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Pathophys > Cancer 2a > Flashcards

Cancer 2a Flashcards

1
Q

Cancer

A

uncontrolled proliferation of cells that serves no physiologic fxn

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2
Q

neoplasm

A

any new growth

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3
Q

benign

A

encapsulated and well-differentiated

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4
Q

malignant

A

invasive and dedifferentiated

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5
Q

tumor

A

reserved for malignant cancers

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6
Q

metastasis

A

spread of cancer to other areas of the body-est. of secondary tumors

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7
Q

tumor marker

A

specific biochem marker (hormone, enzyme,gene,antibody) present in or on tumor cells, or in body fluids

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8
Q

Benign cells charcteristics

A

-grow slowly
-well-defined border
-not invasive
-well-differentiated: looks like cells which they arose from
-dividing cells are rare
-does not metastasize

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9
Q

Malignant cells characteristic

A

-grow rapidly
-does not have a border
-invade local structure and tissues
-poorly differentiated, may not be able to determine tissue or origin
-many dividing cells
-can spread distantly through blood and lymph vessels

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10
Q

Normal cells

A

-differentiate
-follow specific instructions
-fulfill roles of cell type
-populations controlled by balance of apoptosis and growth

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11
Q

Cancer cells

A

-break all the rules
-dedifferentiate: cells lose organization and order
-become anaplastic (without form) and pleiomorphic (many shapes, sizes)
-no longer fulfill specified role
-hijack the body’s mechanisms to promote their own survival.

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12
Q

Hallmarks of cancer cells (8 biological capabilities)

A
  1. sustaining proliferative signaling
  2. evading growth suppressors
  3. Enabling replicative immortality
  4. Resisting cell death
  5. Inducing and accessing vasculature
  6. activating invasion and metastasis
  7. avoiding immune destruction
  8. deregulating cell metabolism
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13
Q

Hallmarks of cancer cells -2 enablers of change

A
  1. Genome instability and mutation
  2. Tumor-promoting inflammation
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14
Q

Mutations characteristics

A

-5-6 different pathways are required to transform normal cells to cancer cells
-accumulate with age

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15
Q

Genetic changes (mutations)

A

-DNA changes
-Epigenetic changes
-microRNA expression

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16
Q

Types of genes prone to mutations

A

-oncogenes
-tumor suppressor genes
-caretaker genes

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17
Q

Point mutation

A

change of single nucleotide

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18
Q

nucleotide insertions/deletion

A

changes way that the gene is “read”
-think adding a random letter to a word

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19
Q

chromosomal rearrangement

A

may lead to the production of new or altered protein

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20
Q

gene amplification

A

increases copy number of genes and hence gene effects

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21
Q

gene silencing

A

turns off a gene’s effect

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22
Q

exogenous sequence

A

from virus, can alter fxn

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23
Q

Oncogenes

A

normally signal proliferation-signal cell to divide
-common ex. RAS

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24
Q

RAS

A

a “molecular switch” that initiates proliferation
-point mutation turn the switch on permanently

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25
Q

Chronic myeloid leukemia (CML)

A

result of novel protein that promotes uncontrolled growth

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26
Q

Chromosomal translocation

A

2 chromosomes fuse together in the middle of 2 different genes
ex. bcr on chromosome 9
abl on chromosome 22
resulting protein –> promotes myeloid cell proliferation

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27
Q

N-myc

A

-a normal oncogene
-fetal brain development
-( in neurblastma cells?)

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28
Q

Gene amplification

A

leads to hundreds of copies of
gene–>exaggerated proliferation signal

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29
Q

Tumor-suppressor genes

A

normally halt proliferation- tell the cell to stop dividing
-mutation makes these genes inactive.

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30
Q

Tumor-suppressor gene types

A

-RB1(retinoblastoma)
-p53
-APC
-BRCA1 (breast cancer)

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31
Q

requires ___mutation because we have __alleles for each gene

A

2, 2

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32
Q

RB1 (retinoblastoma gene)

A

-normally strongly inhibits division
-inactivation leads to uncontrolled proliferation (point mutation)
-requires 2 mutations to inactivate both copies of genes

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33
Q

p53 gene

A

-normally guardian of the genome
-activated by cell stress
-when a cell is damages, p53 tells it to repair or die.
-mutated p53 gene found in nearly every human cancer ever studied
-activated caretaker gene

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34
Q

Caretaker genes

A

-normally maintain genomic integrity
-conducts DNA repair; repair mismatched not, signal-strand breaks, dbl-strand breaks.
-mistakes during replication or exposure to radiation/chemicals
-loss of fxn leads to incr mutation rates
-MANY of the genes implicated in cancer

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35
Q

epigenetic changes

A

-alter expression of genes without mutating sequence

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36
Q

Meythlation

A

addition of methyl molecules to DNA blocks transcription
-STOP signal-no transcription
-DNA can be directly methylated, silencing tumor-suppressor genes or activation oncogenes

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37
Q

methylation of _____promotes cancer

A

tumor suppressor genes

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38
Q

demethylation of _____ promotes cancer

A

oncogene

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39
Q

Acetylation

A

-allows gene expression
-alters histones and chromatin
-GO signal

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40
Q

microRNA (miRNA)

A

-short sequences 22 nt that bind to mRNA
-Inhibiting translation into protein
-changes in miRNA abundance can change expression of genes

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41
Q

Oncomirs

A

miRNAs that stimulate progression of cancer

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42
Q
  1. Sustaining proliferative signaling
A

-induced angiogenesis
-lots of proliferation =lots of blood flow and nutrients needed
-tumor cells release growth factors

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43
Q

Growth factors

A

released by tumor cells:
-Vascular endothelial growth factor (VEGF)
-Platelet-derived growth factor (PDGF)
-Basic fibroblast growth factor (bFGF)

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44
Q
  1. Evading growth suppression
A

-contact inhibition
-anchorage dependence
-due to loss of cadherin and integrin expression

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45
Q

Contact inhibition

A
  • in normal stop dividing after forming a complete monolayer bc of contact
    -in cancer cells that will keep dividing and pile on each other
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46
Q

Anchorage dependence

A

-Non-cancerous cells only proliferate when attached to a surface. they cannot divide in soft agar bc they cannot attach
-cancer cells are anchorage-independent can proliferate in soft agar

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47
Q

telomeres

A

-are repeated sequences at the ends of chromosomes
-maintain chromosome stability during replication
-normal cells can only divide a finite amount of times –> Hayflick limit–>senescence (stops dividing)

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48
Q

Telemore shortening is prevented in stem cells bc of

A

an enzyme, telomerase

49
Q
  1. Enabling replicative immortality
A

-telomers
-cancer stem cells regain the ability to synthesize telomerase. and avoid senescence

50
Q
  1. Resisting cell death
A

-apoptosis normally triggered when cell is stressed/damaged
-able to survive repeated cycles of DNA damage, metabolic stress, hypoxie etc.

51
Q

cancers cells resisting cell death

A

decrease pro-apoptotic signals-p53
increase anti-apoptotic signals-bc12

52
Q

metastasis

A

distal spread of cancer cells, usually through blood and lymph vessels

53
Q

metastasis steps

A
  1. invasion
  2. detachment and intravasation
  3. survival in circulation ( difficult)
  4. extravasation
  5. colonizing distal site
54
Q
  1. invasion
A

local spread of cancer cells
-recruitment of macrophages to primary tumor (TAMs)
-promoting local angiogenesis for nutrient supply
-changes in cell adhesion molecule expression to make cancer cells more mobile–>incr mobility

55
Q
  1. detachment and intravasation
A

-secretion of enzymes that digest extracellular matrix (ECM)-Matrix metalloproteinases (MMPs)
-free cancer cells from stoma
-cancer cells that have undergone epithelial-mesenchymal transition (EMT) are most likely to succeed with this step.
-cancer cells infiltrate local blood vessels

56
Q
  1. survival in circulation
A

-normal cells undergo apoptosis when detached from ECM (anchorage-dependence)
-cancer cells, especially those that have undergone EMT, are resistant to this
-avoid detection by immune cells by attaching to circulation platlets
-very few cancer cells with service circulation (v stressful)

57
Q
  1. extravasation
A

-cancer cells in circulation often stop in narrow vessels or at branch points

58
Q

metastases tends to show up in

A

-liver
-lungs
-brain
-bone

59
Q
  1. colonizing distal site
A

-colonizing a distal site requires an environment that favors the cell’s growth (tumor niche)
-not all cancer cells that arrive at a distal site will survive long enough to form a secondary tumor

60
Q
  1. avoiding immune destruction
A

-tumors produce/secrete cytokines and chemokines that attract macrophages to site
-co-opt macrophages to promote health rather than inflammation

61
Q

THE macrophages THT promote health rather than inflammation:

A

-TAMs (tumor-associated macrophages)
-anti-inflamm effects
-block actions of t cytotoxic cells
-secrete GFs for local tissue remodeling, angiogenesis
-secrete (MMPs) that degrade ECM

62
Q

T-reg cells

A

-predominant lymphocyte
-normally active in wound healing to prevent damage of healthy tissue
-secrete high levels of IL-10
-manipulated in cancer to prevent damage of healthy tissue

63
Q

tumors ____ pro-inflammatory signals and ____ anti-inflamm effects. which allows for __-

A

-suppress, promote
- tumor to expand unimpeded by immune response

64
Q
  1. deregulating cell metabolism
A

metobolic stress
warburg effect:
-despite presence of O2 cancer cells primarily use glycolysis
-many mutations associated with cancer support metabolic shift

65
Q

glycolysis

A

-lactate broken down to produce produce building blocks for cells

66
Q

epithelial cells

A

mature and differentiated

67
Q

mesenchymal cells

A

types of progenitor cell (stem cell)
-not many in adults (kids have more)
-you will see these cells in wound healing
-you will see this in cancer -cell from epithelial to mesenchymal

68
Q

Epithelial-mesenchymal transition (EMT)

A

-occurs in embryonic development
-wound healing/tissue remodeling
-cancer

69
Q

most cancers develop in _____

A

epithelial tissue

70
Q

EMT

A

external signals–>activate transcription factors–>change gene expression and cell behavior

71
Q

EMT makes cells more stem like through:

A

-few adhesion molecules
-no polarity
-able to redifferentiate
-resistance to apoptosis
-unlimited replicative potential

72
Q

EMT Transition driven by cytokine and chemokines of ____

A

tumor microenvironment

73
Q

Tumor growth is enhanced by interaction between cells and local environment:

A

-induced angiogenesis (autocrine signaling)
-Monocytes/macrophages converted to TAMs
-Immune response hijacked to support tumor growth
-appearance of cancer stem cells

74
Q

TAMs

A

tumor-associated macrophages

75
Q

cancer stem cells

A

-cells within tumor are NOT homogenous; mixed populations that may contain cancer cells acting as stem cells
–(this is why cancer treatments are multifaceted)

76
Q

stem cells have the ability to

A

-form new growths
-may explain recurrence of tumors after treatment

77
Q

Tumor niche

A

-idea that certain organs are more inviting for metastases
-aka “seed and soil”-hypothesis that’s some organs are more fertile for metastases to thrive

78
Q

cancer cells change the environment for their benefit through____

A

-recruiting immune cells (TAMs and T reg cells)
-secrete their own growth factors (angiogenesis and tissue remodeling)

79
Q

Adenoma

A

a benign neoplasm derived from glandular cells

80
Q

Carcinoma

A

malignant neoplasm derived from epithelial cells

81
Q

Sarcoma

A

malignant neoplasm derived from mesenchymal cells (fat, muscle)

82
Q

Lymphoma

A

malignant neoplasm derived from lymphocytes

83
Q

Melanoma

A

malignant neoplasm derived from melanocytes

84
Q

Germ cell tumor

A

malignant neoplasm derived from germ cells

85
Q

What causes the mutations to lead to cancer?

A

-mutagen, carcinogen

86
Q

Mutagen

A

-any substance that has potential to cause genetic alteration
-increase risk for cancer but don’t necessarily cause it

87
Q

Carcinogen

A

any substance that contributes to cancer progression
-a type of mutagen

88
Q

examples of carcinogens

A

-workplace exposure (industrial chemicals, paint, solvents)
-environmental (UV tradition, some bacteria, viruses)
-residential (asbestos, processed meat)

89
Q

Viral carcinogens

A

-viruses can lead to cancer directly or indirectly
-human papilloma virus
-Hep B or C

90
Q

human papilloma virus

A

-Direct
-Can be anal, cervical, oropharyngeal)
-virus incorporates its own DNA into host’s cells (stratified epithelium)
-Viral protein (E6) shuts of p53: cell damage w/o apoptosis
-E7 forces cell cycle into replication

91
Q

Hepatitis B or C (liver)

A

-indirect
-Cytotoxicity–> chronic inflammation, oxidative stress, tissue damage
-programming damage mutates cells

92
Q

Bacterial carcinogens

A

Helicobacter pylori

93
Q

Helicobacter pylori

A

-80% have bacteria in stomach (asymptomatic)
-10-20% chance of developing stomach ulcers
-1-2% risk of developing stomach cancer
-uses flagella to burrow through mucus layer
–>infect gastric epithelial cells

94
Q

H. Pylori possible mechanisms for causing cancer

A

-enhanced free radical production increases rate of mutations
-induces local inflammatory response (high levels of TNF-alpha and IL-6) leading to metaplasia of gastric epithelium

95
Q

Inherited carcinogens

A

-breast and ovarian
-non-polyposis colorectal cancers
-li-Fraumeni syndrome

96
Q

Breast and ovarian cancer syndrome

A

-BRCA1 and BCRA2
-also attributed to fallopian cancers, breast cancer in men

97
Q

Hereditary non-polyposis colorectal cancers

A

-involves DNA repair genes
-also endometrial, ovarian, pancreatic, small intestine, stomach, kidney cancers

98
Q

Li-Fraumeni syndrome

A

-mutated p53
-can cause sarcoma, leukemia, and brain, breast,adrenal cortex cancers

99
Q

Where do tumor markers detect cancer?

A

blood, urine, CSF

100
Q

Tumor marker uses:

A

-to screen and identify those at high risk for cancer
-to diagnose specific type of tumor
-to follow clinical course of tumor

101
Q

Prostrate tumors- tumor marker:

A

-prostrate specific antigen (PSA)

102
Q

Liver cell tumors-tumor marker

A

alpha-fetoprotein (AFP)a

103
Q

Adrenal medulla tumor-tumor marker

A

catecholamines (epinephrine)

104
Q

Limitations of tumor markers

A

-false positives are possible
-cancer is heterogeneous-makes different markers prominent in diff ppl
-many cancers don’t have identified markers (high research priority)

105
Q

Cancer treatments

A

-sx removal
-radiotherapy
-chemotherapy
-immunotherapy (active or passive)
-hormonal therapy
-targeted therapy

106
Q

Chemotherapy agents

A

-cytotoxic agents
-take advantage of specific vulnerabilities of cancer cells
-poorly tolerated, can damage healthy cells
-combo of chemo agents typically used bc tumors are heterogenous

107
Q

chemo different classes of drugs

A

have different targets:
-cell growth pathways
-DNA replication
-microtubule structure

108
Q

Chemotherapy agents

A

-alkylating agents
-nitrosoureas
-anti-metabolites
-plant alkaloids

109
Q

Alkylating agents

A

carboplatin, cisplatin
-target DNA, kills all replicating cells

110
Q

Nitrosoureas

A

carmustine
-slow down DNA repair mechanisms

111
Q

Anti-metabolites

A

methotrexate, flururacil
-interfere with DNA/RNA in dividing cells

112
Q

Plant alkaloids

A

paclitaxel, vincristine
-anti-mitotics, prevent cells from entering cell division phase

113
Q

Immunotherapy (active)

A

-direct immune system attack to cancer cells through id of (TAAs) tumor-associated antigens
-immune cells removed from pt
-genetically modified to recognize some tumor-specif marker
-cultured and returned to pt
“anti-cancer vaccine”

114
Q

Immunotherapy (passive)

A

-not as direct as active
-enhancing natural anti-cancer mechanisms
-Tumor targeting antibodies
-cytokines

115
Q

Tumor targeting antibodies

A

-bind tumor cell and initiate cell death or interfere with cells fxn
-can activate complement syeste, to initiate cell death or interfere with cells fxn
-cetuximab: targets EGFR treats head and neck cancers
-rituximab: activates complement system, treats leukemia and lymphoma

116
Q

Cytokines

A

-used adjuvants to other therapies
-Interferons, interleukins

117
Q

Hormonal therapy

A

-used for tumors in hormonal-responsive tissues
-don’t directly kill cells-cut off their ability to respond to hormone signals
-Tamoxifen (breast): competes with substrate for ER, blocks proliferation

118
Q

Aromatase inhibitors

A

-enzyme that converts androgens->estrogens
-block formations of estrogens “starve” dependent cancer
-useful in tumors resistant to tamoxifen
-anatroxole

119
Q

Targeted therpy

A

-small molcule inhibitors that target specific proteins
-receptor kinase inhibitors:
-imatinib-binds to mutated protein to stop
-chronic myeloid leukemia (CML)
-competitively binds to bcr-abl fusion protein
-blocks substrate binding and thus cell proliferation

Pathophys (8 decks)

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