Oncology

Question 1

How does the cell cycle catch mistakes in DNA?

Answer 1

has checkpoints

Question 2

Order of cell cycle

Answer 2

G0, G1, S, G2, M

Question 3

G0 phase

Answer 3

rest phase

Question 4

G1 phase

Answer 4

enter cell cycle and prep for DNA replication–proto-oncogenes are activated

Question 5

S phase

Answer 5

synthesis of chr and chr move to opp poles to prep for division into 2 cells (23 chr at end each with nuclear mem around each)

Question 6

G2 phase

Answer 6

cells prep to divide

Question 7

Mitosis phase

Answer 7

2 daughter cells develop

Question 8

Immune surveillance

Answer 8

• our immune sys surveys bod for foreign subs or “no-self” antigens to attach
• with age, system worsens and reaction declines–mutated cells escape easier

Question 9

Patho of cancer cells

Answer 9

• rapid rep w/o G0 and checkpoints
• altered DNA keeps reproducing; no apoptosis
• constant move thru cycle
• ignore growth inhibitors released by neighboring cells so nothing stops them from going where they want

Question 10

Differentiation

Answer 10

how neoplastic cells resemble normal cells with structure and function

Question 11

anaplasia

Answer 11

lack differentiation
- often malignant cells
- total cell disorganization, abnormal appearance, cell dysfxn

Question 12

Which tumors are more well-differentation?

Answer 12

Benign

Question 13

Rules that cancer cells BREAK

Answer 13

• contact inhibition–push others aside
• not cohesive (mets)
• little communication
• proliferation w/o apoptosis
• avoid “non-self” markers so the sys doesn’t attach

Question 14

Cancer cells are…

Answer 14

UNORGANIZED
VARIABLE SHAPE
MAY DIVIDE
VARIABLE NUCLEUS

Question 15

Benign tumor characteristics

Answer 15

• well-differentiated
• local
• cohesive
• no mets
• no necrotic core–living

Question 16

Malignant tumor char

Answer 16

• poor diff or anaplastic
• break free easily
• slow or rapid growth
• neurotic core esp with age–harder to tx bc can’t get tx in

Question 17

Tumor markers

Answer 17

• hor, enzymes, genes, or antigens in blood, urine, or CSF
• let us follow the clinical course (dec w/ tx)
• can also be present w/o cancer (ex: PSA)

Question 18

Phases of cancer cell grwoth

Answer 18

• initiation–alt of genes (spon) or induced by contract with (carcinogen)
• promotion–cells accum
• progression–more mutate with met potential
• metastasis

Question 19

Cancer genetics

Answer 19

gene mutations are sporadic or hereditary (BRCA)

Question 20

tumor suppressor genes

Answer 20

genes that normally “brake” cell division but can mutate and become inactive, inhibiting the brake

Question 21

Oncogenes

Answer 21

Proto-oncogenes that normally tell the cell to grow and mutate to be permanently “on”–prolif

Question 22

Carcinogens

Answer 22

Substances that cause the development of cancer–start mutations
- can alter DNA
- damage accums

Question 23

3 classes of carcinogens

Answer 23

• known–HPV, HIV, alcohol, virus, tobacco
• probable–nightshift
• possible–insuff evidence; exhaust engine

Question 24

promoting agents

Answer 24

help genes proliferate and encourage further mutation
- hi fat diet
- alc
- tobacco
- hor (estrogen)

Reversible

Question 25

viral-induced cancer

Answer 25

- malignancies assoc with virus--HIV, HPV, Hep B and C - insert gene into host cell and host cell begins manufacturing virus - activate growth - promo paths or inhibit tumor supp in infected cells

Question 26

3 ways cancer can spread

Answer 26

- seeding - tumor erodes and sheds into body cavity - implantation - exposure to adjoining tissue - mets - travel thru lymph or vasc

Question 27

Primary tumor

Answer 27

origin tumor

Question 28

Secondary tumor

Answer 28

metastasis; loos like cells from original site - site depends on location of primary tumor - can make own blood supply and secrete vascular endo Grwoth factor

Question 29

most common sites of secondary tumors

Answer 29

lung, bone, liver, brain

Question 30

Where does colon cancer often met to

Answer 30

liver

Question 31

Where does lung cancer often met to

Answer 31

bone and brain

Question 32

Where does breast cancer met to

Answer 32

everywhere

Question 33

Where does prostate cancer met to

Answer 33

vertebrae

Question 34

Where does melanoma met to

Answer 34

the brain

Question 35

Why is the liver a common site for mets?

Answer 35

all blood flow thru the liver

Question 36

intraperitoneal seeding

Answer 36

Spreads thru the peritoneum to other ab organs

Question 37

lymph spread of cancer

Answer 37

cells can get trapped and die, go dormant, or flourish

Question 38

vasc spread of cancer

Answer 38

penetrate BVs and drain local veins; first stop often liver

Question 39

Classifications of malignancy

Answer 39

1 - well diff 2 - mod diff 3 - poor dif

Question 40

Layman class of tumors

Answer 40

1 - confined to organ of origin 2 - locally invasive 3 - regional spread 4 - spread to distal sites

Question 41

TNM classifications

Answer 41

T - tumor size, location, involvement N - lymph node involvement M - metastasis (N0 none, M1 yes)

Question 42

P53

Answer 42

a tumor suppressor gene that triggers apoptosis