5. In the experiment of cell fusion, when tumor cells were fused with normal cells, the subsequently arising cells lost the ability to form tumors. This observation can be explained as --. a. ras proto-oncogene was inactivated, resulting in no tumor formation b. the arising cancer cells shed or inactivated the tumor suppressor genes, hence cells did not form tumors. c. mitogenic growth factors were removed, hence cells did not proliferate uncontrollably.

5. In the experiment of cell fusion, when tumor cells were fused with normal cells, the subsequently arising cells lost the ability to form tumors. This observation can be explained as --. a. ras proto-oncogene was inactivated, resulting in no tumor formation b. the arising cancer cells shed or inactivated the tumor suppressor genes, hence cells did not form tumors. c. mitogenic growth factors were removed, hence cells did not proliferate uncontrollably.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section12.10: Genomics, Epigenetics,and Cancer

Problem 2GR: Another model, the random model, proposes that any cell in a malignant tumor has the potential to...

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1. VHL is a tumor suppressor because a. it causes cancer cells to become hypoxic b. it inhibits the enzyme proline hydroxylase c. it promotes the degradation of a powerful transcription factor. d. in the absence of VHL, HIF-1 is ubiquitylated by proline hydroxylase 2. NF-1 is a tumor suppressor because A. it inactivates Ras by promoting the hydrolysis of GTP to GDP B. it promotes the methylation of the Ras gene promoter C. it is a phosphatase that dephosphorylates the kinases in the Ras effector pathways D. it inhibits the GEF (guanine exchange factor) that activates Ras please answer both question cause this is my last posting question thank you
4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is mutated in the majority of human cancers (many tumor types). a. For each of the mutations described below (i-iv): is this a mutation you would expect to find when sequencing p53 alleles from tumor cells? Why or why not? i. A missense mutation encoding a hyperactive form of the protein. ii. A deletion of the gene. iii. An insertion in the promoter that increases transcription 10-fold. iv. A nonsense mutation. b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of the gene or a mix of mutant and wild type versions? c. For any of the mutations you said you would expect to find in tumor cells, would you expect tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not? d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various tissues due to inheritance of a loss-of-function mutant allele of…
2. The TP53 gene normally functions as a tumor suppressor by preventing abnormal cell growth but is commonly found mutated in cancer cells, resulting in uncontrolled cell growth. You plan to use genetic tools to remove mutated TP53 from plasma cells. Answer the following questions. B) Is ex vivo or in vivo gene therapy/editing most appropriate? Explain why.
1. True or Flase: Cells must only divide when they receive a signal to divide. 2. BRCA1 is a gene that codes for a tumor suppressor protein. If a person inherits a mutation in BRCA1, it greatly increases his or her risk of developing breast cancer. Are the cancer-causing mutations in the BRCA1 gene more likely to: a) increase expression of the gene b)decrease expression of the gene c)not affect the expression of the gene
Different gene therapy approaches have been studied for cancer gene therapy. These approaches include? (select all that applies) a.immunotherapy, b. anti-angiogenic gene therapy, c.inhibition of tumor invasion, d.induction of apoptosis
The p53 gene was discovered in 1979, but it was not clear whether the gene functioned as an oncogene or a tumor-suppressor gene. Several years later, researchers showed that both p53 alleles are inactivated in some mouse cancers. This evidence suggests A. the p53 gene is an oncogene because inactivated alleles would produce mutated signal transduction proteins that would result in stimulating cell division. B. the p53 gene is an oncogene because the cell would overproduce transcription factors to compensate for the inactive alleles, resulting in increased cell division. C. the p53 gene is a tumor-suppressor gene because inactivated alleles indicate a loss of protein function which allowed the cancer to develop D. the p53 gene is a tumor-suppressor gene because the cell would produce too few transcription factors for gene activation, resulting in decreased cell division.
1. For each of the following genes, categorize them as a tumor suppressor gene or a protooncogene. Please explain each choice. Gene Proto-oncogene or tumor suppressor gene? Explanation Bcl-2 Rb Ras APC p53
A tumor suppressor gene regulates the cell cycle; an example is . Select one: a. positively, p21 b. negatively, cyclin c. positively, retinoblastoma d. negatively, retinoblastoma e. positively, RAS Cycle HW due Jump to. 4) Next pa cancer stem cells
Which of the following steps are correct about multistep tumorigenesis (select all that apply)? A. Mutations in progenitor cells are more likely to develop a neoplastic state compared to mutations in stem cells B. Driver mutations give a cell clone a proliferative advanage C. The rate of mutation /genetic change is constant during tumor progression D. Nutrition/diet may effect rate of tumorigenesis E. All cells within a tumor are biologically equivalent and equally capable of high levels proliferation
g protein D. Growth factor receptor ng Tool 0 Q ing C. Growth factor-binding protein D. Growth factor receptor E. Transcription activator A child with retinoblastoma is found to have a 13q14 deletion. The Rb gene, which resides at this locus, produces which kind of tumor-associated protein? A. Cell cycle regulator B. Growth factor ㅂ분 요 9 12 W □ @ 2 C Edit in Paint 8 60 8 Focus
2. The TP53 gene normally functions as a tumor suppressor by preventing abnormal cell growth but is commonly found mutated in cancer cells, resulting in uncontrolled cell growth. You plan to use genetic tools to remove mutated TP53 from plasma cells. Answer the following questions. A) Which genetic tool is most appropriate for this application, gene therapy or gene editing? Explain why.
12.What is field of cancerization? Explain part A and B of this figure. How does it explain field of cancerization?| (A) mutation mutation mutation mutation morphologically normal morphologically abnormal, hyperplastic, dysplastic, or neoplastic (D) tumor 1 tumor 2 (8) 7,8,9 10 wild-type p53 only G-T45. wt p53 NORMAL PATCH FIELD CARCINOMA 17p 3p, 9p, 8p, 189 11g Figure 11.14 The Biology of Cancer (0 Garland Sdener 2014)