1 Molecular Biology of Cancer • Part 1

Robert A. Kratzke

QUESTIONS

Each of the numbered items below is followed by lettered answers. Select the ONE lettered answer that is BEST in each case unless instructed otherwise.

Question 1.1 Completion of the Human Genome Project has revealed that human cells have a repertoire of genes of which approximate number?

A. 2,500 genes

B. 25,000 genes

C. 250,000 genes

D. 2,500,000 genes

Question 1.2 One of the reasons to use cancer cell culture experiments in preclinical studies of cancers is:

A. Allows evaluation of cancer cell interaction with the tumor microenvironment.

B. Cell cultures are amenable to easily manipulated experimental techniques.

C. Adaptation of cancer cells to growth in culture corresponds exactly to cancer cell growth in vivo.

D. Allows evaluation of cancer cell interaction with the native immune system.

Question 1.3 Which of the following is TRUE with regard to genetic mutations in cancer?

A. Gain-of-function mutations (oncogenes) are generally dominant at the cellular level.

B. Loss-of-functions mutations (tumor suppressor genes) are generally recessive at the cellular level.

C. Ninety percent of germ line mutations in familial cancer syndromes are in tumor suppressor genes.

D. All of the above.

Question 1.4 Which of the following proteins has inhibitory activity in the cell cycle?

A. Cyclin D1

B. E2F

C. p16INK4a

D. Cyclin-dependent kinase 4

Question 1.5 Which of the following contributes to cancer progression?

A. Autophagy

B. Apoptosis

C. Senescence

D. Angiogenesis

Question 1.6 Which of the following prevents successful invasion and metastasis ?

A. Senescence

B. Angiogenesis

C. Evasion of apoptosis

D. Self-sufficiency in growth signals

Question 1.7 Which of the following best describes the term “protooncogene”?

A. A normal cellular gene that has been transduced by a retrovirus that is then mutated following viral replication.

B. A homologue of a known oncogenic element identified in prehistoric specimens.

C. A transforming viral gene that can cause malignant transformation in fibroblasts in vitro.

D. The first oncogene discovered to be associated with human cancer.

E. A viral oncogene that, following infection, is the direct causative agent of human cancer.

Question 1.8 The DNA damage checkpoints are located in which phase of the cell cycle?

A. G1/S

B. S/G2

C. M

D. All of the above

Question 1.9 Which of the following is a potential flaw in microarray studies?

A. Inadequate controls

B. Biased estimation of prediction accuracy

C. Correlation between clusters and clinical outcome

D. All of the above

Question 1.10 Which of the following statements about miRNAs is/are TRUE?

A. Consist of RNA 19 to 24 nucleotides in length

B. Cannot be evaluated in array format as part of clinical studies

C. Alters gene expression and protein translation

D. A and C

Question 1.11 The proteome is which of the following:

A. The set of all expressed gene products at a given time

B. The proteins expressed preferentially in malignant cells

C. The set of all proteins potentially expressed by the genome

D. The set of protonated peptides subject to matrix-assisted laser desorption ionization time-of-flight analysis

Question 1.12 Which one of the following statement is CORRECT with regard to molecular profiling using gene arrays and proteomics?

A. Gene arrays can predict protein–protein interactions.

B. Protein levels and protein function do not correspond directly with gene transcript levels.

C. Polymerase chain reaction can be used to amplify biopsy material for use in gene arrays, whereas no signal amplification technology is standard in protein arrays.

D. All of the above

E. B and C

Question 1.13 Which of the following is TRUE about the peptidome?

A. Included peptides must be less than 50,000 daltons.

B. Consists of fragments of larger proteins.

C. May not be amplified in the circulation.

D. Peptide fragments do not bind blood proteins, such as albumin.

Question 1.14 Which of the following statements is CORRECT?

A. Hereditary nonpolyposis colon cancer syndrome (HNPCC) is associated with a 25% lifetime risk of developing colorectal cancer.

B. Approximately 10% of all cases of colorectal cancer are associated with HNPCC.

C. Microsatellite instability is associated with resistance to 5-fluorouracil chemotherapy.

D. None of the above.

Question 1.15 Which of the following is a DNA hypomethylating agent?

A. Suberoylanilide hydroxamic acid (SAHA)

B. 5-Azacytidine

C. Depsipeptide

D. A and C

Question 1.16 The presence of mutations in p53 has been associated with which of the following properties on cells:

A. Loss of the G2 checkpoint following treatment with DNA-damaging agents

B. Enhanced capacity to undergo apoptosis following exposure to radiation

C. Increased capacity for DNA amplification

D. A and C

Question 1.17 Which of the following is an example of gene amplification found in cancer?

A. N-myc amplification in neuroblastoma

B. C-myc amplification in small cell lung cancer

C. Her2/neu amplification in breast cancer

D. All of the above

Question 1.18 Which of the following is TRUE regarding microsatellite instability in colon cancer?

A. Approximately 15% of patients with hereditary nonpolyposis coli have mutations in MLH1 or MSH2.

B. There is potential resistance to 5-fluorouracil.

C. It has a less favorable prognosis.

D. Evidence is in favor of it occurring only late in sporadic colon cancer cases.

Question 1.19 Which of the following is TRUE about excision repair mechanisms?

A. Increased expression of ERCC1 in non–small-cell lung cancer is associated with response to cisplatin.

B. There are two nucleotide excision repair (NER) pathways.

C. Base excision repair is involved in response to damage from chemicals and radiographs.

D. B and C.

Question 1.20 ATR/CHK1 signaling is associated with all of the following statements,

A. Bone marrow failure

B. Predisposition to squamous cell carcinoma

C. Predisposition to acute leukemia

D. All of the above

Question 1.21 Which of the following syndromes are associated with abnormalities in the double-strand repair?

A. Xeroderma pigmentosum

B. Fanconi anemia

C. Lynch syndrome

D. Bloom syndrome

Question 1.22 Decreased expression of Aurora B kinase could lead to the following:

A. Inability for sister chromatids to separate before anaphase

B. Rapid cell division

C. Aneuploidy

D. Increased disassembly of kinetochore proteins

Question 1.23 Which of the following characterizes cytogenetic abnormalities in most human cancers?

A. Universal (monoclonal) population of cells containing identical cytogenetic abnormalities

B. Completely normal karyotype

C. Heterogeneous complex karyotypes

D. Complete loss of X or Y chromosomes

Question 1.24 The “Hayflick phenomenon,” which is the name given to the limited replicative potential of cells, is thought to arise from which of the following?

A. The sequential loss of genetic material from the ends of chromosomes (telomeres) with each round of division

B. The gradual accumulation of uncorrected genetic defects passed on during division leading to senescence or malignancy

C. The activation of telomerase in aging cells leading to enzymatic loss of genetic material from telomeres

D. Dividing eukaryotic cells outgrowing their vascular supply

Question 1.25 Which of the following statements is TRUE regarding telomerase?

A. It has both a DNA and a protein component.

B. It is a DNA topoisomerase.

C. Telomerase protects the integrity of the chromosomal ends.

D. Overexpression of telomerase is found in all cancer specimens.

Question 1.26 Which of the following will induce a quiescent state?

A. Telomere shortening

B. Prolonged DNA damage

C. High-density growth

D. Oncogene activation

Question 1.27 All of the following is/are evidence for senescence as a tumor suppressor mechanism, EXCEPT:

A. Several “tumor suppressor” proteins that are involved in senescence pathways (e.g., p16INK4a) are mutated in familial cancer syndromes.

B. Mice and humans with impaired p16INK4a and p53 function develop normally other than an age-dependent decrease in cancer and decreased susceptibility to cancer in response to carcinogen exposure.

C. Reestablishment of p53 activity in sarcoma and hepatocellular carcinoma has led to cessation of tumor growth.

D. Growth arrest in lung epithelium has been demonstrated in response to oncogenic events.

E. A, C, and D.

Question 1.28 Which of the following is/are potential therapeutic strategy (ies) to promote apoptosis in cancer cells?

A. Inhibition of p16INK4a activity

B. Inhibition of p16INK4a activity via activation of DNA methyltransferases

C. Activation of MDM2

D. Promotion of p16INK4a-p53 interactions

Question 1.29 Breakage–fusion–bridge cycles lead to the following:

A. Methylation

B. Aneuploidy

C. Amplifications

D. Deletions

E. B, C, and D

Question 1.30 Telomerase-null mice are associated with which of the following?

A. Decreased sensitivity to radiation

B. Decreased sensitivity to chemotherapy that induces double-strand breaks (DSBs)

C. Decreased genomic stability in the presence of p53 deficiency

D. Decreased rate of spontaneous malignancy

Question 1.31 Which of the following are receptor tyrosine kinases?

A. Platelet-derived growth factor receptor

B. Insulin-like growth factor receptor 1

C. cKit

D. All of the above

Question 1.32 Which of the following is TRUE about receptor tyrosine kinases?

A. They are always monomeric.

B. Activation always requires tyrosine phosphorylation in all classes.

C. Different types of ligands can activate the same class of receptors.

D. Different types of ligands induce the same receptor conformational changes on binding.

Question 1.33 Which of the following is TRUE about receptor phosphotyrosine phosphatases?

A. Several ligands for these have been described.

B. They rarely function to antagonize tyrosine kinases.

C. Inactivation could increase intracellular phosphorylation under certain circumstances.

D. Receptor phosphatases containing two catalytic domains are rare.

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