Downloaded by Baktynur Azhybaev ([Link]@gmail.
com)
Test Bank
to accompany
The Cell: A Molecular Approach, Eighth Edition
Geoffrey M. Cooper
Chapter 20: Cancer
TEST FILE QUESTIONS
Multiple Choice
1. A tumor is
a. a malignant growth.
b. any abnormal growth of cells.
c. a benign growth.
d. a cancerous growth.
Answer: b
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Describe tumor progression.
2. Cancer is usually caused by
a. a cancer virus.
b. an inherited oncogene.
c. the stepwise breakdown of normal cell regulatory processes.
d. X rays.
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Describe tumor progression.
3. Tumor initiation occurs in a
a. single protein molecule.
b. single cell.
c. few cells.
d. single tissue.
Answer: b
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Describe tumor progression.
4. A tumor of an epithelial cell is a(n)
a. carcinoma.
b. sarcoma.
c. leukemia.
Downloaded by Baktynur Azhybaev ([Link]@[Link])
d. lymphoma.
Answer: a
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
5. The form of cancer with the highest mortality rate in the United States is
cancer.
a. breast
b. prostate
c. lung
d. colon
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
6. The mechanism by which normal cells stop proliferating as a result of
reduced availability of growth factors is called
a. density dependent inhibition.
b. contact inhibition.
c. differentiation.
d. senescence.
Answer: a
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
7. Which characteristic is commonly the same in both normal cells and cancer cells?
a. Density-dependent inhibition of proliferation
b. Contact inhibition of migration
c. Growth factor requirements
d. Dependence on oxygen and nutrients
Answer: d
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
8. Compared to their normal counterparts, leukemic cells
a. continue to differentiate.
b. fail to proliferate.
c. fail to undergo apoptosis.
d. induce widespread apoptosis.
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Learning Objective: Summarize the properties of cancer cells.
9. In some cases, tumors support their unrestricted proliferation producing a growth
factor that they also respond to. This mechanism is called signaling.
a. endocrine
b. juxtacrine
c. autocrine
d. paracrine
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
10. A tumor promoter is a type of carcinogen that
a. induces apoptosis of healthy cells.
b. decreases chromosomal stability.
c. increases cell proliferation.
d. immortalizes cancer cells.
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Compare cancer induction by chemicals and viruses.
11. Ultraviolet radiation increases the likelihood of a cell becoming malignant
primarily because UV radiation
a. induces melanocytes to express more melanin.
b. breaks DNA into fragments.
c. makes RNA polymerase more error-prone.
d. causes DNA damage that leads to mutations.
Answer: d
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Compare cancer induction by chemicals and viruses.
12. Asbestos increases the risk of mesothelioma and lung cancer because it
a. inhibits differentiation.
b. causes DNA damage.
c. turns on the BRCA oncogenes.
d. acts as a tumor promoter by stimulating cell proliferation.
Answer: d
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Compare cancer induction by chemicals and viruses.
13. Which of the following behaviors most increases the likelihood of developing cancer?
a. Drinking a glass of wine a day
Downloaded by Baktynur Azhybaev ([Link]@[Link])
b. Smoking a pack of cigarettes a day
c. Kissing a person who has cancer
d. Breathing the sawdust from a crown gall tumor
Answer: b
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Compare cancer induction by chemicals and viruses.
14. Oncogenes were first discovered in
a. a chicken retrovirus.
b. a human DNA virus.
c. mouse cancer cells.
d. human cancer cells.
Answer: a
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Explain how retroviral oncogenes were identified.
15. The RNA viruses that most commonly pick up cellular oncogenes are the
a. adenoviruses.
b. retroviruses.
c. papilloma viruses.
d. HIV viruses.
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Explain how retroviral oncogenes were identified.
16. A proto-oncogene is
a. a normal gene from which an oncogene can arise.
b. one that has been picked up by an oncogenic virus.
c. evolving into an oncogene.
d. expressed normally in tumor cells.
Answer: a
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Contrast oncogenes and proto-oncogenes.
17. The viral raf oncogene produces a constitutively active protein because the
a. gene is always on.
b. kinase domain is mutant and cannot be competitively inhibited.
c. regulatory domain has been replaced by viral sequences so the protein cannot be
turned off.
d. GTPase activity is deficient and the protein is always in the GTP form.
Answer: c
Textbook Reference: Oncogenes
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Bloom’s Category: 2. Understanding
Learning Objective: Contrast oncogenes and proto-oncogenes.
18. Which statement describes the first direct evidence for involvement of
cellular oncogenes in human tumors?
a. Normal human cells could be transformed by the src-containing Rous sarcoma viruses.
b. DNA extracted from a human bladder carcinoma was able to transform
recipient mouse cells in culture.
c. DNA extracted from a mouse carcinoma was able to transform recipient human cells
in culture.
d. DNA extracted from a human carcinoma was able to transform recipient chicken
cells in culture.
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
19. The most frequently encountered oncogene in human tumors is
a. fos.
b. myc.
c. ras.
d. src.
Answer: c
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
20. C-myc becomes an oncogene in Burkitt’s lymphoma and several plasmacytomas by a
a. point mutation.
b. duplication.
c. translocation to the immunoglobulin heavy chain locus.
d. deletion of a regulatory sequence.
Answer: c
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
21. The ras proto-oncogene can become an oncogene by a single point mutation
that alters its protein product to have activity.
a. more GTPase
b. constitutive Raf-activation
c. greater nucleotide exchange
d. less nucleotide exchange
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
22. Translocation of a gene can produce a fusion product with uncontrolled protein
kinase activity. An example of this type of fusion protein is
a. Tel/PDGFR.
b. Myc/Max.
c. Fos/Jun.
d. ErbB/Ras.
Answer: a
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
23. What normal cellular process would be affected in a cell line in which Bcl-2
was mutated?
a. Cell cycle
b. Apoptosis
c. cAMP signaling
d. Terminal differentiation
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
24. Loss-of-function mutations can be oncogenic if the mutant gene codes for a
a. telomerase.
b. tumor suppressor protein.
c. cyclin-dependent kinase.
d. DNA synthesis enzyme.
Answer: b
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Contrast tumor suppressor genes and oncogenes.
Questions 25–26. Suppose you were to fuse a tumor cell with a nontumor cell in culture,
grow the daughter cells of the hybrid clone in culture, and then inject them into mice with
defective immune systems.
25. Tumors would likely develop in of the mice.
a. less than 1%
Downloaded by Baktynur Azhybaev ([Link]@[Link])
b. 25%
c. 50%
d. nearly 100%
Answer: a
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 3. Applying
Learning Objective: Contrast tumor suppressor genes and oncogenes.
26. What is the reason for the likely result of the experiment described?
a. Tumorigenicity is dominant.
b. 50% of the cells get a tumor suppressor gene.
c. Tumor suppressor genes are recessive.
d. Tumor suppressor genes are dominant.
Answer: d
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 3. Applying
Learning Objective: Contrast tumor suppressor genes and oncogenes.
27. The first tumor suppressor gene was identified in studies of which human tumor?
a. Burkitt’s lymphoma
b. Retinoblastoma
c. Glioblastoma
d. Promyelocytic leukemia
Answer: b
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Contrast tumor suppressor genes and oncogenes.
28. Nonhereditary retinoblastoma develops only when
a. a somatic mutation inactivates the Rb gene.
b. a somatic mutation activates the Rb gene.
c. two somatic mutations inactivate two separate Rb genes.
d. one germ-line mutation and one somatic mutation inactivate Rb genes.
Answer: c
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Contrast tumor suppressor genes and oncogenes.
29. The product of the human papillomavirus oncogene E7 promotes cancer by
a. inhibiting DNA damage repair pathways.
b. binding and preventing function of Rb protein.
c. ubiquitinating the tumor suppressor p53.
d. enhancing expression of telomerase.
Answer: b
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
30. The tumor suppressor genes Smad2 and Smad4 encode
a. growth factor receptors.
b. GTP-binding signal molecules.
c. transcription factors.
d. inhibitors that bind to transcription factors.
Answer: c
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
31. The normal function of the tumor suppressor protein Rb is to
a. induce apoptosis.
b. inhibit Ras.
c. inhibit progression through the G1 restriction point.
d. inhibit Cdk4/cyclin B activity.
Answer: c
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
32. An increase in p53 activity usually results after a cell receives
a. extracellular growth inhibition signals.
b. DNA damage.
c. heat shock.
d. extracellular growth stimulating signals.
Answer: b
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
33. p53 induces apoptosis by
a. inactivating a growth factor receptor.
b. activating transcription of a Bcl-2 family member.
c. activating transcription of a caspase.
d. directly activating a caspase.
Answer: b
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
34. Apoptosis is induced by p53 when
a. a cell is programmed to die during development.
b. growth factor levels decline to zero.
c. any DNA damage is detected.
d. severe DNA damage is detected and cannot be repaired.
Answer: d
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
35. One function of the tumor suppressor protein p53 is to
a. activate synthesis of p21, a Cdk inhibitor.
b. inhibit phosphodiesterase.
c. stimulate cell cycle progression.
d. phosphorylate cyclin-dependent kinases on an inhibitory site.
Answer: a
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
36. MicroRNAs can act as tumor suppressors by inhibiting expression of all of
the following except
a. Cdk.
b. ras.
c. myc.
d. PTEN.
Answer: d
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
37. Malignant colon cancers are usually the result of
a. inherited mutant oncogenes.
b. inherited mutant tumor suppressor genes.
Downloaded by Baktynur Azhybaev ([Link]@[Link])
c. somatic mutation of an oncogene or tumor suppressor gene.
d. multiple mutations activating oncogenes and inactivating tumor suppressor genes.
Answer: d
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Explain the major types of genetic alterations in
human cancers.
38. What is the cure rate for colon carcinomas that remain localized to their site of origin?
a. 90%
b. 75%
c. 50%
d. 25%
Answer: a
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Explain the importance of early diagnosis.
39. Genetic testing for mutant oncogenes or tumor suppressor genes
a. helps identify high-risk individuals before a tumor develops.
b. offers a definitive indication of which individuals will develop tumors.
c. aids the discovery of other mutations that lead to cancer.
d. is not significantly useful as a healthcare practice.
Answer: a
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
40. Traditional drugs used to treat cancer patients
a. target oncogene function.
b. kill cancer cells specifically.
c. damage DNA or inhibit DNA replication.
d. target tumor suppressor protein function.
Answer: c
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
41. Drugs that inhibit general expression or function of an oncogene will
a. inhibit division of tumor cells only.
b. kill tumor cells only.
c. kill tumor cells as well as normal cells.
d. inhibit cell division of tumor cells and normal cells.
Answer: d
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
42. The therapeutic use of monoclonal antibodies against oncogene proteins is limited to
a. secreted targets, such as growth factors.
b. extracellular targets, such as cell surface receptors.
c. extracellular and cytosolic targets.
d. protein targets.
Answer: b
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
43. Herceptin is a monoclonal antibody against the oncogene protein
a. EGF.
b. Bcr/Abl.
c. ErbB-2.
d. Sis.
Answer: c
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
44. Imatinib (Gleevec) blocks proliferation of chronic myeloid leukemia cells
by inhibiting the protein kinase
a. Bcr/Abl.
b. Cdk/cyclin.
c. MAP kinase.
d. ErbB.
Answer: a
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
Fill in the Blank
1. The process by which tumor cells whose mutations give them a selective
advantage grow preferentially is called .
Answer: clonal selection
Textbook Reference: The Development and Causes of Cancer
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Bloom’s Category: 1. Remembering
Learning Objective: Describe tumor progression.
2. Cancer cells can acquire the capacity for unlimited growth by turning on the gene for
.
Answer: telomerase
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
3. SV40, papillomaviruses, and adenoviruses are tumor viruses.
Answer: DNA
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Compare cancer induction by chemicals and viruses.
4. Herpes viruses (HSV) can induce sarcoma.
Answer: Kaposi’s
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Compare cancer induction by chemicals and viruses.
5. Common human cancers caused by viruses include cervical carcinoma and
cancer.
Answer: liver
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Compare cancer induction by chemicals and viruses.
6. Xeroderma pigmentosum is caused by mutations in genes.
Answer: nucleotide-excision repair
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
7. Many cases of breast cancer can be traced to the and genes.
Answer: BRCA1; BRCA2
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
© 2019 Oxford University Press
Downloaded by Baktynur Azhybaev ([Link]@[Link])
8. treatment of promyelocytic leukemia induces terminal differentiation,
forcing the cancer cells to withdraw from the cell cycle.
Answer: Retinoic acid
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
True/False
1. Transformation can be assayed in cell culture.
Answer: True
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
2. Leukemias arise from cells of the immune system.
Answer: False
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
3. Viruses do not induce tumors in humans.
Answer: False
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Compare cancer induction by chemicals and viruses.
4. SV40, papillomaviruses, and adenoviruses induce transformation by
producing proteins that interact with the tumor suppressor proteins p53 and Rb.
Answer: True
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Compare cancer induction by chemicals and viruses.
5. Oncogenic mutations in ras promote accumulation of the GDP bound form of
the protein.
Answer: False
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
6. Several oncogenes encode antiapoptotic proteins that promote cell survival.
Answer: True
© 2019 Oxford University Press
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the functions of oncogene proteins.
7. BRCA1 and BRCA2 prevent breast cancer by maintaining the integrity of the genome.
Answer: True
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
8. The cure rate for carcinomas detected early, when they have not spread from their
site of origin, is 50%.
Answer: False
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Explain the importance of early diagnosis.
9. Acute promyelocytic leukemia results from a mutated retinoic acid receptor,
effectively blocking cell differentiation and allowing leukemic cells to continue
proliferation. Answer: True
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
10. Cancer patients with mutant p53 can be treated effectively with radiation therapy.
Answer: False
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
11. The sensitivity of tumors to inhibition of activated oncogenes is called
oncogene addiction.
Answer: True
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
12. The first drug developed against a specific oncogene and approved for clinical
use was a monoclonal antibody against ErbB-2.
Answer: True
Textbook Reference: Molecular Approaches to Cancer Treatment
© 2019 Oxford University Press
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Bloom’s Category: 1. Remembering
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
Short Answer
1. How do cancer cells become able to proliferate indefinitely, while normal cells
become senescent after a limited number of cell divisions?
Answer: With each cell division, the chromosomes are replicated, and each time they
replicate, they lose a portion of the repetitive sequence (telomere) on each end. The
enzyme telomerase is able to extend the repetitive sequences but normally is not
expressed at high enough levels to maintain chromosomal length indefinitely.
Telomerase expression is significantly increased in most cancers, allowing these cells to
divide indefinitely.
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
2. When does autocrine induction of cell proliferation occur?
Answer: When a mutation causes a growth factor and its receptor to be expressed by the
same cell
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
3. List three ways in which a proto-oncogene can be activated to become an
oncogene. Answer: (1) Point mutation, (2) gene amplification, and (3) gene
translocation Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Contrast oncogenes and proto-oncogenes.
Questions 4–10. Explain the conditions in which the following oncogene protein products
may be oncogenic.
4. The growth factor EGF
Answer: When it is produced by the same cell that has active receptors for EGF, thereby
creating an autocrine (positive) feedback system to stimulate cell proliferation
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
5. The transcription factors Myc, Fos, or Jun
Answer: When they are expressed at high or constant levels in cells in which they
normally would not be expressed
Textbook Reference: Oncogenes
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
6. The growth factor receptor PDGFR
Answer: When translocation (deletion or mutation) alters the receptor domain so that the
kinase domain becomes constitutively active
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
7. The intracellular signal transducing molecule Ras
Answer: When mutation of its GTPase activity occurs so that it cannot split the
bound GTP and thus continually sends a signal to Raf (to activate the MAP kinase
pathway) Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
8. The Cdk-activating protein cyclin D
Answer: When it is expressed constitutively or at high levels
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
9. The cell-differentiation-inducing receptor ErbA (thyroid hormone receptor)
or PML/RARα (retinoic acid receptor)
Answer: When mutant receptors interfere (compete) with the normal differentiation
receptors
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the functions of oncogene proteins.
10. The tumor suppressor protein p53 or Rb
Answer: When mutant suppressor proteins are not able to prevent cell cycle
progression; or when p53 is not able to induce apoptosis when the DNA is damaged; or
when the cell is infected by viruses
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
11. Name three tumor suppressor genes.
Answer: Any three of the following: BRCA1 or BRCA2, Rb, p53, INK4, PTEN, APC,
TBRII, Smad2, and Smad4
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
DASHBOARD QUIZ QUESTIONS
Multiple Choice
1. What is the difference between a benign tumor and a malignant tumor?
a. A malignant tumor is painful, and a benign tumor is not.
b. A malignant tumor has the ability to spread to other tissues and to initiate tumors
at secondary sites, whereas a benign tumor does not spread.
c. A benign tumor will cause a less severe form of cancer than a malignant tumor.
d. A malignant tumor is caused by a virus, whereas a benign tumor arises spontaneously.
Answer: b
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Explain the difference between benign and malignant
tumors.
Feedback A: Incorrect. Pain is not the distinguishing feature between malignant and
benign tumors; both can be either painless or painful.
Feedback B: Correct! Benign tumors do not spread, and they are better candidates for
removal by surgery. Malignant tumors, on the other hand, can spread throughout the
body, invading other tissues and organs. They are far more destructive and difficult to
treat.
Feedback C: Incorrect. Benign tumors are not considered cancerous.
Feedback D: Incorrect. Both malignant and benign tumors can arise spontaneously or be
caused by viruses.
2. Which statement about cancers is false?
a. Carcinomas are malignancies of epithelial cells.
b. Leukemias are malignancies that arise from blood-forming cells.
c. Lymphomas are malignancies from colon tissue.
d. Sarcomas are malignancies of connective tissue like muscle and bone.
Answer: c
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
Feedback A: Incorrect. This is true.
Feedback B: Incorrect. This is true.
Feedback C: Correct! This is false. Lymphomas are malignancies that arise from cells of
the immune system.
Feedback D: Incorrect. This is true.
3. The type of cancer with highest mortality in the United States is cancer of the
Downloaded by Baktynur Azhybaev ([Link]@[Link])
a. prostate.
b. colon/rectum.
c. breast.
d. lung.
Answer: d
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
Feedback A: Incorrect. Prostate cancer is the most frequently occurring cancer, but it
is not the most lethal.
Feedback B: Incorrect. This is the second most lethal cancer, killing approximately
one- third the number of people as the most lethal cancer.
Feedback C: Incorrect. This is one of the most lethal cancers, but not the most lethal.
Feedback D: Correct! Deaths from lung cancer account for approximately 30% of
all cancer deaths in the United States.
4. Which statement concerning the difference between cancer cells and normal cells is
false?
a. Normal cells display density-dependent inhibition of cell proliferation.
b. Cancer cells have reduced requirements for extracellular growth factors.
c. Malignant cells generally secrete proteases that digest extracellular matrix components.
d. Cancer cells undergo normal differentiation, but excessive proliferation.
Answer: d
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
Feedback A: Incorrect. This is
true. Feedback B: Incorrect. This
is true. Feedback C: Incorrect.
This is true.
Feedback D: Correct! This is false. Cancer cells do not differentiate normally. In fact,
many therapies are designed to push cancer cells toward terminal differentiation where
they would be likely to stop proliferating.
5. Angiogenesis contributes to cancer development by
a. providing nutrients and oxygen to tumors and by facilitating metastasis.
b. initiating a mutation in a gene that causes uncontrolled cell growth.
c. inhibiting apoptosis (programmed cell death).
d. preventing the normal inhibition of growth that occurs when cells make contact.
Answer: a
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the properties of cancer cells.
Feedback A: Correct! Tumors stimulate angiogenesis, or new blood vessel formation,
which brings them nutrients and oxygen. In addition, the blood vessels provide a path of
entry into the circulatory system, from which tumors can spread to other tissues.
Feedback B: Incorrect. Angiogenesis does not occur until after uncontrolled cell growth
Downloaded by Baktynur Azhybaev ([Link]@[Link])
has been initiated.
Feedback C: Incorrect. Inhibition of apoptosis contributes to the development of cancer,
but it is not related to angiogenesis.
Feedback D: Incorrect. A loss of contact inhibition is characteristic of cancerous cells,
but it does not involve angiogenesis.
6. Infection with which of the following viruses is associated with development of
liver cancer in humans?
a. Simian virus 40 (SV40)
b. Hepatitis B viruses
c. Epstein-Barr virus
d. Papillomaviruses
Answer: b
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 1. Remembering
Learning Objective: Compare cancer induction by chemicals and viruses.
Feedback A: Incorrect. SV40 is associated with Merkel cell carcinoma in humans.
Feedback B: Correct! Chronic infection with hepatitis B along with hepatitis C is
associated with a hundredfold increase in the risk of developing liver cancer.
Feedback C: Incorrect. The Epstein-Barr virus is associated with Burkitt’s lymphoma and
nasopharyngeal carcinoma.
Feedback D: Incorrect. Papillomaviruses are associated with cervical cancers.
7. The more than 40 oncogenic retroviruses that have been identified share expression
of all of the following genes except
a. src.
b. pol.
c. env.
d. gag.
Answer: a
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Explain how retroviral oncogenes were identified.
Feedback A: Correct! src is found in some retroviruses, but not all. It encodes a tyrosine
kinase.
Feedback B: Incorrect. pol encodes a viral reverse transcriptase.
Feedback C: Incorrect. env encodes viral envelope glycoproteins.
Feedback D: Incorrect. gag encodes a viral protease.
8. Which statement does not describe a way in which oncogenes incorporated into
viral genomes can differ from their normal cellular counterparts (proto-oncogenes)?
a. They can contain fusions to viral sequences, resulting in structural changes
that deregulate the protein.
b. They can contain point mutations in regulatory domains, resulting in a loss of
protein regulation.
c. They can be present in many tandem copies, as opposed to the single copy present in
Downloaded by Baktynur Azhybaev ([Link]@[Link])
the cell.
d. They can be expressed from much stronger promoters than the normal
cellular promoter.
Answer: c
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Contrast oncogenes and proto-oncogenes.
Feedback A: Incorrect. This is common among viral oncogenes.
Feedback B: Incorrect. Point mutations that deregulate protein activity are common
among viral oncogenes, such as the ras oncogenes.
Feedback C: Correct! Viruses have very compact genomes and do not possess tandem
copies of genes.
Feedback D: Incorrect. Viral promoters are often very strong, and incorporation of a gene
into a virus often brings it under the control of one of these promoters.
9. Burkitt's lymphoma is caused almost exclusively by
a. point mutations in the ras proto-oncogene.
b. translocation of the abl proto-oncogene.
c. translocation of the c-myc proto-oncogene.
d. amplification of the N-myc gene.
Answer: c
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Contrast oncogenes and proto-oncogenes.
Feedback A: Incorrect. Ras mutations are common in colon and lung cancers.
Feedback B: Incorrect. Translocation and fusion of abl to bcr are common in chronic
myelogenous leukemia.
Feedback C: Correct! Burkitt’s lymphoma is caused by a translocation of c-myc to one of
the immunoglobulin gene loci, causing its unregulated expression.
Feedback D: Incorrect. This occurs in neuroblastomas.
10. The PDGF receptor is a proto-oncogene (a normal cellular gene that
becomes oncogenic when mutated). Which statement about the PDGF receptor
is true?
a. The oncogenic mutation occurs at the intracellular amino terminal end of the receptors.
b. The oncogenic mutation constitutively represses the intracellular kinase activity of
the protein.
c. The oncogenic mutation generates a receptor that is no longer dependent on ligand
for activation.
d. The PDGF protein monomer activates cell proliferation via tyrosine kinase activity.
Answer: c
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Contrast oncogenes and proto-oncogenes.
Feedback A: Incorrect. The mutation occurs at the extracellular amino terminal.
Feedback B: Incorrect. The mutation activates intracellular kinase activity.
Feedback C: Correct! Once the Tel/PDGFR fusion protein dimerizes, activity of the
Downloaded by Baktynur Azhybaev ([Link]@[Link])
intracellular kinase domain produces unregulated proliferation even in the absence of
growth factor.
Feedback D: Incorrect. PDGFR fused with Tel create a fusion protein dimer.
11. Oncogenic conversion of the two dimerizing proto-oncogene components of the AP-
1 transcription factor can lead to abnormal cell proliferation. Which two gene products
form the active AP-1 transcription factor complex?
a. Fos and Jun
b. Fos and Myc
c. Myc and Jun
d. Raf and Myc
Answer: a
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
Feedback A: Correct!
Feedback B: Incorrect.
Feedback C: Incorrect.
Feedback D: Incorrect.
12. The translocation that places the transcription factor Tel at the amino terminus of
the PDGF receptor converts PDGFR to an oncogene by
a. constitutive repression of the fusion protein.
b. forming Tel dimers that produce unregulated signals for proliferation.
c. activating the tyrosine kinase domain in monomeric form.
d. increasing the transcriptional activation capability of Tel.
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
Feedback A: Incorrect. Expression level of the fusion protein does not significantly alter
tyrosine kinase activity.
Feedback B: Correct! The Tel portion of the Tel/PDGFR fusion protein forms dimers in
the absence of growth factor binding, leading to activation of tyrosine kinase domains in
the cytoplasmic domain and unregulated proliferative signals from the oncogene protein.
Feedback C: Incorrect. Tyrosine kinases must form dimers and phosphorylate each other
to be activated.
Feedback D: Incorrect. Tel is not an oncogene, and the fusion protein does not travel to
the nucleus.
13. The viral raf gene is oncogenic because
a. it is more highly expressed under control of the viral env promoter.
b. it encodes a constitutively active protein kinase that is missing a regulatory N
terminal domain.
Downloaded by Baktynur Azhybaev ([Link]@[Link])
c. it carries a loss of function point mutation.
d. it carries a gain of function point mutation.
Answer: b
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
Feedback A: Incorrect. Expression levels would not change kinase activity.
Feedback B: Correct! Loss of the N terminal regulatory domain allows Raf to
constitutively activate the growth-promoting ERK signaling pathway.
Feedback C: Incorrect. Viral raf is not altered by a point mutation.
Feedback D: Incorrect. Viral raf is not altered by a point mutation.
14. The majority of oncogene proteins are
a. metabolic enzymes.
b. structural proteins, such as nuclear lamins.
c. proteins involved in cell sorting.
d. components of signaling pathways that regulate cell proliferation.
Answer: d
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Summarize the functions of oncogene proteins.
Feedback A: Incorrect. Metabolic enzymes are not likely to cause cancer when
mutated. Feedback B: Incorrect. Defective structural proteins do not cause cancer.
Feedback C: Incorrect. Defective cell sorting may cause chaos in the cell, but it is
unlikely to cause cancer.
Feedback D: Correct! Defective versions of proteins involved in signaling cell
proliferation are the most common causative agents of cancer.
15. The protein encoded by the PTEN gene acts as a tumor suppressor by
a. phosphorylating p53 and increasing its proapoptotic activity.
b. antagonizing CDK4, 6/cyclin D activity to activate the G1 cell cycle restriction point.
c. dephosphorylating phosphatidylinositol 3,4,5-bisphosphate, thus
antagonizing PI 3 kinase/Akt activity.
d. increasing expression of BRCA1 to protect cells against DNA damage.
Answer: c
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
Feedback A: Incorrect. PTEN is not a kinase and does not target p53.
Feedback B: Incorrect. This is the mechanism of CDK inhibitors, such as p16 and p21.
Feedback C: Correct! PTEN is a phosphatase that dephosphorylates PIP3, rendering Akt
unable to stimulate cell proliferation.
Feedback D: Incorrect. PTEN does not influence BRCA1 or BRCA2 expression.
Downloaded by Baktynur Azhybaev ([Link]@[Link])
16. Which statement about the tumor suppressor gene p53 is false?
a. It plays a role in up to 50% of human cancers.
b. Its loss causes retinoblastoma, a rare childhood cancer of the eye.
c. It blocks cell cycle progression in response to DNA damage.
d. It is required for apoptosis in response to DNA damage.
Answer: b
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
Feedback A: Incorrect. This is true. p53 is mutated in a wide variety of
malignancies. Feedback B: Correct! This is false. A gene called Rb is the cause of
retinoblastoma.
Feedback C: Incorrect. This is true. p53 induces the synthesis of p21, which inhibits the
Cdk/cyclin complex as well as PCNA, thus blocking progression of the cell cycle until
after the damage has been repaired.
Feedback D: Incorrect. This is true. Cells with unrepaired DNA normally die by
undergoing apoptosis. However, cells lacking p53 fail to undergo apoptosis, and thus can
survive and become malignant.
17. PTEN is a tumor suppressor gene in the Akt signaling pathway. Which
statement about PTEN/Akt is false?
a. PIP2 can be oncogenically mutated to induce cell survival.
b. PTEN antagonizes (has the opposite effect) of PI 3-kinase.
c. Akt can be oncogenically mutated to induce cell survival.
d. It is a lipid phosphatase that dephosphorylates PIP3 to PIP2.
Answer: a
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Give examples of the functions of tumor suppressor
gene products in
signal transduction, cell cycle progression, and cell survival.
Feedback A: Correct! This is false. PIP2 is not a protein and cannot be mutated.
Feedback B: Incorrect. This is true.
Feedback C: Incorrect. This is true.
Feedback D: Incorrect. This is true.
18. Which of the following genes has been associated with colon cancer?
a. APC
b. bcl-2
c. Rb
d. erbB-2
Answer: a
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 1. Remembering
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Learning Objective: Explain the major types of genetic alterations in
human cancers.
Feedback A: Correct! APC, as well as other genes, has been linked to colon cancer.
Feedback B: Incorrect. bcl-2 is associated with chronic lymphocytic leukemia.
Feedback C: Incorrect. Rb is associated with retinal blastoma.
Feedback D:
Essay
1. What is a possible reason that carcinomas, which are tumors derived from
epithelial cells, are the most common types of cancer in humans?
Answer: Most cells in adults have ceased to proliferate and have entered the G0, or
quiescent, stage of the cell cycle. In contrast, epithelial cells are continually turned over
and thus continue to divide. Because many of the signals that stimulate cell division are
still active, they may be more susceptible to uncontrolled cell proliferation. Epithelial
cells come into frequent contact with cancer-causing substances from the environment
because they line both the outer (skin) and inner (e.g., the intestinal and respiratory
tracts) surfaces of the body.
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
2. Why are cancer cells less dependent on growth factors than their normal
cellular counterparts?
Answer: 1) Cancer cells frequently secrete their own growth factors in an autocrine
fashion, making them less dependent on growth factors from normal signaling pathways.
2)Oncogenic mutations frequently occur in the signaling pathways themselves, making
the pathways constitutively active and less dependent on any growth factors that would
normally trigger the pathways (in effect, they bypass the initiating event of the cascade
altogether).
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
3. What is the likely reason that antiangiogenic therapies hold so much promise
for treatment of tumors?
Answer: Without angiogenesis, tumors would be limited in size to approximately a
million cells. After that, angiogenesis is required for the tumor to have adequate blood
flow for survival. Blood vessels grow in response to growth factors secreted by the
tumors, which stimulate the endothelial cells to proliferate in the walls of capillaries in
surrounding tissues. This results in the outgrowth of new capillaries into the tumor and
also facilitates metastasis. Thus, drugs that block this angiogenesis could have a dramatic
effect on tumor growth and metastasis. These drugs are currently in clinical trials and
development in many pharmaceutical companies and laboratories.
Textbook Reference: Molecular Approaches to Cancer Treatment
Downloaded by Baktynur Azhybaev ([Link]@[Link])
Bloom’s Category: 3. Applying
Learning Objective: Summarize the properties of cancer cells.
4. Describe how growth of transformed cells in a tissue culture dish differs from
growth of untransformed cells.
Answer: Transformed cells display three properties that untransformed cells do not:
altered morphology, loss of contact inhibition, and loss of density-dependent inhibition of
growth. In a background of untransformed cells, single transformed cells will form a
colony of morphologically altered cells that overgrow the background of normal cells.
These foci of transformed cells can be detected from within a few days to two weeks.
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
5. When observed under a microscope, cancer cells often have a more rounded
morphology than untransformed cells. What accounts for this difference in morphology?
Answer: Cancer cells tend to be less dependent on cell−cell and cell−matrix interactions
for survival. They are often less adhesive to neighbors and/or extracellular matrix, due to
reduced expression of cell surface adhesion molecules, such as E-cadherin. This reduced
adhesiveness of cancer cells results in morphological and cytoskeletal alterations, such
as rounding.
Textbook Reference: The Development and Causes of Cancer
Bloom’s Category: 2. Understanding
Learning Objective: Summarize the properties of cancer cells.
6. Describe how the first oncogene was discovered.
Answer: The src oncogene was discovered in a study of mutant versions of the Rous
sarcoma virus (RSV), which causes tumors in birds. Some of the mutants were able to
replicate normally in birds but did not cause tumors, indicating that (1) viral replication
itself did not cause tumors, and (2) the gene that was mutated was involved in tumor
development. The gene was eventually identified and found to transform avian cells by
itself, and thus was the first oncogene to be discovered. Equally important, studies of src
led to the discovery that retroviral oncogenes are derived from normal genes (proto-
oncogenes) picked up from host cells.
Textbook Reference: Oncogenes
Bloom’s Category: 1. Remembering
Learning Objective: Explain how retroviral oncogenes were identified.
7. What is the most common mechanism by which -catenin is converted from
a protooncogene to an oncogene?
Answer: -catenin acts together with Tcf to activate genes such as c-myc and cyclin D1,
whose products promote survival and cell proliferation. It is responsive to the Wnt family
of protein paracrine hormones. In the absence of Wnt signal, -catenin is
phosphorylated, ubiquitinated, and rapidly degraded by the proteasome. In the presence
of a Wnt signal,
-catenin is not phosphorylated, allowing it to accumulate in the cytoplasm, translocate to
the nucleus, and interact with Tcf to initiate transcription of target genes. Point mutations
Downloaded by Baktynur Azhybaev ([Link]@[Link])
in -catenin that prevent its phosphorylation stabilize it in the absence of Wnts, making
cell proliferation Wnt independent.
Textbook Reference: Oncogenes
Bloom’s Category: 2. Understanding
Learning Objective: Describe the ways in which oncogenes are formed in
human cancers.
8. Explain why the disease retinoblastoma is inherited in a dominant fashion, despite
the fact that it is caused by a recessive (loss-of-function) mutation in the tumor
suppressor gene Rb.
Answer: Statistically, 50% of the progeny of an individual with retinoblastoma
(heterozygous for Rb) will inherit the mutant version of the gene. However, because
human cells are diploid, and loss of Rb function is recessive, not all cells in these
individuals will become cancerous. Loss of the second allele of Rb (the normal copy from
the unaffected parent) by mutation in a single cell, however, results in that cell becoming
cancerous and the subsequent development of disease. Somatic mutations of this allele
are common enough that almost all children who receive one mutant copy of the allele
will lose the normal allele in at least one retinal cell. Inheritance of the disease therefore
follows the pattern for inheritance of a dominant allele. In other diseases caused by
recessive mutations, mutation of both alleles of the disease gene in just few a cells is, on
the whole, insignificant. In the case of Rb, it can be lethal.
Textbook Reference: Tumor Suppressor Genes
Bloom’s Category: 2. Understanding
Learning Objective: Explain the major types of genetic alterations in
human cancers.
9. Why is cancer more often cured when detected early?
Answer: Cancer develops in a stepwise fashion: a cell first begins to proliferate
uncontrollably. This is followed by an increased invasiveness of one of the cell’s
progeny, followed by an increased metastatic potential of one of that cell’s progeny.
Thus, the gradual accumulation of mutations leads to a malignant tumor with metastatic
potential. If the tumor is caught early on, at the stage where it is still just a benign
growth, it can be treated locally by surgery. In addition, the earlier a malignant tumor is
treated, the more likely it will be to respond to radiation and chemotherapy; unlike
normal cells, cells in late-stage tumors often do not cease cell proliferation in response to
these treatments.
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Explain the importance of early diagnosis.
10. What is the therapeutic strategy for using Herceptin to treat breast cancer?
Answer: In about 30% of breast cancers, ErbB-2 (a receptor protein tyrosine kinase) is
overexpressed as a result of amplification of the erbB-2 gene. In vitro, cells that
overexpress ErbB-2 exhibit elevated proliferation. Herceptin is a monoclonal
antibody that binds the extracellular domain of ErbB-2 and blocks proliferation in the
ErbB-2
overexpressing cell lines. In clinical trials, Herceptin was shown to reduce tumor size and
increase human survival, and it became the first antibody to gain FDA approval. It is now
Downloaded by Baktynur Azhybaev ([Link]@[Link])
widely used in treating ErbB-2-overexpressing breast tumors.
Textbook Reference: Molecular Approaches to Cancer Treatment
Bloom’s Category: 2. Understanding
Learning Objective: Describe the basis for selectivity of oncogene-targeted
drugs.
Downloaded by Baktynur Azhybaev ([Link]@[Link])