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General Pathology > Neoplasia Part 2 > Flashcards

Neoplasia Part 2 Flashcards

1
Q

what are the hallmarks of cancer? (8)

A

-Self-sufficiency in growth signals
-Insensitivity to growth inhibition
-Altered cellular metabolism
-Evasion of apoptosis
-Limitless replicative potential
-Sustained angiogenesis
-Ability to invade and metastasize
-Evasion of the immune system

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2
Q

what are the 2 enabling factors of cancer?

A

-Cancer-promoting inflammation
-Genomic instability resulting from defects in DNA repair

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3
Q

how are Oncogenes involved in cancer’s self-sufficient growth?

A

promote autonomous growth

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4
Q

how are Oncoproteins involved in cancer’s self-sufficient growth?

A

lack regulatory elements and don’t depend on external growth

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5
Q

what are the steps in normal cell proliferation, where if one is altered, irregular growth can be promoted? (5)

A
  1. Binding of growth factor to receptor
  2. Transient receptor activation leading to activation of signal transducing proteins on the inside of the membrane
  3. Transmission of the signal via 2nd messengers or signal transduction molecules to the nucleus
  4. Activation of nuclear regulatory factors that then initiate DNA transcription
  5. Progression in the cell cycle culminating in cell division
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6
Q

how does the signaling of growth factors normally act?

A

paracrine fashion

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7
Q

in cancer, how is growth factor signaling altered?

A

autocrine growth loop established

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8
Q

what growth factor is affected in glioblastomas?

A

PDGF

(platelet derived growth factor)

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9
Q

what growth factor is affected in sarcomas?

A

TGF-α

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10
Q

Tumor cells can activate ______ to produce growth factors

A

normal stromal cells

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11
Q

how can Growth Factor Receptors be affected in cancer and which is more common?

A

-Mutant receptors
-Receptor overexpression (more common)

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12
Q

what are 2 examples of specific Growth Factor Receptor overexpression and what specific cancers do they typically lead to?

A

-EGF receptor (ERBB1): epithelial H&N tumors (80-100%)

-HER2/NEU (ERBB2): breast cancers (30%)

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13
Q

how are HER2/NEU breast cancers treated?

A

with receptor antibodies –> Herceptin (which will attack and bind the receptor so no more growth factor is produced = tumor stops growing)

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14
Q

how can Signal Transducing Proteins be affected in cancers? what are 2 examples?

A

Mutation in the genes that couple receptors to their nuclear targets:

-RAS

-ABL

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15
Q

what is the most commonly mutated proto-oncogene growth factor receptor?

A

RAS

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16
Q

what type of enzyme does the ABL proto-oncogene code for?

A

Non-receptor associated tyrosine kinase

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17
Q

what type of cancer are mutations in the ABL proto-oncogene associated with?

A

Chronic myeloid leukemia (CML)

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18
Q

explain the pathophysiology of Chronic myeloid leukemia (CML) and the ABL proto-oncogene?

A
  1. t(9:22) creates BCR-ABL fusion protein with unregulated kinase activity
  2. RAS/RAF pathway activation
  3. MAPK
  4. transcription of MYC protein
  5. cell cycle progresses

(unregulated kinase activity = protein is constantly turned on even without more GF = constantly dividing)

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19
Q

how is Chronic myeloid leukemia (CML) treated?

A

inhibitor of BCR-ABL fusion kinase binds and disables the protein → Gleevec/imatinib

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20
Q

how can Nuclear Transcription Factors be affected in cancer?

A

Growth autonomy can occur from mutant genes that affect transcription

(promotion of growth by affecting cyclins (regulatory) OR CDK activation with repression of their inhibitors)

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21
Q

what are some genes that when mutated can act as Nuclear Transcription Factors to cause autonomous growth in cancer? (5)

A

MYC, MYB, JUN, FOS, REL

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22
Q

how does the MYC gene affect transcription and cause autonomous growth when mutated?

A

-activates cyclin-dependent kinases (CDKs)
-represses CDK inhibitors (CDKIs or CDKNs)

=TOTAL: promote growth by bypassing first checkpoint in growth cycle

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23
Q

what are the common Burkitt lymphoma translocations that affect the MYC Nuclear Transcription Factor and what Ig chain is involved?

A

t(8;14) = (MYC, Ig heavy chain)

[ALSO: t(2;8) = (kappa light chain, MYC) and
t(8;22) = (MYC, lambda light chain)]

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24
Q

what is a major histological identifier for Burkitt lymphoma?

A

“Starry Sky” Pattern –> a lot of fast growing lymphocytes = die fast = MACs come to eat dead cells

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25
Q

what do Tumor Suppressor Genes normally do?

A

Inhibit cell proliferation

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26
Q

what does a disruption in Tumor Suppressor Gene function lead to?

A

growth promotion

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27
Q

for Tumor Suppressor Genes disruption to lead to tumor development, what must occur?

A

Two mutations “hits” required –> to lose function, you have to lose both copies of the gene

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28
Q

what is a Tumor Suppressor Gene mutation that can cause a specific cancer and what is the cancer?

A

RB gene –> retinoblastoma (ocular malignancy)

(40% familial and 60% sporadic forms)

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29
Q

what does the RB gene (a Tumor Suppressor Gene) normally do? (3)

A

-Encodes a DNA-binding protein

-Enforces G1 to S phase transition where cells exit the cell cycle temporarily (quiescence) or permanently (senescence) to differentiate or die (via apoptosis)

-Binds transcription factors associated with cell differentiation (myocyte, macrophage, melanocyte etc.)

(i.e. stops cell from growing and tells it to differentiate)

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30
Q

what phosphorylation state is the RB gene (a Tumor Suppressor Gene) in when inhibiting growth? is anything bound to it?

A

-hypophosphorylated
-E2F is bound

=blocks growth

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31
Q

what phosphorylation state is the RB gene (a Tumor Suppressor Gene) in when promoting growth? is anything bound to it?

A

-hyperphosphorylated
-E2F unbinds

=cell growth

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32
Q

Why is RB not mutated in all cancers?

A

Other genes that control RB phosphorylation can mimic RB loss

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33
Q

what are ways other genes can control RB phosphorylation and mimic RB loss? (3)

A

-Cyclin D or CDK4 overexpression

-Inactivation of CDKIs (e.g. p16)

-Oncogenic DNA viruses (e.g. HPV) deactivate RB (deactivate NOT mutate)

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34
Q

a Central Theme of malignancy is that the loss of cell cycle control through one or more of what 4 key regulators is present in most human cancers?

A

p16, cyclin D, CDK4, RB

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35
Q

what does the TP53 gene normally do?

A

A central monitor of stress, the “guardian of the genome”, protects by:
-activates cell cycle arrest (quiescence)
-induces permanent cell cycle arrest (senescence)
-Triggers apoptosis (if repair fails)

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36
Q

how does the p53 protein normally appear?

A

-short half-life
-bound to the protein MDM2 which targets p53 for destruction

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37
Q

how does the p53 protein do under stress?

A

activates genes that arrest the cell cycle in G1 or G2 and induces DNA repair genes:

-If DNA damage is repaired→ Normal state

-If repair fails → induces apoptosis or senescence

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38
Q

How does p53 arrest the cell cycle?

A

causes transcription of CDKIs (p21) and other molecules which:

-inhibit cyclin/CDK complexes

-prevent phosphorylation of RB

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39
Q

how can altered p53 lead to cancer?

A

DNA damage –> p53-dependent genes not activated –> mutant cells go through cell cycle without repair –> malignancy

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40
Q

what is the Significance of p53 effects in cancers?

A

> 70% of human cancers have defects in

TP53 (gene):

-The rest have defects up or downstream of TP53 gene

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41
Q

how are RB and p53 similar in how viruses affect them? (These are proteins)

A

can be rendered non-
functional by DNA viruses (e.g. HPV, HBV)

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42
Q

describe what happens during the normal Adenomatous Polyposis Colicatenin (APC) Pathway.

A

Normally, APC helps degrade β-catenin (acts as a tumor suppressor gene) –> preventing its translocation to the nucleus and transcriptional activation of growth promoting genes (MYC gene and gene for cyclin D1)

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43
Q

what happens if APC is absent of not functioning?

A

β-catenin is not degraded –> goes to the nucleus and cell proliferation occurs

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44
Q

APC mutations are seen in what type of cancers?

A

colon cancers (70-80%)

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45
Q

when autophagy normally occur and what is it?

A

When nutrients are scarce, normal cells arrest growth and convert own organelles, proteins and membranes into energy

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46
Q

how do neoplastic cells use autophagy?

A

to remain dormant, making them resistant to
cancer treatment which attacks dividing cells.

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47
Q

____ genes can control autophagy and when function is lost, it can cause tumor formation.

A

tumor suppressor genes

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48
Q

What is the Warburg effect?

A

Cancer cells shift glucose metabolism away from mitochrondria to aerobic glycolysis and so glucose is partially broken down and used to produce lipids and nucleic acids so the cancer can divide faster

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49
Q

what 2 type of genes cause downstream effects that favor the Warburg effect of metabolism?

A

-Oncogenes
-loss of tumor suppressor genes

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50
Q

what is Oncometabolism?

A

Mutations in metabolic enzymes involved in the Krebs cycle lead to a new DNA methylation pattern which alters cancer gene expression –> Potential drug targets

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51
Q

what are the 2 pathways for Apoptosis?

A

-intrinsic (activates p53 response)

-extrinsic (T cell destruction of infected cell)

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52
Q

what triggers the intrinsic pathway for Apoptosis? (3)

A

-stress
-cell injury
-radiation DNA damage

53
Q

what are 2 anti-apoptotic genes?

A

BCL-2 and BCL-XL

54
Q

what are 2 pro-apoptotic genes?

A

BAX and BAK

55
Q

what happens when BAX and BAK are activated?

A

Intrinisic pathway: form holes in mitochondrial membrane, releasing cytochrome c → Activation of caspase 3 → Cell death

56
Q

how is BCL-2 correlated to cancers and what type of cancers?

A

Follicular lymphomas (B-cell cancer of lymphocytes) (~85%):

-translocation t(14:18) of the Ig heavy chain (14) and the BCL-2 gene (18)

57
Q

how do Follicular lymphomas (B-cell cancer of lymphocytes) grow and why?

A

Indolent (slow-growing) lymphoma due to reduced cell death (less apoptosis since BCL-2 is anti-apoptotic) and accumulation of B cells

58
Q

why do normal cells die?

A

after 60-70 doublings, telomeres shorten leading to senescence

59
Q

what happens normally if TP53 or RB function is lost?

A

formation of dicentric chromosomes (2 centromeres) = additional DNA breaks during next mitosis = genomic instability = cell death

(safeguard against survival of mutated cells)

60
Q

what happens if TP53 or RB function is lost BUT telomerase is reactivated in these damaged cells?

A

immortality with extensive mutations and development of cancer

61
Q

Tumors require _____ to enlarge beyond ~1-2mm

A

blood supply

62
Q

how do tumors form a blood supply? (2)

A

New vessels sprout from existing vessels or are recruited from bone marrow

63
Q

how does the formation of new vessels (Neovascularization) allow tumors to grow?

A

New endothelial cells promote tumor growth (i.e. secrete PDGF)

64
Q

how does the formation of new vessels (Neovascularization) allow tumors to spread/metastasize?

A

New vessels are leaky which can promote metastasis of tumor cells

65
Q

how is hypoxia related to Neovascularization?

A

↓O2 = hypoxia-induced factor 1 (HIF1α) activates transcription of vascular endothelial growth factor (VEGF)

66
Q

what 4 things influence VEGF transcription?

A

-hypoxia –> HIF1α: activates transcription

-p53: inhibits growth/blocks transcription

-RAS –> MAP kinase pathway AND MYC: allow self-sufficient growth = cells can grow without blood supply?

67
Q

clinically, _____ block VEGF activity and are used to treat multiple cancers

A

Angiogenesis inhibitors (i.e. bevacizumab)

68
Q

what are the 2 phases of Invasion and Metastasis?

A

-Invasion of ECM and vascular dissemination (BVs and lymphatics)

-Homing of tumor cells (decide where they are headed to)

69
Q

what are the steps of invasion of the ECM? (4 steps)

A
  1. Detachment of tumor cells from each other
  2. Degradation of basement membrane (BM)
  3. Attachment to novel ECM components
  4. Migration of tumor cells
70
Q

what is the part of desmosome that attaches epithelial cells together?

A

E-cadherin

(“intercellular glue”, antigrowth properties)

71
Q

E-cadherin function is lost in almost all of these types of cancer?

A

epithelial cancers

72
Q

what does E-cadherin normally bind to, holding it in the cytoplasm?

A

β-catenin

73
Q

what happens when E-cadherin is lost, that will stimulate growth?

A

β-catenin can translocate to the nucleus –> growth stimulated

74
Q

The process whereby epithelial cancer cells obtain characteristics of connective tissue cells and invade

A

Epithelial to Mesenchymal Transition (EMT)

75
Q

what normal molecules are affected in the Epithelial to Mesenchymal Transition (EMT)?

A

transcription factors (i.e. SNAIL, TWIST)

-downregulate E-cadherin

-upregulate intermediate filaments (i.e. vimentin, smooth muscle actin)

76
Q

what happens during Basement Membrane (BM) Degradation?

A

Tumor cells secrete proteolytic enzymes or

induce stromal cells to elaborate proteases (e.g. Matrix metalloproteinases (MMPs))

77
Q

how do MMPs regulate invasion? (2)

A

-remodel the BM
-cause release of growth factors from the extracellular matrix

78
Q

In normal cells, if ______ which attach cells to BM are lost, apoptosis occurs.

A

integrins

79
Q

T/F Cancer cells avoid apoptosis when integrins are lost due to other mutations

A

true

80
Q

Cleavage of ____ and ____ opens binding sites for tumor cells when there is Altered Attachment to the ECM

A

collagen IV and laminin

81
Q

T/F migration of tumor cells is a complex, multi-step process

A

true

82
Q

what directs tumor cell locomotion?

A

tumor cell-derived cytokines (e.g. autocrine motility factors)

83
Q

how do tumor cell-derived cytokines (e.g. autocrine motility factors) direct tumor cell locomotion?

A

Tumor cells signal stromal cells to release paracrine factors to promote movement.

84
Q

how are most tumor cells found in the circulation?

A

alone

(detected in “liquid biopsies”)

85
Q

what protects tumor cells in the blood from immune recognition?

A

Aggregation with platelets

86
Q

Homing of tumor cells requires what? (2)

A

adhesion to vascular
endothelium and movement through BM

87
Q

Many tumors metastasize to first capillary bed whereas others exhibit _____

A

organ tropism

88
Q

Tumor cells are often inefficient at colonizing new sites such that “dormant” micrometastases may survive for long periods without progression. why is this a bad thing?

A

treatments target fast growing cells so these cells aren’t killed

89
Q

Tumor cells secrete cytokines and growth factors which stimulate _____ cells to alter the environment allowing the tumor to _____

A

stromal cells

colonize

90
Q

The immune system helps prevent tumor ____ or ____

A

formation or progression

91
Q

T/F there is an ↑ frequency of cancer in immunocompromised hosts (congenital, transplant, AIDS)

A

true

92
Q

what is the main immune defense against tumor formation?

A

Cell-mediated immunity

93
Q

what cells are involved in the Cell-mediated immunity to fight against tumor formation?

A

-CTLs (CD8+ Cytotoxic T-lymphocytes)
-NK Cells
-Macrophages

94
Q

these cells are the major immune defense mechanism against tumors
(including those caused by oncogenic viruses HPV, EBV)

A

CTLs (CD8+ Cytotoxic T-lymphocytes)

95
Q

although there is no evidence for Humoral immunity/ protective anti-tumor antibodies to spontaneous tumors, how are antibodies used?

A

as some cancer treatments (therapeutic)

96
Q

Tumor cells often express _____ that stimulate the host immune system to kill cancer cells

A

antigens

97
Q

what are 2 examples of how tumor cells express antigens?

A

-Cancer cells transformed by oncogenic viruses (HPV, EBV) express viral proteins

-Unmutated proteins can elicit an immune response

98
Q

Unmutated proteins can elicit an immune response. what is an example?

A

-Cancer-testis antigens: normally expressed only in germ cells in the testis. If expressed in other cell types (i.e. tumor) then the immune system reacts

99
Q

what does an Effective Immune Response against cancer cells look like?

A
  1. Dead cancer cells release “danger signals”

that stimulate innate immune cells (phagocytes and antigen presenting cells)

  1. CTLs are activated to then kill surrounding

tumor cells

100
Q

High levels of ____ and ____ in tumors correlates with better clinical outcomes

A

CTLs and Th1 cells

101
Q

what are 3 ways that cancers can avoid the immune system?

A

-acquired mutations that prevent CTLS from recognizing the tumor cell as foreign
-Tumor cells express factors that actively suppress host immunity
-immune checkpoints bypassed

102
Q

what are normal immune checkpoints?

A

inhibitory pathways that normally help maintain self-tolerance and control the immune response

103
Q

how are immune checkpoints altered by tumor cells?

A

activated by the tumor cell to prevent immune response to tumor growth

104
Q

what are 2 immune checkpoints that we know of that tumor cells can use to evade the immune system? how does each work

A

-PD-L1 (programmed cell death ligand 1): expressed on tumor cell surface = binds to PD-1 receptor on CTL = CTL loses ability to kill tumor cell

-CTLA4 receptor: expressed on CTL –> When bound, this inhibits T cell function

105
Q

how can Checkpoint Inhibitors be used in cancer treatment?

A

Antibodies used to block checkpoints and thereby allow the immune system to kill tumor cells

106
Q

there is a 10-30% response rate when using Checkpoint Inhibitors in what types of cancers>

A

a variety of solid tumors
(melanoma, lung cancer etc.)

107
Q

T/F Checkpoint Inhibitors have Autoimmune adverse effects

A

true

108
Q

this cancer treatment uses endogenous or synthetic substances to improve or restore immune system function to fight cancer

A

Immunotherapy

109
Q

what are the different types of Immunotherapy? (5)

A

-Monoclonal antibodies (inhibitors of PD1, PDL-1,

CTLA-4)

-Non-specific immunotherapies (IFNα, IL-2)

-Oncolytic virus therapy

-T-cell therapy [chimeric antigen receptor (CAR) T

cells engineered to express antibodies on surface creating potent tumor cell killers)

-Cancer vaccines

110
Q

what are the Monoclonal antibodies for cancer therapy that are approved by the FDA that we have to know? (5)

A

-Rituximab
-Herceptin
-Cetuximab
-Pembrolizumab
-Nivolumab

111
Q

what does Rituximab target and what cancer is it indicated for?

A

-targets: CD20 (B-cell marker)

-cancer indication: B-NHL (lymphomas)

112
Q

what does Herceptin target and what cancer is it indicated for?

A

-targets: HER2/neu

-cancer indication: Breast cancer

113
Q

what does Cetuximab target and what cancer is it indicated for?

A

-targets: EGFR

-cancer indication: Head and neck squamous cell carcinomas

114
Q

what 2 monoclonal antibodies are PD-1 antagonists?

A

-Pembrolizumab
-Nivolumab

115
Q

what do Pembrolizumab and Nivolumab target and what cancer are they indicated for?

A

-targets: PD-1

-cancer indication: Melanoma

116
Q

While typically protective, inflammatory cells can modify the tumor microenvironment so it promotes tumor progression. How? (2)

A

-Advanced tumors contain mainly M2 Macrophages = promote angiogenesis, fibroblast proliferation and collagen deposition (healing, repair, cell growth)

-WBCs secrete: GFs, proteases, VEGF, and TGF-β (from M2 Macs.)

117
Q

WBCs secrete growth factors (i.e. EGF). how does this inflammation promote tumor progression?

A

causes cell proliferation

118
Q

WBCs secrete proteases, how does this inflammation promote tumor progression?

A

-liberate growth factors from ECM
-degrade adhesion molecules
-foster invasion

119
Q

WBCs secrete TGF-β (from M2 Macs.), how does this inflammation promote tumor progression?

A

suppresses CTLs

120
Q

T/F Defects in DNA repair have ↓↓ risk for cancer and cause genomic stability.

A

false

Defects in DNA repair have ↑↑ risk for cancer and cause genomic instability.

121
Q

what are 3 types of normal DNA repair and what do they do/fix?

A

-DNA mismatch repair (MMR): fixes single nucleotide mismatches

-Nucleotide excision repair: fixes DNA crosslinks (thymine dimers)

-Homologous Recombination Repair: repairs DNA strand breaks (normally in gametes only)

122
Q

what syndrome is affected by defects in DNA mismatch repair (MMR) and what type of cancers can this lead to?

A

hereditary non-polyposis colon cancer (HNPCC) syndrome → colon cancer

123
Q

repetitive DNA sequences (1-7bp) that are prone to replication errors which are repaired by normal MMR enzymes.

A

Microsatellites

124
Q

how are Microsatellites affected when MMR enzyme function is lost?

A

begin to vary in number = microsatellite instability (MSI)

125
Q

how is microsatellite instability (MSI) used clinically?

A

When detected, MSI is a marker of faulty DNA repair but by itself it does not seem to have any clinical effect

126
Q

what disease is affected by defects in nucleotide excision repair and what type of cancers can this lead to?

A

xeroderma pigmentosum –> skin cancer

127
Q

what diseases are affected by defects in homologous recombination repair and what type of cancers can this lead to? (2)

A

-Fanconi anemia –> bone marrow failure and more susceptible to cancer development (leukemia is common)

-BRCA1, BRCA2 –> mutations in these 2 tumor suppressor genes accounts for 80% of familial breast cancer

128
Q

describe what is meant by Multi-step Carcinogenesis. give an example

A

-Cancer results from accumulation of multiple mutations, including genes that regulate apoptosis and senescence
-Example: Colon Carcinoma

129
Q
A

General Pathology (32 decks)

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