cancer

Question 1

why are intestinal cells lined with villi

Answer 1

increase their surface area

Question 2

villi vs microvilli?

Answer 2

intestinal lining has villi. each individual cell has microvilli. both serve to increase surface area

Question 3

where would you find stem cells?

Answer 3

Between villi in little ‘crypts’ . Stem cells start at very bottom. sitting there maintaining the population of all the cells

Question 4

how do stem cells produce cells for differentiation?

Answer 4

As they divide, they produce a cell for differentiation. Push those cells up. Eventually go up high enough to stop dividing.

Question 5

why are cancer cells said to have transformed phenotypes?

Answer 5

they are doing different things, taking on new shapes than they were before.

Question 6

malignant vs benign

Answer 6

Malignant: ones that will worsen, can lead to death

Benign: enlarging but should not be invasive/dangerous

Question 7

what do we mean when we say cancer cells are immortal?

Answer 7

grow and divide in agar, and never stop dividing. ex:HeLa cells

Question 8

De-differentiation of cancer cells

Answer 8

return to fetal state

• Alpha-fetoprotein- only made at time of birth. However in cancer cells, damaged liver starts regenerating itself, produces AFP again
• Also, if liver develops a cancer, they start developing AFP. Allows you to detect a cancer.
• Colon cancer has one too- CEA. Prostate: PSA. (lots of false positives tho) Present in blood is sign of a cancer

Question 9

Angiogenesis

Answer 9

signal for new blood vessels. As tumor grows, calls for new blood vessels. increase in this is sign of a tumor

Question 10

factors contributing to cancer

Answer 10

genetic + environmental

Question 11

of those with lung cancer, __% are smokers

Answer 11

96

Question 12

latency period for smoking

Answer 12

30 years

Question 13

does the rate of cancer/death by cancer increase with age?

Answer 13

yes

Question 14

oncogenes and tumor suppressor genes

Answer 14

oncogenes: acts like a dominant gene. Only need a mutation in ONE copy. This gene says Divide, divide divide! Unregulated cell division.

tumor suppressor genes: Loss of function mutation in one copy of gene-> no effect. But second mutation knocks out other copy- whatever genes were doing is lost. Then, more chance of having a cancer develop

Question 15

ways to convert proto-oncogene to oncogene

Answer 15

mutation in coding sequence (mutation in coding sequence , produces broken protein, could tell it to divide)

gene amplification (take normal gene, divide wrong, get several copies of it- if each one produces final product, 3x as much of it, increases signal for cell division- just too much of a normal gene)

chromosome rearrangement (weird inversions)

or: virus could disrupt normal regulation or intorduce extra copy of a gene

Question 16

normal cell signal pathway leading to division

Answer 16

Hormone/ growth factor binds. Changes shape of receptor- causes phosphorylation of some protein factor.

When that is phosphorylated, causes another to be phosphorylated, etc- ‘cascade.’

Question 17

how do you get an error in cell signaling pathway that could lead to signaling for unlimited division?

Answer 17

Many signaling pathways. Many multistep pathways. A mutation in any of these genes would screw up this process.

Many genes that could be mutated in this process and start to signal for cancers. Could lead to incidence of so many types of cancers

Question 18

what can happen with retinoblastoma and what is it an example of?

Answer 18

Rb gene- acts like a recessive gene. Both copies need to be mutated or shut off in order for tumor to grow

Question 19

how does retinblastoma protein normally work and what goes wrong in the case of a cancer?

Answer 19

normally, inactive growth factor receptor, only activates to signal ‘divide’ when a growth factor arrives.

Mutatnt form: protein active 100% of the time! So for people with mutation , whether or not growth factor is there or not, you’re signaling DIVIDE

Question 20

p53- normal, abnormal

Answer 20

P53 protein: monitors the DNA to see if there is damaged.

Normal: if sees damage, calls in repair enzyme, fixes. If cant fix it, signals for apoptosis (cell death process).

Abnormal: if you lose this function, damaged DNA is going through replication. produce aneuploidy, broken chromosomes, translocations. mutant p53 is found in MANY (70%) of cancers.

Question 21

___ protein is a suppressor of cell division when DNA is damaged

Answer 21

p53

Question 22

cell cycle checkpoints

Answer 22

G1, G2, metaphase

Cell in G1: when it wants to go to S, division, there is a G1 checkpoint. Is enviroment favorable? Is cell large enough? Is there DNA damage?

G2: another checkpoint before mitosis. Is all DNA replicated? Undamaged? Environment still good? Ok, enter mitosis

During metaphase: are all chromosomes attached to spindle?

Question 23

p53/Rb both act like (dominant/recessive) genes

Answer 23

recessive

Question 24

colon cancer: what does it tell us about multistep cancer

Answer 24

Cancer arises slowly in multiple steps.

Polyps: can be precursors of cancers. When you convert normal epithelium into a hyper prolifitive epithelium, pile up tissue, form polyp, get intermediate polyp- loses its shape, becomes a carcinoma, and then metastasis.

Association between mutation in APC gene – when it get sa mutation, that’s when epithelium becomes a polyp. K-ras converts to intermediate polyp

Question 25

potential therapeutic targets in cancer

Answer 25

target cell surface protein that is the receptor for cancer, shut it off

OR:

Prevent angiogenesis

OR:

Prevent migration to matrix

Question 26

treatement for CML / philadlephia chromosome issue

Answer 26

Gleevec: Competitively inhbits this oncogene

Question 27

chemo vs radiation

Answer 27

• Goal of radiation- eliminate the cancerous area only
• Chemo- blunt force- eliminate growth of ALL dividing cells . Lose hair, intestinal upset as well.

Question 28

monoclonal antibody therapy

Answer 28

Lung cancer- test for more than 100 different mutations that tend to occur in 13 known genes. Based on that try and tailor the treatment. If you see a particular cell marker, can make a monoclonal Antibody that sticks only to that particular target molecule (some messed up receptor or enzyme) and nothing else

Question 29

how do you create monoclonal antibodies

Answer 29

• Isolate target molecule and inject it into mice
• Mice will make an immune response
• Isolate mouse immune cells (making antibodies against that molecule)
• Fuse immune cells w/ myeloma cell- type of bone marrow cancer- makes the immune cells be able to permanently grow. “immortal” in culture. Stil producing the antibodies that target our bad guy.
• Then , harvest the antibodies from the culture medium, use those to attack the tumor
• May want to ‘humanize’ the antibodies by recombinant DNA procedure- take off parts of molecule that are mouse specific, keep the binding part. The individual won’t reject the antibodies.

Question 30

monoclonal atnibody vs gene therapy

Answer 30

•Monoclonal antibody therapy is NOT gene therapy; in gene therapy you’re editing your genes , here you’re training your immune system to attack a target

Question 31

testing for viruses and cancer

Answer 31

If dealing with a virus causing cancer- test for virus. If virus not present, not likely to die. Example: HPV. Pap smears used to test for HPV. If HPV negative, don’t have to worry about getting cervical cancer

Question 32

BRCA1, BRCA2: __ of cancers.

Answer 32

10%

Question 33

BRCA- what is it and why does it cause cancer

Answer 33

•2 separate genes that work along with tumor suppressor activities, also have DNA repair effects- a mutation here inhibits ability to do DNA repair.

Question 34

HER2: __ % of cancers

Answer 34

20%

Question 35

. Immune targeting:

Answer 35

isolate some of the cancer , isolate T-CELLS FROM CANCER. CULTURE THE T CELLS, grow millions. Put T cells back w/ interleukin-2. (white blood cells) stimulate them to divide , hopefully will have an effect on that type of cancer. Pioneered by steven rosenberg, NIH.

Question 36

Car T

Answer 36

chimeric antigen in receptor T cells. Make cells bind even more rapidly than normal targeted cancer therapies. Still not considered gene therapy.