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;
31 Cards in this Set
- Front
- Back
Cancer, in general, results from __ mutations. Hereditary dz comes from __ mutations.
|
Generally, somatic mutations. Hereditary - germ-line.
|
|
Oncogene = ?
|
Genes that promote autonomous cell growth in neoplasms.
|
|
Protooncogene = ?
|
Tightly controlled genes that promote autonomous cell growth in neoplasms.
|
|
__ is the most commonly mutated oncogene.
|
Ras.
|
|
Ras mutation leads to _?
|
Constitutive activation of cell cycle that leads to uncontrolled growth.
|
|
Name the three codons that have issues in Ras mutation.
|
12, 13, and 61.
|
|
__ negatively regulated Ras.
|
GAPs.
|
|
K-RAS mutations are commonly found in what four malignancies?
|
GI, endometrial, lung, and myeloid.
|
|
N-RAS mutations are commonly found in what two malignancies?
|
Myeloid and melanoma.
|
|
H-RAS mutations are commonly found in what malignancy?
|
Bladder cancer.
|
|
Chromosomal translocations cause malignancy through oncoprotein __ and oncogene __.
|
Oncoprotein fusion. Oncogene activation.
|
|
100% of patients with endemic or non-endemic Burkitt lymphoma have this molecular signal of cell growth.
|
c-myc.
|
|
HER2 shows an example of __ __ in breast cancer. This activates __.
|
Gene amplification. Activates oncogenes.
|
|
This protooncogene codes for PDGF.
|
c-SIS.
|
|
Overexpression of PDGF is found in what two malignancies?
|
Astrocytoma and osteosarcoma.
|
|
This oncogene stimulates growth by interacting with receptors that have tyrosine kinase activity.
|
HER2.
|
|
These two oncogenes increase activity by coding for signaling molecules.
|
ABL and Ras.
|
|
How do the MYC genes code for unregulated cell growth?
|
They code for transcription factors that cause dysregulation of other genes critical to cell proliferation or the cell cycle.
|
|
When particular CDKs bind with particular cyclins, __ initiates the cell cycle.
|
Phosphorylation.
|
|
Two-hit hypothesis of tumor suppressor genes.
|
Must lose activity of both alleles for tumor suppressor to be active.
|
|
What is the difference between an oncogene and a tumor suppressor gene? Which one requires one allele to be mutated for tumorigenesis?
|
Oncogenes activate mutations. Tumor suppressor genes inactivate mutations. Oncogenes only need one mutated allele to promote tumorigenesis.
|
|
__ is active when hypophosphorylated; it binds to E2F, blocking the cell cycle at G1 --> S.
|
Rb.
|
|
E_ blocks Rb.
|
E7.
|
|
__ is the most common mutation found in cancer.
|
p53.
|
|
Working p53 increases __ and __.
|
p2 (CDK inhibitor) and BAX (apoptosis).
|
|
This TSG is involved in neurofibromatosis.
|
NF1.
|
|
This TSG is involved in FAP and hepatocellular carcinoma.
|
APC.
|
|
This TSG is involved in Wilms tumor.
|
WT1.
|
|
This TSG is involved in renal ca, pheochromocytoma, and CNS hemangioblastomas.
|
VHL.
|
|
__ is the prototype anti-apoptosis gene.
|
BCL-2.
|
|
BAX promotes __.
|
Apoptosis.
|