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COM MOD 2 > Chapter 7 Key Concepts > Flashcards

Chapter 7 Key Concepts Flashcards

1
Q

Factors that distinguish benign from malignant tumors (4)

A

Degree of differentiation
Rate of Growth
Local invasiveness
Distant Spread

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2
Q

Appearance of benign tumors

A

resemble tissue of origin and are well differentiated

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3
Q

Appearance of malignant tumors

A

less well differentiated or completely undifferentiated (anaplastic)

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4
Q

Functionality of benign tumors

A

retain functions of cells of origin

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5
Q

Functionality of malignant tumors

A

acquire unexpected functions due to derangements in differentiation

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6
Q

Growth of benign tumors

A

slow growing

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7
Q

Growth of malignant tumors

A

grow faster

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8
Q

Structure of benign tumors

A

circumscribed and have a capsule

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9
Q

Structure of malignant tumors

A

poorly circumscribed and invade surrounding normal tissues

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10
Q

Localization of benign tumors

A

remain localized at the site of origin

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11
Q

Localization of malignant tumors

A

metastasize to distant sites

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12
Q

Factors that influence epidemiology of cancer (4)

A

geography, age, race, genetic background

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13
Q

Age when cancer is most common

A

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

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14
Q

Geographic influence on cancers

A

mainly stem from different environmental factors

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15
Q

Important environmental factors in carcinogens (7)

A 
infectious agents
smoking
alcochol
diet
obesity 
reproductive history
exposure to environmental factors
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16
Q

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

A

chronic inflammation
tissue injury
hyperplasia
immunodeficiency

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17
Q

Environmental and genetic influence on cancer

A

important determinants of cancer risk

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18
Q

Proto-oncogenes

A

normal cellular genes whose products promote cell proliferation

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19
Q

Oncogenes

A

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

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20
Q

Oncoprotein

A

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

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21
Q

Expression of growth factors and growth factor receptors

A

set up autocrine signaling loop

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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

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23
Q

EGF receptor tyrosine kinase

A

lung cancer by point mutations

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24
Q

HER2 receptor tyrosine kinase

A

breast cancer by gene amplification

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25
Q

JAK2 tyrosine kinase

A

myeloproliferative disorders by point mutations

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26
Q

ABL nonreceptor tyrosine kinase

A

chronic myelogenous leukemia, acute lymphoblastic leukemia by chromosomal translocation and creation of BCR-ABL fusion gene

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27
Q

RAS

A

many cancer by point mutation

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28
Q

PI3K and BRAF serine/threonine kinases

A

many cancers by point mutations

29
Q

Mechanism for Burkitt lymphoma and some hematologic malignancies

A

increased expression of MYC

30
Q

MYC

A

master transcription factor that regulates genes needed for rapid cell growth by deregulation through chromosomal translocation

31
Q

Mechanism for neuroblastoma

A

gene amplification

32
Q

Mutations that increase CDK4/cyclin D complexes

A

promote cell cycle progression

33
Q

RB when hypophosphorylated

A

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
Q

Cause of RB hyperphosphorylation

A

normal growth factor signaling

causing inactivation and promoting cell cycle progression

35
Q

Mechanism of antiproliferative effect of RB (4)

A

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
Q

Function of p53 protein (5)

A

Monitor of stress in cell
Controls the expression and activity of proteins involved in cell cycle arrest, DNA repair, cellular senescence, and apoptosis

37
Q

What activates p53 (3)

A

Anoxia
Inappropriate signaling by mutated oncoproteins
DNA damage

38
Q

What senses DNA damage

A

complexes containing kinases of the ATM/ATR family

39
Q

ATM/ATR family kinases

A

phosphorylate p53

40
Q

Active p53

A

upregulates expression of proteins and cause cell-cycle arrest at the G1-S checkpoint allowing for time to repair

41
Q

Proteins expressed with active p53

A

cyclin-dependent kinase inhibitor p21

42
Q

What if DNA damage cannot be repaired?

A

p53 induces celular senescence or apoptosis

43
Q

TP53 in the majority of human cancers

A

show biallelic loss-of-function mutation in TP53

44
Q

Li-Fraumeni syndrome

A

inherit one defective copy of Tp53 and are at high risk for cancers

45
Q

Virus and p53

A

p53 is inactivated by viral oncoproteins such as E6 protein of HPV

46
Q

APC

A

encodes a factor that negatively regulates the WNT pathways in colonic epithelium by promoting formation of a complex that degrades b-catenin

47
Q

VHL

A

encodes component of ubiquitin ligase that is responsible for degradation of hypoxia-induced factors (HIP)

48
Q

BCR-ABL fusion gene

A

involved in chromosomal translocation in chronic myelogenous leukemia

49
Q

Mutated Familial adenomatous polyposis

A

autosomal dominant disorder
loss of a single normal APC allele
associated with development of colonic polyps and early colon carcinoma

50
Q

Sporadic colon carinomas

A

tumor development

biallelic defects in APC

51
Q

Hypoxia-induces factors (HIP)

A

transcription factors that alter gene expression in response to hypoxia

52
Q

von Hippel-Lindau syndrome

A

autosomal dominant disorder
germline loss-of function mutation of VHL
high risk of renal cell carcinoma and phenochromocytoma

53
Q

Sporadic renal cell carincoma

A

acquired biallelic loss-of mutation

54
Q

Controlling vascularization of tumor cells

A

balance between angiogenic and anti-angiogenic factors that are produced by tumor and stromal cells

55
Q

What triggers angiogenesis?

A

hypoxia through HIF-1a on proangiogenic factor VEGF

56
Q

Factors that regulate angiogenesis (4)

A

p53- induce synthesis of angiogenesis inhibitory thombospondin-1
RAS, MYC, MAPK upregulate VEGF and stimulate angiogenesis

57
Q

Use for VEGF inhibitors

A

treat advanced cancers and prolong clinical course but are not curative

58
Q

4 steps of ability to invade tissues

A
  1. loosening of cell-cell contacts
  2. degradation of ECM
  3. attachment of ECM components
  4. migration of tumor cells
59
Q

How are cell-cell contacts lost?

A

inactivation of E-cadherin

60
Q

How is basement membrane and interstitial matrix degradation mediated?

A

proteolytic enzymes secreted by tumor cells and stromal cells such as matalloproteases and cathepsins

61
Q

Functions of proteolytic enzymes (2)

A

Breakdown basement membrane and interstitial matrix

Release growth factors in ECM and generate chemotactic and angiogenic fragments from ECM glycoproteins

62
Q

How to predict the metastatic site of tumors?

A

location of primary tumor

*many tumors arrest in first capillary bed they encounter

63
Q

Most common first capillary beds that tumors encounter?

A

liver and lung

64
Q

Organ Tropism

A

a specific pattern for the metastatic spread of a cancer

65
Q

Genes that promote epithelial-mesenchymal transitions

A

important in metastasis genes in epithelial tumors

ex. TWIST and SNAIL

66
Q

Tumor cells and immune system

A

tumor cells can recognize immune system as non-self and destroy it

67
Q

What mediates antitumor activity?

A

cell-mediated mechanisms- tumor antigens are presenting on MHC I and recognized by CD8 CTLs

68
Q

Products of different classes of tumor antigens (7)

A

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
Q

How can the tumor avoid the immune system in immunocompetent patients? (3)

A

Selective outgrowth of antigen-negative variants
Loss or reduced expression of HLAs
Immunosuppression mediated by TGFb, PD-1L, galectins

COM MOD 2 (9 decks)

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