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Pathology > Neoplasia (PPT) > Flashcards

Neoplasia (PPT) Flashcards

1
Q

An abnormal mass of tissue the growth of which exceeds and is uncoordinated with that of normal tissue and persists in the same excessive manner after cessation of stimuli which evoked the change

A

Neoplasia

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2
Q

This means new growth

A

Neoplasm

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3
Q

Onco means

A

Tumoe

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4
Q

Term used to describe malignant epithelial tumor

A

Carcinoma

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5
Q

Term used to describe malignant mesenchymal tumor

A

Sarcoma

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6
Q

Nomenclature of tumors are based on its

A

Biologic behavior

Tissue of origin

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7
Q

Types of biologic behavior

A

Benign

Malignant

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8
Q

Different tissue of origin

A

Epithelial
Mesenchymal
Mixed
Teratoma

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9
Q

Characteristics of squamous cell carcinomas

A

Lots of desmosomes and tonofilaments on EM
Lone apoptosis
Keratin pearls
Tumor cells are strikingly similar to normal squamous epithelial cells

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10
Q

Two types of mixed tumors

A

With mixed differentiation
Teratoma
Aberrant differentiation (not true neoplasms)

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11
Q

Example of tumors with mixed differentiation

A

Pleomorphic adenoma

Wilm’s tumor

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12
Q

Carcinosarcoma

A

Tumors with mixed differentiation

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13
Q

Tumor comprised of cells from more than one germ layer

A

Teratoma

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14
Q

Arise from totipotent cells (usually gonads)

A

Teratoma

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15
Q

Benign cystic teratoma of ovary

A

Most common teratoma

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16
Q

Aberrant differentiation that is characterized by disorganized mass of tissue whose cell types are indiginous to the site of the lesion

A

Hamartoma

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17
Q

Aberrant differentiation characterized by ectopic focus of normal tissue (heterotopia)

A

Choriostoma

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18
Q

Misnomers in neoplasia

A

Hepatoma: malignant liver tumor
Melanoma: malignant skin tumor
Seminoma: malignant testicular tumor
Lymphoma: malignant tumor of lymphocytes

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19
Q

Benign tumor composed of smooth muscle cells

A

Leiomyoma

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20
Q

Characteristics of Leiomyoma

A

Display typical characteristics of benignity, well-delineation, non-necrotic and non-invasive

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21
Q

Analogy. Fat cells
Lipoma: __________
Liposarcoma: ___________

A

Lipoma: Mature fat cells
Liposarcoma: Immature fat cells (lipoblasts)

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22
Q

Bulky tumor affecting the femur

A

Osteosacroma

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23
Q

Defining feature of osteogenic sarcoma

A

Malignant osteoid

Matrix secreted by osteoblast

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24
Q

Features of rhabdomyosarcoma

A

Anaplastic tumor
Marked cellular and nuclear pleomorphism
Hyperchromatic nuclei
Tumor giant cells

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25
Q

True or False.
As the cell population expands, a progressively higher percentage of tumor cells leaves the replicative pool by reversion to G0, differentiation, and death.

A

True

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26
Q

Danger signals of cancer

Mnemonic: CAUTION US

A 
Change in bowel  or bladder habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or  lump (breast or elsewhere)
Indigestion or difficulty of swallowing
Obvious change in a mole or a wart
Nagging cough or hoarseness
Unexplained anemia
Sudden unexplained weight loss
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27
Q

True or False.
Presence of the danger signs/symptoms do not necessarily mean one has cancer. But having these symptoms should compel one to see a physician.

A

True

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28
Q

Estimated highest cancer incidence in males and females

A

Males: Prostate
Female: Breast

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29
Q

Estimated highest cancer death in males and females

A

Male: Lungs
Females: Lungs

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30
Q

True or False.

The occurrence of cancers is related to components of the environment.

A

True.

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31
Q

In both sporadic and familial form of retinoblastoma, mutations happen on the

A

Retinal cells

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32
Q

Defective gene in retinoblastoma

A

RB gene

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33
Q

Transfer of defective RB gene in familial form retinoblastoma is based on what type of heredity

A

Autosomal dominant

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34
Q

Triggered pathways of apoptosis and mechanisms used by tumor cells to evade cell death

A

CD95 receptor–induced and DNA damage

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35
Q

Role of APC

A

Regulate the stability and function of B-catenin

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36
Q

Biologic behavior of tumors depend on

A

Rate of Growth
Degree of Differentiation
Local Invasion
Presence or absence of Metastasis

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37
Q

Hallmark of malignancy

A

Metastasis

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38
Q

Benign or Malignant.

Well-circumscribed

A

Benign

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39
Q

Benign or Malignant.

Ill-defined.

A

Malignant

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40
Q

Benign or Malignant.

Encapsulated

A

Benign

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41
Q

Benign or Malignant.

Irregular margins

A

Malignant

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42
Q

Benign or Malignant.

Well-differentiated

A

Benign

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43
Q

Benign or Malignant.

Anaplastic

A

Malignant

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44
Q

Benign or Malignant.

Pushing margins

A

Benign

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45
Q

Benign or Malignant.

Presence of invasion/metastasis

A

Malignant

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46
Q

Benign or Malignant.

Absence of metastasis

A

Benign

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47
Q

Rate of growth in neoplasia is determined by

A

Doubling time of the tumor cells
Fraction of tumor cells that are in the replicative pool
Rate at which cells are shed and lost in the growing lesion

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48
Q

Fraction of tumor cells that are in the replicative pool

A

Growth fraction

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49
Q

Provides surveillance mechanisms for ensuring that critical transitions occur in the correct order with fidelity in their completion

A

Cell growth checkpoint

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50
Q

Cause cell cycle arrests by promoting inhibitory pathways or inhibiting activation pathways

A

Cell growth checkpoint

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51
Q

p53 activation in response to DNA damage which in turnm activate p21 (CDK inhibitor

A

Cell growth checkpoint

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52
Q

Mechanism of apoptosis

A

Abnormal mitochondrial membrane permeability ➡️ allows escape of cytochrome-c into the cystosol ➡️ activates proteolytic enzymes (caspases) ➡️ execution of the process ➡️ removal of dead cell fragments by phagocytosis without inflammatory reactions

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53
Q

Crucial event that initiates apoptosis

A

Abnormal mitochondrial membrane permeability

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54
Q

True or False.

Apoptosis goes through several complex phases

A

True

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55
Q

Apoptotic pathway that is the result of increased mitochondrial permeability and release of pro-apoptotic molecules intocytoplasm (no death receptors)

A

Intrinsic (mitochondrial) pathway

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56
Q

Types of injury that initiate the intrinsic pathway

A

Radiation, toxins, free radicals, hypoxia, withdrawal of growth factors or hormones

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57
Q

Injury to the mitochondria stimulates the production of these anti-apoptotic components

A

Bcl-2

Bcl-x

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58
Q

Intrinsic pathway can be inhibited to protect virally infected cells from Fas apoptosis by

A

FLIP

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59
Q

True or False.
In intrinsic pathway, death agonists cause changes in the inner mitochondrial membrane, resulting in the mitochondrial permeability transition (MPT) and release of cytochrome c and other pro apoptotic proteins into the
cytosol, which activate caspases. AIF, Apoptosis-inducing factor.

A

True

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60
Q

Mechanism of extrinsic (death-receptor-initiated pathway of apoptosis)

A
  1. Fas cross linked to FasL.
  2. 3 death domains (FAD) come together and form binding site for and adaptor protein.
  3. FADD attached to death receptors binds inactive caspase-8 which come together and autocatalytically activated to active caspase-8
  4. Cascade of other caspase activates executioner caspases.
  5. Apoptosis initiated
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61
Q

Lack of differentiation

A

Anaplasi

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62
Q

The extent to which parenchymal cells resemble comparable normal cells, both morphologically and functionally

A

Differentiation

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63
Q

Disordered growth

Disordered maturation

A

Dysplasi

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64
Q

Characteristics of Anaplasia

A 
Pleomorphism
Hyperchromaticity
Increased nucleocytoplasmic ratio
Abnormal (atypical) mitotic figures
Loss of polarity (loss of orientation)
Presence of multiple or enlarged nucleoli
Formation of tumor giant cells
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65
Q

Malignant cells confined to epithelial lining (intraepithelial and intramucosal), limited by the basement membrane

A

In-situ

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66
Q

Malignant cells have breached basement membrane and are in the sub-epithelial stroma, lamina propria or submucosa

A

Invasive

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67
Q

Examples of intraepithelial neoplasia

A

Cervical, valvular, vaginal

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68
Q

Local invasion include

A

Invasion through basement membrane,
Invasion into lamina propria
Invasion through muscularis mucosa

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69
Q

Metastasis include

A

Contiguous invasion to adjacent organ
Seeding of body cavities/fluids
Lymphatic spread
Hematogenous spread

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70
Q

Sequence of events in invasion of intracellular matrix

A
  1. Detachment of tumor cells (E-cadhedrins)
  2. Attachment to matrix components (Laminin, Fibronectins)
  3. Degradation of extracellular matrix (Collagenase, cathepsin D)
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71
Q

Vascular dissemination/homing

A

Vascular/lymphatic drainage in microenvironment

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72
Q

Eight fundamental physiological changes in the neoplastic cell
Mnemonic: SA3LISE

A 
Self-sufficiency in growth signals
Ability to invade and metastasize
Ability to evade host response
Altered cellular metabolism
Limitless replicative potential Insensitivity to growth-inhibitory signals
Sustained angiogenesis
Evasion of APOPTOSIS
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73
Q

Mechanism of cell proliferation

A
  1. Binding of growth factor to receptor on the cell membrane
  2. Stimulation of GF to activate several signal transducing proteins on the membrane
  3. Transmission of signals via 2nd messengers or cascade of signal transduction molecules
  4. Induction and activation of nuclear regulatory factors that initiate DNA transcription
  5. Entry and progression of the cell into the cell cycle resulting in cell division
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74
Q

True or False.

Disorder of cell growth and behavior, must be defined at the cellular and molecular level.

A

True

75
Q

Predominant cause of sporadic cancers

A

Somatic mutations (frequently due to environmental factor)

76
Q

Other causes of sporadic cancers

A

Age
Heredity
Acquired preneoplastic disorders

77
Q

In very young and very old individuals

A

Somatic mutations increase

Immune competence decrease

78
Q

Familial cancer are commonly seen in

A

Early age, tumors among close relatives or multiple or bilateral tumors

79
Q

True or False.

Nonlethal genetic damage lies at the heart of carcinogenesis.

A

True.

80
Q 
True or False.
Nongenetic damage (or mutation) may be acquired by the action of environmental agents, such as chemicals, radiation, or viruses, or it may be inherited in the germ line.
A

True.

81
Q

True or False.
The genetic hypothesis of cancer implies that a tumor mass results from the clonal expansion of a single progenitor cell that has incurred genetic damage (i.e., tumors are monoclonal).

A

True

82
Q

Four classes of normal regulatory genes

A
  1. growth-promoting proto-oncogenes,
  2. growth-inhibiting tumor suppressor genes,
  3. genes that regulate programmed cell death (i.e., apoptosis)
  4. genes involved in DNA repair-are the principal targets of genetic damage
83
Q

Tumor suppressor genes that release breaks on cell proliferation, also called promoters

A

Rb

p53

84
Q

Tumor suppressor genes that ensures integrity of the genome, also called caretakers

A

DNA repair genes

85
Q

Genes that regulate apoptosis

A

Proto-oncogenes

86
Q

Dominant genes that may also behave as tumor suppressor genes

A

Proto-oncogenes

87
Q

Two general groups to tumor suppressor genes

A

Promoter genes

Caretaker genes

88
Q

The traditional tumor suppressor genes, such as RB or p53, where mutation of the gene leads to transformation by releasing the brakes on cellular proliferation.

A

Promoters

89
Q

Responsible for processes that ensure the integrity of the genome, such as DNA repair.

A

Caretaker genes

90
Q

True or False.

Mutation of caretaker genes does not directly transform cells by affecting proliferation or apoptosis.

A

True

91
Q

True or False.
DNA repair genes affect cell proliferation or survival indirectly by influencing the ability of the organism to repair nonlethal damage in other genes, including proto-oncogenes, tumor suppressor genes, and genes that regulate apoptosis.

A

True

92
Q

True or False.
A disability in the DNA repair genes can predispose cells to widespread mutations in the genome and thus to neoplastic transformation.

A

True

93
Q

Encode proteins that normally inhibit cell proliferation

A

Tumor suppressor genes

94
Q

Cel surface protein of tumor suppressor genes

A

DCC (cell adhesion)

95
Q

Signal transduction protein of tumor suppressor genes

A

NF-1 (GTPase activator)

96
Q

True or False.
Most oncogenic RAS are mutations with a single base pair change that alters an amino acid at position 12, 13, or 61 in the protein product.

A

True.

97
Q

Proteins that regulate transcription

A

p53, pRb

98
Q

True or False.
RAS mutations destroy GTP-ase activity but retains GTP-binding activity, and current thinking is that these stay locked “on”, telling the transformed cell, “Keep dividing!”

A

True

99
Q

Genes that promote autonomous cell growth in cancer cells

A

Oncogenes

100
Q

They are derived by mutations in proto-oncogenes and are characterized by the ability to promote cell growth in the absence of oncoproteins

A

Oncogenes

101
Q

Normal growth-promoting signals products that resemble the normal products of proto-oncogenes except these are devoid of important regulatory elements, and their production in the transformed cells does not depend on growth factors or other external signals

A

Oncoproteins

102
Q

Most commonly activated by point mutations.

A

RAS

103
Q

Mutations in these locations interfere with GTP hydrolysis that is essential to convert RAS into an inactive form

A

Three hotspots which encode residues either within the GTP-binding pocket or the enzymatic region essential for GTP hydrolysis

104
Q

When mutations in the three hotspots occur

A

RAS is trapped in its activated GTP-bound form

The cell is forced into a continuously proliferating state

105
Q

True or False.

A

All signal transduction pathways enter the nucleus and have an impact on a large bank of responder genes that orchestrate the cells’ orderly advance through the mitotic cycle

106
Q

Ultimate consequence of signaling through oncogenes like RAS or ABL is

A

inappropriate and continuous stimulation of nuclear transcription factors that drive growth-promoting genes

107
Q

Consequence of mutations affecting genes that regulate transcription of DNA

A

Growth autonomy

108
Q

Gene that can either activate or repress the transcription of other genes

A

MYC gene/protein

109
Q

Activate MYC

A

Growth-promoting genes, including cyclin-dependent kinases (CDKs)

110
Q

Repress MYC

A

CDK inhibitors

111
Q

Mechanism by which MYC promotes turmorigenesis

A

Increasing expression of genes that promote progression through the cell cycle and repressing genes that slow or prevent progression through the cell cycle

112
Q

Dysregulation of the MYC gene resulting from a t(8;14) translocation occurs in

A

Burkitt lymphoma, a B-cell tumor

amplified in breast, colon, lung, and many other cancers

113
Q

Amplified in neuroblastomas and small-cell cancers of lung

A

The related N-MYC and L-MYC genes

114
Q

Governor of proliferation

A

Rb gene

115
Q

First tumor suppressor gene discovered

A

Rb gene

116
Q

Product of Rb gene

A

DNA-binding protein that is expressed in every cell type examined, where it exists in an active hypophosphorylated and an inactive hyperphosphorylated state

117
Q

The importance of the Rb lies in

A

its enforcement of G1, or the gap between mitosis (M) and DNA replication

118
Q

Initiation of DNA replication requires the activity of

A

Cyclin E/CDK2 complexes

119
Q

Expression of cyclin E is dependent on the

A

E2F family of transcription factors

120
Q

True or False.
Early in G1, Rb is in its hypophosphorylated active form, and it binds to and inhibits the E2F family of transcription factors, preventing transcription of cyclin E.

A

True

121
Q

Hypophosphorylated RB blocks

A

E2F-mediated transcription

122
Q

One of the most commonly mutated genes in human cancers

A

p53

123
Q

Mutations in p53 causes

A

Activation of temporary cell cycle arrest
Induction of permanent cell cycle arrest
Triggering of programmed cell death

124
Q

Temporary cell cycle arrest

A

Quiescence

125
Q

Permanent cell cycle arrest

A

Senescence

126
Q

Programmed cell death

A

Apoptosis

127
Q

In other words, mutation on the p53 gene causes

A

Quiescence
Senescence
Apoptosis

128
Q

Gene that senses DNA damage and assists in DNA repair by causing G1 arrest and inducing DNA repair genes

A

P53

129
Q

A cell with damaged DNA that cannot be repaired is directed by p53 to either enter ___________ or undergo ____________.

A

senescence

apoptosis

130
Q

Guardian of the genome

A

p53

131
Q

Mechanisms of cellular aging

A

DNA Damage
Decreased cellular replication
Reduced regenerative capacity of tissue stem cells
Accumulation of metabolic damage

132
Q

DNA damage occurs through

A

Faulty DNA repair genes

Calorie restriction

133
Q

Incomplete replication and progressive shortening of telomeres that causes decreased cellular replication

A

Replicative senescence

134
Q

Distinctive form of cellular metabolism with high level of glucose uptake and increased conversion to lactose fermentation via glycolytic pathway

A

Warburg effect

135
Q

Aerobic glycolysis

A

Warburg effect

136
Q

Provides rapidly dividing cells with metabolic intermediates needed for synthesis of cellular components

A

Warburg effect

137
Q

Gene damage that further leads to clonal proliferation

A

Carcinogenesis

138
Q

Mechanisms of carcinogenesis

A

Point mutation
Chromosomal translocation
Chromosome deletion
Gene amplification

139
Q

DNA-binding protein proto-oncogenes

A

MYC family

140
Q

Present in all eukaryotes, whose protein products are intranuclear and bind to DNA itself, enabling DNA synthesis

A

MYC

141
Q

Activation is usually by amplification (excess copies of a gene) and/or translocation rather than by mutation

A

MYC

142
Q

MYC causes

A

Gene amplification

143
Q

Targets of genetic damage

A

Growth-promoting proto-oncogenes
Growth inhibiting cancer suppressor genes
Apoptosis-regulating genes

144
Q

True or False.
The related neu (once erb2, now HER2) is amplified in many carcinomas, notably adenocarcinomas, especially of the breast, and the degree of amplification strongly correlates with bad outcome.

A

True

145
Q

True or False.

Carcinogenesis is a multistep process that causes tumor progression.

A

True

146
Q

Neoplastic cell arise from a SINGLE CELL

30 population doubling time produce 109 cells = 1 gram

A

Clonality

147
Q

Acquisition of permanent, irreversible qualitative changes in one or more characteristics of a neoplasm

A

Progression

148
Q

Cellular genes that can become activated to become cancer causing oncogenes
Encode proteins involved in normal differentiation or proliferation

A

Proto-oncogenes

149
Q

Inhibitor of apoptosis

A

Bcl-2

150
Q

True or False.
Tumor-suppressor genes keep cells benign, even when the oncogenes are activated. To lose their anti-cancer effect, BOTH copies must be altered.

A

True

151
Q

Biology of tumor growth

A

Tumor angiogenesis, progression and heterogeneity

152
Q

Components of tumor angiogenesis

A

Vascular endothelial growth factor
Basic fibroblast growth factor
Anti-angiogenic factors

153
Q

Factors causing tumor progression and heterogeneity

A

Increased aggressiveness
Genetic instability/random mutations
Loss of p53, DNA repair genes

154
Q

Recognition and destruction of NON-SELF tumor cells upon their appearance

A

Immune surveillance

155
Q

Components of immune surveillance

A

CD8+cytotoxic T cells (CTLs)
Natural killer cells
Macrophages
Humoral mechanism

156
Q

Major defense mechanism againts tumors

A

CTLs

157
Q

Categories of antigens

A

Tumor specific antigens

Tumor-associated antigens

158
Q

Tumor cells escape immunosurveillance by

A

Selective outgrowth of antigen negative variants
Loss or reduced expression of HLA antigens
Tumor-induced immunosuppression
No co-stimulation/no sensitization
Apoptosis of cytotoxic T-cells

159
Q

Mechanisms of immune surveillance escape by tumor cells

A

Mutation
Downregulate MHC molecules on tumor cell surface
Lack of CO-stimulation molecules, e.g., (CD28, ICOS)
Immunosuppressive agents
Antigen masking
Apoptosis of cytotoxic T-Cells (CD8); damn tumor cell KILLS the T-cell

160
Q

Mechanism of the activation of proto-oncogenes

A

Point mutation
Chromosome rearrangments
Gene amplification

161
Q

DNA sequences within eukaryotic cells that seem to be involved in the development and maintenance of tumors

A

Oncogenes

162
Q

Genes that direct the synthesis of proteins that under some conditions transform a benign host cell into a cancer cell

A

Oncogenes

163
Q

Proto-oncogene minus its regulatory sequences, or with a characteristic mutation, or in an excessive number of copies (“amplification”)

A

Viral oncogene

164
Q

Capable of causing cancer by themselves, and hence are very different from their normal counterparts (i.e., have been damaged several times)

A

Viral oncogene

165
Q

Examples of viral oncogene

A

Human Papilloma virus
Epstein-Barr Virus
Hepatitis B virus

166
Q

HPV type that causes squamous cell carcinoma in the cervix

A

HPV 16 and 18

167
Q

HPC type that causes genital warts

A

HPV 6 and 11

168
Q

Diseases caused by EBV

A

Burkitt’s lymphoma: t(8,14)
Nasopharyngeal carcinoma
Lymphoma in AIDS

169
Q

Hepatitis B virus causes

A

Hepatocellular carcinoma

170
Q

Grading of neoplasia depends on

A

Differentiation of tumor (well, moderate, pootly differentiated)

171
Q

Staging of neoplasia depends on

A

Timor size
Node involvement
Presence or absence of metastasis

172
Q

Better method for prognosticating neoplasias

A

TNM system

173
Q

Soft tissue tumors which are definitionally high grade

A 
Ewing’s sarcoma
Rhabdomyosarcoma
Angiosarcoma
Pleomorphic liposarcoma
Soft tissue osteosarcoma
Mesechymal chondrosarcoma
Demspolastic small cell tumor
174
Q

Grading of low grade soft tissue tumors

A 
Well-differentiated liposarcoma
Atypical lipomatous tumor
Dermatofibrosarcoma protuberans
Infantile fribrosarcoma
Angiomatoid MFH
175
Q

Atypically proliferating

A

Boderline tumors/low malignant potential

176
Q

Criteria for Borderline Serous Tumors or APST

A
  1. Stratification and budding in > 10% of tumor
  2. Cribriform and micropapillary pattern less than 5mm area (if >5mm =>MPSC, micropapillary serous carcinoma)
  3. Mitoses < 4 per 10 high power fields
  4. Absence of stromal invasion
177
Q

Laboratory Diagnosis of Cancer

A

Morphologic methods
Biochemical assays
Molecular diagnosis
Molecular profiling

178
Q

Morphologic methods used to diagnose cancer

A

Cytology
Immunohistochemistry
Flow cytometry

179
Q

Biochemical assay used to diagnose cancer

A

Tumor markers

180
Q

Molecular diagnostics used to diagnose cancer

A

PCR/FISH

181
Q

Molecular profiling used to diagnose cancer

A

DNA-microarray

182
Q

Examples of cytologic procedures

A

Cervial pap’s smear
Fine needle aspiration biopsy
Frozen section diagnosis

183
Q

In immunohistochemistry, the basic batteries used to differentiate tumors include

A

Cytokeratine
Vimentin
LCA
S-100/NSE

Pathology (5 decks)

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