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Pathology Final > Lecture 10 - Neoplasia > Flashcards

Lecture 10 - Neoplasia Flashcards

1
Q

a hallmark to cancer is growth signal autonomy.
what is this mediated by and what does it mean?

A

cancer cells can divide WITHOUT the normal external signals required for division

mediated by mutated ONCOGENES

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2
Q

a hallmark of cancer is insensitivty to grwoth inhibitory signals

this is an issue with what?

A

issue with tumor suppressor genes

cancer cells unaffected by inhibitory growth signals

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3
Q

evasion of PCD is a hallmark of cancer

what does this mean

A

pcd = programmed cell death (apoptosis)

in normal cells, excessive DNA damage would induce apoptosis, but not in cancer cells

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4
Q

relate cancer cells to cellular senescence

A

normal cells reduce the length of their telomeres with new division

cancer cells maintain the length of their telomeres

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5
Q

relate angiogenesis to cancer cells

A

sustained angiogenesis is a hallmark of cancer bc most cancer cells require the growth of new blood vessels in the tumo

the normal inhibitory and stimulatory signals are not required in cancer cells

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6
Q

explain the migration of normal cells and of cancer cells

A

normal cells generally do NOT migrate (except in embryo development)

cancer cells invade other tissue and other organs (metastasi)

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7
Q

explain the metabolic pathways of cancer cells

A

they use abnormal metabolism to satisfy a high demand for energy and nutrients

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8
Q

true or false

cancer cells are able to avoid the immune system

A

true

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9
Q

severe ______ abnormalities are found in most cancers

A

chromosomal

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10
Q

relate inflammation to cancer

A

local chronic inflammation is associated with many types of cancer

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11
Q

what is a Ras protein

A

transmits growth signals

if mutated, can be an oncogene bc there is continuous stimulation of cell prolferation

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12
Q

name 4 potential oncogenes

A

Myc
Ras
Fos and Jun
Androgen and Estrogen receptors

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13
Q

explai what Myc is

A

a gene (oncogene) that is involved in cellular proliferation and energy production. can facilitate tumor cell invasion. can also activate cell death

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14
Q

explain how Fos and Jun are oncogenes

A

they produce AP-1 which binds to DNA

this allows the cancer cells to proliferate and metastise and perform angiogenesis for their survival

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15
Q

explain how androgen and estrogen receptors can be oncogenes

A

they are both receptors as well as transcription factors

that allow cell proliferation, and are involved in breast tumorigenesis and prostate tumorigenesis

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16
Q

what 2 things allow the cell to progress through the cell cycle and perform mitosis and thus drive cell proliferation?

A

CDK (cyclin dependent kinases)
and cyclin

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17
Q

how many key checkpoints are there in the cell cycle?

A

1-4

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18
Q

how are the cyclins activated?
what happens when the cyclins are activated?

A

cyclins are activated when the cell receives signals from growth factors, cytokines, etc

triggers cell proliferations and expression of genes that PROMOTE progression through the cell cycle and cell division is promoted

protooncogenes increased to promote cell cycle progression

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19
Q

what can INHIBIT cyclins?
what happens when cyclins are inhibited?

A

DNA damage, DNA replication errors, oxidant injury can inhibit the cyclins

p53 may be activated (tumor suppressor gene)

CKIs (cyclin kinase inhibitors) are activated:

INK proteins activated
Cip/Kip
Rb proteins

all activated to BLOCK CELL CYCLE PROGRESSIOn to prevent the proliferation of cells that have damaged DNA and prevent a tumor from forming

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20
Q

name 5 inhibitors of the cell cycle that are induced when DNA damage occurs

A

p53
CKI’s (cyclin kinase inhibitors) which are:
Kip/Cip
Rb families
INK

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21
Q

what are the 3 major families of CKIs

A

INK4
Cip/Kip proteins
Rb families

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22
Q

INK4 proteins bind and block….

A

CDKs 4, 6

and block the cell cycle from progressing into G1

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23
Q

Cip/Kip proteins bind and block…..

A

CDK2
CDK1

take up where INK4 left off and inhibits rest of the cell cycle

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24
Q

Rb family members inhibit….

A

CDK2

bind E2F transcription factors, which drive entry and transit through the S phase of the cell cycle by triggering Cyclins A and E

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25
Q

what are the 4 stages of the cell cycle

A

G1
S
G2
M

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26
Q

what is E2F?

A

a family of transcription factors that drives the cell to proliferate through the transcription of cyclins A and E

it is inhibited by the Rb family of proeins

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27
Q

true or false

E2F pushes the cell to proliferate

A

true - when not bound to Rb

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28
Q

what liberates E2F from Rb?
what does this cause?

A

CDK 2,4,6, and cyclins D and E double phosphorylates Rb

causes the cell cycle to progress bc E2F is liberated

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29
Q

NORMALLY, with no cell damage, p53 is kept at ___ levels

A

low

30
Q

explain the condition of p53 under normal cell conditions

A

is polyubiquinated by E3 ubiquitin ligase and is thus degraded by proteasomes

not a lot can be detected in normal cells

31
Q

explain what happens to p53 when DNA is damaged or DNA replication is stalled

A

protein kinases ATM and ATR recognize this damage and work with CHk1 and Chk2 to PHOSPHORYLATE P53

when phosphorylated, p53 dissociates from MDM2 (the E3 ubiquitin ligase) and goes to the nucleus where it promotes cell cycle arrest through increasing producion of one of the members of the Cip/Kip family of CKIs (cyclin kinase inhibitors)

32
Q

after p53 has translocated to the nucleus and blocked cell cycle progression, what happens if the DNA is repaired?
what happens if it’s not repaired?

A

if repaired, the block is removed and cell cycle proceeds

if cannot be repaired, p53 triggers apoptosis

33
Q

what is PTEN

A

a tumor suppressor gene

34
Q

true or false

inhibitors of cyclins are tumor suppressor genes

A

TRUE - bc they block cell cycle from happening when DNA is damaged

35
Q

what will happen if the activity of PTEN is decreased?

A

tumor genesis is promoted

36
Q

explain cellular senescence and how it relates to cancer

A

normally, progressive mitoses causes the telomeres to shorten and p53 and Rb cause apoptosis after repeated cycles

in a cancer cell, the telomeres do not shorten with each division but instead get weaker and weaker and eventually control of the cell cycle is lost, ends of chromosomes are uncapped and thus UNSTABLE to produce a polyp, (benign).

this can survive to produce a malignant tumor by activating telomerases

37
Q

name a potential anti cancer drug that is related to cellular senescence

A

a drug that inhibits telomerases can prevent a benign tumor from becoming malignant

bc premalignant cells survive by activating telomerases

38
Q

what is VEGF

A

vascular endothelial growth factor - stimulates the formation of new blood vessles

39
Q

explain VEGF-stimulated tumor angiogenesis

A

increased oncogene expression and decreased tumor suppressor activity results in increased VEGF

these VEGF’s bind and activate VEGF receptors.

VEGFs also stimulate the endothelial cells to make filopodia and produce ECM proteases so that they can migrate through the ECM

binding to VEGF receptors stimulates the recruitment of pericytes which stabilize the newly formed blood vessels and limits the installation of basement membrane

the new vessel is leaky, and provides oxygen and nutrients less effectively. the vessel makes invasion and metastasis easier

40
Q

name a potential kind of drug that can stop cancer progression, related to angiogenesis

A

create a drug that inhibits VEGF to prevent the formation of new blood vessels that promote metastasis

41
Q

differentiate between normal physiologic blood vessel formation and tumor blood vessel formation

A

normal - no gaps

tumor - many gaps to allow cancer cells to circulate easily

tumor cells pose as endothelial cells

42
Q

true or false

normal cells do not typically migrate

A

true - (except embyronic development)

cancer cells do migrate and invade other tissues

43
Q

explain the process of tumor invasion and metastasis

A

-acquire the ability to bind ECM

-crosses the basement membrane through undergoing EMT (epithelial-mesenchymal transition)

-tumor cells produce proteolytic enzymes to degrade the ECM

-tumjor cells move through ECM and penetrate blood vessels and lymphatics by secreting kinases that increase the permeability or proteases to degrade

–some tumor cells exit the vessels and establish micrometastases at a site of the body that grows into a metastatic tumor

44
Q

what is extravasation

A

trans-endothelial migration

45
Q

how can circulating tumor cells survive in the blood?

A

NK cells try to destroy them, but…

-these NK cells may be inhibited by neutrophils

-the tumor cells may be covered in platelets which protects them from being recognized by the NK cells

46
Q

what are MMPs and how are they related to cancer progression

A

matrix metalloproteinases

allow extravasation of cancer cells from the blood vessels and into the surrounding tissue

47
Q

true or false

metabolism is not very different in cancer cells compared to normal cells

A

false - it is

48
Q

cancer cells have _____– glucose consuption

what is this called?

A

increased - to fuel their rapid growth and proliferation

Warburg Effect

49
Q

explain how cancer cells alter in their production of ATP

A

they favor glycolysis over oxidative phosphorylation

50
Q

explain the difference in lactate production between normal cells and cancer cells

A

cancer cells have enhanced lactate production bc it’s a byproduct of glycolysis – leading to acidic envionment that promotes tumor invasion and metastasis

51
Q

cancer cells exhibit increased Glutamine dependency

why?

A

to fuel TCA cycle

52
Q

explain the altered lipid metabolism of cancer cells

A

increased lipogenesis and lipid uptake – to fulfill demands of membrane genesis and signaling and energy storage

53
Q

true or false

the pentose phosphate pathway is downregulated in cancer cells

A

FALSE - heightened

to generate NAPDH and ribose-5-phosphate

these are their antioxidants that serve as both defense mechanisms and can produce nucleotides for cancer DNA replication

54
Q

explain the mitochondrial dysfunction of cancer cells

A

altered in morphology and function – impaired oxidative phosphrylation and increased reliance on glyclysis

55
Q

PTEN controls……

A

cellular metabolism

56
Q

HOW does PTEN control cellular metabolism

A

by downregulating mTOR

makes it impossible for cancer sells to generate biosynthetic building blocks they need for their proliferation

increased glycolysis, increased amino acid transport, decreased TCA

57
Q

True or false

PTEN upregulates mTOR

A

false - downregulates

58
Q

how does p53 regulate cellular metabolism?
what activates p53?

A

increased metabolic stress activates AMPK which activates p53

results in decreased glycolysis, decreased fatty acid synthesis, and increased oxidative phosphorylation

so that cancer cells can’t get the nutrients they need

59
Q

explain tumor heterogeneity

A

the tumor cells close to blood vessels kind of behave like normal cells bc they generate ATP mostly by oxidative phosphorylation and show ANABOLISM

they cannabalize catabolic products from other further tumor cells - autophgy - to get nutrients

in tumor stromal cells - net catabolic metabolism - goal is to get nutrients

60
Q

tumor cells closest to blood vessels are _____ and furhest are ____
what is the term for this

A

close to blood vessels = anabolic. they cannabalizze the catabolic products from furhter tumor cells and stromal cells

far from blood vessels = catabolic

called tumor heterogeneity

61
Q

what is the difference between tumor specific antigens and tumor associated antigens?

A

tumor specific antigens = present ONLY on tumor cells. thus, they can be recognized by CD4+

tumor associated antigens are NOT unique to tumors - can’t help in immune response but can be useful for diagnostics and therapy

62
Q

name 5 immune cells that can help with stopping tumor progression

A

CD4+ (cytotoxic)
helper t cells
NK cells
killer macrophages
B cells/plasma cells

63
Q

name 3 common ways that can lead to the inactivation of tumor suppression

A

-mutation in the tumor suppressor gene

-chromosome loss (if carries tumor suppressor genes)

-abnormal methylation of CpG islands near promoter regions of the tumor suppressor genes

64
Q

true or false

DNA is constantly damaged and repaired

A

true - this is normal

if a repair process malfunctions however, there is risk for mutation and potential cancer development if mutation occurs at a tumor suppressor gene

65
Q

how is a single strand break in DNA repaired

A

base excision repair

66
Q

how is a double strand break in DNA repaired?
what 3 cancers may occur if this repair process doesn’t work?

A

through homologous recombination

pancreas
breast
ovarian

67
Q

what is an adduct?
how is it repaired? what 2 cancers can occur if not repaired

A

complex that forms when a chemical binds to DNA

repaired through nucleotide excision repair

zerodema
pigmentosum

68
Q

a base repair mismatch can result in what 2 cancers?

A

colon and rectal

69
Q

define a proto-oncogene

A

a normal gene that can become an oncogene if mutated

70
Q

name 4 common genetic changes that can result in proto-oncogene formation

A

missense mutations
gene amplifications
chromosomal translocations
retroviral insertions

71
Q

name a common proto-oncogene

A

Ras

if continually activated, there is continuous stimulation of cell proliferation

72
Q
A

Pathology Final (11 decks)

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