Exam 4 Part 4

Question 1

Cons of ESC use

Answer 1

potential for rejection if not your own DNA
Potential for tumor formation
ethical issues, legal issues
work with human ESC is still in its infancy

Question 2

inducible pluripotent stem cells

Answer 2

differentiated cells stably transfected with certain genes revert to an ESC-like state
may present a way around the ethical dilemmas
permulation of adult stem cells an ESC

Question 3

formation of iPSCs

Answer 3

take culture of fibroblasts from adult skin
introduce DNA encoding three key transcription regulators
the resulting iPSCs can be used to make any other cell (except extra embryonic stuff)
can be a tool to study genetic diseases in several differentiated cell types

Question 4

what you thin of when you hear cancer

Answer 4

death, tumors, mutation, stages, HeLa, $$, uncontrolled growth, research, CELL BIOLOGY

Question 5

Cancer Stage I

Answer 5

uncontrolled proliferation (benign and malignant)

Question 6

Cancer Stage II

Answer 6

dediffrentiation/loss of function
look more like SC and loose physiological function
can be used to ID cancer

Question 7

Cancer Stage III

Answer 7

invasiveness (malignant only)

moves into other parts of tissue (local movement)

Question 8

Cancer Stage IV

Answer 8

metastasis (malignant only)
distal migration, has gone into the blood/lymph
gets in the way of normal cell functions

Question 9

malignant neoplasm

Answer 9

evil new growth

tumor

Question 10

carcinomas

Answer 10

cancers of epithelial cells: lung, breast, colon

Question 11

sarcomas

Answer 11

cancers of supporting tissues: bone, muscle cartilage, fat

Question 12

lymphomas/leukemias

Answer 12

cancers of the lymphatic or blood origin. Leukemias are not solid state

Question 13

cancer cell properties

Answer 13

undifferentiated, anchorage-independent growth, immortal, extremely variable chromosome numbers, less sensitive to cell density and extracellular signals, reactivated telomerase, usually highly migratory and invasive, secrete growth factors and other chemicals, normal systems of cell regulation are disrupted

Question 14

how cancer spreads

Answer 14

1 - series of mutations are needed to move the cell to an undifferentialed state and mass
2- new blood vessel blood growth is needed

Question 15

angiogenesis

Answer 15

creation of new blood vessels

cancer cells are hypoxic or secrete MMP to cause blood vessels to come to them

Question 16

chorioallantoic assay

Answer 16

CAM look at the blood vessels forming around a retina tumor

Question 17

vascular endothelial growth factor

Answer 17

VEGF - allows for angiogenesis -binds to its receptors on blood vessel endothelial cells

Question 18

metalloprotease

Answer 18

MMP -cell secrete this - digests the ‘scaffold’ andallows for new vessels to travel to a distal site

Question 19

what allows for migration/metastasis?

Answer 19

degradation of cell-cell contacts (cadherins)
change in the state of cell-matrix contacts (integrins)
activation of proteases (plasminogen, MMPs)
potential hijack of inflammatory systems/blood cells

Question 20

hijack of inflammatory systems/blood cells

Answer 20

uses signals to make cells like WBCs to leave blood stream, can also mask itself from the immune system by using things like platelets

Question 21

selecting for tumors

Answer 21

we can select for the tumors that are genetically able to survive and thrive in the blood by taking the few that make it to places by the lungs and reinjecting it

Question 22

where metastasizing cancers usually go

Answer 22

lungs or liver - places with extensive capillary beds
OR places with favorable growth conditions like prostate to bone
-sometimes there is a molecular signature

Question 23

what causes cancer

Answer 23

caused by carcinogen/radiation
caused by a virus (insert DNA and disrupt normal DNA)
caused through inheritance
caused through spontaneity

Question 24

proto-oncogene

Answer 24

normal gene that has the potential to cause cancer

Question 25

oncogene

Answer 25

proto–oncogene that has mutated to become a gain-of-function mutation to cause cancer
stuck accelerator

Question 26

tumor suppressor gene

Answer 26

normal gene that when mutated can cause cancer with a loss of function mutation
need to have both alleles mutate
broken brakes when mutated

Question 27

inherited mutations

Answer 27

speed up the development of cancer

Question 28

ways a proto-oncogene becomes an oncogene

Answer 28

mutation in coding sequence
gene amplification (extra protein)
chromosome rearrangement (nearby regulatory DNA sequence causes normal protein to be overproduced, OR fusion to actively transcribed gene produces hyperactive fusion protein)

Question 29

commonalities in proto-oncogenes

Answer 29

growth factors, receptors (often for growth factors, often kinases, refractory to signal), small GTPases (stuck in GTP), non-receptor protein kinases (imbalance of regulation
transcription factors (overproduction)
cell cycle/cell death regulators

Question 30

usual causes of cancer in young people

Answer 30

inherited mutations, exposed to something (tanning beds, etc)
bad luck

Question 31

non-specific cancer treatment

Answer 31

kill or remove the cells
usually surgery or extreme use of drugs that will kill anything that grows fast
has nasty side-effects

Question 32

specific cancer treatments

Answer 32

treatments that target just the tumor like enhancing the immune system, MAB, hormone therapy, repair and replacement (stem cells)

Question 33

gleevec

Answer 33

targets a specific kinase that occurs in a specific leukemia