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WVSOM
Oncology
Question | Answer |
---|---|
Typically induces cell transformation | Proto-oncoogene |
The development of cancer cells.Cancer cells commonly inactivate inhibitor growth signals, evade apoptosis, have a limitless replicative potential, invade tissue, a sustained mutagenesis and undergo angiogenesis | Oncogenesis |
Growth factors/receptors, Signal Transduction pathways, Transcription factors, Cell cyle control proteins, DNA repair enzymes, Apoptosis Proteins | Examples of oncogenes |
Point mutation, Chromosomal translocation, Multiple copies of DNA, Frame shift mutation | Mechanisms in which proto-ocogenes become oncogenes |
Regulates the G1 phase of the cell cycle | Cyclin D |
Cyclin D binds to | CDK 4/6 |
Inhibitors of the cell cycle. Help to control the progession through the cell cycle | Cylin Dependent Inhibitors (CDI) |
The formation of cyclin D/CDK 4/6 complex is inhibited by | p15, p16, p18, p19 |
Most cyclin/cdk complexes are inhibited by | p21 |
p21 is activated by | p53 |
This monitors DNA damage and activates p21 to inhibit cell division | p53 |
A monomeric G protein and a proto-oncogene | Ras |
An example of a tumor suppressor | Retinoblastoma (Rb) |
DNA repair is initiated by | p53 |
Tumor suppressor genes become oncogenic by | Deletions, Point mutations, DNA methylation |
A loss-of-function mutation is an example of | tumor suppressors |
A gain-of-function mutation is an example of | proto-oncogenes |
Ras directly activates | Raf |
MEK directly activates | MAPK |
MAPK activates | Fos (a transcription factor) |
Ras induces cell proliferation | True |
Hedgehog is a proto-oncogene | True |
The EGF receptor is an example of a proto-oncogene | True |
The mitochondrial pathway and the membrane receptor pathway are two type of mechanisms that induce | Apoptosis |
Activation of caspase-8 induces apoptosis | True |
Activation of the ... receptor activate apoptosis through the activation of caspase-8 | Death |
The activation of the ... pathway is elicited through the activation of Apaf-1, Cyt c, ATP, and pro-caspase-9 | Mitochondrial |
Bcl-2 is an | Anti-apoptotic protein |
Bax is a | Pro-apoptotic protein |
The idea that more than one mutation is required for a normal cell to become a tumor | Multiple Hit Hypothesis |
Benzopyrene (cigarettes), Aflatoxin B, Reactive oxygen species, DNA crosslinking agents, and Alkylating agents are chemicals that can cause | DNA damage |
The inability to repair thymine dimers which are caused by UV irradiation | Xeroderma pigmentosum |
Multiple TTAGGG repeats found at the ends of chromosomes | Telomeres |
The enzyme responsible for creating telomeres and is often inactivated in adult cells but activated during oncogenesis | Telomerase |
Defined as a limited capacity to divide before cells enter a non-proliferate state | Senescence |
Caused by a translocation of the myc gene from chromosome 8 to 14 | Burkitt Lymphoma |
Caused by a translocation between chromosomes 9 and 22 | Chronic Myelogenous Leukemia |