Ch 23 - Cancer Genetics

Which statement explains why colon cancer is an example of clonal evolution? Colon cancer develops due to sequential mutation of multiple genes. Colon cancer has no known genetic cause. Colon cancer is not treatable at any stage of the disease. Mutations in one gene cause colon cancer.

Colon cancer develops due to sequential mutation of multiple genes. Colon cancers develop by acquiring sequential mutations that increase the severity of the cancer, as defined by clonal evolution.

If you think a particular gene is overexpressed in hereditary pancreatic cancer, would you compare the gene expression patterns of the hereditary tumor to the gene expression pattern of normal, noncancerous tissue, tissue from a nonhereditary pancreatic tumor, or both?

both noncancerous tissue and nonhereditary tumor If your gene is only overexpressed in the hereditary tumor, it is likely playing an important role in the hereditary form of the cancer.

Human papillomaviruses are found in 95 percent of women with _____ cancer.

cervical About 95 percent of all women with cervical cancer are infected with human papillomavirus (HPV).

Assuming that the rest of the genome is normal, cells with an inactivating mutation in one copy of a tumor-suppressor gene with the second copy of the gene still wild-type are most likely to_____.

continue normal divisions for this cell type The cell is heterozygous for the mutation, which is usually recessive, so there will be no abnormal effect.

What result might you expect if you overexpressed let-7 miRNA in cancer cells expressing high levels of Ras? decrease in Ras protein levels no change in Ras protein levels increase in Ras protein levels increase in the levels of active MAP kinase

decrease in Ras protein levels Let-7 miRNA negatively regulates expression of the Ras protein.

Which virus is associated with liver cancer?

hepatitis B virus People affected by hepatitis B have an increased risk of liver cancer.

Which virus is associated with cervical, penile, and vulvar cancers?

human papillomavirus (HPV) HPV is associated with cervical, penile, and vulvar cancers.

What type of epigenetic event would be expected to silence tumor-suppressor genes?

hypermethylation Around 5 percent to 10 percent of normally unmethylated CpG islands located at promoters become abnormally methylated in cancer cells. This excess methylation may inhibit transcription of tumor-suppressor genes, thus stimulating the development of cancer.

The retinoblastoma (RB) protein serves as the guardian of the G1/S cell cycle checkpoint by inhibiting which molecule from activating transcription of genes necessary for DNA replication?

E2F The cell is prevented from passing through the G1/S checkpoint by the retinoblastoma protein, which binds to a transcription factor called E2F and keeps it inactive.

During the cell cycle, levels of which of these will fluctuate and eventually lead to the G2 to M transition?

mitosis-promoting factor Near the end of G2, the amount of active MPF reaches a critical level, which commits the cell to divide.

Colorectal cancer is thought to originate as tumors called:

polyps. Initially, these polyps are microscopic, but in time they enlarge, and their cells acquire the abnormal characteristics of cancer cells.

Which mutation in a gene associated with colorectal cancer causes increased cell division?

ras When ras is mutated, the protein it produces continually relays a stimulatory signal for cell division even when growth factors are absent.

What is the most likely mechanism by which hypermethylation is thought to cause cancer?

reduced expression of tumor-suppressor genes Around 5 percent to 10 percent of normally unmethylated CpG islands located at promoters become abnormally methylated in cancer cells. This excess methylation may inhibit transcription of tumor-suppressor genes, thus stimulating the development of cancer.

What system allows an external signal to trigger a cascade of intracellular reactions that produce a specific response?

signal transduction Signal transduction is the transmission of molecular signals from a cell's exterior to its interior.

Breast cancer is associated with mutations in ________ genes, as opposed to being associated with a virus.

BRCA

How can cancer be a genetic disease but rarely inherited?

Cancer is caused by multiple mutations in genes, but it is rarely inherited because the mutations needed typically happen in somatic cells over an individual's lifetime. Since the occurrences of mutations are in somatic cells, it is seldom seen passed down from generation to generation.

________ are abnormal cells that divide without control.

Carcinomas

Which virus is associated with Burkitt lymphoma, nasopharyngeal cancer, and Hodgkin lymphoma?

Epstein-Barr virus Epstein-Barr virus is one of the most common human viruses in the world.

If a cell-surface receptor involved in the Ras signal-transduction pathway is mutated to a continuously activated form, which of these events could occur?

MAP kinase will always activate transcription of downstream genes

What is the distinction between a benign tumor and a malignant tumor?

Malignant tumors invade other tissues. If the cells invade other tissues, the tumor is said to be malignant.

_________ is a cancer that causes patches of abnormal tissue to grow under the skin and is associated with the human herpes virus.

Kaposi sarcoma

Which observation supports the idea that chromosome mutations are a result of cancer? Many different types of chromosomal mutations are found in a variety of cancers. Different chromosomal mutations are associated with different gene mutations. Specific gene mutations are associated with particular types of cancer. The same chromosomal mutation is present in a particular type of cancer.

Many different types of chromosomal mutations are found in a variety of cancers. At least three types of chromosome rearrangements—deletions, inversions, and translocations—are associated with certain types of cancer.

If a person is exposed to a chemical mutagen that damages their DNA in such a way as to predispose them to cancer, will this person pass this cancer predisposition down to their children?

Maybe, if the cancer-causing mutations happen in germ line cells, there is a chance that the cancer could be passed down to their children. The defect can occur in either somatic or sex cells.

Why does it make sense that most cancer cells have mutations in genes that control the cell cycle?

Most cancer cells grow uncontrollably, so it makes sense that genes involved in regulating growth would be mutated. In a cancer cell, one or more of these growth signals has been disrupted, which causes the cell to proliferate at an abnormally high rate.

_____ are mutations that arise randomly in the process of tumor development and do not contribute to cancer progression.

Passengers Passengers are mutations that arise randomly in the process of tumor development and do not contribute to cancer progression.

The ____ gene is involved with cell cycle regulation and the onset of HPV.

RB

What role does telomerase play in cancer formation and progression?

Telomerase prevents cell death triggered by shortened telomeres and is constitutively active in many cancers. In many tumor cells, sequences that regulate the expression of the telomerase gene are mutated, allowing the enzyme to be expressed, and the cell is capable of unlimited cell division, which allows cancer cells to divide indefinitely.

Which of these statements is TRUE concerning the function of proto-oncogenes? They make products that act as signals to inhibit DNA replication. They make products that act as cell checkpoint regulators, which prevent entry into the next stage of the cell cycle if damaged DNA has not yet been repaired. They make products that repair DNA at sites of lesions. Their products are components of cell growth pathways.

Their products are components of cell growth pathways. Proto-oncogenes are normal cellular genes that regulate cell growth and differentiation, which often encode products such as growth factors and their receptors.

Why are tumor-suppressor genes more difficult to identify than oncogenes?

To contribute to cancer, both copies of the tumor-suppressor gene must be mutated. Heterozygotes are often predisposed to cancer because the inactivation or loss of the one remaining normal allele is all that is required to completely eliminate the tumor-suppressor gene product.

All of these are examples of the "two-hit hypothesis," EXCEPT: a cell acquires two mutations that cause it to become a tumor. a cancer cell first acquires its mutation and then causes neighboring cells to mutate. a cell has an inherited mutation and then acquires the second mutation. a cell inherits two mutations that cause it to become a tumor.

a cancer cell first acquires its mutation and then causes neighboring cells to mutate. Cells that travel to other sites in the body, where they establish secondary tumors, have undergone metastasis.

Chronic myelogenous leukemia is often associated with which of these events?

a translocation Most people with chronic myelogenous leukemia have a reciprocal translocation between the long arm of chromosome 22 and the tip of the long arm of chromosome 9.

What is a possible result of a chromosome mutation?

activation of tumor-suppressor genes Chromosome mutations result in the inactivation of tumor-suppressor genes.

What does "loss of heterozygosity" mean?

when, in an individual with one mutated copy of a tumor suppressor, the wild-type tumor-suppressor gene is mutated and now the individual has two copies of the mutated tumor-suppressor gene A common mechanism for the loss of heterozygosity is a deletion on the chromosome that carried the normal copy of the tumor-suppressor gene.