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Pathology Final > Lecture 10 - Neoplasia > Flashcards

Lecture 10 - Neoplasia Flashcards

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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
what are the 4 stages of the cell cycle
G1 S G2 M
26
what is E2F?
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
27
true or false E2F pushes the cell to proliferate
true - when not bound to Rb
28
what liberates E2F from Rb? what does this cause?
CDK 2,4,6, and cyclins D and E double phosphorylates Rb causes the cell cycle to progress bc E2F is liberated
29
NORMALLY, with no cell damage, p53 is kept at ___ levels
low
30
explain the condition of p53 under normal cell conditions
is polyubiquinated by E3 ubiquitin ligase and is thus degraded by proteasomes not a lot can be detected in normal cells
31
explain what happens to p53 when DNA is damaged or DNA replication is stalled
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
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?
if repaired, the block is removed and cell cycle proceeds if cannot be repaired, p53 triggers apoptosis
33
what is PTEN
a tumor suppressor gene
34
true or false inhibitors of cyclins are tumor suppressor genes
TRUE - bc they block cell cycle from happening when DNA is damaged
35
what will happen if the activity of PTEN is decreased?
tumor genesis is promoted
36
explain cellular senescence and how it relates to cancer
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
name a potential anti cancer drug that is related to cellular senescence
a drug that inhibits telomerases can prevent a benign tumor from becoming malignant bc premalignant cells survive by activating telomerases
38
what is VEGF
vascular endothelial growth factor - stimulates the formation of new blood vessles
39
explain VEGF-stimulated tumor angiogenesis
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
name a potential kind of drug that can stop cancer progression, related to angiogenesis
create a drug that inhibits VEGF to prevent the formation of new blood vessels that promote metastasis
41
differentiate between normal physiologic blood vessel formation and tumor blood vessel formation
normal - no gaps tumor - many gaps to allow cancer cells to circulate easily tumor cells pose as endothelial cells
42
true or false normal cells do not typically migrate
true - (except embyronic development) cancer cells do migrate and invade other tissues
43
explain the process of tumor invasion and metastasis
-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
what is extravasation
trans-endothelial migration
45
how can circulating tumor cells survive in the blood?
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
what are MMPs and how are they related to cancer progression
matrix metalloproteinases allow extravasation of cancer cells from the blood vessels and into the surrounding tissue
47
true or false metabolism is not very different in cancer cells compared to normal cells
false - it is
48
cancer cells have _____-- glucose consuption what is this called?
increased - to fuel their rapid growth and proliferation Warburg Effect
49
explain how cancer cells alter in their production of ATP
they favor glycolysis over oxidative phosphorylation
50
explain the difference in lactate production between normal cells and cancer cells
cancer cells have enhanced lactate production bc it's a byproduct of glycolysis -- leading to acidic envionment that promotes tumor invasion and metastasis
51
cancer cells exhibit increased Glutamine dependency why?
to fuel TCA cycle
52
explain the altered lipid metabolism of cancer cells
increased lipogenesis and lipid uptake -- to fulfill demands of membrane genesis and signaling and energy storage
53
true or false the pentose phosphate pathway is downregulated in cancer cells
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
explain the mitochondrial dysfunction of cancer cells
altered in morphology and function -- impaired oxidative phosphrylation and increased reliance on glyclysis
55
PTEN controls......
cellular metabolism
56
HOW does PTEN control cellular metabolism
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
True or false PTEN upregulates mTOR
false - downregulates
58
how does p53 regulate cellular metabolism? what activates p53?
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
explain tumor heterogeneity
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
tumor cells closest to blood vessels are _____ and furhest are ____ what is the term for this
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
what is the difference between tumor specific antigens and tumor associated antigens?
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
name 5 immune cells that can help with stopping tumor progression
CD4+ (cytotoxic) helper t cells NK cells killer macrophages B cells/plasma cells
63
name 3 common ways that can lead to the inactivation of tumor suppression
-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
true or false DNA is constantly damaged and repaired
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
how is a single strand break in DNA repaired
base excision repair
66
how is a double strand break in DNA repaired? what 3 cancers may occur if this repair process doesn't work?
through homologous recombination pancreas breast ovarian
67
what is an adduct? how is it repaired? what 2 cancers can occur if not repaired
complex that forms when a chemical binds to DNA repaired through nucleotide excision repair zerodema pigmentosum
68
a base repair mismatch can result in what 2 cancers?
colon and rectal
69
define a proto-oncogene
a normal gene that can become an oncogene if mutated
70
name 4 common genetic changes that can result in proto-oncogene formation
missense mutations gene amplifications chromosomal translocations retroviral insertions
71
name a common proto-oncogene
Ras if continually activated, there is continuous stimulation of cell proliferation
72

Pathology Final (11 decks)

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