ADVANCED PATHOPHYSIOLOGY EXAM NEW VERSION LATEST UPDATE WITH ACCURATE ANSWERS GUARANTEED PASS BEST STUDYING MATERIAL WITH 1OO+ QUESTIONS

Autocrine stimulation is the ability of cancer cells to do what? a. Stimulate angiogenesis to create their own blood supply b. Encourage secretions that turn off normal growth inhibitors c. Secrete growth factors that stimulate their own growth d. Divert nutrients away from normal tissue for their own use - ANSWER C. Cancer cells must have mutations that enable them to proliferate in the absence of external growth signals. To achieve this, some cancers acquire the ability to secrete growth factors that stimulate their own growth, a process known as autocrine stimulation. The other options describe other activities of cancer cells, but not autocrine stimulation. A student studying biology asks the professor to describe how the ras gene is involved in cancer proliferation. What explanation by the professor is best? a. It suppresses the action of the tumor-suppressor genes. b. It changes the way the growth promotion genes work. c. A mutation in this gene allows continuous cell growth. d. It activates a cell surface receptor that allows signaling to the nucleus . - ANSWER C. Up to one-third of all cancers have an activating mutation in the gene for an intracellular signaling protein called ras. This mutant ras stimulates cell growth even when growth factors are missing. The remaining options do not describe how ras contributes to cancer formation and growth. How does the ras gene convert from a proto-oncogene to an oncogene? a. Designating a chromosome that has a piece of one chromosome fused to a piece of another chromosome b. Duplicating a small piece of a chromosome, repeatedly making numerous copies c. Altering one or more nucleotide base pairs d. Promoting proliferation of growth signals by impairing tumor-suppressor genes - ANSWER C A point mutation is the alteration of one or a few nucleotide base pairs. This type of mutation can have profound effects on the activity of proteins. A point mutation in the ras gene converts it from a regulated proto-oncogene to an unregulated oncogene, an accelerator of cellular proliferation. Fusion, duplications, and proliferation of growth signals are not the cause of a ras gene converting to an oncogene. Inherited mutations that predispose to cancer are almost invariably what kind of gene? a. Proto-oncogenes b. Oncogenes c. Tumor-suppressor genes d. Growth-promoting genes - ANSWER C. Inherited mutations that predispose to cancer are almost invariably in tumor-suppressor genes. At present, no research supports the other options as factors related to how inherited mutations cause cancer. In a normal, nonmutant state, what is an oncogene referred to as? a. Basal cell b. Target cell c. Caretaker gene d. Proto-oncogene - ANSWER D In its normal nonmutant state, an oncogene is referred to as a proto-oncogene. A basal cell is in the innermost surface of epithelial tissue. Target cells are the recipients of mutations or substances. A caretaker gene is responsible for the maintenance of genomic integrity. The professor explains to students that oncogenes are genes that are capable of what? a. Undergoing mutation that directs the synthesis of proteins to accelerate the rate of tissue proliferation b. Directing synthesis of proteins to regulate growth and to provide necessary replacement of tissue c. Encoding proteins that negatively regulate the synthesis of proteins to slow or halt the replacement of tissue d. Undergoing mutation that directs malignant tissue toward blood vessels and lymph nodes for metastasis - ANSWER A. Oncogenes are independent of normal regulatory mechanisms; thus the cell is driven into a state of unregulated constitutive expression of proliferation signals and uncontrolled cell growth. Burkitt lymphomas designate a chromosome that has a piece of chromosome 8 fused to a piece of chromosome 14. This is an example of which mutation of normal genes to oncogenes? a. Point mutation b. Chromosome translocation c. Gene amplification d. Chromosome fusion - ANSWER B. Chromosome translocations, in which a piece of one chromosome is translocated to another chromosome, can activate oncogenes. One of the best examples is the t(8;14) translocation found in many Burkitt lymphomas; t(8;14) designates a chromosome that has a piece of chromosome 8 fused to a piece of chromosome 14. A point mutation is the alteration of one or a few nucleotide base pairs. Gene amplification is the result of repeated duplication of a region of a chromosome, so that instead of the normal two copies of a gene, tens or even hundreds of copies are present. Chromosome fusion occurs during translocation. In childhood neuroblastoma, the N-myc oncogene undergoes which type of mutation of normal gene to oncogene? a. Point mutation b. Chromosome fusion c. Gene amplification d. Chromosome translocation - ANSWER C. Amplifications are the result of the duplication of a small piece of a chromosome over and over again; consequently, instead of the normal two copies of a gene, tens or even hundreds of copies are present. The N-myc oncogene is amplified in 25% of childhood neuroblastoma. Why are two "hits" required to inactivate tumor-suppressor genes? a. Each allele must be altered, and each person has two copies, or alleles, of each gene, one from each parent. b. The first hit stops tissue growth, and the second hit is needed to cause abnormal tissue growth. c. Tumor-suppressor genes are larger than proto-oncogenes, requiring two hits to affect carcinogenesis. d. The first hit is insufficient to cause enough damage to cause a mutation. - ANSWER A. A single genetic event can activate an oncogene, acting in a dominant manner in the cell. However, each person has two copies, or alleles, of each gene, one from each parent. Therefore two hits are required to inactivate the two alleles of a tumor-suppressor gene, allowing the process to become active. The remaining options do not describe the reason two hits are required. How do cancer cells use the enzyme telomerase? a. To repair the telomeres to restore somatic cell growth b. As an intracellular signaling chemical to stimulate cell division c. To switch off the telomerase to enable cells to divide indefinitely d. To switch on the telomerase to enable cells to divide indefinitely - ANSWER D Cancer cells, when they reach a critical age, somehow activate telomerase to restore and maintain their telomeres and thereby make it possible for cells to divide over and over again. What are characteristics of benign tumors? a. Benign tumors invade local tissues. b. Benign tumors spread through the lymph nodes. c. Benign tumors cause systemic symptoms. d. Benign tumors include the suffix -oma. - ANSWER D Benign tumors are usually encapsulated and well-differentiated. They retain some normal tissue structure and do not invade the capsules surrounding them or spread to regional lymph nodes or distant locations. Benign tumors are generally named according to the tissues from which they arise and include the suffix -oma. Benign tumors do not cause systemic symptoms What does the health professions student learn about benign tumors? a. The resulting pain is severe. b. Benign tumors are not encapsulated. c. Benign tumors are fast growing. d. The cells are well-differentiated. - ANSWER D. A benign tumor is well-differentiated with its tissue appearing similar to the tissue from which it arose. The other options are characteristic of a malignant tumor.