Practice Exam 2 PDF

1. What is the primary function of immunotherapy in cancer treatment? a) To directly kill cancer cells. b) To help the immune system recognize and attack cancer cells. c) To prevent the spread of cancer cells to other parts of the body. d) To reduce the side effects of chemotherapy and radiation the...

1. What is the primary function of immunotherapy in cancer treatment? a) To directly kill cancer cells. b) To help the immune system recognize and attack cancer cells. c) To prevent the spread of cancer cells to other parts of the body. d) To reduce the side effects of chemotherapy and radiation therapy. 2. Which of the following is NOT a step in the development of metastatic cancer? a) Inappropriate mitosis b) Escape from apoptosis c) Acquisition of a blood supply d) Increased cell adhesion 3. How do cytotoxic T-cells primarily eliminate infected cells? a) By releasing antibodies that bind to the infected cells. b) By engulfing and digesting the infected cells. c) By inducing apoptosis in the infected cells. d) By producing cytokines that attract other immune cells. 4. What is the primary role of regulatory T-cells? a) To suppress cytotoxic T-cells that recognize normal cellular proteins. b) To activate cytotoxic T-cells to attack cancer cells. c) To produce antibodies that target cancer cells. d) To promote the growth of new blood vessels to support tumor growth. 5. What experimental evidence suggests that the immune system regulates tumorigenesis? a) Mice with enhanced immune systems show increased rates of cancer. b) Mice with defective immune system genes have an increased rate of cancer. c) Immunization with tumor antigens has no effect on tumor growth. d) Transplant patients show a decreased incidence of cancer. 6. What is the significance of tumor-infiltrating lymphocytes (TILs) in cancer? a) TILs always indicate a positive immune response against the tumor. b) TILs could be recruited to either help or attack the tumor. c) TILs are only found in benign tumors. d) TILs have no impact on tumor growth or progression. 7. Why might immune recognition of tumors often be a late step in oncogenesis? a) Tumors actively suppress the immune system in early stages. b) The immune system is generally tolerant to cancer cells. c) Tumors may only trigger an inflammatory response after significant growth and spread. d) Cancer cells are genetically identical to normal cells. 8. Which of the following is NOT a mechanism by which tumor cells can evade the immune system? a) Hiding their identity b) Avoiding apoptosis c) Increasing MHC protein expression d) Inducing immune cell apoptosis 9. What are stromal cells? a) Cells of the connective tissues. b) The main cells that comprise the major organs of an organism c) Cells that circulate in the blood and lymph. d) Cells that line the surfaces of the body. 10. How do stromal cells aid in cancer progression? a) By suppressing the immune response. b) By directly killing healthy cells. c) By releasing growth factors that stimulate tumor growth. d) By preventing the formation of new blood vessels. 11. What is the function of PDGF in tumor development? a) To suppress the growth of stromal cells. b) To inhibit the production of ECM. c) To attract fibroblasts that produce ECM and enhance cell proliferation and migration. d) To trigger apoptosis in tumor cells. 12. What is anoikis? a) The process of new blood vessel formation. b) The spread of cancer cells to distant sites. c) Cell death What is a) The process by which tumor cells suppress blood vessel growth. ○ b) The release of VEGF from the ECM, allowing it to stimulate angiogenesis. ○ c) The transformation of normal cells into cancer cells. ○ d) The spread of cancer cells from the primary tumor to distant sites. 16. Why does inhibiting VEGF inhibit tumor progression? ○ a) VEGF directly promotes the growth and division of cancer cells. ○ b) VEGF is essential for the formation of new blood vessels that support tumor growth. ○ c) VEGF suppresses the immune system's response to cancer cells. ○ d) VEGF promotes the spread of cancer cells to distant sites. 17. What is a characteristic of tumor vasculature that distinguishes it from normal vasculature? ○ a) Tumor vasculature is highly organized and efficient. ○ b) Tumor vasculature is often poorly organized and leaky. ○ c) Tumor vasculature is less permeable than normal vasculature. ○ d) Tumor vasculature is not essential for tumor growth. 18. What is Avastin (bevacizumab)? ○ a) A chemotherapy drug that directly kills cancer cells. ○ b) A drug that stimulates the immune system to attack cancer cells. ○ c) A humanized monoclonal antibody against VEGF. ○ d) A drug that prevents the spread of cancer cells to distant sites. 19. What is the main concern about prostate cancer screening? ○ a) It may lead to the diagnosis and treatment of cancers that would not have caused harm. ○ b) It is not effective at detecting early-stage prostate cancer. ○ c) It is associated with significant side effects. ○ d) It is very expensive and not widely available. 20. What is the primary cause of death in most cancer patients? ○ a) Metastatic cancers. ○ b) Primary tumors. ○ c) Complications from chemotherapy and radiation therapy. ○ d) Weakened immune systems. 21. Which of the following cancers is known for its high metastatic potential? ○ a) Prostate cancer. ○ b) Colon cancer. ○ c) Breast cancer. ○ d) Skin cancer. 22. What is the basal lamina? ○ a) A layer of cells that line the surfaces of the body. ○ b) A type of immune cell that attacks cancer cells. ○ c) A matrix of densely woven extracellular proteins that separates epithelial tissues from underlying connective tissues. ○ d) A network of blood vessels that supplies nutrients to tissues. 23. What is the relationship between tumor size and metastasis? ○ a) Tumors must reach a certain size before they can metastasize. ○ b) Tumor size correlates with metastasis, but it is not strictly determinative. ○ c) Smaller tumors are more likely to metastasize than larger tumors. ○ d) There is no relationship between tumor size and metastasis. 24. What is the epithelial-to-mesenchymal transition (EMT)? ○ a) The process by which cancer cells become more specialized. ○ b) The spread of cancer cells to distant sites. ○ c) A process that occurs normally during wound healing and development, in which epithelial cells lose their cell-cell adhesion and gain migratory and invasive properties. ○ d) The formation of new blood vessels to support tumor growth. 25. What are the roles of Snail and Twist genes in cancer? ○ a) They promote cell-cell adhesion and inhibit cell migration. ○ b) They suppress the immune system's response to cancer cells. ○ c) They are transcription factors that regulate many different EMT genes, contributing to the acquisition of invasive behaviors. ○ d) They induce apoptosis in tumor cells. 26. How do cancer cells exploit healthy cells during metastasis? ○ a) By directly killing healthy cells to create space for tumor growth. ○ b) By absorbing nutrients from healthy cells. ○ c) By inducing wound-response behaviors in neighboring cells, triggering EMT and the release of MMPs. ○ d) By using healthy cells as a shield against the immune system. 27. What are matrix metalloproteinases (MMPs)? ○ a) Proteins that promote cell-cell adhesion. ○ b) Enzymes that degrade the extracellular matrix, facilitating tumor cell invasion. ○ c) Growth factors that stimulate tumor cell proliferation. ○ d) Signaling molecules that suppress the immune response. 28. What is the significance of breaching the basal lamina in cancer? ○ a) It allows tumor cells to access nutrients and oxygen more easily. ○ b) It prevents tumor cells from metastasizing. ○ c) It marks the transition from a usually benign tumor to a usually malignant tumor, as tumor cells can then invade surrounding tissues and blood vessels. ○ d) It triggers apoptosis in tumor cells. 29. Why are the capillaries of the lung often the first location that metastatic cells arrive at? ○ a) Lung tissue provides an ideal environment for tumor growth. ○ b) The lungs are highly vascularized, and circulating tumor cells are more likely to get trapped in the small capillaries of the lungs. ○ c) The immune system is less active in the lungs. ○ d) Cancer cells have a specific affinity for lung tissue. 30. What are some of the challenges that cancer cells face when surviving in the bloodstream? ○ a) High levels of nutrients and growth factors. ○ b) Lack of immune surveillance. ○ c) Lack of solid matrix for attachment, tissue-specific growth factor requirements, and fluid shear forces. ○ d) Easy access to distant tissues. 31. What is extravasation? ○ a) The process of cancer cells entering the bloodstream. ○ b) The process of cancer cells leaving the bloodstream and invading a new tissue. ○ c) The formation of new blood vessels to support tumor growth. ○ d) The death of cancer cells due to lack of nutrients. 32. What are micrometastases? ○ a) Small, non-cancerous growths. ○ b) Single cells or clumps of cancer cells that have spread to a new tissue but have not yet formed a macroscopic tumor. ○ c) The primary tumor that forms at the site of origin. ○ d) Benign tumors that do not invade surrounding tissues. 33. What is the "seed and soil" model of metastasis? ○ a) All cancer cells have the same metastatic potential. ○ b) Cancer cells (seeds) may be distributed widely, but they will only grow (germinate) in a suitable environment (soil). ○ c) The primary tumor determines the location of metastases. ○ d) Metastasis is a random process. 34. Why are bones a common site of metastasis for some cancers? ○ a) Bones are not well-protected by the immune system. ○ b) Bone tissue provides an ideal environment for tumor growth. ○ c) Cancer cells have a specific affinity for bone tissue. ○ d) The ECM in bones is rich in growth factors that can be released by osteoclasts. 35. What is the significance of Peyton Rous's discovery of the Rous Sarcoma Virus (RSV)? ○ a) It proved that all cancers are caused by viruses. ○ b) It provided the first experimental evidence that a virus could cause cancer. ○ c) It led to the development of the first vaccine against cancer. ○ d) It demonstrated that cancer is a genetic disease. 36. How did scientists distinguish between bacteria and viruses in the early 20th century? ○ a) By their shape and size under a microscope. ○ b) By filtration experiments, as viruses were small enough to pass through filters that retained bacteria. ○ c) By their genetic material. ○ d) By their ability to cause disease. 37. What is a focus in the context of tissue culture cells? ○ a) A type of immune cell that attacks cancer cells. ○ b) A cluster of transformed cells with altered morphology, often rounded and exhibiting loss of contact inhibition. ○ c) A type of growth factor that promotes cell proliferation. ○ d) A region of DNA damage. 38. What is the difference between c-src and v-src? ○ a) c-src is a viral gene, while v-src is a cellular gene. ○ b) c-src is the normal, unmutated version of the src gene, while v-src is the mutated, oncogenic version. ○ c) c-src is a tumor suppressor gene, while v-src is an oncogene. ○ d) c-src is only found in chickens, while v-src is found in all vertebrates. 39. What is the difference between acute transforming viruses and slowly transforming viruses? ○ a) Acute transforming viruses induce cancer rapidly, while slowly transforming viruses take a longer time to cause cancer. ○ b) Acute transforming viruses only infect certain types of cells, while slowly transforming viruses can infect any cell type. ○ c) Acute transforming viruses cause benign tumors, while slowly transforming viruses cause malignant tumors. ○ d) Acute transforming viruses are more common than slowly transforming viruses. 40. What is insertional mutagenesis? ○ a) A mutation that occurs spontaneously during DNA replication. ○ b) A type of mutation caused by exposure to radiation. ○ c) A mutation caused by the integration of foreign DNA, such as a virus or transposon, into the host genome. ○ d) A mutation that inactivates a tumor suppressor gene. 41. What is the significance of the LMO2 gene in the context of gene therapy? ○ a) It is the gene that was targeted for replacement in the gene therapy trial. ○ b) It is a tumor suppressor gene that was accidentally inactivated by the retroviral vector. ○ c) It is a known oncogene for T-cell leukemias, and the retroviral vector integrated near this gene in some patients, leading to leukemia development. ○ d) It is the gene that encodes the gamma-C protein. 42. Why was Kaposi's Sarcoma (KS) initially thought to be a familial disease? ○ a) It was highly contagious and spread easily within families. ○ b) Before the AIDS epidemic, it occurred mostly in men of Mediterranean and Jewish descent, suggesting a genetic predisposition. ○ c) It was caused by a mutation in a tumor suppressor gene. ○ d) It could only be transmitted through direct contact with infected blood. 43. How does Hepatitis C increase the risk of liver cancer? ○ a) Chronic infection causes inflammation in the liver, which is associated with cirrhosis and eventually liver cancer. ○ b) The virus directly integrates its DNA into the host genome, causing mutations. ○ c) It suppresses the immune system's response to cancer cells. ○ d) It promotes the growth of new blood vessels to support tumor growth. 44. What is the significance of BRCA1 and BRCA2 genes in cancer? ○ a) They are oncogenes that promote cell proliferation. ○ b) They are viral genes that can cause cancer. ○ c) Mutations in these genes significantly increase the risk of developing breast and ovarian cancers. ○ d) They are genes that regulate the immune system's response to cancer cells. 45. What is genomic instability? ○ a) The ability of the genome to repair DNA damage. ○ b) The normal variation in DNA sequence between individuals. ○ c) An increased tendency for mutations and chromosomal abnormalities to occur in cells, a hallmark of cancer cells. ○ d) The activation of oncogenes and inactivation of tumor suppressor genes. 46. How are stem cells protected from genomic instability? ○ a) They divide rapidly, diluting out any mutations. ○ b) They are not exposed to mutagenic agents. ○ c) They have mechanisms such as transit-amplifying divisions, tissue organization, apoptotic priming, expression of Mdr1 proteins, and bias in DNA replication. ○ d) They have enhanced DNA repair mechanisms. 47. What is depurination? ○ a) A type of spontaneous DNA damage in which a purine base is lost from the DNA molecule. ○ b) The addition of a methyl group to a cytosine base. ○ c) The formation of a double-strand break in DNA. ○ d) The conversion of cytosine to uracil. 48. How can oxidative species contribute to cancer development? ○ a) They promote the repair of DNA damage. ○ b) They can generate DNA double-strand breaks and other types of DNA damage. ○ c) They enhance the immune system's response to cancer cells. ○ d) They inhibit the growth of new blood vessels to support tumor growth. 49. What is the AMES test used for? ○ a) To diagnose cancer in patients. ○ b) To identify potential carcinogens (cancer-causing agents). ○ c) To measure the rate of cell proliferation. ○ d) To assess the effectiveness of cancer treatments. 50. What is loss of heterozygosity (LOH)? ○ a) The duplication of a chromosome. ○ b) The loss of one allele of a gene, often a tumor suppressor gene, making the remaining allele more vulnerable to mutation. ○ c) The translocation of a piece of one chromosome to another chromosome. ○ d) The activation of an oncogene