- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
44 Cards in this Set
- Front
- Back
|
How does the number of oncogenes present affect the possible tumor growth
|
two oncogenes are more effective at creating tumors than one, and some combinations of oncogenes are more effective than others
|
|
What can we attribute tumor growth to in singly-transgenic mice?
|
inefficient repair mechanisms (consistent with a shorter life span)
|
|
Describe the role of active tumor suppressor gene products
|
Inhibit growth and suppress transformation in the normal cell
|
|
How are tumor suppressor gene deficiencies inherited?
|
Recessive, both copies must be missing in order to lack function
|
|
Describe the specific function of tumor suppressor gene
|
regulate gene transcription in genes whose function is to inhibit proliferation
|
|
Describe characteristics of metastasis cells
|
Cells which have proliferated through mutation and selective pressure and developed the ability to migrate and grow in distant sites
|
|
Name the 6 stages of metastasis
|
1) Primary Tumor
2) Invasion 3) Intravasation 4) Circulating tumor cells 5) Extravasation 6) Metastasis |
|
What is required to convert a normal cell to a tumor cell?
|
Multiple genetic defects
|
|
What is the primary cause of death among cancer patients?
|
Metastasis. Cells eventually invade other organs and take over the body
|
|
What determines where certain tumor cells will metastasize?
|
unknown at this point, but perhaps tissue specific factors play a role (autopsies have proven that they don't just arise at the next downstream organ) "seed and soil hypothesis"
|
|
Describe the survival of metastatic cells in circulation
|
Not very efficient. Only about 1 in 10,000 go on to create a secondary tumor location, all the rest die
|
|
What is the key feature of invasion, intravasation, and extravasation?
|
They all have the ability to invade through the stroma, basement membrane, and blood vessel walls
|
|
Describe the 3-step hypothesis that accounts for the invasive properties of cells undergoing invasion, intravasation, and extravasation
|
1) tumor cell binding (to basement membrane)
2) proteolysis of ECM 3) Migration of tumor cell |
|
When, in terms of adhesion, is cancer invasion optimal?
|
At intermediate adhesion
|
|
Why are cancer cells with no adhesion not effective?
|
No migration, no growth
|
|
Describe the effects of metalloprotease inhibitors on cancer
|
Modest effects by themselves
|
|
What is the effect of treating cancer with a metalloproteinase and a chemotherapeutic agent?
|
Significantly fewer deaths due to cancer
|
|
What aids in attaching tumor cells to the basement membrane?
|
laminin receptors
|
|
What is the role of integrins in extravasation?
|
They are cell surface proteins which aid to bind a variety of adhesion molecules and thus allowing binding to endothelium and beginning extravasation
|
|
What sequence is readly recognized by integrins?
|
Arg-Gly-Asp
|
|
How do tumors move through extracellular matrix?
|
by hydrolzying it
|
|
What is the main serine protease produced by tumor cells?
|
plasminogen activator (typically urokinase type, uPa)
|
|
What is the function of plasminogen activator
|
activates it to plasmin, which in turn hydrolyzes the extracellular matrix (degrades it allowing for tumor invasion)
|
|
Describe the function of metastatic mice lacking uPa?
|
no plasminogen activator, no metastatic melanoma
|
|
What is the function of interstitial collagenase?
|
to hydrolyze collagen I, II and III
|
|
How do tumors move through extracellular matrix?
|
by hydrolyzing it
|
|
What is the main serine protease produced by tumor cells?
|
plasminogen activator
|
|
What is the function of plasminogen activator
|
activates it to plasmin, which in turn hydrolyzes the extracellular matrix
|
|
Describe the function of metastatic mice lacking uPa?
|
no plasminogen activator, no metastatic melanoma
|
|
What is the function of interstitial collagenase?
|
to hydrolyze collagen I, II and III
|
|
What is the functionof Type IV and V-specific collagenases?
|
To break down the basement membrane
|
|
Describe the presence of type IV collagenase in both highly metastatic variants and tumorigenic nonmetastatic variants
|
Tumorigenic nonmetastatic variants have significantly less type-IV collagenase than highly metastatic variants do
|
|
What are autocrine motility factors?
|
induce motility by receptor-coupled phosphoinositide-specific phospholipase C
|
|
What effect does autocrine motility factor have on calcium?
|
activates phosphoinositide metabolism which increases calcium
|
|
What is the result of autocrine motility factor increasing amounts of calcium in the cell?
|
The calcium acts to remodel the actin cytoskeleton via gelsolin
|
|
Describe the process of gene knockout
|
Ability to insert a heterozygous or homozygous gene into an animal using selective markers and recombination
|
|
What is homologous recombination?
|
the mutated gene is inserted onto a plasmid at the site of the endogenous gene. This mutated gene is then inserted into the endogenous site of the DNA
|
|
Describe how homologous recombination is viewed in mice
|
Use a black marker and insert into a white mouse. Information is taken up if the mouse turns out to black and white striped. Then, the chimeric mice are cross over and over until black mice occur.
|
|
What is the function of DCC7?
|
involved in cell adhesion
|
|
What makes metastatic cells especially difficult to treat?
|
after they arise from the primary tumor, they develop new properties different from the primary tumor
|
|
What is the theoretical mechanism of action in metalloproteinase inhibitors?
|
proteinases are used to migrate and invade distant tissue. Metalloproteinase inhibitors aim to stop the migration and invasion.
|
|
Why can't we overrun the body with metalloproteinases in an attempt to stop metastasis?
|
Proteinases within the body are needed to break down the collagen fibers and extracellular matrix
|
|
What can inhibit the effect of autocrine motility factors?
|
pertussis toxin
|
|
What is the advantage to using gene knockout?
|
By isolating certain genes of interest, we can specifically note the result of a particular mutations
|
