Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease Mechanisms > Ch 7: Neoplasm > Flashcards

Ch 7: Neoplasm Flashcards

1
Q

define neoplasm

A

new, abnormal proliferation of cells
can be benign or malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what two cell types are neoplasms made of

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is differentiation

A

extend to which the neoplastic parenchymal cells resemble normal parenchymal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is well-differentiated

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is poorly-differentiated

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define anaplasia

A

cells that lose their organization and differentiation
poorly differentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a sarcoma

A

malignant tumor of mesenchymal origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is a carcinoma

A

malignant tumor of epithelial origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the two main phases of the normal cell cycle

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the two components of the M phase

A

mitosis and cytokinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is mitosis

A

nuclear division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is cytokinesis

A

division of everything in the cell except for the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens during interphase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens during the S phase

A

labile cells entering
DNA is replicating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens during G2 (gap 2) phase

A

producing more proteins and centrioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are 2 examples of permanent cells

A

neurons and cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are two examples of labile cells

A

epidermis and GI epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

cyclin dependent kinases (CDK)
cyclins
cell cycle inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are cyclin dependent kinases (CDK)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are cyclins

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do cell cycle inhibitors do

A

enforce the cell cycle checkpoints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

explain how a growth factor can lead to cell growth

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the two families of cell-cycle inhibitors

A

CIP/KIP and INK4/ARF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the three types of CIP/KIP cell-cycle inhibitors and what do they do

A

p21, p27, and p57
inhibit cyclins from binding to CDK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the two types of INK4/ARF cell-cycle inhibitors and what do they each do

A

p16 (INK4) - competes with CDK4 for binding to cyclin D
p14 (ARK) - prevents p53 degradation by inhibiting MDM2 activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is a proto-oncogene

A

normal genes within your body that promote cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is an oncogene

A

mutated or over expressed version of proto-oncogene that cause excessive cell growth
considered dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is a tumor suppressor gene

A

genes that stop cell proliferation
recessive - two mutations to change the function
ex. TP53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is an oncoprotein

A

protein encoded by oncogene
oncogene will increase or alter function of oncoprotein to increase cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the 5 types of oncoproteins

A

GFR
RAS
PI3K
MYC
D cyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are three ways in which an oncogene can become activated

A

gene amplification
point mutation
chromosome rearrangement (translocation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the PDGFB gene

A

platelet derived growth factor beta
important growth factor involved in certain cancers like glioblastomas

38
Q

what are the two main types of growth factor receptor genes

A

ERBB2 (HER) and PDGFRP

39
Q

what is paracrine stimulation

A

growth factor stimulates itself and neighboring cells

40
Q

what is autocrine stimulation

A

cell releases growth factor which binds to its own receptors

41
Q

which two proteins involved in signaling transduction can be mutated to become oncogenes

A

ABL and RAS

42
Q

what is a Philadelphia chromosome

A

translocation of ABL into BCR gene
fusion of these genes leads to over activation of tyrosine kinase and therefore growth factor signaling pathways

43
Q

what is MYC

A

a nuclear regulatory protein that can be mutated to become an oncogene
mutation in this leads to Burkitt lymphoma

44
Q

what is CCND1 (cyclin D1)

A

a cell cycle regulator that helps to activate cyclin dependent kinases
can become an oncogene once mutated

45
Q

a mutation in the PDGFB leads to which type of cancer

A

astrocytoma

46
Q

what controls cell-cycle checkpoints

A

tumor supressor proteins
ex. RB and p53

47
Q

what is retinoblastoma

A

malignant tumor of the retina caused by mutations in 2 normal Rb gene
two forms: sporadic and familial

48
Q

what is the familial form of retinoblastoma

A

40% of cases
child inherits one defective Rb gene
another Rb gene undergoes spontaneous mutations

49
Q

what is the sporadic form of retinoblastoma

A

60%
two Rb mutations in somatic cells (not inherited)

50
Q

what is a negative regulator of G1/S cell cycle

A

RB gene and Rb protein

51
Q

what do the BRCA1 and 2 genes do

A

repair double-stranded breaks in DNA

52
Q

what is the normal function of the RB gene and Rb protein and what happens when it goes array

A

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
Q

what does the neurofibromin-1 (NF1) gene do

A

tumor supressor gene that inhibits RAS/MAPK signaling

54
Q

what does the TP53 gene and p53 protein do

A

stop cell cycle during G1 and cause DNA repair or apoptosis of a damaged cell

55
Q

what is p53

A

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
Q

how does p53 control cell cycle arrest during G1

A

induce transcription of p21 which is a cell-cycle inhibitor

57
Q

how does p53 repair DNA damage

A

using GADD45 protein

58
Q

how does p53 cause apoptosis

A

promotes BAX

59
Q

how is p53 regulated

A

by MDM2 enzyme
degrades p53 once it’s no longer needed

60
Q

what is cellular senescence

A

stops cell from dividing and shuts it down
down by p53

61
Q

what is TP53’s 2 main roles in causing cancer

A

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
Q

what is the Warburg effect

A

tumor cells undergo a metabolic switch to aerobic glycolysis
increase uptake of glucose which converted to lactate
produces 2ATP and metabolic intermediates

63
Q

why do cancer cells practice the Warburg effect instead of using oxidative phosphorylation

A

lactate and metabolite products are more efficient for lipid and molecular building block production

64
Q

what are the two mechanisms of how cancer cells resist apoptosis

A

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
Q

what is PUMA

A

pro-apoptotic protein

66
Q

what are the two ways cancer cells practice immortality

A

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
Q

how do cancer cells practice angiogenesis

A

increase angiogenic factors or loss of angiogenic inhibitors

68
Q

how does hypoxia trigger angiogenesis

A

transcription factors release cytokines like VEGF and bFGF
leads to proliferation of endothelial cells and new growth of vessels

69
Q

how do proteases affect angiogenesis

A

influence balance angiogenic and antiangiogenic factors

70
Q

what is meant by neoplastic progression

A

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
Q

what are the three ways in which cancer can spread to other areas of the body

A

direct seeding
lymphatic spread
hematogenous spread

72
Q

what is hematogenous spread of tumor

A

cells detach from the tumor
go through and degrade the extra-cellular membrane
access capillaries to migrate to distant site

73
Q

how do cancer cells survive as they’re traveling through the blood

A

bind to platelets to protect them

74
Q

what is direct seeding and which cancers use this method most

A

metastasis method where cancer cells penetrates into a neutral open field
seen in ovarian carcinomas that spread to peritoneal surfaces

75
Q

what are the 3 most common sites of metastasis of the colon/pancreas/stomach

A

liver, lung, and nodes

76
Q

what are the 5 most common sites of metastasis of the breast

A

nodes, lung, bone, liver, and chest wall

77
Q

what are the 4 most common sites of metastasis of the lung

A

brain, liver, nodes, and bone

78
Q

what is the most common site of metastasis of the prostate

A

bone

79
Q

what are the 3 most common sites of metastasis of melanoma

A

liver, brain, and lung

80
Q

what are the three ways in which tumor cells can evade host immune response

A

loosing expression of antigens
loosing expression of MHC molecules
producing immunosuppressive cytokines or ligands

81
Q

how does UV light cause cancer

A

causes two thymine bases to bind by covalent bonds (thymine dimers)
typically rare because your body eliminates these cells

82
Q

what is the repair mechanism for X-ray, oxygen radical, alkylating agent, and spontaneous reaction damage

A

base-excision repair (BER)

83
Q

what is the repair mechanism for UV light and polycylcic aromatic hydrocarbon damage

A

nucleotide-excision repair (NER)

84
Q

what is the repair mechanism for X-ray and anti-tumor agent damage

A

recombinational repair (HR, EJ)

85
Q

what is the repair mechanism for replication errors

A

mismatch repair

86
Q

what is the nucleotide excision repair pathway

A

enzyme repairs DNA damage where several genes are involved
mutation in this pathway can lead to xeroderma pigmentosum (skin cancer)

87
Q

what is epigenetic modification

A

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
Q

what is DNA methylation

A

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
Q

where do you see the most methylation in cancers

A

promotor region of many tumor suppressor genes

90
Q

do oncogenes use hyper or hypomethylation

A

hypomethylation

91
Q

do tumor supressor genes use hyper or hypomethylation

A

hypermethylation

92
Q

what is the relationship between transcription and methylation

A

the more methylation you have, the less transcription

Disease Mechanisms (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions