Chapter 20: Cancer Overview Flashcards
1
Q
cancer results from the breakdown of
A
normal regulatory mechanisms that govern the cell
2
Q
in cancer what results from accumulated abnormalities in multiple cell regulatory systems?
A
loss of growth control
3
Q
define tumor
A
any abnormal pproliferation of cells
4
Q
characteristics of a benign tumor
A
- remains confined to original location
- no invading/ spreading to distant body sites
5
Q
characteristics of a malignant tumor
A
- capable of invading healthy tissue
- capable of metastasis
6
Q
what are the 3 basic types of cancer?
A
- carcinomas
- sarcomas
- leukemias/lymphomas
7
Q
carcinomas are malignancies of
A
epithelial cells
8
Q
sarcomas are solid tumors of
A
connective tissues
muslce, bone, cartilage, fibrous tissue
9
Q
tumors are further classified according to
A
- tissue of origin
- type of cell involved
10
Q
provide 2 examples of cancers that describe the type of cells involved
A
- fibrosarcomas: fibroblasts
- erythroid leukemias: precursors of RBCs
11
Q
most cancers develop late in life…why?
A
- cells become malignant
- mutations accumulate over time
12
Q
normal tissue is a composite of cells in which different X chromosomes have been
A
inactivated
13
Q
as normal tissue cells proliferate each displays the same patterm of X activation…what is it?
A
- X1: inactive
- X2: active
14
Q
tumors begin to develop from a
A
single initially altered cell
15
Q
what are the 4 types of growth patterns?
A
- hypertrophy
- hyperplasia
- dysplasia
- neoplasia
16
Q
characterists of hypertrophy
A
- increase cell size
- normal organization
17
Q
characteristics of hyperplasia
A
- increase cell #
- normal organization
18
Q
characteristics of dysplasia
A
disorganized growth
19
Q
characteristics of neoplasia
A
- disorganized growth
- net increase in dividing cells
20
Q
what are the 3 stages of carcinogenesis?
A
- initiation
- promotion
- progression
21
Q
the initiation stage of carcinogenesis constitutes…
A
a mutation
22
Q
as a tumor progresses it increases its
A
growth rate & malignancy
23
Q
what is an examples of tumor progression?
A
colon carcinoma
24
Q
the proliferation of colon epithelial cells give rise to a small benign
A
adenoma/polyp
25
colon selection leads to
- adenoma growth
- increase size
- increase proliferative potential
| malignant carcinoma
26
what are the 8 characteristics of cancer?
1. density-dependent inhibition
2. reduced dependence on GFs
3. abnormal/blocked differentiation
4. reduced cell adhesion
5. angiogenesis
6. protease secretion & metastasis
7. resistance to apoptosis
8. capacity for unlimited replication
27
describe density-dependednt inhibition
- normal cells multiply until they reach an optimal density
- tumor cells continue to proliferate uncontrollably
28
normal fibroblast cell migration is self-limited by
cell contact
| tumor cells are not inhibited by cell contact
29
in leukemic cells differentiation is blocked at a stage where they still have the ability to
continue proliferating
30
what facilitated metastasis?
reduced cell adhesion
31
malignant cells secrete proteases that digest
extracellular matix components allowing invasion into connective tissue, blood vessels, lymphatic ducts
32
resistance to apoptosis is often caused by a
pathway mutation
33
the capacity for unlimited replication is a result of
telomerase expression
34
focus assay takes advantage if what 3 properties of transformed cells?
1. altered morphology
2. loss of contact inhibition
3. loss of density-dependent inhibition
35
list some examples of carcinogens
- UV radiation
- chemical toxins
- mutagens
- tumor promoters
- viruses
36
UV radiation is likely to cause
skin cancer
37
list 4 examples of chemical toxins
1. tobacco
2. asbestos
3. benzenes
4. aflatoxin
38
mutagens damage
DNA
39
list examples of tumor promoters
- phorbol esters
- endocrine disruptors
- hormones
40
what are the steps of tumor viruses in permissive cells
virus replication
cell lysis
release of virus particles
41
what are the steps of tumor viruses in non-permissive cells
virus replication
some cells are permanently transformed
42
80% of human cancers are NOT induced by
viruses
43
what is considered the prototype of a highly oncogenic retrovirus
RSV
44
studies of RSV lead to the
identification of the first viral oncogene
45
what are the 4 things found in RSV genones?
1. virion structural proteins
2. reverse transcriptase integrase
3. envelope glycoproteins
4. Src tyrosone kinase
46
what are the 3 genetic sources of cancer?
- oncogenes
- tumor suppresor genes
- DNA repair genes
47
what are known as the accelorators in cancer
oncogenes
48
what are known as the brakes in cancer?
tumor suppresor genes
49
what are known as the mechanics of cancer?
DNA repair genes
50
oncogenes are normally
growth promoting
51
oncogenes as a normal gene is called
proto-oncogene
52
oncogenes when mutated induce
transformation
53
oncogenes can be
viral or cellular
54
tumor suppressor genes when mutated can NOT arrest
proliferation
| Rb, p53
55
human oncogenes are usually homologous of
viral counterparts
56
oncogenes result from
- single point mutations
- chromosomal translocations
| genes of regulatory mechanisms Ras
57
DNA extracted from human bladder carcinoma induced the
transformation of transfected mouse cells in culture
58
Ras mutants cannot carry out
GTP hydrolysis
| results in constitutively active protein
59
what is the single point mutation of Ras
Gly is substituted for Val
60
oncogenes proteins act as
- GFs (EGF)
- GF receptors (ErbB)
- intracellular signaling molecules (Ras/Raf)
61
Ras/Raf oncogenes constitutively activate the
ERK MAP kinase pathway
62
describe the translocation of c-myc
proto-oncogene is translocated from C8 to the IgH on C14
63
the translocation of c-myc results in
Burkitt's lymphoma
| malignancy of antibody producing B cells
64
Tel/PDGF oncogene encodes a fusion protein where the extra-cellular domain of the normal receptor is replaced by the
Tel transcription factor
65
in Tel/PDGF oncogene activation the helix-loop-helix induces
dimerization of PDGFr & continuous activation of the protein kinase
66
what is the prototype of a tumor suppressor gene
Rb
67
tumor suppressor genes target
cyclin D/Cdk4,6
68
tumor suppresor genes where first identified as the product of a gene responsible for
retinoblastoma
69
unphosphorylated Rb binds to the
E2F transcription factor
70
Rb binding to the E2F transcription factor prevents
- transcription of genes for DNA replication
- passage through the G1 checkpoint into S phase
71
phosphorylated Rb cannot bind
E2F
72
E2F then activates
gene transcription triggering the onset of S phase
73
when retinoblastoma is hereditary the 1st mutation is already present in the
germ line
74
when retinoblastoma is nonhereditary the 1st mutation is present after the
first somatic division
75
what are characteristics of retinoblastoma?
- thickening of optic nerve
- displaced retina
