Cancer - Campbell Flashcards
Name two drugs first used in 1940 to treat acute lymphocytic leukemia that are still in use today. What metabolic pathway or pathways do they inhibit? What differentiates them from the most recently developed cancer therapies?
6-mercaptapurine (6-MP): Purine synthesis inhibitors and affects DNA replication
Methotrexate: Affects purine and thymidine synthesis
These older drugs are different from most recently developed cancer therapies in that they take the “shotgun”/ broad approach, whereas newer ways use targeted therapies.
Cushing syndrome is caused by an overgrowth of cells in the adrenal gland that produce cortisol. The tumor that results leads to overproduction of cortisol and increased drinking, eating, urination and enlarged, distended abdomen, “skull-like” look head. These tumors do not typically invade other tissues, remaining confined to an enlargement of the original area. Would Cushing syndrome be characterized as a cancer because it involves a tumor?
No. (By Bill)
Which of the following can sometimes be involved in the genesis of a cancer? (may have more than one answer)
A. Bacteria. B. viruses. C. inherited predispositions D. gene defects E. environmental causes (e.g. excess sunlight, some chemicals)
A. Bacteria
B. Viruses
C. inherited predispositions
E. environmental causes (e.g. excess sunlight, some chemicals)
Which of these is always involved in cancer?
A. Bacteria.
B. viruses.
C. inherited predispositions
D. gene defects
E. environmental causes (e.g. excess sunlight, some chemicals)
D. gene defects
When the gene for ras has a certain mutation, it gains activity (has increased function). Defects in this gene are also associated with cancer. Is the normal ras gene a tumor suppressor, an oncogene, an anti-oncogene, or a proto-oncogene? (more than one answer be correct)
Proto-oncogene
Protos are the normal form of growth signaling genes that can become oncogenes throug gain of function.
By Bill
When the gene for ras has a certain mutation, it gains activity (has increased function). Defects in this gene are also associated with cancer. Is the mutant ras gene a tumor suppressor, an oncogene, an anti-oncogene, or a proto-oncogene?
Oncogene (A normal gene can be a proto, but only after gaining a function (mutation) does it become an oncogene)
by Bill
When the APC gene has a certain mutation, it loses activity (has reduced function). Defects in this gene are also associated with cancer. Is the normal APC a tumor suppressor, an oncogene, an anti-oncogene, or a proto-oncogene (more than one answer may be correct)?
Anti-oncogene / tumor suppressor
Same thing! Normal activity must decrease cancer if reduced activity increases it! (By Bill)
When the APC gene has a certain mutation, it loses activity (has reduced function). Defects in this gene are also associated with cancer. Is the mutant APC a tumor suppressor, an oncogene, an anti-oncogene, or a proto-oncogene? (more than one answer may be correct)
I think it may still be an anti-oncogene, because although it has lost function , it is still functioning in some capacity. Maybe?
By Bill
What does the gene p53 do? What happens when it gets knocked out (i.e. “loss of function)”?
Gene p53 regulates the checkpoint between G1 and S phase in the cell cycle. When gene p53 is knocked out, cancer occurs.
The loss of function of what two genes have a 1% relationship to colorectal cancer?
HMLH1 and HMSH2 are DNA repair genes that become defective and result in cancer
BRCA1 is a gene discovered in 1994 that when even one defective copy is inherited predisposes to breast and ovarian cancer, and to a lesser extent pancreatic cancer. BRCA1 has a role in cell cycle arrest in response to DNA damage (i.e. BRCA1 participates in halting cell division while certain types of DNA damage are being repaired. Would this make BRCA1 a proto-oncogene, an oncogene, or an anti-oncogene?
BRCA1 is an anti oncogene.
By Bill
The human platelet derived growth factor receptor beta (PDGFRbeta) is a receptor involved in vascular system development. One of its normal roles is in promoting proliferation of vascular smooth muscle cells surrounding endothelial cells of developing blood vessels. Explain why it might be a proto-oncogene and how it might become an oncogene.
It is a proto-oncogene because it normally promotes cell proliferation. If its function was enhanced it could go out of control and become an oncogene.
By Bill
Make a list of all examples from class of cell cycle control genes, all growth signal transduction genes, and all DNA repair genes that when defective may contribute to the development of cancer. Which are cell cycle, which are growth signaling and which are DNA repair genes?
Cell Cycle Control-
P53 (controls checkpoint between G1-S)
Growth Signal Transduction-
HER2
DNA Repair-
hMLH1
hMSH2
(Bill)
Name some characteristics of matrix metalloproteinase proteins. What process associated with cancer are matrix metalloproteinases involved in?
Characteristics: enzymes that cut proteins in the extracellular matrix that require metal ions to function.
Involved in Metastasis. (By Bill)
Explain the mechanism discussed in class by which cancer cells may evade apoptosis.
Cancer cells evade apoptosis by up-regulating XIAP (x-linked inhibitor of apoptosis).