Molecular Biology of Cancer • Part 2

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2 Molecular Biology of Cancer • Part 2


Viralkumar Vaghani and George R. Simon


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 2.1 The correct order of mitosis is:


A. Prometaphase, metaphase, anaphase, telophase, prophase


B. Prometaphase, metaphase, prophase, anaphase, telophase


C. Prophase, prometaphase, metaphase, anaphase, telophase


D. Telophase, anaphase, prophase, metaphase, prometaphase


Question 2.2 The cyclin responsible for facilitating the progress of the cell into and through mitosis is:


A. Cyclin A


B. Cyclin B


C. Cyclin D


D. Cyclin E


Question 2.3 Which of the following are means of regulating cyclin-dependent kinases (CDKs)?


A. Positive regulatory acetylation


B. Negative regulatory phosphorylation


C. CDK inhibitors


D. B and C


E. A and C


Question 2.4 Which of the following is necessary for the G1/S-phase transition?


A. Cyclin B-CDK1 complex accumulation


B. Cyclins E and A accumulation


C. Dephosphorylation of T14 and Y15


D. CDK1 activation along with binding of CDC20 to anaphase promoting complex/cyclosome (APC/C)


Question 2.5 Which of the following has no role in cell-cycle exit?


A. Downregulation of CDKs and cyclins


B. Activation of APC/C


C. Reduction in protein synthesis


D. A and C


E. B and C


Question 2.6 Activation of antimitogenic signaling involves the following molecules:


A. Transforming growth factor (TGF)-β


B. Interferon (IFN)-α


C. Upregulation of CDK inhibitors and downregulation of cyclins


D. All of the above.


Question 2.7 Select the FALSE statement regarding microRNAs?


A. microRNAs encode protein kinases that regulate cell cycle.


B. They regulate mRNA expression.


C. There is at least five clusters of microRNAs targeting mRNA that encodes cell-cycle regulatory proteins.


D. miR-15a/16 cluster targets cyclin E1 and cyclin D1.


Question 2.8 Of the genes listed below, select the gene that is involved in both cell-cycle regulation and DNA repair?


A. TP53


B. NBS1


C. PTTG1


D. CHK2


Question 2.9 Replicative senescence is initiated by means of:


A. Downregulation of cyclins


B. p53 activation


C. Progressive telomere shortening


D. Upregulation of IFNs


Question 2.10 Genes that encode negative regulators of growth and proliferation are:


A. Protooncogenes


B. Oncogenes


C. S-phase genes


D. Tumor suppressor genes


Question 2.11 Select the syndrome that is associated with a mutation in the gene encoding Nbs1, leading to microcephaly and a strong predisposition to lymphoid malignancies?


A. Nijmegen disease


B. Von Hippel–Lindau (VHL) syndrome


C. Familial malignant melanoma syndrome


D. Li–Fraumeni syndrome


Question 2.12 Type I cell death is also known as:


A. Autophagy


B. Apoptosis


C. Necrosis


D. Autolysis


Question 2.13 Which of the following proteins serve as are ligands for the death receptor pathway?


A. TNFα


B. Fas


C. Noxa


D. A and C


E. A and B


Question 2.14 Taxanes specifically target this BH3-only Bcl-2 protein:


A. Nbk/Bik


B. Bim


C. Puma


D. Bad


Question 2.15 RAF is inhibited by which of these therapeutic agents that induce apoptosis?


A. Sorafenib


B. Imatinib mesylate


C. Bortezomib


D. Taxanes


Question 2.16 Bcl-2 small molecule inhibitors like ABT-737 induce apoptosis by:


A. Binding to the BH3-binding pocket.


B. Inhibiting tyrosine kinase activity of Bcr/Abl restoring Bim function.


C. Stimulating Bim expression


D. Blocking proteasome degradation of Bim


Question 2.17 Angiogenesis inhibitors theoretically induce apoptosis by which of the following means?


A. Tyrosine kinase inhibition


B. Histone deacetylase inhibition


C. Inhibition of antiapoptotic proteins


D. Nutrient deprivation


Question 2.18 Type II programmed cell death, autophagy, is regulated by:


A. mTOR in the PI3-kinase/AKT pathway


B. Bax/Bak


C. BH3-only proteins


D. APC/C


Question 2.19 Autophagy has a role in the following:


A. Recycling of normal cellular components.


B. Protection against aging.


C. Cell lysis caused by surrounding inflammation.


D. A and B.


E. A and C.


Question 2.20 Select the property that is specific to apoptosis?


A. Rapid cellular swelling


B. Lysosome activation


C. Loss of plasma membrane integrity


D. Release of intracellular components to the extracellular compartment


Question 2.21 The Warburg effect describes:


A. Exponential cell growth in response to an exogenous stimulant.


B. Inefficient energy production by most cancer cells, resulting in rapid adenosine triphosphate (ATP) depletion and necrotic cell death.


C. Initiation of neoplasia requires two somatic mutations for initiation of sporadic neoplasms and hereditary neoplasms require a genetic plus a somatic mutation.


D. Sculpting of normal human tissues as a result of cell death.


Question 2.22 Bevacizumab is:


A. A monoclonal antibody to basic fibroblast growth factor (bFGF).


B. A monoclonal antibody to vascular endothelial growth factor (VEGF).


C. A monoclonal antibody to phospholipid lipid growth factor (PLGF).


D. A monoclonal antibody to epidermal growth factor receptor (EGFR).


Question 2.23 The first step in tumor angiogenesis is:


A. A localized degradation of the surrounding basement membrane of a parental venule.


B. Paracrine signaling causing increased leakiness of a parental venule’s basement membrane.


C. An inflammatory response causing recruitment and activation of leukocytes that mediate angiogenesis


D. Release of endothelial cell (EC) progenitors from the bone marrow


Question 2.24 Which of the following functions is ascribed to pericytes?


A. Paracrine signaling


B. Mediation of resistance to antiangiogenic therapy


C. Enhances endothelial survival


D. All of the above


Question 2.25 Tumor vasculature is characterized by?


A. Increased dilation


B. Increased red blood cell (RBC) flow


C. Increased tortuosity


D. A and B


E. A and C


Question 2.26 Functions ascribed to VEGF are?


A. Stimulation of endothelial cell division


B. Migration of endothelial cells.


C. Enhancing endothelial cell survival.


D. A and B


E. A, B and C


Question 2.27 VEGF is inducible by many factors, of which the most important may be:


A. H1F1α


B. TSP-1


C. pVHL


D. p53


Question 2.28 Which of the following is thought to promote tumor angiogenesis?


A. TSP-1


B. IL-6, IL-8


C. DLL4


D. Vasohibin


Question 2.29 Metronomic low-dose chemotherapy describes:


A. Continuous low-dose treatment with chemotherapeutics


B. Pulse dosing with low doses of chemotherapeutics


C. Continuous low-dose treatment with intermittent pulse dosings of chemotherapeutics


D. Treatment of refractory tumors with continuous low doses of chemotherapeutics in conjunction with metronidazole


Question 2.30 Which of the following is/are potential toxicity(ies) of antiangiogenic agents?


A. Hypertension


B. Aplastic anemia


C. Arteriothrombotic event


D. A and B


E. A and C


Question 2.31 Which of the following factors is/are associated with risk of metastasis?


A. Tumor grade


B. Depth of invasion beyond normal cellular compartments


C. Lymphovascular invasion


D. All of the above


Question 2.32 The percentage of tumor cells that can give rise to metastases is?


A. <0.01%


B. 1%


C. 20%


D. >80%


Question 2.33 Genes that can mediate tumorigenic functions and secondarily serve metastatic-specific functions either in a general way or with particular organ selectivity is best known as:


A. Tumorigenic genes


B. Metastasis progression genes


C. Metastasis virulence genes


D. Protooncogenes


Question 2.34 Cells that mediate the breakdown of the basement membrane allowing for tumor invasion are known as:


A. Carcinoma-associated fibroblasts


B. Pericyte-derived fibroblast


C. Tumor-associated macrophages (TAMs)


D. Dendritic cells


Question 2.35 Cellular loss of this molecule leads to decreased cellular attachment and enhanced tumor invasion/motility:


A. E-cadherin


B. β-Catenin


C. α-Tubulin


D. Ankyrin


Question 2.36 The following are the selective pressures experienced by circulating tumor cells (CTCs)


A. Shear stress


B. Nitric oxide


C. Nutrient deprivation


D. A, B, and C


Question 2.37 Which of the following molecules are known to assist in the extravasation of CTCs?


A. Ezrin


B. VEGF


C. CXCL12


D. CXCR4


E. All of the above


Question 2.38 Osteoblastic bone metastases are characteristic of which type of cancer?


A. Breast


B. Prostate


C. Lung


D. Renal cell


Question 2.39 Which of the following cancers rarely metastasize to the liver?


A. Colon cancer


B. Breast cancer


C. Prostate cancer


D. Melanoma


Question 2.40 The stochastic model of tumor heterogeneity is best described as:


A. Every cell has equal potential to initiate and sustain tumor growth, but most cells do not proliferate extensively because of the low cumulative probability of permissive events.


B. Cancer stem cells (CSCs) are biologically distinct from the bulk cell population, which does not possess tumor-initiating activity.


C. Tumors are heterogeneous secondary to random, acquired mutations.


D. Tumors are pressured into heterogeneity by variable pressures applied to the tumor.


Question 2.41 The hierarchy model of tumor heterogeneity is best described as:


A. Every cell has equal potential to initiate and sustain tumor growth, but most cells do not proliferate extensively because of the low cumulative probability of permissive events.


B. CSCs are biologically distinct from the bulk cell population, which does not possess tumor-initiating activity.


C. Tumors are heterogeneous secondary to random, acquired mutations.


D. Tumors are pressured into heterogeneity by variable pressures applied to the tumor.


Question 2.42 The drug vemurafenib (PLX4032) targets which gene in the MAPK/ERK pathway?


A. RAS


B. BRAF


C. BIM


D. ERK


Question 2.43 Which of the following agents targets tumor metabolic pathways?


A. Pemetrexed


B. 5 FU


C. Temsirolimus


D. All of the above


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Mar 13, 2017 | Posted by in ONCOLOGY | Comments Off on Molecular Biology of Cancer • Part 2

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