Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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- Which one of the following events is unlikely to beassociated with cancer?a. mutation of a cellular proto-oncogene in a normaldiploid cellb. a chromosomal translocation with a breakpointnear a cellular proto-oncogenec. deletion of a cellular proto-oncogened. mitotic nondisjunction in a cell carrying a deletionof a tumor-suppressor genee. incorporation of a cellular oncogene into a retroviruschromosomearrow_forwardOne example of an oncogene is ras. Ras is a G protein that is activated when growth factors bind to a G protein-coupled receptor. The mutated form of ras binds to GTP but does not allow the GTP to be broken down to GDP. Ras is involved in both the G1G1 and G2G2 checkpoints. What happens to cells that have this mutated form of ras? A. They divide when they should not. B. They don’t divide when they should. C. They enter mitosis without going through the S phase of the cell cycle. D. They enter cytokinesis without going through the M phase of the cell cycle.arrow_forwardOrder the listed proteins in the correct order so that cell proliferation is activated as the endpoint. 1. ERK1/2 2. MEK1/2 3. a MAPKKK 4. hepatocyte growth factor 5. c-MET 6. a GEF 7. Rasarrow_forward
- When the antigen-presenting cells binds to the T-cell, it will cause the T-cell to increase the amount of a protein called perforin, which is secreted to kill nearby cells. Which of these could INCREASE the amount of a functional perforin proteins produced? a. Increased methylation of DNA near the site of the gene b. Increased binding of a repressor, that decreases the binding affinity between TFIID and DNA c. Increased production of a small RNA that is complementary to perforin mRNA d. Increased O-linked glycoslyation of perforin proteins in the Golgiarrow_forwardWhich of the following statements concerning p53 is NOT correct? O a. p53-dependent transcription of target genes leads to cell cycle arrest or cell death (apoptosis). O b. O C. Loss of p53 function results in loss of checkpoint controls. Loss of p53 function creates an environment that is permissive for genome instability--that is, more damaged cells with chromosome aberrations and mutations survive and propagate. d. p53 is a tumor suppressor protein which is largely responsible for protecting cells from cancer- causing DNA-damaging agents.arrow_forwardCompare and contrast oncogenes and supressor genes. Give an example of a gene of each kind and a cancer type associated with mutations in said gene.arrow_forward
- A patient comes into your clinic exhibiting generic cancer symptoms. In order to help form a diagnosis, you ask about patient history and they tell you that they worked for years in an agricultural job, primarily in handling food for large bovine animals and then later working with insect pesticide treatment of grain fields. You decide to test for elevated levels of the environmental agent(s) in their body and focus your cancer diagnosis on based on the established associations of epigentic effects and cancer. O nickel and cadmium; stomach and skin cancer O benzene; breast, prostate and thyroid cancer O polycyclic aromatic hydrocarbons and benzene; lung, breast, stomach and skin cancer O arsenic and endocrine disruptors; skin, bladder, liver and kidney cancerarrow_forwardMost forms of cancer involvea. the activation of a single oncogene.b. the inactivation of a single tumor-suppressor gene.c. the activation of multiple oncogenes.d. the activation of multiple oncogenes and the inactivation ofmultiple tumor-suppressor genes.arrow_forwardCells in a tumor contain mutated copies of a particular gene that promotes tumor growth. Gene therapy can be used to introduce a normal copy of this gene into the tumor cells. Would you expect this therapy to be effective if the mutated gene were an oncogene? A tumor-suppressor gene? Explain your reasoning.arrow_forward
- An oncogene is produced from a that has acquired a .a. proto-oncogene, loss-of-function mutationb. proto-oncogene, gain-of-function mutationc. tumor-suppressor gene, loss-of-function mutationd. tumor-suppressor gene, gain-of-function mutationarrow_forwardOn the image, you can see the results of a DNA microarray used for cancer prognosis, where tissue samples from healthy and cancerous tissues were analyzed. cDNA from healthy cells and cancer cells were labeled with green and red fluorescence, respectively, mixed equally, and hybridized with the chip. It is known that gene A is more highly expressed in breast cancer type I, while genes B and C have lower expression in type II, which is highly aggressive. Based on the gene expression levels shown in the image, the cancer sample does not correspond to either type I or type II breast cancer, why is that?arrow_forwardPlease answer subquestions 1.a and 1.b Question 1.a: A mutation in MAPK makes it constitutively active. If cells are treated with the control treatment (no EGF) will be observed. When cells are treated with EGF will be observed. A. No proliferation; proliferation B. Proliferation; proliferation C. No proliferation; no proliferation D. Proliferation; no proliferation Question 1.b: In order to prevent a specific event (step), from occurring in a pathway (e.g, the phosphorylation of MAPKK), you should target the portion of the cascade with an inhibitor. A. Downstream B. Extracellular C. Nuclear D. Upstreamarrow_forward
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