A student has identified Gene X as mutated in many liver tumors. The student transfects primary hepatocytes extracted from a biopsy of a normal liver and finds no evidence of cell proliferation of the cells. In contrast, when they transfect the liver cell line (HEPG2) they see evidence of proliferation. Explain the different results (limit 4-5 sentences).

A student has identified Gene X as mutated in many liver tumors. The student transfects primary hepatocytes extracted from a biopsy of a normal liver and finds no evidence of cell proliferation of the cells. In contrast, when they transfect the liver cell line (HEPG2) they see evidence of proliferation. Explain the different results (limit 4-5 sentences).

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 21QP

See similar textbooks

Similar questions

Although slow acting retroviruses lack oncogenes, retroviral infection can activate proto oncogenes leading to oncogenesis. a. Describe the mechanism of proto-oncogenes activation that can result from with infection with slow acting retroviruses. b. In what other ways can proto-oncogenes be converted to oncogenes?
For the following diseases, describe the best technique for diagnosing them. Please make sure you include how you would tell someone with the disease from someone without the disease. B. Factor V Leiden thrombophilia is caused by a point mutation at position 1691 in exon 10 of the Factor V clotting factor gene that changes an arginine into a glutamine. This change removes one of the cleavage sites for activated protein C and leads to an increased tendency to clot.
Our understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? What is an oncogene? How does if differ from a proto-oncogene? Why are retroviruses prone to accumulating oncogenes? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation
Our understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation.
/20. In class, we discussed diffferent types of genetic change that can cause a normal gene (proto- oncogene) to become a cancer-causing gene (oncogene), Which of the following would not be a cause? A) translocation or transposition (movement of DNA within the same genome) B) gene ampliffication (increased number of copies of a given gene) C) epigenetic change D) point mutation that changes the gene's product E) loss of telomeres during DNA replication ancer?
Loss of p53 function occurs in the majority of human tumors. 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.
What is the Philadelphia chromosome? Briefly describe how it causes chronic myeloid leukemia.
The p53 protein was discovered through its association with SV40 T antigen and assumed initially to be an oncoprotein. a. What is the current consensus as the function of p53 and what evidence caused this change in view? b. How does the effect of mutation in the p53 gene differ from the effect of mutation in the RB gene what is the molecular basis for this difference ?
Pinpointing a disease gene requires a combination of approaches. Mutations in the XIAP gene are known to cause a serious condition called X-linked lymphoproliferative disease (XLPD). In the case of XLPD, in which the blood contains too many lymphocytes (white blood cells of the immune system), crowding out the oxygen-carrying red blood cells and damaging the liver. When compairing the XIAP amino acid sequence of one affected patient to other human and animal standard RefSeq, the patient has an amino acid substitution at position 203, from cystenine (C) to tyrosing (Y). This evolutionary conservation suggests Group of answer choices that the standard RefSeq does not provide enough information to determine a possible cause of XIAP function. mutations in the XIAP gene and XLPD are not associated. that the mutation in the affected patient has no impact on XIAP function. that the mutation in the affected patient might alter XIAP function.
Part 3C: Below is data from a pedigree trace of patients affected with mouse model of pancreatic cancer, and below are the observations regarding a new gene called 318 that is found on chromosome 5. Patient II-4 has two copies of loss of function variant alleles (or is homozygous for loss-of-function variant 318 allele). Patient I-2 has one copy of loss of function variant and one copy of unaffected allele (is heterozygous for loss-of-function variant 318 allele). Patient II-1 has two copies of unaffected allele (or is homozygous for unaffected 318 allele). |-1 1-2 Il-1 Il-2 Il-3 |l-4 II-5 II-1 III-2 III-3 Based upon data above, what is the mode of inheritance for mouse model for pancreatic cancer? Why?
1. a)Proteins that stimulate/promote progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. b)Proteins that inhibit progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. c)What is the difference between a proto-oncogene and an oncogene? d)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.
1) Given the image below, describe what is happening at each of the 3 sections (i.e. 1, 2, and 3) . [In section 1, the gene donor is providing..., In section 2..., In section 3...]