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general path > neoplasm I > Flashcards

neoplasm I Flashcards

1
Q

What is a neoplasia

A

“New Growth”; lack of responsiveness to normal growth controls

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2
Q

what is the study of neoplasms

A

Oncology

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3
Q

what is a benein neoplasms

A

a localized, non spreading neoplasm

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4
Q

what is a malignant neoplasm

A

Cancer

with the potential to invade and destroy adjacent normal tissue and spread to distant sites

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5
Q

survivability to benign and malignant neoplasm

A

Benign can be fixed via surgical removal

Malignanat neoplasms can lead to death, especially without treatment

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6
Q

spread of mailgnant neoplasms to distant sites

A

Metastasis

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7
Q

what is the parenchyma

A

transformed or neoplastic cells

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8
Q

what is a stroma

A

The supporting tissue of the tumor i.e. the non-neoplastic blood vessels and connective tissue supplied by the host

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9
Q

can benein tumors be lethal

A

yes, can crush important parts of brain or body

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10
Q

how would one name a nenign tumor

A

Adding the suffix “-oma” to the end

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11
Q

what is an Adenoma

A

A benign gland-forming epithelial tumor or tumor derived from glandular tissue

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12
Q

what is a papilloma

A

A benign surface epithelial tumor characterized by numerous finger-like progections

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13
Q

how would one name a malignant mesenchymal neoplasms

A

Add the suffix Sarcoma to the root word describing the parenchymal tissue of origin

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14
Q

how would one name a malignancy of epithelial origin

A

Carcinomas

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15
Q

what is a lymphoma

A

A malignancy of lymphocytic origin

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16
Q

what is melanoma

A

Malignancy of melanocytic origin

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17
Q

what is a hamartoma

A

Proliferation of tissue normally found at the site

- still dissordered

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18
Q

how series is a Hamartoma

A

Can regress, and will self heal

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19
Q

what is a choristoma

A

A collection of tissue not normally found in that anatomic site

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20
Q

what is a teratoma

A

A neoplasm derived from more than 1 germ layer

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21
Q

how bad is a teratoma

A

Can range from benign to aggressive

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22
Q

what is melanoma

A

malignancy of melanocytes

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23
Q

what is mesothelioma

A

pleural malignancy

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24
Q

what is seminoma

A

testicular malignancy

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25
Q

what are more differentiated, benign or malignant neoplasms

A

Beneign are generally well-differentiated (look like the cells from which they rose)
- rare and normal appearance of mitosis
Malignant neoplasms: can be well differentiated to poorly differentiated

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26
Q

what are malignancies composed of poorly differentiated cells

A

Anaplastic

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27
Q

what characterizes anaplasia

A 
Pleomorphism
Nuclear hyperchromatism
increased nuclear/cytoplasmic ratio compared to normal cels
Atypical nuclei
numerous and atypical mitoses
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28
Q

what is pleomorphism

A

variation in cell shape and size

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29
Q

what is nuclear hyperchomatism

A

Intensely baseophilic nuclei

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30
Q

what is dysplasia

A

Altered growth pattern

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31
Q

what does dysplasia normally refer to

A

Epithelium that is not neoplastic but may become cancerous eventually.

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32
Q

what do dysplasia cells normally look like

A

microscopic alterations similar to cancer cells

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33
Q

what is the most severe form of epithelial dysplasia

A

Carcinoma-in-situ

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34
Q

what is carcinoma-in-situ

A

has all the microscopic features of cancer , but the atypical cells have not invaded into the host

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35
Q

what is the benifit of well differentiated tumors compared to undifferentiated tumors

A

Still able to retain some functional capability

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36
Q

what grows faster, benign or maliganant tumors

A

Malignant grow much faster

  • well differentiated grow slow
  • poorly differentiated grow fast
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37
Q

how can dysplasia causes problems

A

slowly grow as dysplasia to become carcinoma in situ

eventually cross the basement membrane as a seed bed from which cancer can occur

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38
Q

what happens if tumors outgrow their blood supply

A

results in areas of ischemic necrosis

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39
Q

what would someone say by saying something is paraneoplastic

A

can cause problems due to secondary effects of the neoplasms such as PR

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40
Q

what type of tumor tends to have a capsule

A

Benign tumors

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41
Q

what is the capsule that tends to form around a benign tumor made of

A

A compressed band of fibroud connect tissue at the periphery of the tumor

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42
Q

do all benign tumors have a capsule

A

No (hemangioma and neurofibroma are exceptions

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43
Q

how do cancers grow

A

progressive infiltration
invasion
destruction
penetration of surrounding tissues

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44
Q

what is the most reliable means of distinguishing the malignant nature of a tumor

A

infiltrative quality

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45
Q

what is metastasis

A

the process in which portion of a malignancy break free and travel to distant sites where they form new tumor masses

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46
Q

what establishes a tumor as being malignant unequivovally

A

metastasis

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47
Q

what determines if a tumor can metastasize

A

the type of tumors

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48
Q

which tumors metastasize

A

osteosarcoma

melanoma

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49
Q

what tumors tend not to metastasize

A

basal cell carcinoma

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50
Q

how often do tumors tend to metastases

A

30% are large

20% have small metastases

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51
Q

what increases the tendency of metastasis

A

greater anaplasia

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52
Q

how do malignancies spread

A

Seeding within body cavities
spreading within the Lymphatic
Hematogenous spread

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53
Q

wheree do lymphatic spread

A

seen with carcinomas, resulting in lymph node metastases

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54
Q

what preferes hematogenous spread

A

Sarcomas

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55
Q

where do metastics deposites spread via hematogenous spread

A

lung and liver

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56
Q

what is hematogenous spread

A

spread via the blood

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57
Q

what is the incidence of cancer

A

1.69 million new cases

600,00 deaths a year

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58
Q

what gender is increasing in cancer

A

leveled for males

More females have taken up smoking, so greater rate

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59
Q

what gender is dying more via cancer

A

more Cancer deaths in males over 50 years
less deaths in females
- due to papsmears (decreased uterine cervix cancer)

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60
Q

at what age does cancer frequency increase

A

greater than 55 years

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61
Q

does the environment have an effect on cnacer

A

Yes

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62
Q

how much does cancer affect children under `15 years old

A

account for 10% of deaths in us (second to car accidents)

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63
Q

what are the hereditary aspects of cancer

A

Inherited cancer syndroms
Defective DNA repair syndromes
Familial cancers

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64
Q

what kind of dissorder is an inhereted cancer syndrom

A

autosomal dominant

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65
Q

examples of inherited cancer syndroms

A

Retinoblastoma

Multiple endocrine neoplasia (Men)

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66
Q

what kind of dissorder is defective DNA repair syndromes

A

Autosomal recessive

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67
Q

examples of Defective DNA repair sydromes

A

xeroderma pigmentosum

ataxia telangiesctasia

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68
Q

what are examples of familial cancers

A

Breast
Ovarian
colon

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69
Q

when do hereditary disease tend to show themselves

A

early age of onset(especially defective DNA repair)

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70
Q

how often do Hereditary disases tend to have an identifiable basics

A

about 10%

- most often a co roll

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71
Q

why do familial cancers tend to show themsevlves

A

early age at onset

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72
Q

what are characters of familial cancers

A

tumors arising in 2+ close relatives of the index case

Multiple or bilateral tumors

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73
Q

what is an acquired preneoplastic disorder

A

Persistent regenerative cell replication

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74
Q

where does acquired preneoplastic disorders tend to show themselves

A

Squamous metaplasia and dysplasia of bronchial mucosa
Endometrial hyperplasia and dysplastic proliferation
Leukoplakia of oral mucosa, vulva, or penis
Vilous adenomas of the colon

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75
Q

what lies at the heart of cancinogenesis

A

Nonlethal genetic damge

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76
Q

how many cells does Cancers come from

A

arise from one geneticall altered cells

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77
Q

what are the normal regulatory genes that are the principle targets of genetic damge

A

Protooncogenes
Cancer suppressor genes
Apoptosis regulatory genes

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78
Q

what happens if DNA repair genes are disables

A

the frequency of mutations increases

rate of neoplastic transformation increases

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79
Q

can carciongenesis occur with one mutation

A

No, a multistep process both photypicaly and genetically

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80
Q

what do cancers tend to produce that encourages their own growth

A

Self-sufficiency in growth signals

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81
Q

what are the protein products of oncogenes

A

Oncoproteins

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82
Q

what are protooncogenes

A

Growth promoting genes

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83
Q

what tends to be included/neded from cancer to occur

A 
Evade apoptosis
Self-sufficincy in growth signals
Insensitivity to anti-growth signals
Tissue invasion and metastasis
Limitless replicative potential
Sustained angiogenesis
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84
Q

what is the difference between proto-oncogenes and oncogenes

A

Proto-oncogenes lack reguatlion

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85
Q

what happens when a proto-oncogen is mutated, or its regulator is mutated

A

uncontrolled promotion of cell growth

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86
Q

what oncogenes can lead to uncontrolled promotion of cell growth

A 
Growth factors
GRowth factor receptors
signal transuding proteins
nuclear transcription factors
Cyclins and cyclin-dependent kinases
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87
Q

how might a protooncogene be transformed to an oncogenes

A
  • Structural mutation of the gene, resulting in an abnormal product
  • altered regulation of gene expression, resulting in increased production of a normal growth promoting protein
88
Q

what is growth factor needed for

A

Stimulation to undergo proligeration

89
Q

what is Glioblastoma

A

Platelet derived growth factor (PDGF)

90
Q

what does Some sarcomas need for growth and self-sufficiency

A

TGFa (tumor growth factor alpha)

91
Q

how can receptors aid in growth signal self-sufficiency

A

Mutation and overexpression of growth factor receptors (ERB B1 and B2
- lead to response even if no growth factor

92
Q

what do mutant receptor proteins cause

A

Deliver continuous mitogenic signal

93
Q

what does overexpression of growth factors lead to

A

Makes cancer cells hyperresponsive to even normal GF

94
Q

what is often times mutated to lead to growth factor protblems

A

RAS oncogenes(30% of tumors have this mutation)

95
Q

how does Mutant RAW cause a problem

A

Growth signals are normally turned off quickly, but mutant RAS remains active leading to constant cell proliferation

96
Q

what nuclear transcription factor tends to be the most affected to cause GRowth self-sufficiency

A

MYC

97
Q

what does MYC gene dysregulation lead to

A
  • overexpression, leading in continuous activation of cyclin-dependent kinases (CDKs) driving the cell to devide
  • repressed CDK inhibitors
98
Q

how Does Burkitt lumphoma lead to an increase in MYC oncogene

A
  • chromosome 8 and 14 switch a little bit and MYC is found on chromosome 14 next to the Ig gene
  • Ig is constanatly being synthesized so MYC is also then synth often
99
Q

what is the roll of Cyclins/cyclin-dependent Kinases

A

Orderly progresssion of cell cycle after activation by binding to cyclins

100
Q

what regulates CDK’s

A

two families of CDK inhibitors

101
Q

dysregualtion of CDK’s leads to what

A

Favors cell proliferation

- more and more transcription factors

102
Q

what do tumor suppressor genes do

A

Inhibit cell proliferation

103
Q

what was the first tumor suppressor gene found

A

RB gene

104
Q

what does the RB gene product do

A

Regulates transcription

105
Q

what is the Knudson’s two hit hypothesis

A

Two mutation in the genome of a cell required to induce retinoblastoma

106
Q

what is needed for retinoblastoma to develop

A

Both of the normal allels of the RB locus must be inactivated

107
Q

how does RB mutation pass in familial cases

A

Childinherits one defective copy of the RB gene and the other allele is normal
-normal RB gene undergoes somatic mutation leading to a tumor developing

108
Q

where do most retinoblastomas come from

A

60% of retinoblastomas are sporadic

others are familail, inhherited as autosomal dominant

109
Q

what do we understand better, tumor suppressor genes or oncogenes

A

we better understand oncogenes

110
Q

what do tumor suppressor genes regulate

A

Cell cycle
cell adhesion
singal transduction

111
Q

what does Active PRb do

A

binds transcription factors that regulate the cell cycle

112
Q

what happens when pRb is phosphorylated

A

transcription factors are released, leading to DNA synthesis

113
Q

what happens if pRb is mutated

A

cell cycle has no breaks, and transcription factors go wild

114
Q

what genes is the single most common target for genetic alteration in human tumors

A

TP53 tumor suppressor gene

115
Q

commonness of tp52 tumor suppressor gene genetic alteration in human tumors

A

single most common target,

- homozygous loss of TP52 in nearly all cancers

116
Q

what usually leads to loss of TP53 gene

A

somatic mutation
- or -
one aberrant TP53, leading to increased rate of cancer

117
Q

what is Fraumeni syndrom

A

having one aberrant TP53 gene

118
Q

what is the action of TP53

A
  • slow down DNA replication when mutations have affected the DNA
  • activates the transcription of DNA repair enzymes
  • apoptosis if cell cannot be repaired
119
Q

what happens without a normal TP53 gene

A

cell incorporates the mutation in its genome and results in cancer

120
Q

does one gene aid in evading apoptosis

A

No, many genes

121
Q

what is the prototypic anti-apoptosis gene

A

BCL2

(other genes are TP53 and c-myc)

122
Q

what are the characteristisc of tumors that grow via apoptotic evasion

A

slow grwoing and low grade due to not ding, instead of quick prolieration

123
Q

why would there be a surplus of BCL2

A

translocation from chromsome 18 to Ig heavy chain locus on chromosome 14

124
Q

how large can tumors get without vasculatur

A

cannot exceed 1-2 mm

125
Q

what does angiogenesis facilitate that is bad

A

metastases to provide access to the vasculature

126
Q

what are the major 2 phases of metastasis

A
  • Invasion of the ECM

- vascular dissemination and adhesion/homing of tumor cells

127
Q

what are the steps of invasion of the ECM

A
  • tumor cells detach from each other
  • attach to ECM components (BM and CT) including collagens, glycoproteins and proteoglycans
  • Degrade matrix components and basement membrane
  • Migrate to vascular channels
128
Q

what may happen to a tumor once in circulation

A
  • vulnerable to destruction by the host immune cells

- Adhere to vascular endothelium, following by basement membrane transmigration

129
Q

how can distribution of tumor metases be predicted

A

by location of the primary tumor and its vascular or lymph drainage

130
Q

how often is organ tropism seen in metastasis

A

Sometimes, but never involved skeltal muscle

131
Q

why does organ tropism seen in skeletal muscle

A
  • Organ-specific endothelial adhesion molecules bind tumor cell lingants
  • Chemokine receptors on tumor cells home to sites where specific ligands and readily produced.
132
Q

what are some environmental carcinogens

A

ionizing radiation
Sunlight
Dietary agents

133
Q

what is hereditary nonpolyposis colon cancer syndrome

A

familial cancer of the colon

- result from defective genes involved in DNA mismtach repair and evidence of microsatellite instability

134
Q

what does xeroderma pigmentosum lead toc

A

increase in skin cancers

135
Q

what is xeroderma pigmenosum

A

the inability to repair UV damage

136
Q

what are examples of fragile DNA diseases

A

Bloom syndrome
Ataxia telangiectasia
Fanconi anemia
Familial breast cancer

137
Q

what does sunlight normmaly due to DNA

A

pyrimidine(thymadine) cross-linking in DNA which halts replication

138
Q

does fragile DNA need only a couple mutations to induce cancer

A

No, still needs lots

139
Q

how do tumors change after time

A

More aggressive locally and hreater metastatic potential

140
Q

what are some karyotypic changes that occur

A

Balanced translocation
Deletions
GEne amplifactaions

141
Q

how common are balanced transolocations

A

extremely common

- especially in hematopoietic neoplasms

142
Q

how similar are tumor cells in one tumor mass

A

may be heterogeneous

143
Q

benifit of tumors being heterogeneous

A

able to survive certain therapies, invade host tissue or metastasize with greater efficiency

144
Q

what is the second most prevalent form of keryotypic abnormality

A

Deletions

145
Q

what deletions are most common in oral cancer

A

3p, 9p, and 17p

146
Q

what did percival pott do

A

Described scotal skin cancer in chimney sweep, attributing it to chronic exposure to soot

147
Q

are chemical carcinogens natural or synthetic

A

both

148
Q

what are the actions of carcinogens

A

directly with DNA (direct-acting agents)

most are indirect with some metabolic conversion

149
Q

what are indirect carcinogens called

A

Procarcinogens

150
Q

what are the active end-products of procarcinogens

A

Ultimate carcinogens

151
Q

what are the characteristics of tumors that survive chemo

A

Low control
Need little to grow
non antigenic/ recognixable

152
Q

3 major classes of cariogenic agents

A

Chem
Radiant energy
Oncogenic viruses

153
Q

are chemical carcinogens electrophiles or neutralphiles

A

electrophiles

154
Q

what do chemical carcinogens react with

A

DNA
RNA
cell proteins

155
Q

what are chemicals called promoters

A

have little inherent mutagenicity

drive cells to divide and immortalize DNA alterations

156
Q

how do alcohol and cigarates work together to increase cancer

A

alcohol makes it easier for the carcinogens to enter

157
Q

what happened to dentists that help patients film for radiographs

A

Developed squamous cell carcinoma of the index finer

158
Q

how has cancer affected those who mine radioactive ores

A

10x high lunger cancer

159
Q

what happened to the survivors of the atomic bomb

A

had markedly increased incidence of leukemia as well as other cancers

160
Q

how long is the latent periods for radiation exposure and time of cancer

A

long (7-12 years)

161
Q

latency of atomic bomb survivor cancer

A

8-12 years

162
Q

what kind of virus is Human T-cell leukemia virus Type I

A

RNA oncogenic virus

163
Q

how often does Human T-cell leukemia virus type I cause leukemia

A

only in 3-5% of individuals who are infected after 20-50 years of latency

164
Q

what do f DNA oncogenic viruses do

A

transforming DNA viruses that form stable associations with the host cell genome

165
Q

what cancers can HPV cause

A

some types do benign squamous papillomas or veruca vulgaris

ulterine cnacer and oropharyngeal cancer

166
Q

what can Epstein barr virus do

A

Burkitt lymphoma
B cell lymphoma in immunosuppressed patients
Hodgkin lymphoma
nasopharyngeal carcinoma

167
Q

what can Hep B do

A

Linked to hepatocelular carcinoma

168
Q

what are tumor antigens

A

Tumor-specific antigens and tumor associated antigens

169
Q

what are the antitumor effector mechanisms

A

Cytotoxic T cells (CD8+)
Nat Killer cells
Macrophages
Humoral factors

170
Q

what shows that immunosurveillance is a real thing

A

Increased frequency of cancer observed in immunocompromised

171
Q

what are tumor specific antigens

A

antigens only associated with tumor cells

172
Q

what is the cancer-testis antigens

A

MAGE-1 (melanoma-associated antigen)

173
Q

what are tumor associated antigens

A

found on normal cells

overexpressed on tumors

174
Q

what are antigesn that represent a specialized function of cells

A

Differentiation-specific antigens

175
Q

what kind of antigen is prostate specific antigen

A

Tumor associated antigen

176
Q

where is prostate-specific antigen

A

in association with both normal and enoplastic prostatic epithelium, but more in neoplastic state

177
Q

what does Cytotoxic T lymphocytes do to fight cancer (CD8+)

A

play a role against virus-induced neoplasms

- burkitt’s lymphoma

178
Q

what do Natural Kiler cells do

A

Lymphocytes that kill tumor cell without prior sensitization

179
Q

the first line of defnse against tumors

A

Natural killer cells

180
Q

what is the action of macrophages

A

Collaborate with T cells and NK cells to destroy tumor cells

181
Q

how do macrophages kill tumors

A

Act by using mechs that destroy microbes

Produce TNF-alpha

182
Q

how much do immunocompromised people have cancer

A

200x more often

183
Q

why do immunocompromised tend to have more cancer

A
  • selective outgrowth of antigen-negative variants
  • loss or reduced expression of histocompatibility antigens
  • lack of co-stimulation
  • Immunosuppression
184
Q

what does it mean by saying that selective outgrowth of antigen negative nariants in immunocompromised people lead to more cancer

A

Subclones that are most immunogneic to host are destroyed, leading to relatively antigen-negative subclones

185
Q

what does it mean by saying that loss or reduced expression of histocompatibility antigens in immunocompromised people lead to more cancer

A

tumor cells dont express normal levels of HLA class I, escaping attack of cytotoxic T cells

186
Q

what does it mean by saying that loss of costimulation in immunocompromised people lead to more cancer

A

t cells need co-stimulatory molecule to initate immune response to foreign antigen

187
Q

can carcinogenic agents suppress the immun system

A

Yeh

188
Q

can benign tumors be serious

A

Yeh

189
Q

When can cancer lead to a change in hormone prouction

A

adenomas and carcinomas arising from beta cells can produce hyperinsulinism
- fetal

190
Q

what kind of tumors tend to produce too much insulin

A

Well differentiated benign tumors

191
Q

when would a tumor cause ulveration

A

when a tumor expands to the point of breaking through the epithelium surface

192
Q

when can ulceration cause a problem

A

bleeding and secondary infection

193
Q

where is cachexia seen

A

In cancer patients

194
Q

what does Cachexia lead to

A

Progressive loss of body fat and lean body mass
accompanied by profound weakness, anorexia, and anemia
- wasting

195
Q

when does Cachexia present itself

A

terminal

196
Q

how often are paraneoplastic syndroms found

A

10-15% of cancer patients

197
Q

why are paraneoplastic syndroms important

A

May represent an early manifestation of occult disase
May pose significant clinical problems for affected patients
May mimic metastatic disease and thereby confound treatment

198
Q

what is a prognosis

A

defining a grade and stage of a malginicy to predict the course of a disease

199
Q

what does grading cancer show

A

Assess aggressiveness of a malignancy

  • differentiation
  • number of mioses
200
Q

what is grade I vs Grade IV cancer

A

Grade I: most differentiated

Grade IV: least differentiated

201
Q

what is staging of cancer

A

estimating cancer size of extent

  • size of primary lesion
  • presence of metastatic lesion
  • presence of lymph node involvement
202
Q

what unit is used for squamous cell carcinoma of head and neck staging

A

T: primary tumor diameter(1-4)
N: regional lymph node involvement (0-3)
M: metastases (0-1)

203
Q

what is more valuable for prognosis staging of Grade

A

Staging

204
Q

what is incisional biopsy

A

Portion of lesion taken for microscopic examination

205
Q

excisional biops

A

Entire lesion was removed for microscopic examination

206
Q

how useful is electron microscopy

A

Only for a limited number of cases

207
Q

when is frozen section biopsy done

A

Done at time of definitve surgery in the hospital

208
Q

Pros and cons of Frozen section biopsy

A

Quick but prone to erros

209
Q

pros and cons of fine needle aspiration biopsy

A

Needs expertise in obtaining

Expertese in analyzing

210
Q

when is fine needle aspiration biopsy useful

A

evaluating superficial and deep seated masses

211
Q

when is cytologic (papanicolaou) smears done

A

Screening for cervical Ca

Supplemnted by HPV test

212
Q

what is Immunocytochemistry

A

Specific antibody-guided detection of tumor-specific or associated antigens to determine the precise classifciation or subclass of a tumor

213
Q

when is Flow cytometry done

A

Classifcation of leukemias and luymphomas

214
Q

what is done for Flow cytometry

A

Surface markers and DNA ploidy analysis

215
Q

what do biochemical assays look for

A

Tumor associated enzymes, hormones and other tumor markers in blood
- prostate-specific antigen

216
Q

what is molecular diagnosis

A

Use of fluorescent in-situ hybridization or PCR to create personalized medicine

general path (16 decks)

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