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FoundSci III > Neoplasia V > Flashcards

Neoplasia V Flashcards

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1
Q

Neoplastic clonal expansions is because of__________ x3

A
  1. Activation of protooncogenes
  2. inactivation of tumor suppressor genes
  3. Decreased apoptosis due to imbalance between pro and anti apoptotic genes
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2
Q

What is the gene product and associated condition of the tumor suppressor gene APC?

A

Negative regulator of Beta catenin/WNT path

Colorectal cancer

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3
Q

What is the gene product and associated condition of the tumor suppressor gene BRCA1/BRCA2?

A

DNA repair protein

Breast, ovarian, and pancreatic cancer

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4
Q

What is the gene product and associated condition of the tumor suppressor gene Rb?

A

Inhibits E2F, blocks G1 to S phase

Retinoblastoma

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5
Q

What is the gene product and associated condition of the tumor suppressor gene TP53?

A

activates p21, blocks G1 to S phase

Most human cancers

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6
Q

What is the gene product and associated condition of the tumor suppressor gene VHL?

A

Inhibits hypoxia inducible factor 1a

von Hippel Lindau disease

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7
Q

What is the gene product and associated condition of the tumor suppressor gene WT1?

A

Transcription factor that regulates urogenital development

Wilms tumor (nephroblastoma)

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8
Q

______ and _______ are components of WNT signaling path

A

APC

Beta catenin

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9
Q

What is the function of the WNT signaling pathway?

A

Controls tissue proliferation in adult bone marrow, skin, intestine

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10
Q

How does APC normally function in the WNT pathway?

A

APC protein downregulates Beta catenin and prevents its accumulation

No proliferation

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11
Q

What occurs when WNT activates the WNT receptor?

A

Inactivation of APC which increases levels of Beta-catenin

Beta catenin translocates to nucleus

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12
Q

What occurs with continuous WNT signaling?

A

FAP

Nonfamilial colorectal CA and sporadic adenomas

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13
Q

What are the functions of p53?

A
  1. tumor supressor
  2. cell cycle arrest at G1/S - acts via p21 (inhibits cyclin/CDK4)
  3. Apoptosis - induces pro-apoptotic genes (BAX)
  4. Anti-angiogenic - inhibits VEGF and promotes thrombospondin production
  5. Promotes cell senescence
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14
Q

What can activate p53 in a normal cell?

A

DNA damage

Hypoxia

Telomere shortening and loss of function

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15
Q

What can occur once p53 is activated and binds to DNA? x3

A
  1. p21 activated and leads to G1 arrest
  2. GADD45 activated (DNA repair) and DNA successfully repaired. If unsuccessful, apoptosis occurs
  3. BAX activated and apoptosis occurs
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16
Q

What occurs in a cell with mutations or loss of p53?

A

No cell arrest and No DNA repair or senescence

Mutant cells then mutate and get malignant tumor

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17
Q

How does HPV interact with p53?

A

HPV E6 inhibits p53 and prevent apoptosis and growth arrest. Increases telomerase expression

HPV E7 inhibits p53, p21, and RB-E2F which also prevent apoptosis and growth arrest

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18
Q

What are the 3 cancers associated with Rb gene mutations?

A
  1. Retinoblastoma
  2. Osteosarcoma
  3. Soft tissue sarcoma
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19
Q

This disease commonly occurs in children and leads to progressive blurred vision with uni or bilateral leukocoria. Features will also be diffuse growth of small round blue cells with dark rounded nuclei and flexner-wintersteiner rosettes, mitotic figures, and microcalcifications.

A

Retinoblastoma

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20
Q

What is Knudson’s Two-hit hypothesis?

A

For retinoblastoma

Both alleles of Rb locus must be inactivated for it to occur

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21
Q

In familial cases of retinoblastoma, what occurs with mutation?

A

First hit in all somatic cells of the body - one defective copy inherited from affected parent.

Second hit in retinal cells - lose normal Rb gene and get retinoblastoma

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22
Q

What occurs with mutation in sporadic cases of retinoblastoma?

A

Mutation occurs and cells become homozygous for mutant tumor suppressor genes and leads to cancer

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23
Q

Heterozygous cells for Rb are _________

A

normal

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24
Q

What are the functions of VHL gene?

Study These Flashcards
A

Tumor suppressor gene on chromosome 3p

Part of ubiquitin ligase complex - regulates nuclear transcription via HIF-1a

25
What disease is VHL associated with?
VHL syndrome
26
Carcinogenesis is a ________ of successive mutations
accumulation
27
Tumor cells have upregulated ____________ and limitless replicated __________ activity
telomerases
28
What occurs in a cancer cell with telomerase?
Maintains the telomere length Prevent cell cycle arrest and apoptosis
29
What is the warburg effect?
Aerobic glycolysis Cancer cells demonstrate a distinct form of metabolism characterized by high levels of glucose uptake and increased conversion of glucose to lactose via the glycolytic path
30
________ refers to reversible, heritable changes in gene expression that occur without mutation.
Epigenetics
31
Epigenetic changes involve __________ and modification of __________, both of which affect gene expression
DNA methylation histones
32
DNA methylation ________ expression
reduces
33
Histone modification leads to the _________ of DNA into heterochromatin
compaction
34
P-glycoprotein is also know as _______. Classically seen in ________
MDR1 - multidrug resistance protein 1 Adrenocortical carcinoma
35
P-glycoprotein is used to ___________, including chemo agents
pump out toxins
36
__________ are laminated, concentric spherules with dystrophic calcification.
Psammoma bodies
37
Psammoma bodies can be seen in ________ x5
Papillary thyroid carcinoma Papillary renal cell carcinoma Serous papillary cystadenocarcinoma of ovary Meningioma Malignant mesothelioma
38
What are carcinogenic agents and give 4 examples?
Agents that cause genetic damage and induce neoplastic change. Chemical carcinogen Radiation Viral and bacterial carcinogen Hormonal carcinogen
39
__________ are highly reactive electrophiles that remove electrons from DNA, RNA, or proteins and cause cell damage.
Chemical carcinogens
40
Chemical carcinogens are act ________ and ___________
Directly - act without modification Indirectly - require activation
41
What are the 2 steps involved in chemical carcinogenesis?
1. Initiation 2. Promotion
42
_________ involve chemical that initiate carcinogenesis, produce cell alteration, can't form tumors alone, permanent DNA damage, and is rapid and irreversible.
Initiation of chemical carcinogenesis
43
__________ involves inducing tumors in initiated cells. Non-tumorigenic by themselves (do not affect DNA, reversible)
Promotion
44
What are 3 examples of chemical carcinogens?
1. Polycyclic aromatic hydrocarbons 2. Aromatic amines and Azo dyes 3. Naturally occurring chemical carcinogen
45
___________ come from combustion of tobacco and smokes meats and fish.
Polycyclic Aromatic Hydrocarbons
46
Polycyclic aromatic hydrocarbons lead to cancers of _________
Lung Bladder
47
Aromatic amines and azo dyes cause carcinogenicity where?
Liver
48
Beta-naphthylamine, an example of aromatci amine or azo dye, causes what cancer?
Bladder
49
What is an example of a naturally occurring chemical carcinogen?
Aflatoxin B1
50
Where is aflatoxin B1 from and what does it cause?
Mycotoxin produced by fungus Aspergillus flavus in improperly stored corn, rice, and peanuts. Leads to hepatocellular carcinoma (p53 mutations)
51
Where are nitrosamines from and what do thy cause?
Formed in GI tract Associated with gastric cancer Reaction of amines and nitrite
52
Asbestos leads to _____
mesotheliomas
53
Chromium and nickel can lead to _____
lung cancer
54
Arsenic can lead to ______
skin cancer
55
What are examples of promoters of chemical carcinogenesis?
1. Estrogen 2. Diethyl-stilbesterol 3. High dietary fat and increased bile acids
56
Estrogen as a promoter can lead to
liver tumors
57
Diethyl stilbesterol can lead to _______
post-menopausal endometrial CA Vaginal cancer in women exposed in utero
58
High dietary fat and increased bile acids can lead to ______
colon CA

FoundSci III (22 decks)

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