Exam 4 part 4 Flashcards Preview

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Flashcards in Exam 4 part 4 Deck (31):
1

benign

tumor stays inside boundary of normal structure

2

malignant

glandular tumor, destroys duct integrity and spreads

3

metastases

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

4

carcinomas

derive from epithelial cells
Ex: breast, digestive organs

5

sarcomas

derive from connective tissue or muscle cells

6

leukemias and lymphomas

derive from white blood cells

7

carcinogenesis

production of cancer

8

causes of mutations

1. radiation- X rays, radon, UV light
2. mutagens- chemicals in environment, viruses

9

# of mutations for cancer

five mutations

10

cancer cells lose _________

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

11

angiogenesis

development of new blood vessels
tumors induce this

12

Warburg effect

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

13

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

1. tumor
2. tumor
3. homeostasis

14

overactive or over expressed forms of these gene promote cancer

proto-oncogenes, when active they're called oncogenes

15

inactive forms of these genes contribute to cancer development

tumor suppressor genes

16

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

DNA maintenance genes

17

overactivity mutation

gain of function, oncogene enabled

18

underactivity mutation

loss of function, tumor suppressor gene inactivated

19

ways a photo-oncogene can be activated

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

20

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

hyperactive protein made in normal amounts

21

regulatory mutation (proto-oncogene)

normal protein greatly overproduced

22

gene amplification (proto-oncogene)

normal protein greatly overproduced (multiple of the same gene)

23

chromosome rearrangement (proto-oncogene)

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

24

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

Rb gene

25

two oncogenes that increase cancer chances

Ras and Myc

26

function of Rb

inhibits entry into the S-phase
binds to E2F

27

Rb pathway

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

28

p53

transcription factor protein for many genes, including p21

29

p21

protein p21 inhibits G1/S and S-Cdk

30

p53 pathway

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
5. p21 protein binds S-Cdk, inactivates it

31

PTEN

phosphatase, tumor suppressor