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Pathology > Neoplasia (Handout) > Flashcards

Neoplasia (Handout) Flashcards

1
Q

Fundamental and shared characteristics of cancer

A
  1. Genetic disoder caused by DNA mutations
  2. Genetic alterations in cancer cells are heritable. As a results, cells harboring these alterations are subject to Darwinian selection.
  3. Mutations and epigenetic alternations impart to cancer cells a set of properties are referred collectively as cancer hallmarks.
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2
Q

Four major classes of genes involved in cancer

A

Oncogenes
Tumor suppressor genes
Genes that regulate apoptosis
Genes that regulate interactions between tumor cells and host cells

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3
Q

Genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth

A

Oncogenes

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4
Q

Genes that normally prevent uncontrolled growth and when mutated or lost, allow transformed phenotype to develop

A

Tumor suppressor genes

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5
Q

Functions of tumor suppressor genes

A

Governors

Guardian

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6
Q

Breaks on cell proliferation

A

Governors

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7
Q

Senses genomic damage

A

Guardians

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8
Q

Some these genes initiate and choreograph a complex “damage control response” that leads to the cessation of proliferation or apoptosis if the damage is too great

A

Guardian genes

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9
Q

Enhances cell survival rather than stimulating proliferation per se

A

Genes that regulate apoptosis

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10
Q

Genes that are recurrently mutated or functionally altered in certain cancers

A

Genes that regulate interactions between tumor cells and host cells

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11
Q

Benign and malignant tumors are differentiated based on

A

degree of differentiation, rate of growth, local invasiveness and distant spread

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12
Q

Benign or malignant.

Resemble the tissue of origin and are well-differentiatied

A

Benign

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13
Q

Benign or malignant.

Poorly or completely undifferentiated (anaplastic)

A

Malignant

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14
Q

Benign or malignant.

Tend to be slow growing

A

Benign

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15
Q

Benign or malignant.

Grow faster

A

Malignant

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16
Q

Benign or malignant.

Well circumscribed and have a capsule

A

Benign

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17
Q

Benign or malignant.

Poorly circumscribed and invade the surrounding normal tissues

A

Malignant

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18
Q

Benign or malignant.

Remain localized to the site of origin

A

Benign

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19
Q

Benign or malignant.

Locally invasice and metastasize to distant sites

A

Malignant

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20
Q

Mutations that alter the function of cancer genes and thereby directly contribute to the development or progression of a given cancer

A

Driver mutations

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21
Q

Acquired mutations that are neutral in terms of fitness and do not affect cellular behavior

A

Passenger mutations

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22
Q

Can either activate or inactivate the protein products of the genes depending on their precise position and consequence

A

Point mutations

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23
Q

True or False.
Point mutations that convert proto-oncogenes generally produce a gain-of-function by altering amino acid residues ina domain that normally hold the person’s activity in check (RAS gene).

A

True

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24
Q 
True or False.
Point mutations (also insertions and deletions) in tumor suppressor genes reduce or disable the function of the encoded proteins (TP53).
A

True

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25
Q

May be produced by chromosomal translocations or inversions

A

Gene rearrangement

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26
Q

Some gene reaarangements result in overexpression of proto-oncogenes by removing then form their normal regulatory elements and placing them under control of an inappropriate hightly active promoter or enhancer

A

Gene rearrangements

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27
Q

Other oncogenic gene rearrangments create fusion genes encoding novel chimeric proteins

A

Gene rearrangements

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28
Q

Another prevalent abnormality in tumor cells

Removal of specific regions of chromosomes may result in the loss of particular tumor suppressor genes

A

Deletions

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29
Q

Proto-oncogenes may be converted to oncogenes by ___________, with consequent overexpression and hyperactivity of otherwise normal proteins.

A

Gene amplification

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30
Q

Two clinically examples of gene amplification

A

NMYC neuroblastoma

HER2 gene in breast cancers

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31
Q

Defines as a number of chromosomes that is not a mutiple of the haploid sate

A

Anueploidy

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32
Q

In human, this is a chromosome that is not a multiple of 23

A

Aneuploidy

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33
Q

This was remarkably common in cancers, paticularly carcinomas, and was proposed of carcinogenesis

A

Aneuploidy

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34
Q

Effects of aneuploidy

A

Errors in mitotic checkpoint

Increase the copy number of key oncogenes and decrease potent tumor suppressors

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35
Q

Noncoding single-stranded RNAs, approximately 22 nucleotides in legnth

A

MicroRNAs (miRNAs)

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36
Q

Negative regulators of genes

A

MicroRNAs

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37
Q

MiRNAs inhibit gene expression posttranscriptionally thru

A

Translation suppression
mRNA cleavage (in some cases)

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38
Q

Reversible/heritable changes in gene expression that may occur without mutation

A

Epigenetics

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39
Q

Epigenetics involve posttranslational modifications of __________ and ______________ both affecting gene expression.

A

Histones and DNA methylation

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40
Q

Along their course, cancers generally become more aggressive and acquire greater malignant potential, referred to as

A

Tumor progression

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41
Q

The acquisition of the genetic and epigenetic alterations that confer these hallmarks may be accelerated by ___________________________.

A

Cancer-promoting inflammation and by genomic instability

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42
Q

These are considered as enabling characteristics because they promote cellular transformation and tumor progression

A

Cancer-promoting inflammation and by genomic instability

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43
Q

True or False.

All cancers display eight fundamental changes in cell physiology which are considered hallmarks of cancer.

A

True

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44
Q

Hallmarks of Cancer

A
  1. Self-sufficiency in growth signals
  2. Insensitivity to growth-inhibitory signals
  3. Altered cellular metabolism
  4. Evasion of apoptosis
  5. Limitless replicative potential (immortality)
  6. Sustained angiogenesis
  7. Invasion and metastasis
  8. Evasion of immune surveillance
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45
Q

Normal cellular genes whose products promote cell proliferation

A

Proto-oncogenes

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46
Q

Mutant or overexpressed versions of proto-oncogenes that function autonomously w/o requirement for normal growth-promoting signals

A

Oncogenes

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47
Q

Mechanisms of uncontrolled proliferation by oncogenes

A

a. Stimulus-independent expression of growth factors and their receptors (autocrine loop) (“self-stimulation”)
b. Mutation in genes encoding growth factor receptors/tyrosine kinases -> constitutive signaling
c. Amplification of EGF receptor family genes (such as HER2 in Breast Cancer)
d. Fusion of portions of ABL tyrosine kinase + BCR protein gene = BCR-ABL fusion gene that encodes a constitutively active tyrosine kinase (as seen in certain leukemias)
e. Mutations in genes encoding signaling molecules (RAS commonly is mutated in human cancers and normally flips between resting GDP-bound state and active GTP-bound state. Mutation block hydrolysis of GTP to GDP, leading to unchecked signaling)
f. Overproduction or unregulated activity of transcription factors
g. Translocation of MYC in some lymphomas leads to overexpression and unregulated expression of its target genes controlling cell-cycling
h. Mutations that inactivate cyclin genes or inactivate negative regulators of cyclins and cyclin-dependent kinases

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48
Q

Drive the cell cycle by phosphorylating various substrates and normally are controlled by CDK inhibitors.

A

Complexes of cyclins with CDKs

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49
Q

True or False.

A

Mutations in genes encoding cyclins, CDKs, and CDK inhibitors result in uncontrolled cell cycle progression and are found in a wide variety of cancers including melanomas and brain, lung, and pancreatic cancers.

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50
Q

True or False.
It is now accepted that loss of normal cell cycle control is central to malignant transformation and that at least one of the four key regulators of the cell cycles is mutated in most human cancers.

A

True

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51
Q

Four key regulators of the cell cycle

A

p16, cyclin D, CDK4, RB

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52
Q

Governor of the cell cycle

A

Rb

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53
Q

One defective copy of RB gene is present in the germ line
Only one additional somatic mutation is needed to completely eliminate RB function

A

Familial retinoblastoma

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54
Q

Exerts anti-proliferative effects by controlling the G1 to S transition of the cell cycle

A

Rb gene

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55
Q

In its active form, RB is ___________________ and binds to ______________________.

A

Hypophosphorylated; E2F transcription factors

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56
Q

This interaction prevents transcription of genes like cyclin E that are needed for DNA replication, and so cells are arrested in G1.

A

Binding of RB to E2F transcription factors

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57
Q

Inactivation of Rb gene

A

Growth factor signaling leads to cyclin D expression > activation of cyclin D-CDK4/6 complexes > inactivation of RB by phosphorylation > release of E2F

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58
Q

Fundamental to malignant transformation

A

Loss of cell cycle control

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59
Q

True or False.
Almost all cancers have a disabled G1 checkpoint due to mutation of either RB or genes that affect RB function such as cyclin D, CDK4, and CDKIs.

A

True

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60
Q

Many oncogenic DNA viruses (like ___________) encodes proteins (like __________) that bind RB and render it nonfunctional.

A

HPV; E7

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61
Q

Guardian of the Genome

A

TP53

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62
Q

This encode p53

A

TP53

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63
Q

Central monitor of stress in the cell

A

TP53

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64
Q

TP53 is activated by

A

Anoxia, inapporpriate oncogene signalling or DNA damage

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65
Q

Activated p53 ontrols the expression and activity of genes involved in

A

Cell cycle arrest, DNA repair, cellular senescence, and apoptosis

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66
Q

Mechanism of p53 activation

A

DNA damage – activation of p53 by phosphorylation – transcription of CDKN1A (P21) - prevention of RB phosphorylation – G1-S block in cell cycle

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67
Q

Main effect of the G1-S block in cell cycle

A

Allows the cell to repair DNA damage

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68
Q

True or False.

In unrepairable DNA damage, p53 induces cellular senescence or apoptosis.

A

True

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69
Q

Individuals inherit one defective copy of TP53 in the germ line, wherein only one additional mutation is required to lose normal p53 functioning

A

Li-Fraumeni syndrome

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70
Q

Patients with Li-Farumeni syndrome are prone to develop a

A

Wide range of tumors

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71
Q

Incapacitation of p53 by HPV is achieved by

A

Binding to the proteins encoded by these viruses

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72
Q

True or False.

70% of human tumors demonstrate biallelic mutations in TP53.

A

True

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73
Q

Inhibits proliferation of cells by activation of growth-inhibiting genes and suppression of growth-promoting genes

A

TBG-Beta

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74
Q

Growth inhibiting genes

A

CDKI

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75
Q

Growth promoting genes

A

MYC

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76
Q

Function of TGF-beta is compromised in tumors by

A

Receptor mutations (Colon, stomach, endometrium) and mutational inactivation of SMAD genes that transduce TGF–Beta signaling in the pancreas

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77
Q

Maintains contact inhibition that is lost in malignant cells

A

E-cadherin

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78
Q

Possess anti-proliferative capabilities that regulate the destruction of beta catenin proteins

A

APC gene

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79
Q

When APC is lost, ______________ will not be destroyed leading to its translocation to the nucleus where it acts as a growth-promoting transcription factor

A

Beta–catenin

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80
Q

Inherited presence of a germ line mutation in the APC gene and sporadic loss of sole normal allele leading to the development of colonic polyps at a young age.

A

Familial Adenomatous Polyposis Syndrome

81
Q

Polyps in the FAPS evolve into _____________.

A

Colon cancers

82
Q

True or False.

Somatic loss of the APC gene is seen in approximately 70% of sporadic colon cancers.

A

True

83
Q

Even in the presence of ample oxygen, cancer cells demonstrate a distinctive form of cellular metabolism characterized by high levels of glucose uptake and increased conversion of glucose to lactose (fermentation) via the glycolytic pathway.

A

Warburg effect

84
Q

Number of ATP produced by Warburg effect

A

2 ATP

85
Q

True or False.
Even though it yields only 2 ATP, the multiple number of cancer cells making those ATP create enough energy to continue living and replicating.

A

True

86
Q

This explains why tumor cells are glucose hungry

A

Warburg effect

87
Q

Form of pro-growth metabolism that favors glycolysis over oxidative phosphorylation, provides rapidly dividing cells with metabolic intermediates needed for synthesis of cellular components (while oxidative phosphorylation does not)

A

Warburg effect

88
Q

True or False.
Warburg effect is not cancer-specific, and is induced in normal cells by exposure to growth factors and becomes fixed in cancer cells.

A

True

89
Q

Triggers warburg effect

A

Metabolic reprogramming is produced by signaling cascades downstream of growth factor receptors, the very same pathways that are deregulated by mutations in oncogenes and tumors suppressor genes in cancers

90
Q

Inducers of warburg metabolism

A

Oncoproteins - RAS, MYC, mutated growth factor receptors

91
Q

Oppose warburg metabolism

A

Tumor suppressors - PTEN, NF1, P53

92
Q

State of severe nutrient deficiency in which cells arrest their growth and cannibalize their own organelles, proteins, and membranes as carbon sources for energy production

A

Autophagy

93
Q

True or False.
Cancer cells may accumulate mutations to avoid autophagy, or may corrupt the process to provide nutrients for continued growth and survival.

A

True

94
Q

Some oncoproteins such as mutated IDH act by causing the formation of high levels of “_______________” that alter the epigenome, thereby leading to changes in gene expression that are oncogenic.

A

Oncometabolites

95
Q

Tumors may be resistant to programmed cell death, as a consequence of inactivation of _____ or activation of _______________.

A

P53; anti-apoptotic genes

96
Q

Evasion of cell death by cancers mainly involves acquired abnormalities that interfere with the

A

intrinsic (mitochondrial) pathway of apoptosis

97
Q

Most common apoptotic abnormalities involve

A

Loss of TP53 function

98
Q

Mechanism of loss TP53 function

A

TP53 mutations or overexpression of MDM2
Prevents upregulation of PUMA

99
Q

A p53 inhibitor

A

MDM2

100
Q

Another cause of evasion of apoptosis

A

Overexpression of anti-apoptotic members of the BCL2 family (BCL2, BCL-XL, and MCL1)

101
Q

Protect cells from the action of BAX and BAK, the proapoptotic members of the BCL2 family

A

BCL2, BCL-XL and MCL-1

102
Q

True or False.
In a large majority of follicular B-cell lymphomas, BCL2 levels are high because of a (14;18) (q32;q21) translocation that fuses the BCL2 gene with the regulatory elements of the transcriptionally active immunoglobulin heavy chain gene.

A

True

103
Q

Induce the death of cancer cells by stimulating the intrinsic pathway of apoptosis and are being developed as therapeutic agents

A

Inhibitors of the MDM2 (which activate p53) and inhibitors of BCL2 family members

104
Q

Most normal human cells have a capacity of at most _____ doublings.

A

70 doublings

105
Q

After the 70th doubling, cells lose the ability to divide and enter replicative senescence.

A

Progressive shortening of telomeres at the ends of chromosomes

106
Q

activate cell cycle checkpoints, leading to senescence

A

Shortened telomeres

107
Q

DNA repair pathways are inappropriately activated by shortened telomeres, leading to massive chromosomal instability and mitotic crisis.

A

Disabled checkpoints

108
Q

True or False.

Telomere maintenance is seen in virtually all types of cancers.

A

True

109
Q

Enzyme that is upregulated in 85-95% of cancers which keeps the telomere count of cancer cells.

A

Telomerase

110
Q

When tumor cells reactivate telomerase, they

A

Stave off mitotic catastrophe and achieve immortality

111
Q

A few tumors use other mechanisms to lengthen their telomeres which depend on DNA recombination.

A

Alternative lengthening of telomeres

112
Q

Vascularization of tumors is controlled by the balance between ____________________________________ that are produced by tumor and stromal cells.

A

angiogenic and anti-angiogenic factors

113
Q

Triggers angiogenesis

A

Hypoxia

114
Q

Growth factors involved in angiogenesis

A

HIF-1α acts on the transcription of the proangiogenic factor VEGF

115
Q

Mechanism of angiogenesis

A

Hypoxia ➡️ stabilized HIF-1α ➡️ activated transcription of VEGF ➡️ angiogenesis

116
Q

p53 induces synthesis of the angiogenesis inhibitor

A

thombospondin-1

117
Q

upregulate VEGF expression and stimulate angiogenesis

A

RAS, MYC, and MAPK signaling

118
Q

used to treat a number of advanced cancers and prolong clinical course, but not curative

A

VEGF inhibitors

119
Q

Ability to invade tissues, a hallmark of malignancy

A

Invasion and metastasis

120
Q

Four steps of invasion and metastasis

A
  1. Loosening of cell–cell contacts
  2. Degradation of ECM
  3. Attachment to novel ECM components
  4. Migration of tumor cells.
121
Q

lost by the inactivation of E-cadherin through a variety of pathways

A

Cell-cell contacts

122
Q

Basement membrane and interstitial matrix degradation is mediated by proteolytic enzymes secreted by tumor cells and stromal cells, such as

A

MMPs and cathepsins

123
Q

release growth factors sequestered in the ECM and generate chemotactic and angiogenic fragments from cleavage of ECM glycoproteins

A

Proteolytic enzymes

124
Q

True or False.
The metastatic site of many tumors can be predicted by the location of the primary tumor. Many tumors arrest in the first capillary bed they encounter (lung and liver, most commonly).

A

True

125
Q

True or False.
Some tumors show organ tropism, probably due to activation of adhesion or chemokine receptors whose ligands are expressed by endothelial cells at the metastatic site.

A

True

126
Q

True or False.

Cells can be recognised by the immune system as non-self and are destroyed.

A

True

127
Q

True or False.

Anti-tumor mechanism are mediated predominantly by cell-mediated mechanisms.

A

True

128
Q

Presented on the cell surface by MHC class I molecules and are recognized by CD8+ cells

A

Anti-tumor activity

129
Q

Different classes of tumor antigens includes products of

A

Mutated genes
Overexpressed or aberrantly expressed proteins
Tumor antigens produced by oncogenic viruses

130
Q

True or False.
Immunosuppressed patients have an increased risk for cancer development, particularly types caused by oncogenic DNA viruses.

A

True

131
Q

Mechanisms by which tumors may avoid the immune system

A

Selective outgrowth of antigen-negative variants
Loss or reduced expression of histocompatibility molecules
Immunosuppression mediated by expression of certain factors (e.g., TGF-β, PD-1 ligands) by the tumor cells

132
Q

True or False.
Antibodies that overcome some of these mechanisms of immune evasion are approved for treatment of patients with advance forms of cancer.

A

True

133
Q

Etiology of cancer:

_________________ inflict genetic damage, which lies at the heart of carcinogenesis.

A

Carcinogenic agents

134
Q

Three classes of carcinogenic agents:

A

Chemicals
Radiant energy
Microbial products

135
Q

Chemical carcinogens have ________________________________ that directly damage DNA, leading to mutations and eventually cancer.

A

Highly reactive electrophile groups

136
Q

do not require metabolic conversion to become carcinogenic

A

Direct-acting agents

137
Q

not active until converted to an ultimate carcinogen by endogenous metabolic pathways.

A

Indirect-acting agents

138
Q

may influence carcinogenesis by altering the conversion of indirect-acting agents to active carcinogens.

A

Polymorphisms of endogenous enzymes such as cytochrome P-450

139
Q

Examples of direct-acting agents

A

alkylating agents used for chemotherapy

140
Q

Examples of indirect-acting agents

A

benzo(a)pyrene, azo dyes, aflatoxin

141
Q

act by stimulating cell proliferation. Increased proliferation may occur through direct effects of tumor promoters on target cells or may be secondary to tissue injury and regenerative repair

A

Tumor promoters

142
Q

Because malignant transformation results from mutations, most chemical carcinogens are mutagenic acting as ________________ (induction of cell proliferation is a sine qua non of tumor promotion) which can be augmented by non-tumorigenic ___________________.

A

Initiators; promoters

143
Q

True or False.
Application of an initiator may cause mutational activation of an oncogene, such as RAS, but with subsequent application of promoters leads to clonal expansion of initiated (mutated) cells.

A

True

144
Q

True or False.

Initiated clone cells accumulates additional mutations, developing eventually into a malignant tumor.

A

True

145
Q

True or False.

Sustained cell proliferation increases the risk for mutagenesis, and hence promotes neoplastic transformation.

A

True

146
Q

Whatever its source, ___________is an establish carcinogen.

A

Radiation

147
Q

Sources of radiation

A

UV rays of sun, radiographs, nuclear fission, radionuclides

148
Q

Three causes of ionizing radiation

A

o chromosome damage
o chromosome rearrangement
o point mutations (less frequently)

*any of which may affect cancer genes and thereby drive carcinogenesis

149
Q

UV rays in sunlight induce the formation of ____________ within DNA, leading to mutations that can give rise to _________________________________ of the skin.

A

pyrimidine dimers; squamous cell carcinomas and melanomas

150
Q

Oncogenic RNA viruses

A

HTLV-1

HCV

151
Q

Another term for Human T-cell leukemia/Lymphoma Virus

A

Human T-Lymphocytic virus

152
Q

causes adult T-cell leukemia/lymphoma (ATLL) that is endemic to Japan and the Caribbean

A

HTLV-1

153
Q

a viral protein found in a unique region called pX encoded in the HTLV-1 genome

A

Tax gene

154
Q

Stimulates proliferation, enhances cell survival, and interferes with cell cycle controls; essential for viral replication, because it stimulates transcription of viral RNA from the 5’ long-terminal repeat

A

Tax gene

155
Q

alters the transcription of several host cell genes and interacts with certain host cell signaling proteins. By doing so, this gene contributes to the acquisition of several cancer hallmarks.

A

Tax gene

156
Q

Although this proliferation initially is _______________, the proliferating T cells are at increased risk for secondary mutations that may lead to the outgrowth of a ___________________.

A

polyclonal; monoclonal leukemia

157
Q

True or False.

All types of hepatitis are RNA viruses except for HBV, which is a DNA virus.

A

True

158
Q

Another type of oncogenic RNA virus

A

Hepatitis C Virus (HCV)

159
Q

Oncogenic DNA virus

A

HPV
EBV
HBV

160
Q

Associated with benign warts, as well as cervical cancer (Squamous Cell Carcinoma of the Cervix)

A

Human Papilloma Virus (HPV)

161
Q

Oncogenicity of HPV is related to expression of two viral oncoproteins:

A

E6 and E7

162
Q

Action of E6 and E7

A

E6 binds to p53
E7 binds RB tumor suppressors

Neutralizes the action of the genes

163
Q

True or False.
E6 and E7 from high risk strains of HPV (which gives rise to cancers) have higher affinity for their targets than do E6 and E7 from low risk strains of HPV (gives rise to benign warts).

A

True

164
Q

EBV is implicated in the pathogenesis of

A 
Burkitt’s lymphomas  
Lymphomas in immunosuppressed patients 
Hodgkin lymphoma 
Uncommon T-cell and NK cell tumors 
Nasopharyngeal carcinoma 
subset of Gastric Carcinoma
sarcomas (rarely)
165
Q

Certain EBV gene products contribute to oncogenesis by stimulating _______________________________________. Concomitant compromise of immune competence allows ________________________, leading eventually to development of lymphoma.

A

normal B-cell proliferation pathways

sustained B-cell proliferation

166
Q

True or False.

Between 70% to 85% of hepatocellular carcinomas worldwide are caused by HBV or HCV

A

True

167
Q

The oncogenic effects of HBV and HCV are _________________, but the dominant effect seems to be _____________________________________, with hepatocellular injury, stimulation of hepatocyte proliferation, and production of reactive oxygen species that can damage DNA.

A

multifactorial; immunologically mediated chronic inflammation

168
Q

The _______________ of HBV and the HCV core protein can activate a variety of signal transduction pathways that also may contribute to carcinogenesis.

A

HBx protein

169
Q

H. pylori infection has been implicated in both

A

gastric adenocarcinoma and MALT lymphoma

170
Q

The mechanism of H. pylori–induced gastric cancers is ___________________, including immunologically mediated chronic inflammation, stimulation of gastric cell proliferation, and production of ______________________ that damage DNA.

A

Multifactorial; reactive oxygen species

171
Q

It is thought that H. pylori infection leads to ______________________________ and that eventually _______________________________ emerges as a result of accumulation of mutations.

A

polyclonal B-cell proliferations; monoclonal B-cell tumor (MALT lymphoma)

172
Q

Effects of tumor on host

A
  1. Location of tumor
  2. Paraneoplastic syndrom
  3. Cancer cachexia
173
Q

Location of tumor

A

Ulceration
Obstruction
Loss of blood supply

174
Q

systemic symptoms that cannot be explained by tumor spread or by hormones appropriate to the tissue, are caused by the ectopic production and secretion of bioactive substances

A

Paraneoplastic syndrome

175
Q

Symptom complexes that occur in patients with cancer and that cannot be readily explained by local or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the tumor

A

Paraneoplastic syndrome

176
Q

Bioactive substances that are secreted in paraneoplastic syndrome

A

ACTH, PTHrP, or TGF-α

E.g. lung cancer producing ACTH

177
Q

Progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia; draining the body’s nutrients for it to survive

A

Cancer cachexia

178
Q

Clinical aspects of neoplasia

A
  1. Effects of tumor on host
  2. Grading
  3. Staging
179
Q

Determined by cytologic appearance/differentiation; behavior and differentiation are related, with poorly differentiated tumors having more aggressive behavior

A

Grading

180
Q

True or False.

The closer it looks like the original epithelium, the lower the grade.

A

True

181
Q

Grading levels of neoplasia

A 
Well-differentiated (Grade I)
Moderately differentiated (Grade II)
Poorly differentiated (Grade III)
182
Q

Extent of tumor

A

Staging

183
Q

Determined by surgical exploration or imaging based on size, local and regional lymph node spread, and distant metastases

A

Staging

184
Q

True or False.

Staging has greater clinical value than grading because it is the better prognosticating factor.

A

True

185
Q

TNM (Tumor, Nodes, Metastasis) system

A

STAGE 1: 0-2cm, non-palpable, non-recognizable tumor
STAGE 2: 2-5cm
STAGE 3: > 5cm
STAGE 4: metastasis, even if not palpable

186
Q

Laboratory diagnosis of cancer

A

Morphologic methods
Immunohistochemistry
Flow cytometry

187
Q

Clinical and radiologic data are invaluable for optimal pathologic diagnosis.
The specimen must be adequate, representative, and properly reserved.

A

Morphologic methods

188
Q

Morphologic methodology

A

Cytologic preparations

Tissue preparations

189
Q

Cytologic preparations

A

Pap smear

FNAB

190
Q

Tissue preparations

A 
Frozen sections
Tissue core needle biopsy
Incision biopsy
Excision biopsy
Radical resection biopsy
191
Q

Immunohistochemistry includes

A

Detection of cytokeratin
Hormone production
Enzyme production

192
Q

Fluorescently labeled antibodies against cell surface molecules and differentiation antigens used to obtain the phenotype of malignant cells

A

Flow cytometry

193
Q

Molecular diagnostics of cancer

A
  1. Diagnosis of malignancy
  2. Prognosis and behavior
  3. Detection of minimal residual disease
  4. Diagnosis of hereditary predisposition to cancer
  5. Therapeutic decision-making
194
Q

Molecular profiling of tumors

A

“OMICS”

195
Q

complete draft of the sequence of the human genome, released in 2003
Advances have enabled the systematic sequencing and cataloging of the genomic alterations in various human cancers, and effort sponsored by the National Cancer Institute called the Cancer Genome Atlas

A

Human Genome Project

196
Q

assess epigenetic modifications genome-wide

A

Epigenetic

197
Q

quantify all of the RNAs expressed in a cell population

A

Transcriptome

198
Q

measure many proteins simultaneously

A

Proteome

199
Q

take a snapshot of all the cell’s metabolites

A

Metabolome

Pathology (5 decks)

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