea

A

burkitt lymphoma

149
Q

nasopharyngeal carcinomas are endemic where

A

southern china, africa and inuits in artic

150
Q

HBV causes cancer how

A

indirect: activates NFkB for apotosis hepatocytes
direct: HBx gene TFs and signal tranduction

151
Q

Helicobacter pylori is common in what cancers

A

gastric adenocarcinomas and gastric lymphomas

152
Q

gastric lymphomas arise from what lymphocyte

A

B cell origin associated with MALTomas

153
Q

what is histo fro H. pylori gastric adenocarcinoma

A

have T reactive cells to H pylori but also poly clonal B cell proliferation

154
Q

What cells kill latent DNA virus Ag

A

CD8

155
Q

what proteins are at higher levels in melanomas

A

GM2 GD2 and GD3

156
Q

what protein is higher expressed in breast cancer

A

MUC1

157
Q

What IL activat eNK to kill tumors

A

2 and 15

158
Q

how do macrophages kill tumors

A

ROS and TNF

159
Q

What Ab are used to Tx lymphomas

A

monoclonal Ab CD20 (B cell)

160
Q

How do tumor cells evade immune system

A 
loss MHC R
lack costimulation for binding
T cell inhibitory R CTLA4
Ag masking via glycocalyx
Apoptosis CTLs
161
Q

what cancer is assoc with HMWkeratin

A

squamous cell carcinoma

162
Q

how do most neoplasms cause hyper Ca

A

PTH related protein

163
Q

what is acanthosisnigircans

A

gray black patches of verruvous hyperkeratosis on skin

164
Q

what is hypertrophic osteoarthropathy and what Pts do you see it with

A

new bone on distal long bones, clubbing of digits

seen with bronchogenic carcinoma

165
Q

What is trousseau syndrome and what cancers can lead to it

A

migratory thrombophebitis

usually carcinomas of lung or pancreas

166
Q

Acute DIC is most common with what

A

acute promyelocytic leukemia and prostatic adenocarcinoma

167
Q

nonbacterial thrombotic endocarditis is seen with what

A

vegetations of mucin secreting adenocarcinomas

168
Q

What is the grade of a tumor

A

level of differentiation of tumor and number of mitoses or architectural features

169
Q

what is the stage of a tumor

A

size o primary lesion, spread and presence of blood bourne metastasis

170
Q

What is the TNM rating

A

T0-4 N0-3 M0-2

171
Q

when is needle aspiration used

A

palpable lesions like breast, thyroid and nodes

172
Q

what is immunohistochemistry used for

A

determination site of origin and detection of certain R or Ab

173
Q

flow cytometry is used with what cancers primarily

A

leukemias

174
Q

PCR we can differentiate what

A

monoclonal vs polyclonal

175
Q

what is comparative genomic hybridization used in

A

gains/losses tumors

176
Q

What is the most useful analyses of tmors

A

molecular progiles

177
Q

Increased IgG and kappa chain is key to what disease

A

Mult myelmoa

Patho I (6 decks)

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