20. Traditional cancer treatments are surgery, radiation, and chemotherapy. Newer approaches block hormone receptors, stimulate cell specialization, block telomerase, and inhibit angiogenesis. A genomic approach identifies mutations and differences in gene expression that define cancer subtypes.
7. Define dedifferentiation.
8. List the processes and pathways that are abnormal in cancer.
9. Describe what happens as a cancer grows beyond the original tumor.
10. Explain what is inaccurate about the statement “cancer cells are the fastest dividing cells in the body.”
11. Describe four ways that cancer can originate at the cell or tissue level.
12. Define cancer stem cell.
13. Distinguish between a proto-oncogene and an oncogene.
18.2 Characteristics of Cancer Cells
5. A tumor cell divides more frequently or more times than cells surrounding it, has altered surface properties, loses the specializations of the cell type it arose from, and produces daughter cells like itself.
6. A malignant tumor infiltrates tissues and can metastasize by attaching to basement membranes and secreting enzymes that penetrate tissues and open a route to the bloodstream.
From there, a cancer cell can travel, establishing secondary tumors.
18.3 Origins of Cancer Cells
7. Cell specialization and position within a tissue are important determinants of whether cancer begins and persists.
8. Cancer stem cells can divide to yield cancer cells and abnormally differentiated cells.
9. A cell that dedifferentiates and/or turns on expression of
“stemness” genes can begin a cancer.
10. A mutation that enables a cell to divide continually can alter the percentages of cells in a tissue that can divide, resulting in an abnormal growth.
11. Chronic repair of tissue damage can provoke stem cells into producing an abnormal growth.
18.4 Cancer Genes and MicroRNAs
12. Cancer is often the result of activation of proto-oncogenes tooncogenes, and inactivation of tumor suppressor genes.
Mutations in DNA repair genes cause cancer by increasing the mutation rate.
13. Proto-oncogenes normally promote controlled cell growth, but are overexpressed because of a point mutation, placement next to a highly expressed gene, or transcription
Review Questions
1. Explain the connection between cancer and control of the cell cycle.
2. Explain why not all cells whose chromosomes have long telomeres are cancer cells.
3. Explain how the cell cycle is controlled from both inside and outside the cell.
4. Explain why cancer is usually a genetic disease at the molecular and cellular levels, but not at the whole-body level.
5. Explain why it is important to know whether a cancer is sporadic or inherited.
6. List four characteristics of cancer cells.
www.mhhe.com/lewisgenetics9
Answers to all end-of-chapter questions can be found at www.mhhe.com/lewisgenetics9. You will also find additional practice quizzes, animations, videos, and vocabulary flashcards to help you master the material in this chapter.
20. Explain how comparing mutations in cells from the same cancer type at different stages can reveal the sequence of genetic changes behind the cancer.
21. Explain how mutations differ from gene expression changes in cancer.
22. Describe a way that exploring the genome of cancer cells reveals information not apparent from focusing on one type of cancer or one gene associated with cancer.
23. Distinguish among population, case-control, and prospective studies to identify environmental factors in cancer.
24. Explain how a cancer treatment that targets cell surface receptors works.
25. Explain why not all cancers affecting the same cell type respond the same way to a particular drug.
14. Describe two ways that oncogenes are activated.
15. Explain how an oncogene is associated with a gain of function and a mutation in a tumor suppressor gene is associated with a loss of function.
16. Explain how retinoblastoma, a p53 -related cancer, inherited stomach cancer, and BRCA1 breast cancer have similar causes.
17. Explain how microRNAs can affect oncogenes and tumor suppressor genes.
18. Distinguish between gatekeeper and caretaker genes in cancer.
19. Describe how a form of inherited colon cancer illustrates that several mutations can contribute to causing the disease.
8. Colon, breast, ovarian, and stomach cancers can be prevented by removing the affected organ. Why is this approach not possible for chronic myeloid leukemia?
9. A vegetarian develops pancreatic cancer and wants to sue the nutritionist who suggested she follow a vegetarian diet. Is her complaint justified? Why or why not?
10. MammaPrint is a DNA microarray-based test of the expression of seventy genes implicated in breast cancer. Certain patterns are significantly more common in cancers that spread, creating a “signature” that doctors can use to guide treatment decisions. Cite an advantage and a shortcoming of this test.
11. The discovery of cancer stem cells suggests a new type of treatment—develop a drug that stops self-renewal. Explain how such a drug might work, and what an adverse effect might be.
12. Colorectal cancer is diagnosed in half a million people worldwide each year. In 4 percent of diagnosed individuals, the cancer is part of a familial cancer syndrome, such as Lynch syndrome (MIM 114400). Genetic testing for Lynch syndrome targets mismatch repair genes, and costs about $3,000. What information would be valuable to decide if it is practical to test for Lynch syndrome for all cases of newly diagnosed colon cancer?
13. A mutation in a gene called FLT3, which encodes a tyrosine kinase receptor, causes acute myelogenous leukemia, which has a five-year survival rate of 20 percent. A new drug blocks the receptor on white blood cells. Explain how it works.
14. Rose and Angela are 4- year-old identical twins. Rose develops leukemia, but Angela does not. How is this possible?
Applied Questions
1. An individual can develop breast cancer by inheriting a germline mutation, then undergoing a second mutation in a breast cell; or by undergoing two mutations in a breast cell, one in each copy of a tumor suppressor gene. Cite another type of cancer, discussed in the chapter, that can arise in these two ways.
2. How do the mechanisms of the drugs Gleevec and Avastin differ?
3. A young black woman thinks that she cannot get a BRCA form of breast cancer because she isn’t Jewish. Is she correct?
4. von Hippel-Lindau syndrome (MIM 193300) is an inherited cancer syndrome. The responsible mutation lifts control over the transcription of certain genes, which, when overexpressed, cause tumors to form in the kidneys, adrenal glands, and blood vessels. Is the von Hippel-Lindau gene an oncogene or a tumor suppressor? Cite a reason for your answer.
5. The BRCA2 gene causes some cases of Wilms’ tumor and some cases of breast cancer. Explain how the same tumor suppressor mutation can cause different cancers.
6. Ads for the cervical cancer vaccine present the fact that a virus can cause cancer as startling news, when in fact this has been known for decades. Explain how a virus might cause cancer.
7. A tumor is removed from a mouse and broken up into cells.
Each cell is injected into a different mouse. Although all the mice used in the experiment are genetically identical and raised in the same environment, the animals develop cancers with different rates of metastasis. Some mice die quickly, some linger, and others recover. What do these results indicate about the characteristics of the original tumor cells?
Case Studies and Research Results
19. Elsie finds a small lump in her breast and goes to her physician, who takes a medical and family history. She mentions that her father died of brain cancer, a cousin had leukemia, and her older sister was just diagnosed with a tumor of connective tissue. The doctor assures her that the family cancer history doesn’t raise the risk that her breast lump is cancerous, because the other cancers were not in the breast. Is the doctor correct?
20. Lung cancer is classified as “small cell” or “non–small cell”
based on the appearance of cancer cells under a microscope.
However, non–small cell lung cancers fall into three subgroups, based on gene expression patterns. Suggest two ways that this information might be used.
17. Go to http://cancergenome.nih.gov and describe a recent discovery. Describe the type of cancer and how genomic information either confirms what was already known about particular genes that cause the cancer, or adds to or changes what was known.
18. Consult the websites for the pharmaceutical companies that market Herceptin, Gleevec, Avastin, or any other cancer drug and explain how the drug works.
Web Activities
15. Go to the Cancer Quest website ( www.cancerquest.org ).
From the menu on the left, click on Cancer Genes. Select an oncogene or tumor suppressor gene and describe how, when mutant, the gene causes cancer.
16. Go to www.cancer.gov . Click on “search for clinical trials.”
Select a type of cancer from the drop-down menu, and then click “genetic.” Read about a clinical trial and describe the genetic predisposition or changes that are being studied.
Improving Pig Manure
Pig manure presents a serious environmental problem. The animals do not have an enzyme that would enable them to extract the mineral nutrient phosphorus from a compound called phytate in grain, so they are given dietary phosphorus supplements. As a result, their manure is full of phosphorus. The element washes into natural waters, contributing to fish kills, oxygen depletion in aquatic ecosystems, algal blooms, and even the greenhouse effect. But biotechnology may have solved the “pig poop” problem.
In the past, pig raisers have tried various approaches to keep their animals healthy and the environment clean. Efforts included feeding animal by-products from which the pigs can extract more phosphorus, and giving supplements of the enzyme phytase, which liberates phosphorus from phytate. But consuming animal by-products can introduce prion diseases, and giving phytase before each meal is costly. A
“phytase transgenic pig,” however, is genetically modified to secrete bacterial phytase in its saliva, which enables it to excrete low-phosphorus manure.
A transgenic organism has a genetic change in each of its cells. The transgenic pig has a phytase gene from the bacterium E. coli. Its manure has 75 percent less phosphorus than normal pig excrement.
Genetic Technologies:
Amplifying, Modifying, and Monitoring DNA
Chapter Contents