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 resultir 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 differen 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 resultir 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 differen 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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Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
Which of the following is not true? ○ In a somatic cell, imprinted genes are not expressed because both copies are methylated. DNA methylation at imprinted genes is changed during meiosis. O DNA methylation at silenced genes is changed during cellular differentiation. O Both copies of a silenced gene are methylated and so neither copy is expressed.
Please answer asap
In terms of the cell cycle, what would happen if there was a defect in the Rb protein that made it unable to bind to gene regulatory proteins? (eg. the cell cycle would arrest in late G2 phase)
dont know the order
Match the following statements to the type of gene they describe. ✓Encode proteins that promote cell cycle progression ✓Encode proteins that regulate cell cycle checkpoints ✓Mutations are loss-of-function and recessive ✓Mutations are gain-of-function and dominant ✓RB1 is an example of this type of gene A.proto-oncogene B.tumor suppressor gene
Isothiocyanates arè compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins DNA Damage p53 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells O Have no effect on progression of cervical cancer cells
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?
You are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4B
Protein P, normally stimulates apoptosis or cell death when activated. Consider a cell with a mutation in one allele such that protein P is always expressed and active, while the other allele of gene P is deleted. Which of the following is true for this cell? Gene P is a proto-oncogene, and the phenotype of the cell is transformed. Gene P is a proto-oncogene, and the phenotype of the cell is not transformed. Gene P is a tumor suppressor gene, and the phenotype of the cell is not transformed Gene P is a tumor suppressor gene, and the phenotype of the cell is transformed 로
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 retroviruschromosome
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?