Select the statements that accurately describe different ways that translocations could lead to cancer. A translocation breaks up a gene that encodes a protein required to pass through mitotic checkpoints. The resultin protein cannot function normally. A gene for a protein that is involved in a mitotic checkpoint is placed next to the regulatory sequence of a differer gene. The gene is now expressed at inappropriate times. A translocation breaks up the sequence of a gene for a tumor-suppressor protein. The resulting protein cannot function properly. A new sequence is added to a proto-oncogene. The modified gene now produces a new protein that increases the cell division. A gene for a tumor-suppressor protein is placed next to a regulatory sequence that increases the expression of the

Select the statements that accurately describe different ways that translocations could lead to cancer. A translocation breaks up a gene that encodes a protein required to pass through mitotic checkpoints. The resultin protein cannot function normally. A gene for a protein that is involved in a mitotic checkpoint is placed next to the regulatory sequence of a differer gene. The gene is now expressed at inappropriate times. A translocation breaks up the sequence of a gene for a tumor-suppressor protein. The resulting protein cannot function properly. A new sequence is added to a proto-oncogene. The modified gene now produces a new protein that increases the cell division. A gene for a tumor-suppressor protein is placed next to a regulatory sequence that increases the expression of the

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 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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Select the statements that accurately describe different ways that translocations could lead to cancer. A translocation breaks up the sequence of a gene for a protein that stimulates apoptosis. The resulting protein cannot function properly. A gene for a protein that stimulates apoptosis is placed next to a regulatory sequence that increases the expression of the gene. A translocation breaks up a gene that encodes a protein required to pass through mitotic checkpoints. The resulting protein cannot function normally. A gene for a protein that is involved in a mitotic checkpoint is placed next to the regulatory sequence of a different gene. The gene is now expressed at inappropriate times. A new sequence is added to a proto-oncogene. The modified gene now produces a new protein that increases the rate of cell division.
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
Myc is a family of regulator genes that code for transcription factors. c-myc was the first gene to be discovered in this family, and c-myc is dependent on mitogenic stimulation for its expression and function. c-myc transcribes a number of genes involved in G1/S cell cycle progression, such as CDK4 and cdc25A Which of the following are true for the c-myc gene? Select all that apply In cancer or transformed cells, the c-myc gene mutation would be recessive, and a loss of function mutation The c-myc gene is a tumor suppressor gene In cancer or transformed cells, the c-myc gene mutation would be dominant, and a gain of function mutation The c-myc gene is a proto-oncogene
Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell division
Ras is a proto-oncogene that is within the EGF pathway. The EGF receptor can activate the cell division pathway only when the EGF ligand binds to the receptor. A gain of function mutation occurs in only one copy of the Ras gene. What are all the possible consequences of this? Select all that apply. Group of answer choices The cell will undergo constant cell division The cell will still be normal as only one copy of Ras is mutated. Both copies must be mutated for the cell to undergo constant cell division There will be an increase of EGF ligands present in the cell The EGF receptor will always be active even with no EGF ligands bound and activate the pathway Ras will always be active and activate the proteins downstream that will turn on cell division Ras will be under the influence of the EGF receptor and will only activate if the EGF ligand is bound to the receptor
A cultured mouse cell line has a mutation in a gene encoding a ribosomal protein. The mutant protein impairs the fidelity of translation such that incorrect amino acids are incorporated at higher rates than normal during protein synthesis. It also slows the rate of mRNA translation and increases the duration of the cell cycle, i.e., the mutant cells grow and divide more slowly. Researchers noted that these cells express higher levels of chaperone proteins than normal cells. Which of the following is the most likely explanation for the elevated chaperone levels.
Gene A encodes for a protein A which prevents exit from the G1 phase of the cell cycle. You are studying mutations in gene A. Which of the following are true for gene A? Select all that apply A mutation that gives constitutively active protein A in one allele and a deletion of the entire gene in the second allele will transform the cell Gene A is a proto-oncogene A nonsense mutation that replaces the fourth codon with a stop codon in one allele and a deletion of the entire gene in the second allele will transform the cell Gene A is a tumor supressor gene
p53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?
Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.
According to the multi-hit model, more than one mutation must occur in a cell for cancer to develop. Once an oncogene has been formed by a mutation, what other type of gene must also mutate?
Cancer is a disease that results in uncontrolled cell division. Cancer cells have lost their ability to regulate the cell cycle Which of the following mutations could be found in cancer cells. Select all that apply. A large deletion mutation in a gene that represses cell division large deletion mutation in a gene that stimulates cell division A large deletion mutation in a gene for DNA polymerase A large deletion mutation in a gene that is required to halt cell cycle while the cell repairs its DNA
The protein p53 is activated when the cell's DNA is damaged. p53 helps to arrest the cell cycle in G1, allowing time for the cell to repair its DNA before replicating. p53 does this job by stimulating the synthesis of a protein that inhibits the cyclin-dependent kinase. Mutations that inactivate p53 contribute to 50% of human cancers. Would you classify p53 as a tumor-suppressor gene or a proto-oncogene?