homework 20

Which of the following can give rise to cancer-promoting mutations? -exposure to excess sunlight -DNA replication errors -exposure to ionizing radiation -inhalation of tobacco smoke

-exposure to excess sunlight -DNA replication errors -exposure to ionizing radiation -inhalation of tobacco smoke Explanation: Cancer is fundamentally a genetic disease: it arises as a consequence of pathological changes in the information carried by DNA. Cancer-promoting mutations can be generated by a variety of mutagens. They can also occur spontaneously, due to limitations in the accuracy of DNA replication and repair. Thus, DNA replication errors, exposure to excess sunlight and ionizing radiation, and the inhalation of tobacco smoke can all promote genetic mutations that can lead to cancer.

Many of the genes mutated in individual tumors are involved with which of the following regulatory pathways? -pathways controlling the catabolism of lactose -pathways regulating the cell's response to DNA damage or stress -pathways governing the initiation of cell division

-pathways regulating the cell's response to DNA damage or stress -pathways governing the initiation of cell division Explanation: Many of the genes mutated in individual tumors are involved with pathways governing the initiation of cell division and those regulating the cell's response to DNA damage or stress. As more is learned about the genetic basis of cancer, certain pathways emerge. Given that cancer is an uncontrolled growth of cells, it is therefore not surprising that mutations that cause cancer commonly occur in pathways that control cell proliferation, growth, survival, and response to DNA damage and stress.

Which statement is true about human cells? A. Unlike normal cells, cancer cells can only divide a limited number of times in culture. B. Cancer cells lose the ability to produce the enzyme telomerase. C. Cancer cells tend to lack telomeres. D. In cancer cells, telomeres grow progressively shorter with each cell division. E. Cancer cells maintain their telomeres by reactivating the enzyme telomerase.

Cancer cells maintain their telomeres by reactivating the enzyme telomerase. Explanation: Cancer cells maintain their telomeres by reactivating the enzyme telomerase. Reactivation of telomerase allows cancer cells to break through the proliferation barrier faced by normal, human cells that have turned off telomerase. By re-expressing telomerase, cancer cells avoid the progressive telomere shortening that would otherwise occur as the cells proliferate. In normal human somatic cells that have stopped expressing telomerase, telomeres grow progressively shorter with each cell division. Cells of the germ line, however, continue to express this enzyme to ensure that gametes and the subsequent generation inherit elongated telomeres that are associated with "young chromosomes."

How is β-catenin involved in cancer? A. It is a proto-oncogene because mutations in β-catenin make the protein more active in its association with DNA polymerase during S phase. B. It is a tumor suppressor because overactivation of both copies of Brca1 or Brca2 allows cancer cells to ignore cell-cycle checkpoints. C. It is a tumor suppressor because the inactivation of both copies of it allows cancer cells to continue to survive and divide, even in the presence of damaged DNA. D. It is a proto-oncogene because mutations in β-catenin make the protein resistant to degradation, promoting cell proliferation.

It is a proto-oncogene because mutations in β-catenin make the protein resistant to degradation, promoting cell proliferation. Explanation: β-catenin is a proto-oncogene. Activating mutations in β-catenin make the β-catenin protein resistant to degradation, promoting cell proliferation. After migrating from the cytoplasm into the nucleus, β-catenin binds to the TCF transcription regulator, creating a complex that activates transcription of various Wnt-responsive genes, including genes whose products stimulate cell proliferation. Therefore, β-catenin exerts its effect as a transcriptional regulator, and is not involved directly with DNA polymerase. p53 and Brca1/Brca2 are tumor suppressors; the inactivation of both copies of these genes allows cancer cells to continue to survive and divide in the presence of massively damaged DNA.

Which of the following is most consistent with the data contained within these karyotypes? A. The karyotype on the right is most likely from a young tumor because it is still demonstrating genetic stability. B. The karyotype on the right is most likely from an advanced tumor due to its significant evidence of genetic instability. C. The karyotype on the left is most likely from an advanced tumor due to its significant evidence of genetic instability. D. The karyotype on the left is not likely that of human and the karyotype on the right is from a normal human male.

The karyotype on the right is most likely from an advanced tumor due to its significant evidence of genetic instability. Explanation: The karyotype on the left appears to be from a normal human female. The chromosomes in these karyotypes are "painted" with a combination of fluorescent stains that give each chromosome a different color. The karyotype on the right is most likely from an advanced tumor due to its significant evidence of genetic instability. Cancer cells often have highly abnormal chromosomes, reflecting genetic instability. The advanced cancer karyotype shows multiple translocations, including two instances of a translocation of material from chromosome 6 to chromosome 4, one of which also includes a piece of chromosome 1. Whereas the normal cell contains 46 chromosomes, the breast cancer cell has 51; several of its chromosomes are missing, and it has an extra copy of a handful of chromosomes—along with 6 copies of chromosome 19. This demonstrates a significant level of genetic instability and suggests that this cell line has been undergoing mutation for some time; this is not a young tumor.

Which of the following is not a key behavior of cancer cells? A. Most are genetically unstable, with a greatly increased mutation rate. B. They can often proliferate indefinitely. C. They are less prone than normal cells to kill themselves by apoptosis. D. They are abnormally invasive. E. They consume neighboring cells to fuel their excessive proliferation.

They consume neighboring cells to fuel their excessive proliferation. Explanation: Cancer cells have an abnormal metabolism that fuels their excessive growth and proliferation. However, they do not ingest neighboring cells as a source of nutrients. Some cancer cells are abnormally invasive because they lack the cadherin molecules that would otherwise hold them in their proper place. In addition to their genetic instability, with a greatly increased mutation rate due to inactivation of DNA repair mechanisms, cancer cells often reactivate the gene that encodes telomerase and thereby avoid the progressive shortening of telomeres at the ends of chromosomes with each cell division. This shortening would otherwise limit extensive cell proliferation. This telomere lengthening allows cancer cells to proliferate indefinitely.

Cancer is fundamentally which type of disease? A. an infectious disease B. a genetic disease C. a disease of obesity D. a human disease E. an environmental disease

a genetic disease Explanation: Cancer is best described as a genetic disease. Cancer arises as a consequence of changes to DNA. These changes to the DNA nucleotide sequence are collectively referred to as mutations. Although viruses play a part in some human cancers, such as cervical cancer and HPV, cancer itself is not an infectious disease. Obesity and environmental factors can increase the risk of cancer, but they are not the mechanistic causes of cancer.

Cancerous cells can accumulate mutations more quickly for all the following reasons EXCEPT A. a mutation in a gene involved in DNA replication. B. a mutation in a cell proliferation gene. C. a mutation in a DNA repair gene. D. a mutation that causes mistakes in mitosis.

a mutation in a cell proliferation gene. Explanation: Cancer cells often develop genetic instability and have elevated mutation rates due to mutations in the processes that prevent mutation: DNA repair, DNA replication, mitosis, and cell-cycle checkpoints. Cell proliferation mutations change cancer cell growth, but don't necessarily change mutation rates.

What does the small drug molecule called imatinib (trade name Gleevec) do to help treat cancer cells? A. blocks the activity of a hyperactive tumor suppressor B. encourages the activity of a hyperactive tumor suppressor C. encourages the activity of a hyperactive mutant kinase D. blocks the activity of a hyperactive mutant kinase

blocks the activity of a hyperactive mutant kinase Explanation: Imatinib blocks the activity of a hyperactive mutant kinase. In chronic myeloid leukemia (CML), the growth of the cancer cells depends on a mutant intracellular signaling protein (a tyrosine kinase) that causes the cells to proliferate and survive when they should not.

Which type of mutation would not typically convert a proto-oncogene into an oncogene? A. chromosomal deletion of the region containing the proto-oncogene B. mutation in the coding sequence that leads to the production of a hyperactive protein C. chromosomal rearrangement that leads to the production of a hyperactive protein D. gene amplification E. chromosomal rearrangement that leads to overproduction of the normal proto-oncogene protein

chromosomal deletion of the region containing the proto-oncogene Explanation: A chromosomal deletion of the region containing the proto-oncogene will not typically convert a proto-oncogene into an oncogene because it would decrease that gene's function. Proto-oncogenes are converted to cancer-promoting oncogenes by mutations that increase the gene's activity. All of the other choices represent a gain of function that can convert a proto-oncogene to an oncogene.

Which type of mutation would not be involved in the inactivation of a tumor suppressor gene? A. loss-of-function mutation in tumor suppressor gene B. duplication of the gene C. chromosomal deletion of a region containing the tumor suppressor gene D. loss of a whole chromosome containing the tumor suppressor gene E. silencing of the gene's activity by epigenetic changes

duplication of the gene Explanation: A duplication of the gene would not be involved in the inactivation of a tumor suppressor gene. Gene duplication would provide an additional copy of a tumor suppressor gene. Such gain-of-function mutations would not inactivate the tumor suppressor gene. Because tumor suppressor genes act in a recessive manner, both alleles must be mutated in order for the cancer phenotype to display. Each of the following mechanisms would be involved in the inactivation process over time for a tumor suppressor gene: loss of a chromosome containing a tumor suppressor gene; deletion of the chromosomal region containing a tumor suppressor gene; silencing of a tumor suppressor gene by epigenetic changes; and a loss-of-function mutation.

In most cases, how many mutations are required for a normal cell to turn into a cancer cell? A. generally only one B. more than three C. Cancers are not caused by mutations.

more than three Explanation: More than three mutations are typically required for a normal cell to turn into a cancer cell. Precisely how many mutations it takes to make a cancer cell is a matter of debate, but for most full-blown cancers it could be at least 10—and they have to affect the right type of genes. However, it should be noted that proto-oncogenes and tumor suppressor genes behave differently in the number of mutations required for their cancer-causing effects.

An oncogene is different from a tumor suppressor gene in that A. oncogene mutations more rarely lead to cancer. B. oncogenes have mutations causing decreased activity of the protein. C. oncogenes have mutations causing increased activity of the protein. D. mutation of the gene can contribute to cancer.

oncogenes have mutations causing increased activity of the protein. Explanation: Oncogenes are mutations in genes that lead to increased activity of the protein and lead to the cell changes that promote excessive proliferation and cancer cell phenotypes.

Which cancer-causing gene can be activated by a single mutation in only one allele? A. proto-oncogene B. tumor suppressor gene C. DNA repair gene

proto-oncogene Explanation: The cancer-causing gene that can be activated by a single mutation in only one copy is referred to as a proto-oncogene. Proto-oncogenes can be activated to form oncogenes with a single mutation. This type of gain-of-function mutation can stimulate cell survival, proliferation, or both. Inactivating a single DNA repair gene would leave a second, functional copy intact and both copies of a tumor suppressor gene must be inactivated to cause cancer. These loss-of-function mutations are generally recessive: both copies of the gene must be lost or inactivated to contribute to cancer development.

The rate of cell turnover varies in different tissue types. T/F

true Explanation: The rate of cell turnover varies in different tissue types. For example, cell turnover is very slow in nervous tissue, yet extremely rapid in the intestinal epithelium, where cells are replaced every few days. Most other cell types fall between these two extremes. Bone, for example, has a turnover time of about ten years.

Which class of cancer-critical gene must be inactivated to promote the development of cancer? A. proto-oncogene B. tumor suppressor gene C. oncogene

tumor suppressor gene Explanation: A tumor suppressor gene is the class of cancer-critical gene that must be inactivated to promote the development of cancer. Because of their loss-of-function, recessive nature, both copies of a tumor suppressor gene must be inactivated to contribute to cancer development. On the other hand, proto-oncogenes must be activated to produce cancer-causing oncogenes.

Some types of cancer run in families: individuals in such predisposed families are prone to develop these cancers early in adult life. Mutations in which type of cancer-critical gene would most likely be responsible for "hereditary" cancers that are not immediately present in the phenotype of offspring but develop as age increases? A. proto-oncogenes B. either proto-oncogenes or tumor suppressor genes C. tumor suppressor genes D. Mutations in cancer-critical genes cannot be inherited because cancer is not a hereditary condition.

tumor suppressor genes Explanation: Cancers that run in families are often caused by mutations in a tumor suppressor gene. Affected individuals generally inherit one normal copy of the gene and one mutant copy. The unaffected gene is sufficient to keep their cells behaving normally, but in each cell a single mutation can cause a total loss of the gene's function. Individual tumors arise from cells in which a mutation has inactivated the remaining good copy of the gene. In contrast, mutation in proto-oncogenes can lead to an increase in the rate of the cell cycle and therefore cell division. For many of the cancer-critical genes, the most dangerous mutations are ones that render the encoded protein hyperactive. These gain-of-function mutations have a dominant effect: only one gene copy needs to be mutated to promote the development of cancer.