Exam 4 part 4

Question 1

benign

Answer 1

tumor stays inside boundary of normal structure

Question 2

malignant

Answer 2

glandular tumor, destroys duct integrity and spreads

Question 3

metastases

Answer 3

secondary tumors derived from cells that break off the primary tumor.

Question 4

carcinomas

Answer 4

derive from epithelial cells

Ex: breast, digestive organs

Question 5

sarcomas

Answer 5

derive from connective tissue or muscle cells

Question 6

leukemias and lymphomas

Answer 6

derive from white blood cells

Question 7

carcinogenesis

Answer 7

production of cancer

Question 8

causes of mutations

Answer 8

1. radiation- X rays, radon, UV light

2. mutagens- chemicals in environment, viruses

Question 9

of mutations for cancer

Answer 9

five mutations

Question 10

cancer cells lose _________

Answer 10

contact inhibition, no longer grow in a single layer of cells, pile on top of each other.

Question 11

angiogenesis

Answer 11

development of new blood vessels

tumors induce this

Question 12

Warburg effect

Answer 12

tumor cells down-regulate oxidative phosphorylation, even when oxygen is present
Take up large quantities of glucose, nucleic acids, proteins, and lipids for tumor growth

Question 13

1. normal cell division, decreased apoptosis=
2. increased cell division, normal apoptosis=
3. normal cell division, normal apoptosis=

Answer 13

1. tumor
2. tumor
3. homeostasis

Question 14

overactive or over expressed forms of these gene promote cancer

Answer 14

proto-oncogenes, when active they’re called oncogenes

Question 15

inactive forms of these genes contribute to cancer development

Answer 15

tumor suppressor genes

Question 16

could be considered a third class of cancer-critical genes
mutations in these promote genome instability

Answer 16

DNA maintenance genes

Question 17

overactivity mutation

Answer 17

gain of function, oncogene enabled

Question 18

underactivity mutation

Answer 18

loss of function, tumor suppressor gene inactivated

Question 19

ways a photo-oncogene can be activated

Answer 19

1. deletion or point mutation in coding sequence
2. regulatory mutation
3. gene amplification
4. chromosome rearrangement

Question 20

deletion or point mutation in coding sequence (proto-oncogene)

Answer 20

hyperactive protein made in normal amounts

Question 21

regulatory mutation (proto-oncogene)

Answer 21

normal protein greatly overproduced

Question 22

gene amplification (proto-oncogene)

Answer 22

normal protein greatly overproduced (multiple of the same gene)

Question 23

chromosome rearrangement (proto-oncogene)

Answer 23

1. nearby regulatory DNA sequence causes normal protein to be overproduced
2. fusion to actively transcribed gene produces hyperactive fusion protein

Question 24

gene encodes a regulator of the cell cycle, without it, cell division is uncontrolled

Answer 24

Rb gene

Question 25

two oncogenes that increase cancer chances

Answer 25

Ras and Myc

Question 26

function of Rb

Answer 26

inhibits entry into the S-phase

binds to E2F

Question 27

Rb pathway

Answer 27

1. P16 (Cdk inhibitor) stop cell cycle
2. cyclin D-Cdk complex (deactivates Rb)
3. Rb (inhibits E2F on DNA)
4. E2F (activated allows expression of gene for S-phase

Question 28

p53

Answer 28

transcription factor protein for many genes, including p21

Question 29

p21

Answer 29

protein p21 inhibits G1/S and S-Cdk

Question 30

p53 pathway

Answer 30

1. damage DNA
2. ATM/ATR kinase activates
3. Chk1/Chk2 activates, phosphorylates p53
4. Mdm2 releases active p53
5. p53 binds to p21 gene
6. p21 protein binds S-Cdk, inactivates it

Question 31

PTEN

Answer 31

phosphatase, tumor suppressor