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BIO 130.01 Genetics, Lecture > Chapters 16: Genetics of Cancer > Flashcards

Chapters 16: Genetics of Cancer Flashcards

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1
Q

True or False. Cancer is a genetic disease at the germ cell layer, characterized by the presence of gene products derived from mutated or abnormally expressed genes.

A

False. Somatic level

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2
Q

True or False. Although some mutated cancer genes may be inherited, most are created within somatic cells that then divide and form tumors.

A

True

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3
Q

True or False. Another important difference between cancers and other genetic diseases is that cancers mainly arise from a single mutation in a single gene, but not from the accumulation of many mutations.

A

False. Cancers mainly arise from accumulation of many mutations.

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4
Q

What are the cellular functions affected by cancer?

A
  1. repair of DNA damage
  2. cell division
  3. apoptosis
  4. cellular differentiation
  5. migratory behavior
  6. cell-cell contact
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5
Q

It is clinically defined as a large number of complex diseases, up to a hundred, that behave differently depending on the cell types from which they originate and the types of genetic alterations that occur within each type.

A

Cancer

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6
Q

True or False. Cancers vary in their ages of onset, growth rates, invasiveness, prognoses, and responsiveness to treatments. However, at the molecular level, all cancers exhibit common characteristics that unite them as a family.

A

True

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7
Q

What are the two fundamental properties of cancer?

A
  1. Abnormal cell growth and division (proliferation)

2. defects in the normal restraints that keep cells from spreading and colonizing other parts of the body (metastasis)

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8
Q

If a cell simply loses genetic control over cell growth, it may grow into a multicellular mass namely?

A

Benign tumor

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9
Q

A secondary tumor that arose from the primary site of the tumor is called?

A

Metastases

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10
Q

If cells in the tumor also have the ability to break loose, enter the bloodstream, invade other tissues, and form secondary tumors, then it is referred to as?

A

Malignant

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11
Q

True or False. Although malignant tumors may contain billions of cells, and may invade and grow in numerous parts of the body, all cancer cells in the primary and secondary tumors are clonal.

A

True

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12
Q

Patients diagnosed with this disease show reciprocal translocation between chromosome 8 (with translocation breakpoints at or near the c-myc gene) and chromosomes 2, 14, or 22 (with translocation breakpoints at or near one of the immunoglobulin genes).

A

Burkitt lymphoma

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13
Q

Each Burkitt lymphoma patient exhibits unique breakpoints in his or her c-myc and immunoglobulin gene DNA sequences; however, all lymphoma cells within that patient contain identical translocation breakpoints. Draw a conclusion from this information.

A

This demonstrates that all cancer cells in each case of Burkitt lymphoma arise from a single cell, and this cell passes on its genetic aberrations to its progeny.

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14
Q

Patients with Burkitt lymphoma exhibit mutations in what genes?

A

Reciprocal translocation between the c-myc gene located at chromosome 8 and immunoglobulin gene located in either chromosome 2, 14, or 22

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15
Q

According to the cancer stem cell hypothesis, most of the cells within tumors do not proliferate. Those that do proliferate and give rise to all the cells within the tumor are known as?

A

cancer stem cells

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16
Q

These cells are undifferentiated cells that have the capacity for self-renewal—a process in which the stem cell divides unevenly, creating one daughter cell that goes on to differentiate into a mature cell type and one that remains a stem cell.

A

Stem cells

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17
Q

This model predicts that every cell within a tumor has the potential to form a new tumor.

A

Random or stochastic model

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18
Q

Mutations in the human gene is mainly due to?

A

Intrinsic error rates of DNA replication

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19
Q

True or False. If a single mutation were sufficient to convert a normal cell to a malignant one, then cancer incidence would appear to be dependent of age.

A

False

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20
Q

The process that involves the development of malignant tumor is called?

A

tumorgenesis

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21
Q

The first step in the development of colorectal cancer involves the conversion of normal epithelial cells into a small cluster of cells known as?

A

Adenoma or polyp

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22
Q

This gene encodes a protein involved in the normal differentiation of intestinal cells. What gene is this?

A

adenomatous polyposis coli (APC) gene

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23
Q

The conversion of normal intestinal epithelial cells into adenoma or polyp involves inactivating mutations in what gene?

A

adenomatous polyposis coli (APC) gene

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24
Q

This gene is involved with regulating cell growth. It is usually the second gene that is being affected during the 2nd step progression of the development of colorectal cancer.

A

Kras gene

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25
Q

True or False. Mutation in the Kras gene causes the Kras protein to become constitutively active, resulting in unregulated cell division.

A

True

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26
Q

The cell containing the APC and Kras mutations grows and expands to form a larger intermediate adenoma of approximately 1 cm in diameter. This process is referred to as?

A

Clonal expansion

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27
Q

The third step in the development of colorectal cancer involves the transformation of a large adenoma into a malignant tumor called?

A

carcinoma

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28
Q

The transformation of a large adenoma into a malignant tumor requires acquisition of defects in several genes, including?

A

p53, PI3K, and TGF-Beta

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29
Q

This kind of mutation gives a growth advantage to a tumor cell.

A

Driver mutation

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30
Q

The remainder of the mutations may be acquired over time, perhaps as a result of the increased levels of DNA damage that accumulate in cancer cells, but these mutations have no direct contribution to the cancer phenotype.

A

Passenger mutations

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31
Q

These terms describe the genes that usually acquire driver mutations that lead to cancer.

A

Oncogene and tumor-suppressor gene

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32
Q

The high level of genomic instability seen in cancer cells is known as?

A

mutator phenotype

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33
Q

Leukemic white blood cells from patients with this disease bear a specific translocation, in which the C-ABL gene of chromosome 9 is translocated into the BCR gene on chromosome 22.

A

chronic myelogenous leukemia (CML)

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34
Q

Leukemic white blood cells from patients with this disease bear a specific translocation, in which the C-ABL gene of chromosome 9 is translocated into the BCR gene on chromosome 22 creating a structure known as the Philadelphia chromosome.

A

chronic myelogenous leukemia (CML)

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35
Q

The normal ABL protein is a ______ that acts within signal transduction pathways, transferring growth factor signals from the external environment to the nucleus.

A

Protein kinase

36
Q

True or False. The BCR-ABL protein is an abnormal signal transduction molecule in CML cells, which stimulates these cells to proliferate even in the absence of external growth signals.

A

True

37
Q

Patients with this disease have an increased risk of developing colon, ovary, uterine, and kidney cancers due to mutations in genes controlling DNA repair.

A

hereditary nonpolyposis colorectal cancer (HNPCC)

38
Q

Mutations in any of these genes causes a rapid accumulation of genome-wide mutations and the subsequent development of cancers. These genes are involved in hereditary nonpolyposis colorectal cancer (HNPCC), and control DNA mismatch repair.

A

MSH2, MSH6, MLH1, and MLH3

39
Q

Is the study of factors that affect gene expression but not alter the nucleotide sequence of DNA.

A

Epigenetics

40
Q

True or False. Cancer cells contain altered DNA methylation patterns. Overall, there is much more DNA methylation in cancer cells than in normal cells.

A

False. DNA methylation is much less in cancer cells.

41
Q

True or False. Histone modifications are also disrupted in cancer cells. Genes that encode histone acetylases, deacetylases, methyltransferases, and demethylases are often mutated or aberrantly expressed in cancer cells.

A

True

42
Q

These cells are those that are specialized for specific functions, such as photoreceptor cells of the retina or muscle cells of the heart.

A

Differentiated cells

43
Q

The process of transmitting growth signals from the external environment to the cell nucleus is known as

A

Signal transduction

44
Q

True or False. Cells in the G0 phase of the cell cycle can often be stimulated to reenter the cell cycle by external growth signals. These signals are delivered to the cell by molecules such as growth factors and hormones that bind to cell-surface receptors, which then relay the signal from the plasma membrane to the cytoplasm.

A

True

45
Q

What are the cell cycle checkpoints?

A
  1. G1/S
  2. G2/M
  3. M
46
Q

At the ______, the cell monitors its size and determines whether its DNA has been damaged. If the cell has not achieved an adequate size, or if the DNA has been damaged, further progress through the cell cycle is halted until these conditions are corrected.

A

G1/S checkpoint

47
Q

The second important checkpoint is the ________, where physiological conditions in the cell are monitored prior to mitosis. If DNA replication or repair of any DNA damage has not been completed, the cell cycle arrests until these processes are complete.

A

G2/M checkpoint

48
Q

At this checkpoint, both the successful formation of the spindle-fiber system and the attachment of spindle fibers to the kinetochores associated with the centromeres are monitored.

A

M checkpoint

49
Q

In addition to regulating the cell cycle at checkpoints, the cell controls progress through the cell cycle by means of two classes of proteins which are?

A
  1. cyclins

2. cyclin-dependent kinases (CDKs)

50
Q

This CDK/cyclin complex phosphorylates a number of proteins that bring about the events of early mitosis, such as nuclear membrane breakdown, chromosome condensation, and cytoskeletal reorganization. Its action is prevalent in the G1 phase.

A

CDK1/cyclin B

51
Q

This CDK/cyclin complex activates proteins that stimulate transcription of genes whose products (such as DNA polymerase d and DNA ligase) are required for DNA replication during S phase. Its action is prevalent in the G1 phase.

A

CDK4/cyclin D

52
Q

Is a genetically controlled process whereby the cell commits suicide. This happens if DNA or chromosomal damage is so severe that repair is impossible.

A

Apoptosis

53
Q

Apoptosis involves several steps that hold constant for damaged cells and cells that are being eliminated during development. These are?

A
  1. DNA becomes fragmented
  2. internal cellular structures are disrupted
  3. cell dissolves into small spherical structure known as apoptotic body
  4. apoptotic bodies are engulfed by the immune system’s phagocytic cells
54
Q

A series of proteases called ______ are responsible for initiating apoptosis and for digesting intracellular components.

A

caspases

55
Q

The gene categories are often found to be mutated or misexpressed in cancer cells.

A
  1. Proto-oncogenes

2. Tumor-suppressor gene

56
Q

These genes encode transcription factors that stimulate the expression of other genes, signal transduction molecules that stimulate cell division, and cell-cycle regulators that move the cell through the cell cycle.

A

Proto-oncogenes

57
Q

True or False. In cancer cells, one or more proto-oncogenes are altered in such a way that the activities of their products cannot be regulated in a normal fashion.

A

True

58
Q

When a proto-oncogene is mutated or abnormally expressed and contributes to the development of cancer, it is known as an?

A

Oncogene

59
Q

True or False. Oncogenes are proto-oncogenes that
have experienced a gain-of-function alteration. As a result, only one allele of a proto-oncogene needs to be mutated or misexpressed in order to contribute to cancer. Hence, oncogenes confer a dominant cancer phenotype.

A

True

60
Q

These are genes whose products normally regulate cell-cycle checkpoints or initiate the process of apoptosis.

A

Tumor-suppressor gene

61
Q

True or False. In normal cells, proteins encoded by tumor-suppressor genes enhance progress through the cell cycle in response to DNA damage or growth-suppression signals from the extracellular environment.

A

False. Tumor-suppressor genes suppresses progress through the cell cycle

62
Q

This gene family encodes signal transduction molecules that are associated with the cell membrane and regulate cell growth and division. Protein products of this gene family normally transmit signals from the cell membrane to the nucleus, stimulating the cell to divide in response to external growth factors.

A

ras gene family

63
Q

Ras proteins alternate between an inactive (switched off) and an active (switched on) state by binding either what molecules?

A

guanosine diphosphate (GDP) to switch off or guanosine triphosphate (GTP) to switch on

64
Q

It is the most frequently mutated gene in human cancers — mutated in more than 50 percent of all cancers. This gene encodes a transcription factor that represses or stimulates transcription of more than 50 different genes.

A

p53 gene

65
Q

True or False. Normally, the p53 protein is continuously synthesized but is rapidly degraded and therefore is present in cells at low levels.

A

True

66
Q

What are the types of cellular stress events that bring about rapid increases in the nuclear levels of activated p53 protein?

A
  1. chemical damage to DNA
  2. double-stranded breaks in DNA induced by ionizing radiation
  3. the presence of DNA repair intermediates generated by exposure of cells to ultraviolet light.
67
Q

True or False. In normal cells, p53 can arrest the cell cycle at the G1/S and G2/M checkpoints, as well as retard the progression of the cell through S phase. It accomplishes this by enhancing cyclin/CDK complexes and promotes the transcription of other genes involved in these phases of the cell cycle.

A

False. p53 inhibits cyclin/CDK complexes and regulates the transcription of other genes

68
Q

True or False. The p53 protein can also instruct a damaged cell to commit suicide by apoptosis. It does so by activating the transcription of genes whose products control this process. In cancer cells that lack sufficient p53, these gene products are not synthesized and apoptosis may not occur.

A

True

69
Q

Because of the importance of the p53 gene to genomic integrity, it is often referred to as?

A

the “guardian of the genome.”

70
Q

The loss or mutation of this gene contributes to the development of many cancers, including those of the breast, bone, lung, and bladder.

A

RB1 (retinoblastoma 1) tumor-suppressor gene

71
Q

This is an inherited disorder in which tumors develop in the eyes of young children. In the familial form of the disease, individuals inherit one mutated allele of the RB1 gene and have an 85 percent chance of developing retinoblastomas as well as an increased chance of developing other cancers.

A

retinoblastoma

72
Q

True or False. All somatic cells of patients with hereditary retinoblastoma contain one mutated allele of the RB1 gene. However, it is only when the second normal allele of the RB1 gene is lost or mutated in certain retinal cells that retinoblastoma develops.

A

True

73
Q

Is a tumor-suppressor protein that controls the G1/S cell-cycle check-point. The pRB protein is found in the nuclei of all cell types at all stages of the cell cycle.

A

retinoblastoma protein (pRB)

74
Q

True or False. When cells are in the G0 phase of the cell cycle, the pRB protein is phosphorylated and binds to transcription factors such as E2F, inactivating them.

A

False. At G0 phase pRB protein is non-phosphorylated

75
Q

Explain how pRB regulates progression from G0 phase to G1 to S phase.

A
  1. In G0 phase, pRB protein is non-phosphorylated and is bound to transcription factor E2F thereby inhibiting it.
  2. When growth signals are received, CDK4/cyclin D1 phosphorylates pRB, and the pRB releases the E2F which then induces the expression of over 30 genes whose products are required for the transition from G1 into S phase.
  3. After cells traverse S, G2, and M phases, pRB reverts to a nonphosphorylated state, binds to regulatory proteins such as E2F, and keeps them sequestered until required for the next cell cycle.
76
Q

In order to leave the site of the primary tumor and invade other tissues, tumor cells must dissociate from the primary tumor and secrete proteases that digest components of what structures?

A
  1. extracellular matrix

2. basal lamina

77
Q

Are composed of proteins and carbohydrates, surround, and separate body tissues, form the scaffold for tissue growth and inhibit the migration of cells.

A
  1. extracellular matrix

2. basal lamina

78
Q

Metastasis is controlled by a large number of gene products, including?

A
  1. cell-adhesion molecules
  2. cytoskeleton regulators
  3. proteolytic enzymes
79
Q

This is responsible for cell–cell adhesion in normal tissues. Lower concentrations of this protein are observed in epithelial cancer cells.

A

E-cadherin glycoprotein

80
Q

True or False. It has been shown that the level of aggressiveness of a tumor correlates negatively with the levels of proteolytic enzymes expressed by the tumor.

A

False. correlates positively

81
Q

High levels of this proteolytic enzymes are observed in many highly malignant tumors.

A

metalloproteinases

82
Q

True or False. In addition, malignant cells are susceptible to the normal controls conferred by regulatory molecules such as tissue inhibitors of metalloproteinases (TIMPs).

A

False. they are not susceptible

83
Q

Most inherited cancer-susceptibility alleles occur in tumor-suppressor genes, and are transmitted in a Mendelian dominant fashion thus are sufficient in themselves to trigger the development of cancer.

A

False. Cancer - susceptibility alleles follow dominant Mendelian pattern but not sufficient in themselves to trigger cancer

84
Q

The phenomenon whereby the second, wild-type, allele is mutated in a tumor is known as?

A

loss of heterozygosity.

85
Q

Although the vast majority of colorectal cancers are sporadic, about 1 percent of cases result from a genetic predisposition to cancer known as?

A

familial adenomatous polyposis (FAP)

86
Q

True or False. The normal function of the APC gene product is to act as a tumor suppressor controlling growth and differentiation.

A

True

BIO 130.01 Genetics, Lecture (16 decks)

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