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BMS2021 > The Molecular Basis of Cancer > Flashcards

The Molecular Basis of Cancer Flashcards

1
Q

What are the two main characteristics of cancer cells?

A
  1. Reproduce despite normal constraints that inhibit cell proliferation and clonal expansion
  2. Cancer cells invade and colonize territories normally reserved for other cells
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2
Q

How do cancer cells look physically different to other cells?

A

Enlarged nucleus, changes to cytoskeleton and loss of specialised features

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3
Q

Tumours that remain localised and look like the tissues they came from are likely to be…

A

Benign

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4
Q

Tumours that do not resemble the tissue of origin and invade surrounding tissue are likely to be…

A

Malignant

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5
Q

Cancer cells appear different than surrounding normal cells, divide at a ______ rate, have a _____ metabolic rate and invade new tissues

A

Faster; high

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6
Q

Cancers that invade other tissues and spread to other parts of the body are said to be…

A

Metastatic

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7
Q

What is the growth factor responsible for angiogenesis?

A

VEGF

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8
Q

What are the two ways that DNA damage can be acquired?

A

Inherited and acquired

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9
Q

Why does cancer incidence increase with age?

A

Cumulative exposure to mutagens

DNA repair systems worsen

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10
Q

What are compounds or chemical that produce cancer called?

A

Carcinocens

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11
Q

How likely a mutation will lead to cancer is called its…

A

Penetrance

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12
Q

Genes that promote cancer are called…

A

Oncogenes

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13
Q

Genes that act to prevent cancer are called…

A

Tumour suppressor genes

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14
Q

Genes that repair mutated DNA are called…

A

Mismatch repair genes

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15
Q

What are the five major classes of oncogenes?

A 
Growth factors
Growth factor receptors
Intracellular signalling proteins
Transcription factors
Cell cycle control proteins
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16
Q

How are proto-oncogenes altered by viruses?

A

Insertion of the viral gene either upstream of the proto-oncogene or within the coding sequence

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17
Q

Mutations of tumour suppression genes that code for cell adhesion/recognition can lead to…

A

cell losing their adhesion to their neighbours and spreading

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18
Q

Mutations of tumour suppression genes that code for enzymes in DNA repair can lead to…

A

production of mutant proteins that no longer repair DNA causing mutations to accumulate

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19
Q

Mutations of tumour suppression genes that inhibit cell division can lead to…

A

Mutant proteins being produces that no longer block cell division

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20
Q

What is the two-hit hypothesis for cancer?

A

In order to get cancer, both alleles of a tumor supressor gene must be mutated

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21
Q

What are the role of tumour supressor genes?

A

To prevent cells from progressing through the cell cycle - allowing repair of damaged DNA

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22
Q

A rare childhood tumour of the retina with high penetrance is called…

A

Retinoblastoma

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23
Q

What does hereditary retinoblastoma result in tumour in both eyes?

A

The mutated gene is in all cells so is therefore expressed in the retinas of both eyes

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24
Q

What are the six ways of losing the remaining copy of a normal tumor suppressor gene?

A 
Nondisjunction (chromosome loss)
Nondisjunction and duplication
Mitotic recombination
Gene conversion
Deletion
Point mutation
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25
Q

Which tumour suppressor is responsible for holding the cell at G1 checkpoint?

A

p53

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26
Q

50% of all tumour show mutations and loss of function of _____

A

p53

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27
Q

What cellular responses does p53 induce?

A

Cell cycle arrest
Senescence
Cell differentiation
Apoptosis

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28
Q

How does p53 activation inhibit cell growth?

A

Either through cell-cycle arrest or induction of apoptosis

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29
Q

What are the different types of chromosomal mutations?

A 
Deletion of gene
Chromosome loss
Gain of chromosome
Duplication of gene
Inversion
Translocation
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30
Q

How can chromosomal translocation lead to cancer?

A

Relocation of an oncogene next to a novel regulatory element

Formation of a hybrid oncogene

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31
Q

True or False:

Chromosomal translocation is an acquired somatic event only

A

True

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32
Q

True or False:

Chromosomal translocation is clonal

A

True

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33
Q

What techniques can be used to detect chromosomal translocation?

A

Karyotype
PCR
FISH
Southern Blot

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34
Q

What are the two types of leukemia’s and what is there untreated life expectancy?

A

Acute (3-4 months untreated)

Chronic (years untreated)

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35
Q

What cancer is produced by only one mutation?

A

Chronic myeloid leukemia

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36
Q

True or False:

Chronic Myeloid Leukemia is curable

A

True

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37
Q

What cells have the mutation in chronic myeloid leukemia?

A

Myeloid progenitors

38
Q

What chromosomal translocation causes chronic myeloid leukemia?

A

Reciprocal translocation of Abl tyrosine kinase from chromosome 9 to BCR on chromosome 22. Results in a Ph chromosome (shortened chromosome 22)

39
Q

The chromosomal translocation of chronic myeloid leukemia can be detected by what techniques?

A

Standard cytogenetics
FISH
PCR

40
Q

True or False:

Abl tyrosine kinase is found in the cell membrane

A

False; it is found in the cell

41
Q

What drug inhibits the activity of Abl tyrosine kinase and is therefore a treatment for CML?

A

STI-Gleevac

42
Q

How does STI-Gleevac inhibit the activity of Abl tyrosine kinase?

A

It functions by blocking the binding of ATP to the bcr-abl tyrosine kinase, inhibiting its activity. In the absence of tyrosine kinase activity, substrates required for Bcr-Abl function cannot be phosphorylated and subsequenct cellular events are abrogated

43
Q

How does the Bcr-Abl tyrosine kinase cause CML?

A

The Bcr-Abl tyrosine kinase is a constituitively active kinase which functions by binding ATP and transferring phosphate from ATP to tyrosine residues on various substrates. This causes the excess proliferation of myeloid cells characteristic of CML

44
Q

What are some genes that encode for growth factors or their receptors?

A

PDGF

Erb-B

45
Q

What are some genes that are involved in cell signalling?

A

K-ras

N-ras

46
Q

What are some genes for transcription factors that activate genes?

A

c-myc
N-myc
L-myc

47
Q

What is ABL?

A

a proto-oncogene located on chromosome 9 that encodes a tyrosine kinase. It is negatively regulated by its SH3 domain and deletion of the SH3 domain turns ABL into an oncogene. The t(9;22) translocation results in the head-to-tailfusionof theBCRandABLgenes, leading to afusion genepresent in many cases of chronicmyelogenous leukemia

48
Q

Define angiogenesis

A

the growth of new blood vessels that tumours need to grow. This process is caused by the release of chemicals by the tumour and by the host cells near the tumour

49
Q

Define anti-angiogenics

A

drugs that prevent the growth of new blood vessels and therefore restrict the size that a tumour can grow

50
Q

Define ATP-competitive inhibitors

A

a molecule that binds to an enzyme and decreases its activity

51
Q

Define benign

A

referring to a tumour that does not invade surrounding tissue or spread to other parts of the body

52
Q

Define BRC1

A

a human tumour suppressor gene that encodes a protein that is responsible for repairing DNA. Point mutations or larger deletion and duplication mutations can result in the protein being dysfunctional, and leads to a high penetrance for breast and ovarian cancer

53
Q

Define cancer

A

A term for diseases in which abnormal cells divide without control and can invade nearby tissues

54
Q

Define carcinogen

A

any substance, radionuclide, or radiation that promotes carcinogenesis, the formation of cancer. This may be due to the ability to damage the genome or to the disruption of cellular metabolic processes

55
Q

Define cell-cycle arrest

A

when a cell stops at a cell cycle checkpoint after detecting defects in the DNA. This prevents the accumulation of mutations and development of cancer

56
Q

Define chemotherapy

A

a type ofcancer treatment that uses one or more anti-cancer drugs (chemotherapeutic agents) as part of a standardizedchemotherapy regimen

57
Q

Define chromosomal translocation

A

achromosomeabnormality caused by rearrangement of parts between nonhomologouschromosomes. A gene fusion may be created when thetranslocation joins two otherwise-separated genes, it is detected on cytogenetics or a karyotype of affected cells

58
Q

Define chronic myeloid leukemia

A

a cancer of thewhite blood cells. It is a form ofleukemia characterized by the increased and unregulated growth of predominantlymyeloid cells in thebone marrowand the accumulation of these cells in the blood. It results from a chromosomal translocation where parts of chromosome 9 and 22 swap, creating the BCR-ABL gene, which codes for tyrosine kinase, and the Ph chromosome

59
Q

Define clonal expansion

A

The explosive increase in the number of lymphocytes, both B cells and T cells

60
Q

Define cell proliferation

A

An increase in the number of cells as a result of cell growth and cell division

61
Q

Define cytogenic remission

A

a molecular response that occurs in CML patients undergoing treatment where the cells no longer have the Ph chromosome

62
Q

Define DNA virus

A

avirusthat hasDNAas its genetic material and replicates using aDNA-dependent DNApolymerase.

63
Q

Define familial aggregation

A

the clustering of certain traits, behaviours, or disorders within a givenfamily.Family aggregationmay arise because of genetic or environmental similarities

64
Q

Define FISH

A

Fluorescence in situ hybridization (FISH) is atestthat “maps” the genetic material in a person’s cells. This testcan be used to visualize specific genes or portions of genes.FISH testingis done on breast cancer tissue removed during biopsy to see if the cells have extra copies of the HER2 gene.

65
Q

Define fusion protein

A

proteinscreated through the joining of two or more genes that originally coded for separateproteins

66
Q

Define gene amplification

A

an increase in the number of copies of agene without a proportional increase in othergenes. This can result from duplication of a region of DNA that contains agenethrough errors in DNA replication and repair machinery as well as through fortuitous capture by selfishgeneticelements

67
Q

Define growth factors

A

molecules that typically act as signalling molecules between cells. Examples are cytokines and hormonesthat bind to specific receptors on the surface of their target cells. They often promote cell differentiation and maturation, which varies between growth factors

68
Q

Define haematological remission

A

a molecular response that occurs in CML patients undergoing treatment where BCR-ABL gene can no longer be detected in the blood

69
Q

Define karyotype

A

the number and appearance of chromosomes in the nucleus of a eukaryotic cell

70
Q

Define malignant

A

A term for diseases in which abnormal cells divide without control and can invade nearby tissues

71
Q

Define metastasis

A

the development of secondary malignant growths at a distance from a primary site of cancer

72
Q

Define mismatch repair genes

A

a gene that encodes proteins responsible for regulating DNA mismatch repair. Mutations can be inherited or sporadically and result in the inability to regulate DNA replication resulting in the accumulation of mutations

73
Q

Define mutagen

A

a physical or chemical agent that changes the genetic material, usually DNA, of an organism and thus increases the frequency of mutations above the natural background level

74
Q

Define MYC

A

a family of regulatorgenesand proto-oncogenes that code for transcription factors. In cancer, c-myc is often constitutively expressed resulting in increased expression of cell proliferation genes

75
Q

Define oncogene

A

a gene that has the potential to cause cancer. In tumor cells, they are often mutated and/or expressed at high levels

76
Q

Define p53

A

a tumor suppressor gene that plays a role in apoptosis, genomic stability and inhibition of angiogenesis.

77
Q

Define PCR

A

a technique used inmolecular biologytoamplify a single copy or a few copies of a segment ofDNAacross several orders of magnitude, generating thousands to millions of copies of a particularDNA sequence

78
Q

Define penetrance

A

the proportion of individuals carrying a particular variant (orallele) of agene(thegenotype) that also express an associated trait (thephenotype)

79
Q

Define Ph chromosome

A

Philadelphia translocation(Ph) is a specific genetic abnormality inchromosome 22ofleukemia cancercells (particularlychronic myeloid leukemia(CML) cells). This chromosome is defective and unusually short because ofreciprocal translocation of genetic material betweenchromosome 9and chromosome 22, and contains afusion genecalledBCR-ABL1.

80
Q

Define proto-oncogene

A

A normal gene which, when altered by mutation, becomes anoncogenethat can contribute to cancer.Proto-oncogenesmay have many different functions in the cell. Someproto-oncogenesprovide signals that lead to cell division. Otherproto-oncogenesregulate programmed cell death (apoptosis)

81
Q

Define Ras

A

A family of proteins that are involved in transmitting signals with in cells. Mutations inrasgenes can lead to the production of permanently activated Ras proteins. As a result, this can cause unintended and overactive signaling inside the cell, even in the absence of incoming signals. Because these signals result in cell growth and division, overactive Ras signaling can ultimately lead tocancer

82
Q

Define retinoblastoma

A

a rare form of cancer that rapidly develops from the immature cells of a retina, the light-detecting tissue of the eye

83
Q

Define RNA virus

A

avirusthat hasRNA(ribonucleic acid) as its genetic material. This nucleic acid is usually single-strandedRNA(ssRNA) but may be double-strandedRNA(dsRNA)

84
Q

Define southern blotting

A

a method used in molecular biology for detection of a specific DNA sequence in DNA samples.Southern blottingcombines transfer of electrophoresis-separated DNA fragments to a filter membrane and subsequent fragment detection by probe hybridization

85
Q

Define spontaneous mutation

A

a DNA mutation that can
arise from a variety of sources, including errors inDNAreplication, spontaneous lesions, and transposable genetic elements

86
Q

Define STI-Gleevac

A

a medication used to treat CML that works by stopping the BCR-ABL tyrosine kinase. This can slow growth or result in programmed cell death of certain types of cancer cells

87
Q

Define transcription factors

A

DNA-binding proteins that regulate the expression of an array of target gene that usually have transactivation domains that activate or repress genes)

88
Q

Define tumour supressor genes

A

agenethat protects a cell from one step on the path to cancer. When this genemutates to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other geneticchanges

89
Q

Define tyrosine kinase receptors

A

the high-affinity cell surfacereceptorsfor many polypeptide growth factors, cytokines, and hormones

90
Q

Define VEGF

A

vascular endothelial growth factor; a signal protein produced by cells that stimulates the formation of blood vessels (angiogenesis)

BMS2021 (6 decks)

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