Exam 4 Part 4 Flashcards
Cons of ESC use
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
inducible pluripotent stem cells
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
formation of iPSCs
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
what you thin of when you hear cancer
death, tumors, mutation, stages, HeLa, $$, uncontrolled growth, research, CELL BIOLOGY
Cancer Stage I
uncontrolled proliferation (benign and malignant)
Cancer Stage II
dediffrentiation/loss of function
look more like SC and loose physiological function
can be used to ID cancer
Cancer Stage III
invasiveness (malignant only)
moves into other parts of tissue (local movement)
Cancer Stage IV
metastasis (malignant only)
distal migration, has gone into the blood/lymph
gets in the way of normal cell functions
malignant neoplasm
evil new growth
tumor
carcinomas
cancers of epithelial cells: lung, breast, colon
sarcomas
cancers of supporting tissues: bone, muscle cartilage, fat
lymphomas/leukemias
cancers of the lymphatic or blood origin. Leukemias are not solid state
cancer cell properties
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
how cancer spreads
1 - series of mutations are needed to move the cell to an undifferentialed state and mass
2- new blood vessel blood growth is needed
angiogenesis
creation of new blood vessels
cancer cells are hypoxic or secrete MMP to cause blood vessels to come to them
chorioallantoic assay
CAM look at the blood vessels forming around a retina tumor
vascular endothelial growth factor
VEGF - allows for angiogenesis -binds to its receptors on blood vessel endothelial cells
metalloprotease
MMP -cell secrete this - digests the ‘scaffold’ andallows for new vessels to travel to a distal site
what allows for migration/metastasis?
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
hijack of inflammatory systems/blood cells
uses signals to make cells like WBCs to leave blood stream, can also mask itself from the immune system by using things like platelets
selecting for tumors
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
where metastasizing cancers usually go
lungs or liver - places with extensive capillary beds
OR places with favorable growth conditions like prostate to bone
-sometimes there is a molecular signature
what causes cancer
caused by carcinogen/radiation
caused by a virus (insert DNA and disrupt normal DNA)
caused through inheritance
caused through spontaneity
proto-oncogene
normal gene that has the potential to cause cancer
oncogene
proto–oncogene that has mutated to become a gain-of-function mutation to cause cancer
stuck accelerator
tumor suppressor gene
normal gene that when mutated can cause cancer with a loss of function mutation
need to have both alleles mutate
broken brakes when mutated
inherited mutations
speed up the development of cancer
ways a proto-oncogene becomes an oncogene
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)
commonalities in proto-oncogenes
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
usual causes of cancer in young people
inherited mutations, exposed to something (tanning beds, etc)
bad luck
non-specific cancer treatment
kill or remove the cells
usually surgery or extreme use of drugs that will kill anything that grows fast
has nasty side-effects
specific cancer treatments
treatments that target just the tumor like enhancing the immune system, MAB, hormone therapy, repair and replacement (stem cells)
gleevec
targets a specific kinase that occurs in a specific leukemia
