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LUIV [HS 202] Patho Exam > Trans 10- Neoplasia > Flashcards

Trans 10- Neoplasia Flashcards

1
Q

Neoplasia=

A

“new growth”

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2
Q

o Abnormal mass of tissue
o Uncontrolled, uncoordinated growth with that of the
normal tissue
o Persists in the same excessive manner after
cessation of stimuli

A

Premolecular era

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3
Q

o Disorder of cell growth that is triggered by a series of
acquired mutations affecting a single cell and its
clonal progeny

A

Modern era

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4
Q

neoplastic cells → survival and growth
advantage (excessive proliferation independent of
physiological growth)

A

Mutations

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5
Q

tumor cells arise from a single cell that has
incurred genetic changes (result to cells with the same
genetic makeup)

A

Clonal

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6
Q

o Parenchyma
o Where the classification of the tumor is usually based
on
o Cells that gained mutation and proliferated
o Determines the course of biological behavior

A

Neoplastic cells

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7
Q

o Connective tissue: serves as framework of the tumor
o Blood vessels: to supply nutrition
o Chronic inflammatory cells
o Surround the neoplastic cells
o Essential for growth and spread of the tumor

A

Stroma

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8
Q

§ Abundant collagenous stroma as stimulated by
parenchymal cells
§ Ex: Schirrous (stony hard) in breast cancer

A

Desmoplasia

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9
Q
  • Localized and will not spread to other sites
  • Can be surgically removed
  • Name of cell type from which it originated ends in –oma
A

Benign neoplasms

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10
Q

In mesenchymal tumors, fibrous tissue

A

fibroma

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11
Q

In mesenchymal tumors, cartilage

A

chondroma

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12
Q

In epithelial tumors, derived from glands

A

adenoma

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13
Q

In epithelial tumors, finger-like projections from epithelial surface

A

papilloma

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14
Q

In epithelial tumors, form large cystic masses like in the ovary

A

cystadenoma

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15
Q

Exceptions:

these are malignant

A

melanoma and lymphoma

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16
Q 
• “cancers”
• Invade and destroy adjacent structures
• Spread to distant sites through blood vessels and
lymphatic vessels (metastasis)
• Can cause instant death
A

malignant neoplasms

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17
Q

o Epithelial cell origin (from any of the three germ

layers)

A

carcinoma

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18
Q

tumor cells resemble

stratified squamous epithelium

A

squamous cell carcinoma

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19
Q

neoplastic epithelial cells grow in

glandular pattern

A

adenocarcinoma

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20
Q

o Sar = “fleshy”

o Arise in solid mesenchymal tissues

A

sarcoma

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21
Q

o Arise from blood-forming cells (literally WBCs) or

lymphocytes and their precursors

A

Leukemias or lymphoma

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22
Q
  • Divergent differentiation of a single neoplastic clone

* With two lineages

A

mixed tumors

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23
Q

Contain epithelial components scattered within a

myxoid stroma with cartilage or bone

A

Mixed tumor of the salivary gland

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24
Q

from a single clone

producing both epithelial and myoepithelial cells

A

pleiomorphic adenoma

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25
Q

• Mature or immature cells or tissues belonging to more
than one germ cell layer
• From totipotent germ cells normally present in ovary,
testis or abnormal midline embryonic rests
• May contain variety of tissue types in an unorganized
arrangement

A

Teratoma

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26
Q

cystic tumor
lined by skin full of hair, sebaceous glands and tooth
structure

A

ovarian cystic teratoma

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27
Q

disorganized but benign masses of cells

indigenous to the involved site

A

Hamartoma

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28
Q

disorganized cartilage and

blood vessels

A

pulmonary hamartoma

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29
Q

heterotropic rest of cells

A

choristoma

eg nodule containing pancreatic tissue found in the
stomach, duodenum or small intestine mucosa

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30
Q

4 criteria to distinguish benign from malignant tumors:

A

o Differentiation and Anaplasia
o Rate of Growth
o Local Invasion
o Metastasis

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31
Q

extent to which tumor cells closely

resemble original cells.

A

differentiation

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32
Q

malignant tumors exhibit

A

anaplasia (total disarray of tissue architecture)

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33
Q
  • lack of differentiation

- hallmark of poor differentiated malignancies

A

anaplasia

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34
Q

anaplasia is characterized by

A 
§ Pleomorphism
§ Abnormal nuclear morphology
§ Abundant mitoses
§ Loss of polarity
§ Others: tumor giant cells, necrosis
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35
Q

replacement of a mature cell type with
another mature cell type
o normally reversible but may progress to neoplasia

A

metaplasia

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36
Q

Disordered growth
o premalignant condition (not yet a tumor, might be precedent to the pre-invasive cancer, carcinoma in situ, but may be reversible)
o loss of uniformity of individual cells and architectural orientation
o exhibits pleomorphic, hyperchromatic nuclei, and frequent mitoses, loss of polarity

A

dysplasia

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37
Q

are cohesive, expansile and form a connective tissue capsule making surgical enucleation
easy

A

benign tumors

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38
Q

are invasive, infiltrating and lacking of

well-defined capsule and plane of cleavage

A

malignant tumors

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39
Q

spread of tumor to other sites that are physically discontinuous with the primary tumor

A

metastasis

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40
Q

Unequivocally marks a tumor as

A

malignant

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41
Q

Almost all malignant tumors have the ability to

A

metastasize (Exception: glioma, basal cell carcinoma of the skin)

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42
Q

lymphatics invasion is most common in

A

carcinomas

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43
Q

hematogenous spread is most common in

A

sarcomas

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44
Q

§ favored by carcinomas originating from the kidney
§ Venous or arterial (more frequently through
veins)
§ Lung and liver are common sites because they
receive the systemic & venous outflow

A

Hematogenous spread

45
Q

Differentiation: well-differentiated; typical structure
Rate of growth: gradual
local invasion: no
metastasis: no

A

benign

46
Q

Differentiation: anaplastic; atypical structure
Rate of growth: rapid, erratic
local invasion: yes
metastasis: yes

A

malignant

47
Q

Incidence of cancer in males

A

prostate > lung > colon/rectum

48
Q

Incidence of cancer in females

A

breast >lung > colon/rectum

49
Q

deaths in males

A

lung > prostate > colon/rectum

50
Q

deaths in females

A

lung > breast > colon/rectum

51
Q

Environmental factors that cause cancer

A 
o Infectious agents (ex. HPV)
o Smoking – single most important factor
o Alcohol consumption
o Diet
o Obesity – higher death rates
o Reproductive history
o Environmental carcinogens
52
Q

Carcinomas predominate in the

A

elderly

§ accumulation of somatic mutations
§ decline in immune competence

53
Q

primitive malignancies in children

A

Wilms tumor retinoblastoma

acute leukemias rhabdomyosarcomas

54
Q

§ Proliferation of cells to repair the damage
§ Increase in pool of tissue stem cells susceptible
to transformation
§ Activation of immune cells – reactive oxygen
species
§ ex. H. pylori – lymphoma

A

chronic inflammation

55
Q

Gastric and colonic metaplasia

A

Barrett esophagus

56
Q

Squamous metaplasia

A

bronchial and

bladder mucosa

57
Q

Colonic metaplasia

A

pernicious anemia

58
Q

presenc e of hyperplasia

A

endometrial hyperplasia

59
Q

benign neoplasms

A

villous adenoma

-> 50% may progress to colonic adenocarcinoma

60
Q

those with deficient T cell immunity

A
  • oncogenic viruses

- lymphomas, sarcomas, carcinomas

61
Q

Genetic predisposition and interactions between

environmental and inherited factors examples

A

BRCA1

BRCA2

62
Q

Four basic principles of the molecular basis of cancer

A

non-lethal genetic damage
regulatory genes are involved
carcinogenesis is a multi-step process
monoclonal tumors

63
Q

Genetic damage/mutation may be acquired by
the action of environmental agents (chemicals,
radiation and viruses) or it may be inherited

A

non-lethal genetic damage

64
Q

These normal regulatory genes are the principle

targets of genetic damage.

A

Regulatory genes are involved

65
Q

§ Cancer is a multi-step process at both the
phenotypic and genetic levels resulting from the
accumulation of multiple mutations
§ Cancer does not develop right away because
numerous processes are involved.

A

carcinogenesis is a multi-step process

66
Q

§ Are monoclonal wherein they arise from one
clonal cell
§ A tumor is formed by the clonal expansion of a
single precursor cell that has incurred genetic
damage.

A

Monoclonal tumors

67
Q

o Non-lethal genetic damage at the heart of
carcinogenesis
o May be caused by environmental agents or
spontaneously occur

A

Mutation

68
Q

Four classes of genes that are targets of genetic damage

A
  • Proto-oncogenes and oncogenes
  • Tumor suppressor genes (anti-onco genes)
  • Apoptosis genes
  • DNA-Repair genes
69
Q

§ Normal function is to PROmote cell PROliferation
§ Activation to oncogenes->excessive cell
proliferation
Ø Over-expression of proteins
Ø Gene amplification
Ø Constitutive activation
Ø Ex. eRB-2, ras, abl, mvc

A

Proto-oncogenes and oncogenes

70
Q

Normal function is to INHIBITcell proliferation
§ Damage (“inactivation”) leads to inability to
suppress cell division
§ P-53- involved in tumor formation
§ Rb-13- associated with retinoblastoma
§ APC- adenomatous polypoid gene- polyp in GI
tract

A

Tumor suppressor genes (anti-onco genes)

71
Q

involved in tumor formation

A

P-53

72
Q

associated with retinoblastoma

A

Rb-13

73
Q

adenomatous polypoid gene- polyp in GI

tract

A

APC

74
Q

§ Genes that regulate apoptosis
§ Bcl-2 (anti-apoptosis gene); overexpression leads
to tumorigenesis, involved in gastric lymphoma
§ Bax, bud (pro-apoptosis gene): inactivation leads
to tumorigenesis

A

Apoptosis genes

75
Q

-anti-apoptosis gene
-overexpression leads
to tumorigenesis, involved in gastric lymphoma

A

Bcl-2

76
Q

-pro-apoptosis gene
-inactivation leads
to tumorigenesis

A

Bax, bud

77
Q

is a multi-step process: present on both

the phenotypic and genotypic level.

A

Carcinogenesis

78
Q

are needed to produce a
malignant cell (the more defects, the more
malignant/aggressive the cell)

A

Multiple genetic alterations

79
Q

8 key changes associated with cancer:

A
  1. Self-sufficiency in growth signals
  2. Insensitivity to growth-inhibitor signals
  3. Altered cell metabolism
  4. Evasion of apoptosis
  5. Limitless replicative potential
  6. Sustained angiogenesis
  7. Ability to invade and metastasize
  8. Ability to evade host immune response
80
Q

tumor cells undergo a metabolic
switch -> Synthesis of macromolecules and
organelles

A

Warburg effect

81
Q

Increased glucose leads to increased lactose

conversion

A

glycolytic pathway

82
Q

o Inactivation of P-53

o Activation of anti-apoptotic genes

A

evasion of P-53

83
Q

Continuous expression of

telomerase

A

Evasion of mitotic crisis

84
Q

ability to continually produce stem cells

A

self-renewal

85
Q

Biological hallmarks of malignant tumors

A

ability to invade and metastasize

86
Q

Two steps in the ability to invade and metastasize

A

§ Invasion of basement membrane

§ Vascular dissemination, homing and colonization

87
Q

Invasion of basement membrane

A

downregulation of E-cadherin

activation of proteinases

88
Q

loosening up of

tumor cells

A

downregulation of E-cadherin

89
Q

degradation

of basement membrane

A

MMP’s, cathepsin D,

urokinase, plasminogen activator)

90
Q

3 Types of DNA repair systems

A

§ Mismatch repair
§ Nucleotide excision repair
§ Recombination repair

91
Q

o Familiar cancer: cecum and proximal colon
o Defect in DNA mismatch repair system (“proofreader”)
o Hallmark: microsatellite system instability (also 15% of sporadic cancers)

A

Hereditary Non Polyposis Cancer Syndrome

92
Q

mismatch repair genes

A

MSH2, MLH1

93
Q

o Increases risk for skin cancer after UV exposure
(formation of pyrimidine dimers)
o Defect in nucleotide excision repair

A

Xerdoerma Pigmentosum

94
Q

developmental defects and multiple tumors

A

Bloom syndrome

95
Q

neural symptoms

A

ataxia telangiectasia

96
Q

bone marrow aplasia

A

fanconi anemia

97
Q

chromosomal changes:

Translocation and inversion

A

Lymphomas, Leukemias, Sarcomas, Carcinomas

98
Q

chromosomal changes:

deletions

A

Rb gene: Retinoblastoma

99
Q

Malignancy: Chronic Myeloid Leukemia
Translocation:

A

BCR / ABL

100
Q

Malignancy: Burkitt Lymphoma
Translocation:

A

C-MYC / IGH

101
Q

Malignancy: Mantle Cell Lymphoma
Translocation:

A

CCND1 / IGH

102
Q

Malignancy: Follicular Lymphoma
Translocation:

A

IGH / BLC2

103
Q

Malignancy: Ewing’s Sarcoma
Translocation:

A

EWSR1 / FLI1

104
Q

Multiple copies of proto-oncogene à protein

overexpression

A

gene amplification

105
Q

N-MYC gene

A

neuroblastoma

106
Q

HER2 gene

A

breast cancer

107
Q

o Reversible heritable changes in gene expression without mutation or change in DNA sequence
o Silencing of the gene by methylation or histone
modification

A

Epigenetic Changes

108
Q

carcinogenic agents

A
  • chemical
  • radiation
  • viruses

LUIV [HS 202] Patho Exam (5 decks)

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