Neoplasia Flashcards Preview

PATHOLOGY > Neoplasia > Flashcards

Flashcards in Neoplasia Deck (175):
1

NEOPLASIA DEFINITION

abnormal mass of tissue that's growth exceeds the surrounding normal tissue and grows without stimuli

2

Benign Neoplasm Definition

neoplasm which lacks the ability to invade, destroy tissue and metastasize

3

Malignant Neoplasm Definition

A neoplasm that possesses the ability to invade, destroy tissue and metastasize

4

Cancer definition

referring to all types of malignant neoplasms.

5

Urothelium

Transitional epithelium, lining majority of GU tract

6

Squamous stratified epithelium

multilayered flattened epithelial cells arranged on a basement membrane (mitosis occurs near BM)

7

Polyp

mass arising from a mucous membrane protruding into the lumen of a hollow viscus

8

Poly origin

epithelial cell origin

9

Sessile polyps

flat, arising directly from the mucosal epithelial layer

10

Pedunculated polyps

extending from the mucosa through a fibrovascular elongated stalk + surrounding epithelium

11

Cyst

outer capsule + inner surface lined with epithelium, hollow-cavity filled with mucin

12

Pseudocyst

lacks inner epithelial lining

13

Adeno-

glandular epithelial origin

14

Squamo-

flat, scale-like epithelial origin

15

Papillary

epithelial growth that extend outward as small nipple-like structure or protuberance

16

Papillo-

referring to a epithelial polyp

17

Myxo-

mucin producing mesenchymal origin

18

Rhabdomyo-

skeletal muscle mesenchymal origin

19

Leiomyo-

smooth muscle mesenchymal origin

20

Hemangio-

blood vessel mesenchymal origin

21

Lymphangio-

lymph vessel mesenchymal origin

22

Lympho-

lymphoid organ origin

23

Myelo-

myeloid origin: part of marrow- eosinophil, basophil, neutrophil, and monocyte

24

-oma

Benign neoplasm suffix

25

Carcinoma

malignant epithelial-derived cancer cells

26

Sarcoma

malignant mesenchymal-derived cells

27

Lymphoma

ALL are malignant lymphoid-derived cells

28

Myeloma

ALL are malignant marrow-derived cells

29

Leukemia

ALL are malignant hematologic-derived cells

30

Melanoma

Malignant neoplasm of melanocytic origin

31

Nevi

small benign melanocytic neoplasia

32

Myelodysplastic syndromes

hematologic dysplastic neoplasm

33

Plasmacytomas

discrete, solitary mass of plasma cells extramedullary or in bone

34

plasma cell dyscrasias

expansion of the number of monoclonal bone marrow plasma cells

35

Heterotopia

NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location

36

Choristoma

NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location

37

Hamartoma

NEOPLASTIC; excessive, focal overgrowth of cells and tissues native to the organ in which it occurs

38

Differentiation

degree to which the cellular constituents of a neoplasm resemble mature elements of the cell type

39

Differentiation of benign tumors

Highly differentiated

40

Differentiation of malignant tumors

tend to be less differentiated

41

Poorly differentiated tumors correlates with

advanced malignancy

42

Maturation

Directly related to differentiation; advancement of differentiation

43

Maturation of benign tumors

Very mature

44

Maturation of malignant tumors

tend to be less mature

45

Poorly maturated tumors correlate with

advanced malignancy

46

Dysplasia

Atypical nuclear and cytoplasmic changes which are considered PREmalignant

47

High grade dysplasia =

a lot of cellular atypia

48

Anaplasia

Atypical and aberrant changes within a cell or group of cells reflective of a MALIGNANT neoplastic changes

49

The greater the anaplasia

the more aggressive the tumor and the greater likelihood that the malignant cells become metastatic

50

Neoplastic rate of growth

When cellular replication and survival exceeds cellular loss

51

The greater the differentiation of a tumor, the _________ the growth

SLOWER; greater differentiation correlates with a slow growing tumor

52

In-situ carcinoma growth

Carcinomas begin to grow in the epithelium, but are confined by the basement membrane.

53

Why can't you have in situ sarcomas?

Sarcomas derived from mesenchymal cells are not confined because there is no BM

54

What's the difference between a high-grade dysplasia and in situ carcinoma?

Nothing, virtually impossible to tell

55

Encapsulated

Benign neoplasms: limited cohesive expansion

56

Unencapsulated

Malignant neoplasms: have the capacity for local infiltration and invasion leading to extensive tissue destruction

57

If an in situ carcinoma cell undergoes genetic alterations that allow it to invade the BM, it is now

a microinvasive carcinoma that has the ability to enter vessels if it comes into contact

58

Metastasis

tumor cells ability to leave their primary site or origin (primary neoplasm) and spread to a distant area of the body (separated in space) where they implant and replicate

59

Metastasis can occur via

direct seeding, lymphatic spread or hematogenous spread

60

Metastasis: lymphatic spread

tumor embolus is carried by lymph until it reaches a point where it lodges and begins to grow (generally at regional lymph nodes)

61

Lymphatic spread from breast cancer generally occurs at

axillary lymph nodes

62

Metastasis: Hematogenous spread

tumor embolus is carried by blood vessels, there are no gate keepers - wide-spread

63

Secondary Brain tumor indicates

Hematogenous spread, there is no lymph to brain

64

Metastasis: Direct seeding

the cancer is exposed to a cavity and cancer cells are carried in the fluid within the cavity and carried to another surface

65

Benign Neoplasm Characteristics

Encapsulated, well-differentiated, limited growth due to contact inhibition, freely moveable upon palpation due to capsule, no local invasion

66

Malignant Neoplasm Characteristics

Well-differentiated to undifferentiated, loss of maturity, loss of tissue and cellular organization, nuclear atypia, increased levels of mitoses, large nucleus, tumor giant cells, non-encapsulated, fixed position, often necrotic of hemorrhaging, local invasion, capacity to metastasize

67

Malignant tumor cell features

Large nucleus, abnormal increased mitoses, large, multi-nucleated cells, mitotic figures

68

Grading

Related to degree of differentiation of malignant neoplasm - phenotypic property

69

grade 1 neoplasms

well differentiated

70

Grade 4 neoplasms

poorly differentiated

71

High grade tumors have more

atypical cells and atypical mitotic figures, higher capacity to metastasize

72

Low anaplastic potential

low-grade tumor

73

Staging

classification of a tumor based on the extent of spread throughout the human body as determined by the UICC and AJC

74

Staging considers

tumor size, the degree of regional lymph node involvement and the presence or absence of metastasis

75

AJCC Staging

TNM (tumor size, number of nodes, metastasis)

76

pT2N2 versus T2N2

'p' indicates pathologists staging based on the tissue biopsy; other indicates clinical staging based on diagnostics

77

Incidence of cancer types is due to

environmental (geographical) and genetic determinants

78

Cancer incidence in males

14% lung, 33% prostate, 11% colorectal

79

Cancer incidence in females

33% breast, 12% lung, 11% colorectal

80

Mortality from cancer in males

31% lung, 10% colorectal, 10% prostate

81

Mortality from cancer in females

25% lung, breast 15%, 11% colorectal

82

Autosomal dominant inherited cancer syndromes

means the person is born with a mutation in one gene and only needs to acquire 1 mutation in the other gene throughout life for cancer to develop (1 mutation = increased risk of cancer)

83

Sporadic cancer

requires 2 mutations to occur throughout life, 1 in each chromosome, which is less likely to occur than if born with a mutation

84

Familial Retinoblastoma

pt is heterozygous for Rb gene - when a mutation is acquired sporadically in the normal Rb gene chromosome (usually UV light), the patient becomes homozygous for mutant Rb gene, and retinoblastoma occurs

85

Examples of Autosomal dominant inherited cancer syndromes

Retinoblastoma, MEN syndrome, Familial Adenomatous polyposis, hereditary nonpolyposis colon cancer, Li-Fraumeni Syndrome

86

Li Fraumeni Syndrome

autosomal dominant p53 mutation, predisposes a person to a variety of cancer developments

87

Autosomal Recessive Syndromes of Defective DNA Repair

pt is homozygous for the defective gene, inherits 2 copies of the mutated gene which puts them at increased risk for cancer

88

Examples of Autosomal Recessive Syndromes

Xeroderma pigmentosum, Ataxia-telangiectasia, Fanconi anemia, HNPCC, Bloom Syndrome

89

Familial Clustering

No clear defined transmission pattern, but som egene specificity; early age of onset, tumors in 2+ relatives

90

Acquired Preneoplastic Disorders Include

Preceding inflammatory conditions, viral infection, chemical carcinogenesis, pre-existing benign neoplasm

91

Growth-promoting proto-oncogenes

normal functional gene that regulates growth and differentiation, that when mutated is likely to lead to cancer due to its regulatory functions in a normal cell. Proto-oncogene -> mutation -> oncogene

92

Oncogenes may alter

GFs, GFRs, signal transduction proteins, nuclear regulatory proteins, cell cycle regulators

93

sis gene

oncogene that increases GF production

94

erb-B2 gene

oncogene that increases GF receptors

95

ras gene

oncogene that encodes for a mutated signal transducer protein (constitutively active)

96

myc gene

oncogene coding for mutant TF (nuclear regulatory proteins); active w/o signal transduction

97

Mutation examples

point mutation, chromosomal rearrangement, gene amplification

98

Burkitt's Lymphoma - c-myc mutation type

chromosomal rearrangement of 8 and 14

99

n-myc mutation type

gene amplification

100

anti-oncogenes

regulate nuclear transcription, cell cycle, signal transduction, stimulate cell surface suppressor molecules; normally act as BRAKES to cell cycle

101

Growth inhibiting cancer suppressor genes (anti-oncogenes)

Normally suppress growth, but when mutated can no longer suppress growth

102

Genes which regulate apoptosis

prevent or promote programmed cell death

103

Multi-step carcinogenesis

requires a mutation that activates an oncogene AND suppresses an anti-oncogene, followed by clonal expansion and neoplasm formation

104

Point mutation example

retinoblastoma

105

Examples of anti-oncogenes

Rb, p53, BRCA1-2

106

Clonal expansion characteristic

polyclonal cell population

107

malignant cells have a high number of cells in G1-M phase

G1-M phase

108

Malignant neoplasms have the ability to recruit

angiogenesis

109

Angiogenesis - Proto-oncogenic regulation

Stimulate blood vessel growth.

110

Angiogenesis - Tumor suppressor gene regulation

Normally inhibit blood vessel growth, unless mutated

111

an invasive tumor that has gained the ability to breach basement membrane has likely undergone genetic alteration and now has the ability to bind

laminin of basement membrane

112

monoclonal expansion -->

heterogeneity of the cell population overtime due to mutations in various daughter cells leading to sub-types of cells with various capabilities

113

In situ transformation to invasive carcinoma

Cell must lose adhesion molecules to adjacent cells, obtain an active collagenase to break down ECM, tumor cells then bind to laminin receptors of BM

114

Intravasation

attach and invade the BM of the vessel and migrate through the tight junctions of the endothelial cells

115

Satellite nodules

earliest example of metastasis (intra-organ metastasis)

116

Secondary tumor

arises in a distant location from primary

117

Chemical initiator

causes a change in the cell which makes it susceptible to the development of a neoplasm. Initiation alone is insufficient for neoplasia to occur

118

2 types of initiators

Direct acting agent and Indirect acting agents

119

Indirect acting agents

Require in-vivo metabolic conversion into an active definitive carcinogen (metabolite or free radicals)

120

v-onc

proto-oncogene mutation due to viral transduction

121

c-onc

proto-oncogene mutation due to influences that alter their function in situ

122

p53 is an example of

tumor suppressor (anti-oncogene)

123

Rb is an example of

tumor suppressor (anti-oncogene)

124

BRCA-1/2 is an example of

tumor suppressor (anti-oncogene)

125

Direct acting initiator

Require no chemical transformation to induce their carcinogenic potential

126

chemical initiators are

mutagenic at the molecular level inducing mutations in oncogenes

127

Promoters

themselves are not mutagenic. Rather they stimulate activation and production of enzymes capable of inducing cell growth and proliferation.

128

Examples of direct-acting initiators

alkylating agents, cyclophosphamide, chlorambucil, busulfan, melphalan, immunosuppressants

129

direct-acting initiators are

weak carcinogens

130

Examples of indirect-acting initiators

Polycyclic aromatic hydrocarbons, Aromatic amines/azo dyes, Aflatoxin B1 – Produced by Aspergillus flavus, Nitrosamines and amides

131

Polycyclic aromatic hydrocarbons

indirect-acting initiator, potent carcinogen, can cause skin, colon, lung, bladder cancer, sarcoma

132

Aromatic amines/azo dyes

indirect-acting initiator, activated by the cytochrome P-450 oxygenase activator systems, associated with HCC

133

β-naphthylamine

indirect-acting initiator, present in aniline-dyes, associated with bladder cancer

134

Aflatoxin B1

indirect-acting initiator, Produced by Aspergillus flavus, when Hep B infected person is exposed = increased risk of HCC

135

Nitrosamines and amides

indirect-acting initiator, common food preservatives activated by gut bacteria, gastrointestinal carcinomas

136

Exogenous promoters

Saccharin and cyclamates, Diethylstilbestrol (DES), Exogenous hormones

137

Endogenous Promoters

Hormones, Bile salts/Dietary Fat

138

UV exposure

causes pyrimidine dimers in DNA that overrides the body's inherent Nucleotide Excision Repair (NER) mechanisms

139

UV exposure primarily causes

cutaneous malignancies

140

UV, electromagnetic, particulate, radon

Many can act directly by inducing DNA breaks or indirectly by generating free radicals

141

Cytotoxic viruses

inject their DNA/RNA into a cell, this becomes incorporated into cells DNA and causes mutations/altered genes

142

HPV

DNA oncogenic virus

143

HPV Types 16 and 18 are associated with

invasive squamous cell carcinoma

144

HPV Types 1, 2, 4, 7 are associated with

Benign squamous papillomas

145

HPV Types 6 and 11 are associated with

Genital lesions with low malignant potential

146

Epstein Barr virus (EBV)

DNA oncogenic virus

147

EBV is associated with

Burkitt's Lymphoma, B-cell lymphoma

148

HBV virus

DNA oncogenic virus

149

HBV is associated with

HCC esp in combo with Aflatoxin B1

150

Kaposi virus

DNA oncogenic virus

151

Kaposi virus KSHV is associated with

development of AIDS related Kaposi sarcoma

152

Human T cell leukemia virus (HTLV-1)

RNA oncogenic virus

153

Human T cell leukemia virus (HTLV-1) is associated with

T cell leukemia/lymphoma

154

Hep C virus

RNA oncogenic virus

155

Hep C virus is associated with

HCC

156

Helicobacter pylori

gastric bacteria associated oncogenesis (gastric carcinoma, MALT lymphoma)

157

MALT lymphoma caused by h/ pylori can be treated with

abx

158

Local effects from tumor on host

Effects caused at site due to tumor growth

159

Hormonal effects from tumor on host

tumors may possess the ability to secrete hormones or hormone-like factors

160

Small cell cancer of the lung often secretes

ACTH causing Cushing's Syndrome

161

Cachexia

systemic effect due to tumor, causing increased TNF-alpha and cytokine release, resulting in increased basal metabolic rate, in addition to tumor cells increased need for nutrients

162

Paraneoplastic syndrome

Constellation of physical findings that are in association to products of the tumor

163

migratory thrombophlebitis

Malignancies associated with hypercoagulability

164

Tumor lysis syndrome

group of metabolic complications that can occur after treatment of cancer: hyperkalemia, hyperphosphatemia, hyperuricemia and hyperuricosuria, hypocalcemia, and consequent acute uric acid nephropathy and acute renal failure

165

Anti-tumor defenses include

CTL, NK, Macrophages, immunosurveillance, immunotherapy against tumor antigens

166

Histology

staining and viewing tissue morphology and cells in relation to another

167

Cytology

Cellular staining to look for characteristics of individual cells

168

DNA probe

look for specific DNA sequences characteristic of cancer type

169

Carcinoembryonic Antigen (CEA):

colon cancer

170

Alpha-Fetoprotein (AFP):

HCC

171

Beta Subunit Human Chorionic Gondotropin (β-HCG):

choriocarcinoma

172

CA-125

ovarian cancer

173

Flow cytometry

use to quantify B and T cells

174

exfoliative cytology

scrape away epithelium and stain

175

Fine needle aspiration

insertion of a needle into the neoplasm to collect fluid and cells