Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
25 Cards in this Set
- Front
- Back
What is an oncogene?
|
gain of function muations
|
|
What is a tumor supressor?
|
Loss of function mutation
|
|
An example of Independance from mitogenic stimulation?
|
1. A point mutation causes Ras to become constitutively active increasing production of growth proteins
2. Increase in autocrine GF (TGF-alpha and PDGF) 3. Increase in the # of receptors (EGF receptors like Her2 in breast cancer) *this leads to amplification |
|
An example of Resistance to Growth Inhibition?
|
1. Retinoblastoma and the loss of the RB gene
2. TGF-Beta signaling Pathway (bad TGF-B Receptor and loss of CDK inhibition) 3. SMAD mutations prevent the degradation of of cyclins |
|
What controls cellular differentiation?
|
Myc and MAD
|
|
What happens when Myc activity is increased?
|
Increased: Proliferation and Dedifferentiation
|
|
What happens when Mad is increased?
|
The cell is differentiated and terminal i.e normal
|
|
What is an example of uncontrol cell differentiation caused by an increase in Myc activity?
|
1. Burkittts Lymphoma (cMyc translocation to Ig promoter)
2. Acute Lymphoblastic Leukemia |
|
What does a mutation in the oncogene RET do?
|
constitutively activates the RT-K Receptor
|
|
What type of cancer does a mutation in the oncogene Ras definitely cause?
|
Prostate Cancer
|
|
Cancer sensitivity to anti-growth drugs is strongly dependant on what?
|
cell cycle
|
|
What is an example of cellular imortality?
|
mutations in the Telomerase leads to limitless replication
|
|
What is an angiogenesis inducer?
|
VEGF stimulates VEGF Receptors on endothelium
|
|
Whate are some inhibitors of Angiogenesis?
|
1. Thrombospondin
2. Beta-Interferon 3. CD36 |
|
What are some mechanisms that lead to Invasion and Metastasis?
|
1. Alter Cell to Cell interactions by lowering E-Cadherins and N-CAMs
2. Alter Cell to ECM interaction by changing Integrins 3. Increase Proteases --> destroy ECM and lead to motility |
|
What are some players that SENSE the extracellular enviorment and activation promote Apoptosis?
|
TNF Receptors
|
|
What are some pro-cancer players that SENSE the extracellular enviorment and activation inhbit Apoptosis?
|
IGF Receptors
|
|
What are some players that SENSE the intracellular enviorment and activation promote Apoptosis?
|
p53
|
|
What are some pro-cancer EFFECTORS in the nucleus enviorment upon activation inhbit Apoptosis?
|
BCL-2
|
|
What are some EFFECTORS in the nucleus enviorment upon activation promote Apoptosis?
|
Bax
|
|
What are effectors from the mitochondria that promote Apoptosis?
|
1. Cytochrome C
2. APAF 3. Caspace |
|
What intracellular regulators of apoptosis are controlled by ubiquitination and subsequent destruction in the proteosome?
|
1. BCL-2
2. Caspace |
|
How does ubiquitination of I-kB lead to survival?
|
normally I-kB inhibits NF-kB (anti-apoptotic protein)
|
|
What are mechanism that lead to Genetic Instability?
|
1. mutations in p19 cause p53 to be inhibited by HDM2
2. Mismatch Repair 3. Accumilation of broken and fused chromosomes from bad homologous repair mechanisms |
|
What chemotheraputic drug inhibit the ABL-BCR kinase protein?
|
1. Imatinib
2. Gleevec |