Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)

Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 9QP: What is the difference between a proto-oncogene and a tumor-suppressor gene?

See similar textbooks

Similar questions

Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.
You are looking at the results of a western blot from the lysates of cells harvested from a suspected breast cancer tumor and you see that there is an increased expression of INK4-p16, you suspect that this will______________? Group of answer choices Increase S to G2 phase transition Initiate a cell cycle arrest in G1 Block M to G1 phase transition Promote tumorigenesis
The diosgenin drug (DSG) has been tested on human cholangiocarcinoma cells (bile duct cancer cells). To this aim, the human cholangiocarcinoma cell lines HuCCT1, QBC939, SK-ChA-1, HuH28, RBE, and Mz-ChA-1 have been subjected to different conditions of treatment with DSG, then assessed for their viability using a MTS assay, and their cell cycle progression using flow cytometry (FCM).Note: The MTS assay is based on the reduction of the MTS tetrazolium compound by viable cells to generate a colored formazan dye that is soluble in cell culture media. This conversion is thoughtto be carried out by NAD(P)H-dependent dehydrogenase enzymes in metabolically active cells.The formazan dye is quantified by measuring its absorbance at 490-500 nm. Question : To which kind of biological molecule does this DSG drug resemble? To which kind of properties do you expect for DSG?
The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please explain in details
Would the function of KRAS gene be lost or gained in MDA-MB-231 breast cancer derived cells? Please explain why.
What is the difference between a proto-oncogene and a tumor-suppressor gene?
Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.
Which of the following defects in RAS would be tumorigenic? multiple answers A. Deletion of nucleotide binding domain B. Inactivation of Guanine Exchange Factor (GEF) C. Mutation at amino acid 61 that prevents hydrolysis of bound GTP D. Inactivation of GTPase Protein (GAPS) E. Mutation that prevents binding of GTP
Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.
Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.