Exam 1 - Ch. 12 Flashcards
(116 cards)
1
Q
Cancer
A
Is not a tumor
Is an abnormal growth resulting from uncontrolled
proliferation; it serves no physiologic function.
2
Q
Benign tumors
A
Non-cancerous
Are named according to the tissues from which they
arise and include the suffix, -oma
3
Q
Malignant tumors
A
Cancerous tumors
Are named according to the tissues from which they arise
4
Q
Carcinoma in situ (CIS)
A
Are preinvasive epithelial malignant tumors of glandular
or squamous origin
Have not broken through the basement membrane or
invaded the surrounding stroma
Are not malignant
5
Q
Point mutations
A
Small scale changes
6
Q
Driver mutations
A
“Drive” progression of cancer
7
Q
Passenger mutations
A
Random events
8
Q
Gene amplification
A
Repeated duplication of chromosome → 10s or 100s of gene copies
9
Q
Chromosome translocation
A
Large changes in chromosome structure
Piece of one chromosome is translocated to another chromosome
10
Q
Oncogene
A
Mutant gene that would normally direct protein synthesis and cellular growth - contributes to the development of a cancer
11
Q
Clonal proliferation (expansion)
A
Cancer cell progeny can accumulate faster than nonmutant neighbors. It acquires selective advantage over its neighbors
→↑ growth rate or ↓ apoptosis
12
Q
Malignant transformation
A
Is the process during which a normal cell becomes a cancer cell
13
Q
T OR F: Cancer cells are heterogeneous
A
TRUE
Cancer heterogeneity: due to proliferation and mutation
14
Q
Proto-oncogenes
A
Normal nonmutant genes that code for cellular growth
15
Q
Tumor-suppressor genes
A
Encode proteins that normally negatively regulate proliferation
anti-oncogenes
16
Q
Activation of proto-oncogenes
A
hyperactivity of oncogenes
17
Q
Mutation
A
loss or inactivity of tumor-suppressor genes
overexpression of products that prevent apoptosis, thus allowing continued growth of tumors
18
Q
Growth factor signaling in cancer - Receptors
A
RAS
PI3K
MYC
D cyclins
Are oncoproteins that are activated by mutations in various cancers
19
Q
retinoblastomaprotein(Rb)
A
RB is mutated in childhood retinoblastoma, and in many lung, breast, and bone cancers.
20
Q
Mutation in the TP53 gene (tumor-suppressor gene)
A
“P53 protein is the guardian of the genome”
It monitors intracellular signals related to stress and
activates caretaker genes.
Mutation → Suppression of normal apoptosis.
21
Q
Caretaker genes
A
Maintain genomic integrity.
• Encode proteins that are involved in DNA repair:
• errors in DNA replication
• mutations caused by UVR or ionizing radiation
mutations caused by chemicals and drugs.
22
Q
Genomic Instability
A
- Loss of function of caretaker genes.
- Epigenetic silencing or modulation of gene function.
- Gene expression networks can be regulated by changes in miRNAs (miRs) and ncRNAs.
23
Q
Oncomirs
A
miRs that stimulate cancer development and progression. miRs ↓ the stability and expression of other genes by pairing with mRNA.
24
Q
BRCA1 and BRCA2
A
tumor-suppressors and caretaker genes that repair double-stranded DNA breaks
25
Causes↑↑ risk of breast cancer in both women and men, and ovarian or prostate cancers
Inherited mutations in BRCA1 and BRCA2
26
Chromosome instability (CIN) ↑ in malignant cells may be due to
malfunctions in the cellular machinery that regulates chromosomal segregation at mitosis.
27
Telomeres
protective caps on each chromosome that are held in place by a telomerase
28
T OR F: Cancer cells can activate telomeres
TRUE
→continued division
29
Cancer Metabolism
Cancer cells perform glycolysis
Allows lactate and its metabolites to be used for the more efficient production of lipids and other molecular building blocks needed for rapid cell growth
30
Warburg effect
is the use of glycolysis under normal oxygen conditions
31
Reverse Warburg effect
cancer cells generate large amounts of ATP→
oxidative stress → manipulate and destroy “cancer associated fibroblasts” → secrete metabolites and components → grow cancer cells
32
Chronic inflammation
an important factor in the development of cancer.
Active inflammation predisposes a person to cancer.
By stimulating a wound-healing response that includes proliferation and new blood vessel growth
33
Examples of inflammation as a cause for cancer
Those with ulcerative colitis for 10 years or more have up to a 30-fold ↑ in developing colon cancer.
Hepatitis B (HBV) or hepatitis C (HCV) ↑ the risk of liver cancer.
H. pylori ↑ the risk of stomach cancer.
34
tumor-associated macrophage (TAM)
the key cell that promotes tumor survival
* Blocks cytotoxic T cell and NK cell functions.
* Produces cytokines that help tumor growth and spread.
* Secretes angiogenesis factors.
35
Tumor associated antigens
oncogenes, antigens from oncogenic viruses, oncofetal antigens, and altered glycoproteins and glycolipids
36
Active immunotherapy
Immunization with tumor antigens to elicit or enhance the immune response against a particular cancer
37
Passive immunotherapy
Injecting the patient diagnosed with cancer with antibodies or lymphocytes directed against the tumor-ssociated antigens
38
Cancer invasion
Local spread
• Is a prerequisite for metastasis and the first step in the metastatic process.
Cancer often spreads first to regional lymph nodes through the lymphatic system
39
Metastasis
the spread of cancer cells from the site of the
| original tumor to distant tissues and organs through the body.
40
Metastasis process
Cancer cells secrete protease→ digest the extracellular matrix and basement membranes → create pathways through which cells can move.
• Metastatic cells must be able to withstand the physiologic stresses of travel in the blood and lymphatic circulation.
41
Epithelial-mesenchymal transition (EMT)
a process by which epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell type
42
Paraneoplastic syndromes
Symptom complexes are triggered by a cancer but are not caused by direct local effects of the tumor mass.
43
Cachexia
the most severe form of malnutrition.
| → protein-calorie malnutrition and progressive wasting.
44
Diagnosing and staging of cancer involves
The size of the tumor, the degree to which it has invaded, and the extent of the spread.
45
Stage 1
Is confined to its organ of origin
46
Stage 2
Is locally invasive
47
Stage 3
Has advanced to regional structures.
48
Stage 4
Has spread to distant sites.
49
Tumor Markers
• Are substances produced by benign or malignant cells.
* Hormones • Enzymes • Genes
* Antigens
* Antibodies
50
Tumor markers are used to
screen and identify individuals at high risk for cancer.
diagnose specific types of tumors.
follow the clinical course of cancer.
51
Palliative Surgery
indicated for the relief of symptoms
52
Prophylactic surgery
selected high-risk diseases:
• Mutations of the APC gene have close to a 100% lifetime risk of colon cancer: Colectomy.
• Women with BRCA1/2 mutations have a significantly ↑ risk of breast and ovarian cancer: Prophylactic mastectomy or bilateral salpingo-oophorectomy or both.
53
Radiation Therapy
Is used to kill cancer cells while minimizing the damage to normal structures.
54
Ionizing radiation
Damages cells by imparting enough ionizing radiation to cause molecular damage to the DNA.
Causes irreversible damage to normal cells.
Lifetime radiation dose
55
Brachytherapy
Radiation therapy where Seeds are implanted
56
Induction chemotherapy
Causes shrinkage or the disappearance of
| tumors
57
Adjuvant chemotherapy
Is administered after the surgical excision with
| a goal of eliminating micrometastases
58
Neoadjuvant chemotherapy
Is administered before localized (surgical or radiation) treatment.
59
# Ch. 12 reverse
Is not a tumor
Is an abnormal growth resulting from uncontrolled
proliferation; it serves no physiologic function.
Cancer
60
# Ch. 12 reverse
Non-cancerous
Are named according to the tissues from which they
arise and include the suffix, -oma
Benign tumors
61
# Ch. 12 reverse
Cancerous tumors
Are named according to the tissues from which they arise
Malignant tumors
62
# Ch. 12 reverse
Are preinvasive epithelial malignant tumors of glandular
or squamous origin
Have not broken through the basement membrane or
invaded the surrounding stroma
Are not malignant
Carcinoma in situ (CIS)
63
# Ch. 12 reverse
Small scale changes
Point mutations
64
# Ch. 12 reverse
“Drive” progression of cancer
Driver mutations
65
# Ch. 12 reverse
Random events
Passenger mutations
66
# Ch. 12 reverse
Repeated duplication of chromosome → 10s or 100s of gene copies
Gene amplification
67
# Ch. 12 reverse
Large changes in chromosome structure
Piece of one chromosome is translocated to another chromosome
Chromosome translocation
68
# Ch. 12 reverse
Mutant gene that would normally direct protein synthesis and cellular growth - contributes to the development of a cancer
Oncogene
69
# Ch. 12 reverse
Cancer cell progeny can accumulate faster than nonmutant neighbors. It acquires selective advantage over its neighbors
→↑ growth rate or ↓ apoptosis
Clonal proliferation (expansion)
70
# Ch. 12 reverse
Is the process during which a normal cell becomes a cancer cell
Malignant transformation
71
# Ch. 12 reverse
TRUE
Cancer heterogeneity: due to proliferation and mutation
T OR F: Cancer cells are heterogeneous
72
# Ch. 12 reverse
Normal nonmutant genes that code for cellular growth
Proto-oncogenes
73
# Ch. 12 reverse
Encode proteins that normally negatively regulate proliferation
anti-oncogenes
Tumor-suppressor genes
74
# Ch. 12 reverse
hyperactivity of oncogenes
Activation of proto-oncogenes
75
# Ch. 12 reverse
loss or inactivity of tumor-suppressor genes
overexpression of products that prevent apoptosis, thus allowing continued growth of tumors
Mutation
76
# Ch. 12 reverse
RAS
PI3K
MYC
D cyclins
Are oncoproteins that are activated by mutations in various cancers
Growth factor signaling in cancer - Receptors
77
# Ch. 12 reverse
RB is mutated in childhood retinoblastoma, and in many lung, breast, and bone cancers.
retinoblastomaprotein(Rb)
78
# Ch. 12 reverse
“P53 protein is the guardian of the genome”
It monitors intracellular signals related to stress and
activates caretaker genes.
Mutation → Suppression of normal apoptosis.
Mutation in the TP53 gene (tumor-suppressor gene)
79
# Ch. 12 reverse
Maintain genomic integrity.
• Encode proteins that are involved in DNA repair:
• errors in DNA replication
• mutations caused by UVR or ionizing radiation
mutations caused by chemicals and drugs.
Caretaker genes
80
# Ch. 12 reverse
1. Loss of function of caretaker genes.
2. Epigenetic silencing or modulation of gene function.
3. Gene expression networks can be regulated by changes in miRNAs (miRs) and ncRNAs.
Genomic Instability
81
# Ch. 12 reverse
miRs that stimulate cancer development and progression. miRs ↓ the stability and expression of other genes by pairing with mRNA.
Oncomirs
82
# Ch. 12 reverse
tumor-suppressors and caretaker genes that repair double-stranded DNA breaks
BRCA1 and BRCA2
83
# Ch. 12 reverse
Inherited mutations in BRCA1 and BRCA2
Causes↑↑ risk of breast cancer in both women and men, and ovarian or prostate cancers
84
# Ch. 12 reverse
May be due to malfunctions in the cellular machinery that regulates chromosomal segregation at mitosis.
Chromosome instability (CIN) ↑ in malignant cells
85
# Ch. 12 reverse
protective caps on each chromosome that are held in place by a telomerase
Telomeres
86
# Ch. 12 reverse
TRUE
→continued division
T OR F: Cancer cells can activate telomeres
87
# Ch. 12 reverse
Cancer cells perform glycolysis
Allows lactate and its metabolites to be used for the more efficient production of lipids and other molecular building blocks needed for rapid cell growth
Cancer Metabolism
88
# Ch. 12 reverse
is the use of glycolysis under normal oxygen conditions
Warburg effect
89
# Ch. 12 reverse
cancer cells generate large amounts of ATP→
oxidative stress → manipulate and destroy “cancer associated fibroblasts” → secrete metabolites and components → grow cancer cells
Reverse Warburg effect
90
# Ch. 12 reverse
an important factor in the development of cancer.
Active inflammation predisposes a person to cancer.
By stimulating a wound-healing response that includes proliferation and new blood vessel growth
Chronic inflammation
91
# Ch. 12 reverse
Those with ulcerative colitis for 10 years or more have up to a 30-fold ↑ in developing colon cancer.
Hepatitis B (HBV) or hepatitis C (HCV) ↑ the risk of liver cancer.
H. pylori ↑ the risk of stomach cancer.
Examples of inflammation as a cause for cancer
92
# Ch. 12 reverse
the key cell that promotes tumor survival
* Blocks cytotoxic T cell and NK cell functions.
* Produces cytokines that help tumor growth and spread.
* Secretes angiogenesis factors.
tumor-associated macrophage (TAM)
93
# Ch. 12 reverse
oncogenes, antigens from oncogenic viruses, oncofetal antigens, and altered glycoproteins and glycolipids
Tumor associated antigens
94
# Ch. 12 reverse
Immunization with tumor antigens to elicit or enhance the immune response against a particular cancer
Active immunotherapy
95
# Ch. 12 reverse
Injecting the patient diagnosed with cancer with antibodies or lymphocytes directed against the tumor-ssociated antigens
Passive immunotherapy
96
# Ch. 12 reverse
Local spread
• Is a prerequisite for metastasis and the first step in the metastatic process.
Cancer often spreads first to regional lymph nodes through the lymphatic system
Cancer invasion
97
# Ch. 12 reverse
the spread of cancer cells from the site of the
| original tumor to distant tissues and organs through the body.
Metastasis
98
# Ch. 12 reverse
Cancer cells secrete protease→ digest the extracellular matrix and basement membranes → create pathways through which cells can move.
• Metastatic cells must be able to withstand the physiologic stresses of travel in the blood and lymphatic circulation.
Metastasis process
99
# Ch. 12 reverse
a process by which epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell type
Epithelial-mesenchymal transition (EMT)
100
# Ch. 12 reverse
Symptom complexes are triggered by a cancer but are not caused by direct local effects of the tumor mass.
Paraneoplastic syndromes
101
# Ch. 12 reverse
the most severe form of malnutrition.
| → protein-calorie malnutrition and progressive wasting.
Cachexia
102
# Ch. 12 reverse
Involves the size of the tumor, the degree to which it has invaded, and the extent of the spread.
Diagnosing and staging of cancer
103
# Ch. 12 reverse
Is confined to its organ of origin
Stage 1
104
# Ch. 12 reverse
Is locally invasive
Stage 2
105
# Ch. 12 reverse
Has advanced to regional structures.
Stage 3
106
# Ch. 12 reverse
Has spread to distant sites.
Stage 4
107
# Ch. 12 reverse
• Are substances produced by benign or malignant cells.
* Hormones • Enzymes • Genes
* Antigens
* Antibodies
Tumor Markers
108
# Ch. 12 reverse
used to screen and identify individuals at high risk for cancer.
diagnose specific types of tumors.
follow the clinical course of cancer.
Tumor markers are
109
# Ch. 12 reverse
indicated for the relief of symptoms
Palliative Surgery
110
# Ch. 12 reverse
selected high-risk diseases:
• Mutations of the APC gene have close to a 100% lifetime risk of colon cancer: Colectomy.
• Women with BRCA1/2 mutations have a significantly ↑ risk of breast and ovarian cancer: Prophylactic mastectomy or bilateral salpingo-oophorectomy or both.
Prophylactic surgery
111
# Ch. 12 reverse
Is used to kill cancer cells while minimizing the damage to normal structures.
Radiation Therapy
112
# Ch. 12 reverse
Damages cells by imparting enough ionizing radiation to cause molecular damage to the DNA.
Causes irreversible damage to normal cells.
Lifetime radiation dose
Ionizing radiation
113
# Ch. 12 reverse
Radiation therapy where Seeds are implanted
Brachytherapy
114
# Ch. 12 reverse
Causes shrinkage or the disappearance of
| tumors
Induction chemotherapy
115
# Ch. 12 reverse
Is administered after the surgical excision with
| a goal of eliminating micrometastases
Adjuvant chemotherapy
116
# Ch. 12 reverse
Is administered before localized (surgical or radiation) treatment.
Neoadjuvant chemotherapy
