Chapter 17 Flashcards
1
Q
What is a mass of cell that grew from a single or few mutant cells , escaping normal regulation?
A
tumors
2
Q
What nourish the tumor?
A
growth of new blood vessels
3
Q
Growth is accompanied by
A
angiogenesis (growth of new vessels)
4
Q
Characteristic of benign tumor
A
noninvasive, noncancerous, doesn’t affect other tissues
5
Q
Characteristics of malignant tumor
A
invasive, cancerous, and can metastasize
6
Q
What is metastasis?
A
detaching from the original location and establishing in new body areas
7
Q
what are neoplasms?
A
growing masses of abnormal cells
8
Q
what are the 4 major grouping?
A
a. carcinomas
b. sarcomas
c. hematopoietic neoplasias
d. neuroectodermal neoplasias
9
Q
What are the most common grouping types in human?
A
carcinomas
10
Q
Carcinomas are from epithelial cells of?
A
lung, colon, breast, prostate, stomach, pancreas, and skin
11
Q
Sarcomas are from what tissues involving fibroblasts?
A
mesenchymal tissues
12
Q
examples of sarcomas
A
bone and muscle
13
Q
What groupings are frequent targets?
A
hematopoietic neoplasias
14
Q
examples of hematopoietic neoplasias (3)
A
leukemias, lymphomas, myelomas
15
Q
Examples of neuroectodermal neoplasias (5)
A
neuroblastomas, glioblastomas, neuromas, neurofibrosarcomas, and melanomas
16
Q
Contact inhibition of growth is present in normal or cancer cells?
A
normal cells
17
Q
growth factor requirements are high in normal or cancer cells?
A
normal cells
18
Q
anchorage-dependence is present in normal or cancer cells?
A
normal cells
19
Q
cell cycle checkpoints are intact in normal or cancer cells?
A
normal cells
20
Q
karyotypic profile is normal in normal or cancer cells?
A
normal cells
21
Q
Finite proliferative life spain in normal cells or cancer cells?
A
normal cells
22
Q
What is contact inhibition?
A
normal cells in a tissue culture flask cover the bottom with a monolayer of cells then they stop dividing because they contact one another
23
Q
What layer covers the whole bottom surface of the container?
A
confluent monolayer
24
Q
What cells do not exhibit contact inhibition?
A
cancer cells
25
What cells grow in an anchorage-independent manner?
cancer cells
26
Mortality of normal cells vs cancer cells
normal cells: grow and divided for a limited number of cell divisions before they stop growing
cancer cells: immortality
27
Example of 2 growth factors?
a. PDGF (platelet-derived growth factor)
b. EGF (epidermal growth factor)
28
Most normal cells do not proliferate unless induced to do so by ____
exogenous stimuli like growth factors
29
Cancer cells need ____ in their surroundings to stimulate their own proliferation
smaller amounts of growth factors
30
Chromosome complement in the nuclei of cancer cells is ____
aberrant with some chromosomes missing and others present in excess
31
What are cancer-causing agents that are either physical or chemical?
carcinogens
32
What are agents that cause DNA damage, causing cancer?
mutagens
33
What uses histidine-auxotrophic Salmonella mutants to test if a chemical is mutagenic?
Ames Test 1975
34
Carcinogens affect what cells?
somatic cells
35
If the sector is mutant in somatic tissue, offspring is ___
normal
36
If the sector is mutant in germinal tissue, offspring is _____
normal
37
How can inborn susceptibility to cancer arise?
when mutant genes are passed in germ-line cells
38
Positive regulators that promote normal cell growth and division
proto-oncogenes
39
Negative regulators that serve to constrain proliferation
timor suppressors
40
Proto-oncogenes can be mutated to?
oncogenes, which are cancer causing
41
Tumor suppressors can be mutated, contributing to ______
carcinogenesis
42
Why does tumor suppressor mutation/inactivation contribute to carcinogenesis?
because they can no longer suppress growth
43
What is the virus from a chicken tumor called?
Rous sarcoma virus
44
What is a characteristic of Rous sacroma virus unlike most viruses?
it does not kill cells it infects, rather it transforms them into cells with many of the traits associated with cancer cells
45
RSV
rous sarcoma virus
46
Genome of RSV persists in the progeny cells, thus the cancerous growth becomes ______
heritable trait, passed from one cell to its offspring
47
In 1970s, RSV was classified as ______.
retrovirus with ssRNA genome and src gene
48
src responsible for what?
all of the cancer-inducing properties of RSV
49
src is an _____.
oncogene
50
In 1975, normal version of the src gene was found called
c-src
51
c-src
cellular-src
52
c-src is an ______.
proto-oncogene
53
What is the viral oncogene version of src?
v-src
54
What are 3 other tumor-inducing retroviruses have acquired and altered normal cellular genes in a fashion analogous to the case of RSV?
a. Avian myelocytomatosis virus (myc)
b. Harvey rat sarcoma virus (H-ras)
c. Feline sarcoma virus (fes)
55
myc
Avian myelocytomatosis virus
56
H-ras
Harvey rat sarcoma virus
57
Fes
Feline sarcoma virus
58
class of DNA tumor viruses (dsDNA genomes) causes transformation by
producing cancer-inducing proteins (oncoproteins) unrelated to normal cellular growth-regulating proteins
59
What proteins bind and disturb normal cellular proteins?
cancer-inducing proteins (oncoproteins)
60
5 DNA tumor viruses that produces oncoproteins
a. SV40
b. Epstein=Barr virus (EBV)
c. Papillomaviruses
d. Adenovirus
e. polyoma virus
61
EBV
Epstein=Barr virus
62
In late 1970s, what was found of the transforming oncogenes present in chemically transformed cells?
they are mutant versions of normal proto-oncogenes that have been altered through the mutagenic actions of the chemical
63
Proto-oncogenes can be activated into oncogenes by (2)
a. by their incorporation into retrovirus genome
b. by mutational processes that altered normal genes residing within cellular chromosomes
64
3 type of mutations responsible for proto-oncogene to oncogene
a. simple mutaiton
b. overexpression and gene amplification
c. inversion or translocation
65
Activating mutation will invariably create ____, and influenced ____ even in heterozygous condition.
dominant allele; cell phenotype
66
TSGs
tumor suppressor genes
67
Why do tumor suppressor genes (TSGs) require two mutations?
because an inactivating mutation eliminating one copy of a TSG will create a recessive null allele while the surviving wild-type allele will function properly
68
How often will both TSGs be mutated?
rare
69
Both TSGs will be mutated rarely, except for ____
loss of heterozygosity (LOH)
70
What is loss of heterozygosity?
the conversion of heterozygous genes into a homozygous state
71
How can loss of heterozygosity happen?
via the loss of wild-type gene copy and its replaced by a duplicated copy of the already-mutated copy
72
What is as effective in eliminating TSG function as mutations in the base sequences of the gene?
silencing of one of the gene copies by a process like promoter methylation
73
Disease with one defective TSG copy inherited and the surviving wild-type allele is lost
Hereditary cancer syndromes
74
What is a complex, multistep process in vivo?
cancer formation
75
What has some normal cells, frankly malignant cells, and a number of regions in intermediate states along this spectrum?
cancerous tissue
76
4 example of spectrum in the colon
a. hyperplasia
b. dysplasia
c. large polyps
d. frank carcinomas
77
What is hyperplasia?
excess number of cells
78
What is dysplasia?
cells forming marginally abnormal epithelium inducing relatively undeveloped polyps
79
What are large polyps?
localized, noninvasive growths that often protrude into the cavity
80
What is frank carcinomas?
underlying muscle layer invaded, layer crossed through, and seeded colonies at distant locations
81
Multiple genetic mutations are generally implicated in driving _____
tumor formation
82
What cells cannot be transformed into the tumor cells through the introduction of a single oncogene?
normal cells
83
How many oncogenes are more likely to be associated with tumor?
2
84
What is necessary for oncogenic transgenes to cause tumors?
somatic mutations
85
what happens in response to growth factors and other extracellular signals?
normal cell growth and poliferation
86
Receptors and signaling pathways are involved in?
transmitting/transducing a signal from a ligand into the cell interior
87
Proto-oncogene encoded proteins are found in which steps of the signaling pathways? (4)
a. growth factor
b. growth factor receptor
c. second messengers in cytosol
d. transcription factors
88
Ligand dependent receptor
receptor signals when ligand is present
89
Ligand-independent receptor
receptor constitutively signals even without ligand
90
Normal Ras vs Mutant Ras
Normal Ras: Ras active for brief periods of time
Mutant Ras: Ras constitutively active
91
LIght independent receptor firing occurs via waht 3 mechanisms?
a. autocrine signaling
b. paracrine signaling
c. endocrine signaling
92
What is autocrine signaling?
cells secrete signals which then binds to their own receptors, self-stimulation ensues
93
What is paracrine signaling?
signals from one cell bind to neighboring cells
94
What is endocrine signaling?
signals from some cells enter circulation, go throughout the body
95
Differentiated cells becoming terminally differentiated is called ____
postmitotic
96
What cells have unlimited ability to renew themselves?
stem cells
97
Tumor cells behave similarly to ___
stem cells
98
What is a cell suicide mechanism to facilitate the efficient removal of cells in a tissue during normal development and during adult life?
apoptosis
99
What cells work via apoptosis to eliminate tumorigenic cells before they have a chance to multiply?
immune system's cytotoxic cells Tc and NK
100
G1 cells must pass _____ to commit itself to complete the remainder of cell cycle
restriction point
101
Cells can exit reversibly into what G0 state?
quiescent, nongrowing G0 state
102
Cells can exit irreversibly into what G0 state?
postmitotic, differentiated G0 state
103
What discourage cells from going through the R point?
a. antimitogenic signals
104
What is important in the R point decision?
retinoblastoma gene product (pRb)
105
prb
retinoblastoma gene product
106
Function of Rb when hypophosphorylated
binds E2F and blocks cell from advancing through R point
107
Function of Rb when phosphorylated
releases E2F, thus opening the R point gate and ushering the cell through into late G1
108
In tumors, where Rb gene activity is completely abolished, it results in
no blockage to entering Gq so cell passes freely through R point
109
How can enough spontaneous mutations occur to generate cancer during a human lifetime?
one of the early genes like the component of the DNA repair apparatus or one of the cell cycle checkpoint control components should be mutated
110
What are the 2 examples of early gene mutation to facilitate the development of cancer?
a. loss of p53 function
b. DNA repair defects
111
What happens when p53 loses its function?
cells no longer under the threat of p53-induced apoptosis
112
What are 2 example disease resulting from loss of p53 function?
a. Ataxia telangiectasia
b. Human papillomavirus E6 oncoprotein
113
DNA repair defects function
cells cannot fix damaged DNA
114
What are 3 example diseases resulting from DNA repair defects?
a. Xeroderma pigmentosum (XP)
b. BRAC1 and BRAC2 defective alleles predispose to breast and ovarian carcinomas
c. Hereditary nonpolyposis colon cacner
115
Normal cells enter _____ after they multiply in culture for a limited number of doublings
senescene
116
When can human cells in culture circumvent senescene?
if p53 and Rb tumor suppressor gens are inactivated
117
Normal cells have ____ clock that operates within the cell, independent of extracellular stimuli.
generation-counting ability/cellular
118
The generation counting is the ____ of chromosomes
telomeres at the ends of chromosomes
119
Each cell generation results in the loss of a few of the ______ because of the _____ problem
hexanucleotide repeating units; end-replication
120
Cancer cells depress the expression of _______.
telomerase enzyme
121
Size of tumors are lmited due to (2)
a. lack of access to nutrients and O2
b. inability to remove metabolic wastes and CO2
122
Size of the tumors are limited unless tumor succeeds in?
acquiring a blood vessel network
123
Tumor cells have the ability to secrete _______.
angiogenic growth factors
124
Angiogenic growth factors cause what?
endothelial cells in adjacent normal tissue to proliferate and move toward the tumor mass
125
What happens if tumor cells lack a blood supply?
the death rate is similar to the proliferation rate
126
What in tumor is related to the behavior of the cancer cells?
density of capillaries in tumor
127
Capillary nearness allows
more likely metastasis
128
What are primary tumors?
those that remain where they originate
129
Primary tumors account for ____ cancer deaths
~10%
130
Cancer deaths by primary tumors are due to
cancer metastasis
131
What is the process whereby cancer cells gain access to blood and lymph vessels?
intravasation
132
What is the process where cells escape from the vessel?
extravasation
133
What happens to most cells that leave a tumor die while in circulation?
most of cells that extravasate will fail to survive in their new location
