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Disease Mechanisms > Ch 7: Neoplasm > Flashcards

Ch 7: Neoplasm Flashcards

(92 cards)

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1
Q

define neoplasm

A

new, abnormal proliferation of cells
can be benign or malignant

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2
Q

what two cell types are neoplasms made of

A

neoplastic cells (parenchyma of tumor)
nonneoplastic stroma (CT, blood vessels, and inflammatory cells)

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3
Q

what is differentiation

A

extend to which the neoplastic parenchymal cells resemble normal parenchymal cells

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4
Q

what is well-differentiated

A

neoplastic parenchymal cells that similarly resemble the other parenchymal cells in the area
characteristic of benign tumors

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5
Q

what is poorly-differentiated

A

neoplastic parenchymal cells do not resemble other parenchymal cells in the area
characteristic of malignant tumors

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6
Q

define anaplasia

A

cells that lose their organization and differentiation
poorly differentiated

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7
Q

what is a sarcoma

A

malignant tumor of mesenchymal origin

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8
Q

what is a carcinoma

A

malignant tumor of epithelial origin

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9
Q

what are the two main phases of the normal cell cycle

A

interphase (90% of cycle) and M phase (10% of cycle)

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10
Q

what are the two components of the M phase

A

mitosis and cytokinesis

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11
Q

what is mitosis

A

nuclear division

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12
Q

what is cytokinesis

A

division of everything in the cell except for the nucleus

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13
Q

what happens during interphase

A

cell is growing and preparing for division
split into: G1, S, and G2 phases

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14
Q

what is happening during G1 of the interphase

A

M phase or quiescent (stable/dormant) cells are entering
lots of proteins being made
cells are performing normal, daily metabolic activities and growing

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15
Q

what happens during the S phase

A

labile cells entering
DNA is replicating

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16
Q

what happens during G2 (gap 2) phase

A

producing more proteins and centrioles

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17
Q

what is an example of a quiescent (stable/dormant) cell

A

hepatocytes

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18
Q

what are 2 examples of permanent cells

A

neurons and cardiac myocytes

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19
Q

what are two examples of labile cells

A

epidermis and GI epithelium

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20
Q

what are the 5 steps in the cell cycle

A

G1 phase
S phase
G2 phase
M phase
cytokinesis
“Go Sally Go, Make Children”

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21
Q

what is the first checkpoint of the cell cycle

A

between G1 and S phases
checks for DNA damage
prevent damaged DNA from being made
p53 dependent

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22
Q

what is the second checkpoint of the cell cycle

A

between G2 and M phases
checks for damaged or unduplicated DNA
prevents chromosomal abnormalities
p53 independent/dependent

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23
Q

what are the three things that help to regulate the cell cycle

A

cyclin dependent kinases (CDK)
cyclins
cell cycle inhibitors

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24
Q

what are cyclin dependent kinases (CDK)

A

kinases which drive the cell cycle
available all the time in inactive forms

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25
what are cyclins
molecules (B, E, A, and D) used to activate cyclin dependent kinases (CDK) at different points during the cell cycle only made during certain cycles and then broken down
26
what do cell cycle inhibitors do
enforce the cell cycle checkpoints
27
explain how a growth factor can lead to cell growth
growth factor binds to membrane protein binding activates inactive signal transduction pathway (RAS, MAPK, MYC) active RAS activates other things which leads to production of D cyclins cyclin D binds with CDK4 to make a complex leads to something like Retinoblastoma (Rb) being phosphorylated phosphorylation leads to E2F transcription factor being released cyclin E binds to CDK2 to make a complex complex leads to DNA replication
28
what are the two families of cell-cycle inhibitors
CIP/KIP and INK4/ARF
29
what are the three types of CIP/KIP cell-cycle inhibitors and what do they do
p21, p27, and p57 inhibit cyclins from binding to CDK
30
what are the two types of INK4/ARF cell-cycle inhibitors and what do they each do
p16 (INK4) - competes with CDK4 for binding to cyclin D p14 (ARK) - prevents p53 degradation by inhibiting MDM2 activity
31
what is a proto-oncogene
normal genes within your body that promote cell proliferation
32
what is an oncogene
mutated or over expressed version of proto-oncogene that cause excessive cell growth considered dominant
33
what is a tumor suppressor gene
genes that stop cell proliferation recessive - two mutations to change the function ex. TP53
34
what is an oncoprotein
protein encoded by oncogene oncogene will increase or alter function of oncoprotein to increase cell proliferation
35
what are the 5 types of oncoproteins
GFR RAS PI3K MYC D cyclin
36
what are three ways in which an oncogene can become activated
gene amplification point mutation chromosome rearrangement (translocation)
37
what is the PDGFB gene
platelet derived growth factor beta important growth factor involved in certain cancers like glioblastomas
38
what are the two main types of growth factor receptor genes
ERBB2 (HER) and PDGFRP
39
what is paracrine stimulation
growth factor stimulates itself and neighboring cells
40
what is autocrine stimulation
cell releases growth factor which binds to its own receptors
41
which two proteins involved in signaling transduction can be mutated to become oncogenes
ABL and RAS
42
what is a Philadelphia chromosome
translocation of ABL into BCR gene fusion of these genes leads to over activation of tyrosine kinase and therefore growth factor signaling pathways
43
what is MYC
a nuclear regulatory protein that can be mutated to become an oncogene mutation in this leads to Burkitt lymphoma
44
what is CCND1 (cyclin D1)
a cell cycle regulator that helps to activate cyclin dependent kinases can become an oncogene once mutated
45
a mutation in the PDGFB leads to which type of cancer
astrocytoma
46
what controls cell-cycle checkpoints
tumor supressor proteins ex. RB and p53
47
what is retinoblastoma
malignant tumor of the retina caused by mutations in 2 normal Rb gene two forms: sporadic and familial
48
what is the familial form of retinoblastoma
40% of cases child inherits one defective Rb gene another Rb gene undergoes spontaneous mutations
49
what is the sporadic form of retinoblastoma
60% two Rb mutations in somatic cells (not inherited)
50
what is a negative regulator of G1/S cell cycle
RB gene and Rb protein
51
what do the BRCA1 and 2 genes do
repair double-stranded breaks in DNA
52
what is the normal function of the RB gene and Rb protein and what happens when it goes array
stops cell progression from G1 phase to S phase until they're ready to divide mutations in this gene/protein can lead to DNA damaged cells dividing which can lead to glioblastoma
53
what does the neurofibromin-1 (NF1) gene do
tumor supressor gene that inhibits RAS/MAPK signaling
54
what does the TP53 gene and p53 protein do
stop cell cycle during G1 and cause DNA repair or apoptosis of a damaged cell
55
what is p53
guardian of the genome protein activated by anoxia, inappropriate signaling, or DNA damage regulates cell cycle arrest (G1), DNA repair, cellular senescence, and apoptosis
56
how does p53 control cell cycle arrest during G1
induce transcription of p21 which is a cell-cycle inhibitor
57
how does p53 repair DNA damage
using GADD45 protein
58
how does p53 cause apoptosis
promotes BAX
59
how is p53 regulated
by MDM2 enzyme degrades p53 once it's no longer needed
60
what is cellular senescence
stops cell from dividing and shuts it down down by p53
61
what is TP53's 2 main roles in causing cancer
germline mutation in a TP53 allele or p53 inactivation by viral oncoprotein which causes it to act like a MDM2, p53 is degraded (HPV)
62
what is the Warburg effect
tumor cells undergo a metabolic switch to aerobic glycolysis increase uptake of glucose which converted to lactate produces 2ATP and metabolic intermediates
63
why do cancer cells practice the Warburg effect instead of using oxidative phosphorylation
lactate and metabolite products are more efficient for lipid and molecular building block production
64
what are the two mechanisms of how cancer cells resist apoptosis
intrinsic (mitochondrial) pathway is affected loss of TP53 function or complication of MDM2 prevents up regulation of PUMA or over expression of anti-apoptotic members of the BCL2 family
65
what is PUMA
pro-apoptotic protein
66
what are the two ways cancer cells practice immortality
cancer cells can restore telomeres to continue division by using telomerase they can also inactivate senescence signals (signals that tell them to stop dividing)
67
how do cancer cells practice angiogenesis
increase angiogenic factors or loss of angiogenic inhibitors
68
how does hypoxia trigger angiogenesis
transcription factors release cytokines like VEGF and bFGF leads to proliferation of endothelial cells and new growth of vessels
69
how do proteases affect angiogenesis
influence balance angiogenic and antiangiogenic factors
70
what is meant by neoplastic progression
cancers pick up different mutations along the way as they grow for example, they start off with just angiogenic properties then pick up metastatic and non antigenic properties
71
what are the three ways in which cancer can spread to other areas of the body
direct seeding lymphatic spread hematogenous spread
72
what is hematogenous spread of tumor
cells detach from the tumor go through and degrade the extra-cellular membrane access capillaries to migrate to distant site
73
how do cancer cells survive as they're traveling through the blood
bind to platelets to protect them
74
what is direct seeding and which cancers use this method most
metastasis method where cancer cells penetrates into a neutral open field seen in ovarian carcinomas that spread to peritoneal surfaces
75
what are the 3 most common sites of metastasis of the colon/pancreas/stomach
liver, lung, and nodes
76
what are the 5 most common sites of metastasis of the breast
nodes, lung, bone, liver, and chest wall
77
what are the 4 most common sites of metastasis of the lung
brain, liver, nodes, and bone
78
what is the most common site of metastasis of the prostate
bone
79
what are the 3 most common sites of metastasis of melanoma
liver, brain, and lung
80
what are the three ways in which tumor cells can evade host immune response
loosing expression of antigens loosing expression of MHC molecules producing immunosuppressive cytokines or ligands
81
how does UV light cause cancer
causes two thymine bases to bind by covalent bonds (thymine dimers) typically rare because your body eliminates these cells
82
what is the repair mechanism for X-ray, oxygen radical, alkylating agent, and spontaneous reaction damage
base-excision repair (BER)
83
what is the repair mechanism for UV light and polycylcic aromatic hydrocarbon damage
nucleotide-excision repair (NER)
84
what is the repair mechanism for X-ray and anti-tumor agent damage
recombinational repair (HR, EJ)
85
what is the repair mechanism for replication errors
mismatch repair
86
what is the nucleotide excision repair pathway
enzyme repairs DNA damage where several genes are involved mutation in this pathway can lead to xeroderma pigmentosum (skin cancer)
87
what is epigenetic modification
changing the expression of genes without changing DNA sequences three ways: DNA methylation, nucleosome remodeling, and histone modifications all lead to gene silencing can be passed down
88
what is DNA methylation
a method of epigenetic modification methylation group is added which prevents transcription by shutting off gene expression of whole segments takes two hits to get silencing
89
where do you see the most methylation in cancers
promotor region of many tumor suppressor genes
90
do oncogenes use hyper or hypomethylation
hypomethylation
91
do tumor supressor genes use hyper or hypomethylation
hypermethylation
92
what is the relationship between transcription and methylation
the more methylation you have, the less transcription

Disease Mechanisms (19 decks)

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