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Flashcards in Biochem EX1 - Cancer Deck (13)
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1

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 to head. These tumors do not typically invade other tissues, remaining confined to an enlargement of their original area. Would Cushing syndrome be characterized as a cancer because it involves a tumor?

No. You need invasiveness and metastasis.

2

Which of the following can be involved in the genesis of a cancer? Which of these is always involved in a cancer? (may be more than one correct response to the first question, there is only one correct response to the second).

a) bacteria

b) viruses

c) inherited predispositions

d) gene defects

e) environmental causes (e.g. excess sunlight, some chemicals)

Part 1: All of the above

Part 2: Gene defects

3

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 may be correct)? How about the mutant ras gene (only one answer may be correct)?

The normal gene is a proto-oncogene.

The mutant version is an oncogene.

4

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, anti-oncogene, or a proto-oncogene (more than one answer may be correct)? How about the mutant APC (more than one answer may be correct)?

The normal gene is a tumor suppressor (anti-oncogene)

The mutant gene is a mutant tumor suppressor (mutant anti-oncogene)

5

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. RCA1 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 has an additional role in maintaining chromosomal stability, preventing the chromosomal instability that is characteristic of cancer, but this information is not necessary to answer this study question.)

BRCA-1 is an anti-oncogene.

6

The human platelet derived growth factor receptor β (PDGFRβ ) 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 ecome an oncogene.

It's a protooncogene because it causes cell growth, therefore if you have gain of function it will become an oncogene.

7

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. Know which are cell cycle, which are growth signaling, and which are DNA repair genes.

Cell cycle control - P53, cyclins. loss of function leads to cancer.

 

Growth signal Transduction - HER2 (the receptor for EGF- epidermal growth factor). Gain of function causes cancer.

 

DNA repair - HMCH1 and HMSH2. Loss of function causes cancer.

8

Bcl-2 predisposes to follicular lymphoma when the gene is interrupted by a translocation involving chromosomes 14 and 18. In what way is the Bcl-2 gene “split” in this way consistent with being called an oncogene? In what way is the Bcl-2 gene broken up in this way not an oncogene?

The Bcl-2 gene split is consistent with being called an oncogene because oncogenes occur when there is a gain of function. During translocation, the portion of chromosome 18 where Bcl-2 is located is moved to the very active portion of chromosome 14. The translocation causes a gain of function for Bcl-2.

 

However, it can also not be considered an oncogene due to a loss in function. Bcl-2 is an anti-apoptotic gene. A gain of function of Bcl-2 would result in a loss of function in apoptosis.

9

Explain the mechanism discussed in class by which cancer cells may evade apoptosis (there are actually other mechanisms that apply to other cancers not discussed for lack of time).

The cells have a gene on the X chromosome - called XIAP (x-linked inhibitor of apoptosis). If the cell begins to recognize that it should enter an apoptotic pathway, this protein can stop that process.

10

Name some characteristics of matrix metalloproteinase proteins. What process associated with cancer are matrix metalloproteinases involved in?

The degrade ECM proteins using metals as cofactors.

They are involved in metastasis.

11

Agent 99 is a promising new candidate for cardiovascular disease. Agent 99 stimulates angiogenesis and thus aids blood circulation to areas served by blood vessels that have been blocked by atherosclerosis. Would this make a good cancer chemotherapeutic agent and why?

a) Yes, because in cancer cells apoptosis and angiogenesis are often increased so the cancer cell will not die.

b) No, cancer cells may even benefit from increased blood supply.

c) No, improved cardiac function will increase metastasis.

d) Yes, because it would cure both heart disease and cancer.

e) Yes, and many stimulants of angiogenesis are in clinical trials to test their efficacy in fighting cancer.

b) No, cancer cells may even benefit from increased blood supply.

12

The OSI Pharmaceuticals/Genentech product Tarceva (erlotinib) was approved in the fall of 2004 for the treatment of patients with locally advanced or metastatic non-

small cell lung cancer after failure of at least one prior chemotherapy regimen and advanced pancreatic cancer. Tarceva is a small molecule taken in tablet form that specifically inhibits the kinase activity of human epidermal growth factor receptor (EGFR or HER-1). Will Tarceva likely prove effective and be approved for treatment of other cancers such as small-cell lung cancer and breast cancer, and why?

a) Yes, since the human epidermal growth factor receptor 2 (HER-2) gene is overexpressed in many other cancers, breast cancer being one example.

b) Yes, because Tarceva is a brand new drug designed with all our new knowledge of the molecular basis of cancer to have wide application in cancer chemotherapy.

c) Yes, because p53 is also a plasma membrane-spanning kinase, and is defective in more cancer tumors than any other gene.

d) No, because unfortunately few cancers may be treated by a drug that may be administered in such a convenient form as a tablet.

e) No, because the genes defective in other cancers such as small-cell lung cancer and breast cancer are typically different than those defective in non-small cell lung cancer.

e) No, because the genes defective in other cancers such as small-cell lung cancer and breast cancer are typically different than those defective in non-small cell lung cancer.

13

You are meeting with a breast cancer patient and her family to discuss treatment options. They have heard of Herceptin and inquire about its use. The pathology report or that patient included a biopsy that indicated Herceptin would not be effective. Which of the following would be your best response?

a) Herceptin should be given to this patient despite the pathology report, just in case it works.

b) The pathologist said it shouldn’t be used, and they are the expert.

c) The mechanism of Herceptin is to block a receptor that is overexpressed in some patients. In this patient, the receptor is not overexpressed, so the drug will be of no use.

d) The mechanism of Herceptin is to block a DNA repair enzyme that is overactive in some patients. In this patient, the DNA repair enzyme is not overactive, so the drug will be of no use.

e) Since cancer drugs have few side effects, it would be okay, but expensive (a course of treatment is ~50 k$ to >100 k$), to use if the patient and family really want

 

d) The mechanism of Herceptin is to block a DNA repair enzyme that is overactive in some patients. In this patient, the DNA repair enzyme is not overactive, so the drug will be of no use.