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General Pathology > Neoplasia Part 1 > Flashcards

Neoplasia Part 1 Flashcards

1
Q

cancer = ______ tumors

A

malignant

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2
Q

what is the 2nd leading cause of death in the US?

A

cancer

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3
Q

cancer is a ____ disorder

A

genetic

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4
Q

with cancer being a genetic disorder, what are the 2 ways are the mutations that cause it mostly acquired?

A

-arise spontaneously
-environmental exposure

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5
Q

T/F genetic changes are heritable with the accumulation of mutations leading to characteristic features of cancer; however, actual inherited cancers are infrequent

A

true

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6
Q

the loss of normal growth control where cells become transformed and start doing their own thing

A

neoplasia

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7
Q

what is another name for a neoplasm?

A

tumor

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8
Q

what are the 2 major qualities of neoplasia?

A

parasitic and autonomous

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9
Q

what do the root words of neoplasia mean?

A

“new growth”

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10
Q

study of neoplasms/tumors

A

oncology

(“oncos” = tumor)

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11
Q

neoplasia is a spectrum of diseases, what are the ranges of neoplasms? (4)

A

-benign
-locally aggressive
-intermediate malignant
-malignant

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12
Q

what are the 2 anatomic components of tumors?

A

-parenchyma
-stroma

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13
Q

the tumor component that consists of neoplastic cells

A

parenchyma

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14
Q

the tumor component that consists of the supporting connective tissue and vasculature

A

stroma

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15
Q

which tumor component determines how a tumor is named?

A

parenchyma

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16
Q

the degree of resemblance of tumor cells to parent cells

A

Differentiation

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17
Q

what does “well-differentiated”, in regards to tumor cells, mean?

A

more resemblance to parent cells

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18
Q

what does “poorly differentiated”, in regards to tumor cells, mean?

A

little resemblance to parent cells

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19
Q

what does “anaplasia”, in regards to tumor cells, mean?

A

no resemblance to parent cells

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20
Q

what are other names for “anaplasia”?

A

dedifferentiated and undifferentiated

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21
Q

in a “poorly differentiated” tumor cell, increased/abnormal DNA replication lead to what? (6)

A

-pleomorphism
-nuclear hyperchromatism
-increased nuclear/cytoplasmic ratio
-atypical nuclei
-numerous and atypical mitoses
-prominent nucleoli

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22
Q

what is pleomorphism?

A

when all the cell shapes and sizes are different

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23
Q

a microscopic, potentially reversible, altered growth or maturation pattern

A

dysplasia

(“altered growth”)

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24
Q

what does dysplasia refer to when seen in epithelial tissues?

A

-precancerous (premalignant) state –> may progress to malignancy
-you will see disorderly maturation, pleomorphism, and mitotic activity

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25
Q

what does dysplasia refer to when seen in bone lesions?

A

does NOT imply pre-cancerous state, just means altered growth

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26
Q

what is carcinoma in-situ?

A

dysplastic changes involving the full thickness of the epithelium, but lesion remains confined to the normal tissue and does not pass beyond the basement membrane = “pre-invasive/precancerous”

(NOT cancer but one step away; final step of dysplasia)

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27
Q

in general, how are benign epithelial tumors named?

A

-root word = clinical appearance, anatomic site, or cell type form

  • suffix = “-oma”
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28
Q

what is a papilloma?

A

finger-like epithelial projections overlying cores of vascular fibrous connective tissue that arises from surface epithelium –> benign epithelial tumor

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29
Q

what is an adenoma?

A

benign tumor of glandular epithelium - benign epithelial tumor

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30
Q

what is a papillary cystadenoma?

A

adenoma characterized by adenomatous papillary processes that extend into cystic spaces (i.e. cystadenoma of ovary) - benign epithelial tumor

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31
Q

how are benign mesenchymal tumors named?

A

most often named by tissue of origin + “oma”

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32
Q

benign mesenchymal tumor of fibrous tissue

A

fibroma

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33
Q

benign mesenchymal tumor of cartilaginous tissue

A

chondroma

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34
Q

benign mesenchymal tumor of smooth muscle

A

leiomyoma

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35
Q

benign mesenchymal tumor of skeletal muscle

A

rhabdomyoma

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36
Q

benign mesenchymal tumor of fat

A

lipoma

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37
Q

benign mesenchymal tumor of bone

A

osteoma

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38
Q

benign mesenchymal tumor of blood vessels

A

angioma

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39
Q

what are two examples of benign mixed tumors we learned about?

A

-pleomorphic adenoma (salivary glands)
-fibroadenoma (breast; only the fibrous part is neoplastic)

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40
Q

a benign tumor that involved both the epithelium and connective tissue

A

benign mixed tumors

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41
Q

what is a teratoma?

A

a neoplasm (tumor) with cells derived from more than 1 germ layer (totipotent –> can form many different types of tissue)

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42
Q

what is a hamartoma?

A

disorganized overgrowth of tissue that is native to the site that is generally non-neoplastic (not a tumor bc it does not grow autonomously)

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43
Q

what is a choristoma?

A

disorganized overgrowth of tissue at unexpected site that is non-neoplastic (not a tumor bc it does not grow autonomously)

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44
Q

what is a polyp?

A

a mass that projects above a mucosal surface

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45
Q

what are notable “-oma” exceptions that are actually malignant, rather than benign? (6)

A

-lymphoma
-melanoma
-mesothelioma (lungs)
-seminoma (gonad germ cells)
-glioblastoma (brain)
-hepitoma (hapatocellular-carcinoma; liver)

(Lady Made Miso Soup Gladly Here)

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46
Q

what are notable “-oma” exceptions that are non-neoplastic (i.e. not tumors)? (2)

A

-granuloma (multi-nucleated giant cells, epithelioid histiocytes, lymphocytes)
-hematoma (bruse)

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47
Q

in general, how are malignant epithelial tumors named?

A

-root word: anatomically or cellularly
-suffix: + “-carcinoma”

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48
Q

what is a squamous cell carcinoma?

A
  • malignant epithelial tumor from squamous epithelium (skin, mouth, esophagus, vagina) or areas of squamous metaplasia (bronchi or cervix)
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49
Q

production of squamous cell carcinomas are marked by what?

A

keratin

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50
Q

what is a transition cell carcinoma?

A

malignant epithelial tumor from urinary tract epithelium

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51
Q

what is adenocarcinoma?

A

malignant epithelial tumor from glandular origin (including GI mucosa, endometrium, and pancreas)

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52
Q

adenocarcinomas usually show desmoplasia. what is that?

A

CT growth in reaction to the tumor

(reason why tumors feel firm)

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53
Q

in general, how are malignant mesenchynal tumors named?

A

-root word = anatomically or cellularly
-suffix: + “sarcoma”

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54
Q

malignant mesenchymal tumor of fibrous tissue

A

fibrosarcoma

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55
Q

malignant mesenchymal tumor of cartiaginous tissue

A

chondrosarcoma

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56
Q

malignant mesenchymal tumor of bone

A

Osteosarcoma

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57
Q

malignant mesenchymal tumor of skeletal muscle

A

rhabdomyosarcoma

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58
Q

malignant mesenchymal tumor of smooth muscle

A

leiomyosarcoma

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59
Q

malignant mesenchymal tumor of fat

A

lipsarcoma

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60
Q

malignant mesenchymal tumor of vessels

A

angiosarcoma

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61
Q

what are some eponyms/malignant tumors that have their own special name since they were named after the person that discovered them? (3)

A

-Burkitt Lymphoma
-Hodgkin disease/lymphoma
-Wilm’s tumor

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62
Q

what are 3 ways to name tumors based on their resemblance to tissue of origin and/or degree or differentiation?

A

-well-differentiated (“low grade”)
-moderately differentiated
-poorly differentiated (“high grade”)

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63
Q

what are ways to name tumors based on their appearance under the microscope? (4)

A

cystic, papillary, tubular, solid, etc

(often added to describe variants of a tumor)

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64
Q

Is the following clinical description for benign or malignant tumors:
non-cancerous?

A

benign

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65
Q

is the following clinical description for benign or malignant tumors:
slow growing?

A

benign

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66
Q

is the following clinical description for benign or malignant tumors:
remains localized and does not spread but may cause local damage?

67
Q

is the following clinical description for benign or malignant tumors:
surgically removable?

68
Q

is the following for clinical description benign or malignant tumors:
survivable with good prognosis?

69
Q

is the following clinical description for benign or malignant tumors:
cancer?

70
Q

what is latin for cancer?

71
Q

is the following clinical description for benign or malignant tumors:
rapid growth?

72
Q

is the following clinical description for benign or malignant tumors:
leaves the anatomic compartment to invade and destroy adjacent tissues?

73
Q

is the following clinical description for benign or malignant tumors:
metastasis is a defining feature?

74
Q

what is metastasis?

A

spread of a tumor to a distant site

75
Q

is the following clinical description for benign or malignant tumors:
can cause death due to poor prognosis?

76
Q

is the following gross/microscopic description for benign or malignant tumors:
well-differentiated?

77
Q

is the following gross/microscopic description for benign or malignant tumors:
normal mitosis?

78
Q

is the following gross/microscopic description for benign or malignant tumors:
encapsulated?

79
Q

is the following gross/microscopic description for benign or malignant tumors:
well to poorly differentiated (or anaplastic)?

80
Q

is the following gross/microscopic description for benign or malignant tumors:
atypical mitoses?

81
Q

is the following gross/microscopic description for benign or malignant tumors:
non-encapsulated?

82
Q

the typically growth rate of benign tumors is affected by what factors? (3)

A

-hormones
-blood supply
-pressure constrains

83
Q

how fast do benign tumors grow?

A

very slowly – months to years

84
Q

how fast do malignant tumors grow?

A

fast – variable but can be rapid enough to outgrow blood supply and make its own or cause tissue death (necrosis)

85
Q

describe the local invasion of benign tumors

A

are encapsulated at the periphery so can’t invade much

86
Q

describe the local invasion of malignant tumors

A

they infiltrate and invade –> destructive and have no capsule = can infilatrate

87
Q

what is the hallmark of malignancy?

A

metastasis

88
Q

T/F metastatic capacity depends on tumor type

89
Q

what factors mean a tumor is more likely to metastasize? (2)

A

more anaplastic and larger tumor = more likely to metastasize

90
Q

____% of newly diagnosed malignant tumors have clinically evident metastases

A

30% (early detection is soo important!!!)

91
Q

what are ways that malignancy is spread? (5)

A

-seeding in body cavities
-lymphatic spread
-hematogenous (blood) spread
-neural spread (path of least resistance)
-Batson’s venous plexus, along vertebral column (path of least resistance)

92
Q

how is malignancy of carcinoma typically spread? what are the 2 exceptions to this rule?

A

-lymphatic spread
-exceptions: renal cell carcinoma, hepatocellular carcinoma

93
Q

how is malignancy of sarcoma typically spread?

A

hematogenous (blood) spread

(lungs and liver = secondary sites)

94
Q

What are examples of paths of least resistance

A
  • Neural spread
  • Batson’s venous plexus: along vertebral column = potential spread to the jaw
95
Q

tissue stem cells live within ____ within a tumor

96
Q

what controls stem cell division into additional stem cells or differentiated cancer cells?

A

signals from surrounding niche cells

97
Q

what is the theory surrounding cancer stem cells?

A

if they exist, then they must be eliminated to cure the disease but they may be resistant to therapy or harbor resistance

98
Q

T/F multiple subtypes of oral cancer stem cells have been identified, all with different markers

99
Q

neoplasia epidemiology gives insights into causes. what are examples of possible epidemiological causes? (5)

A

-incidence
-geographic and environmental factors
-age
-heredity
-acquired predisposing conditions

100
Q

T/F for all cancers combined, the incidence (new cases/100,000) and death rate have decreased with some modest individual exceptions

101
Q

what is the life time risk for cancer?

A

1 in 2-3 chance of getting cancer with 1 in 5 chance of dying from cancer in US

102
Q

T/F there is remarkable variation around the world in cancer incidence and death rates

103
Q

T/F the study of populations, habits, dietary features and environmental exposures can identify risk factors for cancer

104
Q

what are some examples of environmental exposures that are associated with an increased cancer risk? (6)

A

-occupation exposure to carcinogens
-chronic sun exposure
-cigarette smoking
-chronic alcohol consumption
-obesity
-oncogenic HPV

105
Q

T/F Young individuals (5-15 years) are most likely to get cancer

A

False

old individuals (55-75 years) are most likely to get cancer

106
Q

in children (0-15 years), cancer accounts for ____% of deaths (leukemia, lymphoma, CNS tumors, bone/ST sarcomas)

107
Q

there are hereditary predispositions for cancer but only ____% of cancers are related to inherited mutations

108
Q

what are two inheritance patterns that have been noted in cancer? give examples of each

A

-autosomal dominant: retinoblastoma, familial adenomatous polyposis

-autosomal recessive: (typically DNA repair genes) xeroderma pigmentosum

109
Q

describe what is meant by “familial cancers of uncertain inheritance”

A

clustering of cancer in families without specific marker genes or predicatale inheritance patterns

110
Q

what are the features of “familial cancers of uncertain inheritance”?

A

-early age at onset
-2+ close relatives with tumors
-multiple/bilateral tumors

111
Q

about ___% of cancers are caused by random mutations during regular cell division

112
Q

are most cancers developed from environment and hereditary factors or just random bad luck?

A

random, bad luck

113
Q

what is meant by “acquired preneoplastic disorder”

A

an acquired disorder that is pre-cancerous / premalignant –> a precursor lesion

(need to closely follow these for early cancer detection)

114
Q

what does the abbreviation “CA” mean?

115
Q

what is the following “acquired preneoplastic disorder” a precursor for?
-smoking induced squamous metaplasia
-dysplasia of bronchial mucosa

A

bronchogenic CA

116
Q

what is the following “acquired preneoplastic disorder” a precursor for?
-endometrial hyperplasia
-endometrial dysplasia

A

endometrial CA

117
Q

what is the following “acquired preneoplastic disorder” a precursor for?
-oral, vulvar and penile leukoplakia

A

squamous cell CA

118
Q

what is the following “acquired preneoplastic disorder” a precursor for?
-villous adenoma of colon

A

colorectal carcinoma

119
Q

what is a. villous adenoma of colon?

A

preneoplastic glandular growth that grows like a polyp

120
Q

are benign tumors premalignant? explain

A

generally no but a few exceptions:
-adenomas of the colon can undergo malignant transformation

121
Q

what defines the molecular basis of cancer

A

carcinogenesis

122
Q

what are the 2 main principles of carcinogenesis?

A

-non-lethal genetic damage
-there are 4 classes of cancer genes that are recurrently affected in cancers

123
Q

what are the 4 classes of cancer genes that are recurrently affected in cancers?

A

-proto-oncogenes
-tumor suppressor genes
-apoptosis regulation genes
-tumor cell/host cell interaction genes

124
Q

What are proto-oncogenes?

A

genes that encode for proteins that stimulate normal cell growth & division (normal versions of oncogenes)

125
Q

what is an oncogene?

A

a mutated proto-oncogene that will stimulate innappropriate growth (tumor)

126
Q

what are the 2 types of tumor suppressor genes and what do they do?

A

-governors/promoters: stop cell proliferation (directly)

-guardians/caretakers: help in DNA repair

127
Q

what are the 2 types of classes of mutations that cause cancer?

A

-driver (pathogenic) mutations
-passenger (neutral) mutations

128
Q

what are driver (pathogenic) mutations?

A

mutations that alter function of cancer-promoting genes to directly influence development or progression of cancer

129
Q

where are driver (pathogenic) mutations found?

A

tightly clustered within cancer genes

130
Q

what are passenger (neutral) mutations?

A

an acquired mutation that does not directly affect formation of cancer

131
Q

where are passenger (neutral) mutations found?

A

widely scattered throughout the genome?

132
Q

since passenger (neutral) mutations do not directly cause cancer, how can they lead to it?

A

they create genetic variants that can provide a selective advantage for tumor cells (i.e. drug resistance)

133
Q

what are some patterns of genetic damage?

A

-point mutations
-balanced translocations
-deletions
-gene amplification
-aneuploidy

134
Q

what type of genetic damage pattern is the RAS oncogene usually affected by in cancer?

A

point mutation

135
Q

what type of cancers are balanced translocations common in? (2)

A

hematopoietic neoplasms and sarcomas

136
Q

what are 3 classic cancers that are caused by balanced translocations?

A

-Chronic myeloid leukemia (CML)
-Burkitt’s lymphoma
-Follicular B-cell lymphoma

(CML is the “Philadelphia chromosome”)

137
Q

what chromosome and gene undergo a balanced translocation in Chronic myeloid leukemia (CML)?

A

Philadelphia Chromosome - BCR-ABL fusion gene

138
Q

what gene undergoes a balanced translocation in Burkitt’s lymphoma?

139
Q

what genes are deletions normally found in? give an example that would lead to a cancer

A

-tumor suppressor genes

-ex: Rb in retinoblastoma

140
Q

T/F the genetics damage pattern of ‘gene amplification’ can increase to hundreds of copies

141
Q

gene amplifications are seen _____ and _____

A

-homogeneously staining regions

-double minutes

142
Q

what are double minutes in gene amplification?

A

extrachromosomal circular DNA fragments

143
Q

what are 2 examples of normal genes that can be altered via gene amplification and the cancers they cause?

A

-MYC –> Neuroblastomas

-HER-2/neu –> breast cancer

(possibly also EGFR –> lung cancer)

144
Q

what is aneuploidy?

A

when there is a number of chromosomes that is not a multiple of the haploid state (i.e. 23)

(he said it technically could be considered gene amplification but with an entire chromosome)

145
Q

aneuploidy is very common in cancers, especially ____

A

carcinomas

146
Q

aneuploidy occurs due to errors of the _____

A

mitotic checkpoint

147
Q

in cancer cells, aneuploidy tends to increase _____ and decrease _____

A

-increase oncogene copies

-decrease tumor suppressor gene copies

148
Q

non-coding single stranded RNAS that are ~22 bases long

A

microRNA (miRNAs)

149
Q

what are some functions of microRNA (miRNAs)? (3)

A

-inhibit gene expression by repressing translation or by mRNA cleavage

-help control cell growth, differentiation, and cell survival

-may promote increased oncogene or decreased tumor suppressor gene expression

150
Q

T/F clinical trials are evaluating the use of microRNA (miRNAs) as therapeutic targets to treat some cancers

151
Q

T/F miRNA-based drugs in combination with first-line agents may be adopted as a new therapeutic modality to treat oral cancer

152
Q

T/F There are thousands of Long non-coding RNAs (lncRNAs) in the cancer genome with specific expression patterns.

153
Q

T/F Long non-coding RNAs (lncRNAs) help regulate cancer development and may be crucial for future studies for targeted therapy

154
Q

what are epigenetic changes?

A

reversible, heritable changes in gene expression without mutation (no DNA mutation involved)

155
Q

what are 3 things that can lead to epigenetic changes?

A

-post-translational modification of histones
-changes in methylation
-mutations in genes that regulate the epigenome (thus, how much methylation occurs)

156
Q

what are 2 forms of changes in methylation that cause epigenetic changes that lead to cancer?

A

-genome-wide hypomethylation in cancer cells –> instability –> induces tumors

-selective promoter hypermethylation –> silences tumor suppressor genes = no expression

(remember, CpG islands)

157
Q

what is an example of selective promoter hypermethylation that silences tumor suppressor genes = no expression

A

CDKI (p16INK4a) altered in many cancers

158
Q

are most neoplasms (tumors) monoclonal or polyclonal?

A

monoclonal

159
Q

(monoclonal/polyclonal) proliferations are almost always non-neoplastic (no tumors)

A

polyclonal

160
Q

T/F Carcinogenesis is a multi-step process leading to tumor progression (increased malignant potential)

161
Q

Clinically evident tumors are most likely (homogeneous/heterogeneous)

A

heterogeneous

162
Q

_____ and _____ lead to more aggressive tumors and less response to therapy over time

A

Evolution and selection

163
Q

explain how to write out genes vs the gene’s protein product

A

-genes: italicized

-proteins: no italicized

(i.e. RB gene vs RB protein or Tp53 gene vs p53 protein)

General Pathology (32 decks)

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