Oncogenes and Tumor Suppressor Genes

Question 1

Neoplasia is the dysregulated cellular ______________, aberrant _____________ and size

Answer 1

Differentiation; proliferation

Question 2

Neoplasia is
a) Reversible
b) Irreversible

Answer 2

b) Irreversible

Question 3

True or false: Cancerous cells proliferate and grow without control

Answer 3

True

Question 4

Differentiation is impeded at which stage of tumorigenesis?

Answer 4

One or multiple stages

Question 5

Selective growth advantage (s) is the difference between _________ and death in a cell population

Answer 5

Birth

Question 6

In normal adult cells in the absence of injury, s is equal to what?

Answer 6

Zero

Question 7

What is dysplasia?

Answer 7

A tissue is out of place

Question 8

True or false: Dysplastic cells are malignant

Answer 8

False, they are pre-malignant

Question 9

What are some hallmarks of cancer?

Answer 9

Evading growth suppressors, avoiding immune destruction, activating invasion and metastasis, resisting cell death

Question 10

An oncogene is a gene that ______________ the selective growth advantage of the cell in which it resides

Answer 10

Increases

Question 11

A proto-oncogene is a normal gene that can become an oncogene due to ____________ or increased _______________

Answer 11

Mutations; expression

Question 12

A tumor suppressor is a gene that, when inactivated by ____________, increases the selective __________ advantage of the cell in which it resides

Answer 12

Mutation; growth

Question 13

Who coined the term “oncogene”?

Answer 13

Robert Huebner and George Todaro

Question 14

What was the first oncogene that was identified?

Answer 14

v-src

Question 15

A driver gene mutation is a mutation that _____________ or ________________ confers a selective growth advantage to the cell in which it occurs

Answer 15

Directly; indirectly

Question 16

True or false: A passenger mutation is a mutation that has direct or indirect effect on the selective growth advantage of the cell in which it occurred

Answer 16

False, it has no direct or indirect effect on the selective growth advantage of the cell in which it occurred

Question 17

What is the difference between a sporadic and a familial mutation?

Answer 17

Sporadic - there needs to be two hits on both alleles for the cancer to develop
Familial - there only needs to be a second hit on a single allele for the cancer to develop because the first hit occurred before birth in one allele

Question 18

In which case of somatic or germ-line mutation does cancer develop faster?

Answer 18

Germ-line mutation

Question 19

What are some oncogenes?

Answer 19

RAS, SRC, Bcl

Question 20

Ras is a ___________ that is frequently mutated in cancer that affects a variety of cancer-driving processes

Answer 20

GTPase

Question 21

What is Ras signaling?

Answer 21

SOS1 activates Ras by activating it from its GDP state to its GTP state
Continuous on state of Ras leads to proliferation through Ras effector pathways

Question 22

What inactivates Ras?

Answer 22

NFI

Question 23

True or false: There are more oncogenes than tumor suppressors

Answer 23

True

Question 24

What is p53?

Answer 24

p53 is a transcription factor that triggers apoptosis, autophagy and cell arrest

Question 25

Where do mutations occur in the genome of p53?

Answer 25

DNA binding domain

Question 26

How does mutant p53 inhibit wild type p53?

Answer 26

TP53 mutation leading to a loss of function of the wild type copy

Question 27

True or false: One single oncogene can cause cancer

Answer 27

False, oncogenes need to collaborate to make cells cancerous, otherwise the cells die or survive

Question 28

What is the role of ARF?

Answer 28

Encodes inhibitors of cyclin and increases p53 by inhibiting MDM

Question 29

If p53 activates p21, the cells go through ______________

Answer 29

Senescence

Question 30

If p53 activates BH3, the cells go through ___________

Answer 30

Apoptosis

Question 31

Which protein blocks senescence?

Answer 31

Myc

Question 32

Which protein blocks apoptosis?

Answer 32

Akt

Question 33

What does senescence mean?

Answer 33

Growing old

Question 34

The Hayflick limit is the number of times a _________ human cell population will _______ until cell _______ stops

Answer 34

Normal; divide; division

Question 35

What are some Hayflick factors?

Answer 35

Short telomeres, high DNA damage, high INK4a

Question 36

What is the role of INK4a?

Answer 36

Activates Rb and leads to apoptosis/senescence

Question 37

Oncogene addiction is a cellular condition in which a cancer cell requires the activity of a specific ______________ or cellular process for growth and survival

Answer 37

Oncogene

Question 38

Which cancer hallmark is linked to cyclin-dependent kinase inhibitors?

Answer 38

Evading growth suppressors

Question 39

What is horizontal resistance?

Answer 39

Second mutation of receptor renders the receptor insensitive to the treatment

Question 40

What is vertical resistance?

Answer 40

Drug binds to receptor, mutation multiplies the number of receptors, meaning the drug has to target more receptors

Question 41

What are some challenges in treating cancer?

Answer 41

A tumor can have many clones of different cells within one mass that need different factors
Cancer cells are able to adapt to various stress factors