Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

COM MOD 2 > Chapter 7 Key Concepts > Flashcards

Chapter 7 Key Concepts Flashcards

(69 cards)

Start Studying
1
Q

Factors that distinguish benign from malignant tumors (4)

A

Degree of differentiation
Rate of Growth
Local invasiveness
Distant Spread

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

Appearance of benign tumors

A

resemble tissue of origin and are well differentiated

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

Appearance of malignant tumors

A

less well differentiated or completely undifferentiated (anaplastic)

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

Functionality of benign tumors

A

retain functions of cells of origin

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

Functionality of malignant tumors

A

acquire unexpected functions due to derangements in differentiation

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

Growth of benign tumors

A

slow growing

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

Growth of malignant tumors

A

grow faster

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

Structure of benign tumors

A

circumscribed and have a capsule

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

Structure of malignant tumors

A

poorly circumscribed and invade surrounding normal tissues

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

Localization of benign tumors

A

remain localized at the site of origin

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

Localization of malignant tumors

A

metastasize to distant sites

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

Factors that influence epidemiology of cancer (4)

A

geography, age, race, genetic background

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

Age when cancer is most common

A

older than 60 years of age but can occur in adults, children, and infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Geographic influence on cancers

A

mainly stem from different environmental factors

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

Important environmental factors in carcinogens (7)

A 
infectious agents
smoking
alcochol
diet
obesity 
reproductive history
exposure to environmental factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can cause increased risk of cancer due to reparative proliferations? (4)

A

chronic inflammation
tissue injury
hyperplasia
immunodeficiency

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

Environmental and genetic influence on cancer

A

important determinants of cancer risk

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

Proto-oncogenes

A

normal cellular genes whose products promote cell proliferation

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

Oncogenes

A

Mutated or overexpressed versions of proto-oncogenes that function autonomously
Lost dependence on normal growth promoting signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Oncoprotein

A

protein encoded by an oncogene that drives increased cell proliferation through one of several mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Expression of growth factors and growth factor receptors

A

set up autocrine signaling loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What constitutive signaling do mutations in growth factor receptors, non-receptor tyrosine kinases, or downstream signaling molecules lead to? (6)

A

Activation of EGF receptor tyrosine kinase
Activation of HER2 receptor tyrosine kinase
Activation of JAK2 tyrosine kinase
Activation of ABL nonreceptor tyrosine kinase
Activation of RAS by point muation
Activation of PI3K and BRAF serine/threonine kinases

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

EGF receptor tyrosine kinase

A

lung cancer by point mutations

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

HER2 receptor tyrosine kinase

A

breast cancer by gene amplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
JAK2 tyrosine kinase
myeloproliferative disorders by point mutations
26
ABL nonreceptor tyrosine kinase
chronic myelogenous leukemia, acute lymphoblastic leukemia by chromosomal translocation and creation of BCR-ABL fusion gene
27
RAS
many cancer by point mutation
28
PI3K and BRAF serine/threonine kinases
many cancers by point mutations
29
Mechanism for Burkitt lymphoma and some hematologic malignancies
increased expression of MYC
30
MYC
master transcription factor that regulates genes needed for rapid cell growth by deregulation through chromosomal translocation
31
Mechanism for neuroblastoma
gene amplification
32
Mutations that increase CDK4/cyclin D complexes
promote cell cycle progression
33
RB when hypophosphorylated
exerts antiproliferative effects by binding and inhibiting E2F transcription factors that regulate genes required for cells to pass through G1/S phase cell cycle checkpoint *inhibits cell cycle progression
34
Cause of RB hyperphosphorylation
normal growth factor signaling | causing inactivation and promoting cell cycle progression
35
Mechanism of antiproliferative effect of RB (4)
Loss of function mutation affecting RB Gene amplification of CDK4 and cyclin D genes Loss of cyclin-dependent kinase inhibitors (p16/INK4) Viral oncoproteins tat bind and inhibit RB (E7 protein of HPV)
36
Function of p53 protein (5)
Monitor of stress in cell Controls the expression and activity of proteins involved in cell cycle arrest, DNA repair, cellular senescence, and apoptosis
37
What activates p53 (3)
Anoxia Inappropriate signaling by mutated oncoproteins DNA damage
38
What senses DNA damage
complexes containing kinases of the ATM/ATR family
39
ATM/ATR family kinases
phosphorylate p53
40
Active p53
upregulates expression of proteins and cause cell-cycle arrest at the G1-S checkpoint allowing for time to repair
41
Proteins expressed with active p53
cyclin-dependent kinase inhibitor p21
42
What if DNA damage cannot be repaired?
p53 induces celular senescence or apoptosis
43
TP53 in the majority of human cancers
show biallelic loss-of-function mutation in TP53
44
Li-Fraumeni syndrome
inherit one defective copy of Tp53 and are at high risk for cancers
45
Virus and p53
p53 is inactivated by viral oncoproteins such as E6 protein of HPV
46
APC
encodes a factor that negatively regulates the WNT pathways in colonic epithelium by promoting formation of a complex that degrades b-catenin
47
VHL
encodes component of ubiquitin ligase that is responsible for degradation of hypoxia-induced factors (HIP)
48
BCR-ABL fusion gene
involved in chromosomal translocation in chronic myelogenous leukemia
49
Mutated Familial adenomatous polyposis
autosomal dominant disorder loss of a single normal APC allele associated with development of colonic polyps and early colon carcinoma
50
Sporadic colon carinomas
tumor development | biallelic defects in APC
51
Hypoxia-induces factors (HIP)
transcription factors that alter gene expression in response to hypoxia
52
von Hippel-Lindau syndrome
autosomal dominant disorder germline loss-of function mutation of VHL high risk of renal cell carcinoma and phenochromocytoma
53
Sporadic renal cell carincoma
acquired biallelic loss-of mutation
54
Controlling vascularization of tumor cells
balance between angiogenic and anti-angiogenic factors that are produced by tumor and stromal cells
55
What triggers angiogenesis?
hypoxia through HIF-1a on proangiogenic factor VEGF
56
Factors that regulate angiogenesis (4)
p53- induce synthesis of angiogenesis inhibitory thombospondin-1 RAS, MYC, MAPK upregulate VEGF and stimulate angiogenesis
57
Use for VEGF inhibitors
treat advanced cancers and prolong clinical course but are not curative
58
4 steps of ability to invade tissues
1. loosening of cell-cell contacts 2. degradation of ECM 3. attachment of ECM components 4. migration of tumor cells
59
How are cell-cell contacts lost?
inactivation of E-cadherin
60
How is basement membrane and interstitial matrix degradation mediated?
proteolytic enzymes secreted by tumor cells and stromal cells such as matalloproteases and cathepsins
61
Functions of proteolytic enzymes (2)
Breakdown basement membrane and interstitial matrix | Release growth factors in ECM and generate chemotactic and angiogenic fragments from ECM glycoproteins
62
How to predict the metastatic site of tumors?
location of primary tumor | *many tumors arrest in first capillary bed they encounter
63
Most common first capillary beds that tumors encounter?
liver and lung
64
Organ Tropism
a specific pattern for the metastatic spread of a cancer
65
Genes that promote epithelial-mesenchymal transitions
important in metastasis genes in epithelial tumors | ex. TWIST and SNAIL
66
Tumor cells and immune system
tumor cells can recognize immune system as non-self and destroy it
67
What mediates antitumor activity?
cell-mediated mechanisms- tumor antigens are presenting on MHC I and recognized by CD8 CTLs
68
Products of different classes of tumor antigens (7)
Mutated proto-oncogenes Tumor suppressor genes Overexpressed or aberrantly expressed proteins Tumor antigens produced by viruses Oncofetal antigens Altered glycolipids and glycoproteins Cell type-specific differentiation antigens
69
How can the tumor avoid the immune system in immunocompetent patients? (3)
Selective outgrowth of antigen-negative variants Loss or reduced expression of HLAs Immunosuppression mediated by TGFb, PD-1L, galectins

COM MOD 2 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions