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M2M exam 3 wk 1 > Carcinogenesis III > Flashcards

Carcinogenesis III Flashcards

1
Q

Oncogenes were discovered in ______

A

certain oncogenic retroviruses.

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2
Q

Retroviruses are

A

RNA containing membrane enclosed viruses that bud from the cell membrane of infected cells and which usually do not kill the infected cell.

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3
Q

The RNA genome consists of _________

A

two identical strands held together by a tRNA molecule.

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4
Q

The gag gene codes for

A

internal virion proteins

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5
Q

When gag genes are the only ones present, the virus does not ______, but _______.

A

cause tumors

replicates through an intermediate proviral DNA and integrates into the host cell genome

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6
Q

Virus can be transmitted as an _______

A

integrated provirus through somatic or sex cells as a cellular gene.

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7
Q

Retroviruses that contain a v-onc segment also have the ability to _______

A

rapidly transform appropriate infected cells to the malignant phenotype. They therefore rapidly induce tumors after infection.

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8
Q

examples of retrovirus with v-onc segments

A
  1. v-src
  2. v-erb
  3. v-abl
  4. v-myc
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9
Q

v-src -

A

v-src - The oncogene of Rous Sarcoma Virus. This caused fibrosarcomas in certain birds.

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10
Q

v-erb

A

v-erb - The oncogene of avian erythroblastosis virus causes erythroblastosis in chickens. Two related genes, erb-A and erb-B have been identified.

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11
Q

v-abl -

A

v-abl - The oncogene found in Abelson leukemia virus from mice.

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12
Q

v-myc -

A

v-myc - This gene is usually fused with a portion of the gag gene. It appears that this gene is capable of eliciting neoplastic transformation of cells.

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13
Q

Cellular Transformation is assayed by:

A

a. Tumor formation in animals after administration of the oncogenic virus.
b. Transformation of cell morphology and growth regulation after infection of cultured cells in vitro. Foci of infected cells developing as transformed clones can be seen and counted

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14
Q 
The protein (pp60v-src) coded by the v-src gene is a \_\_\_\_\_\_\_\_\_. 
Theses proteins then change the properties of the cells by affecting \_\_\_\_\_.
A

membrane bound protein kinase that phosphorylates tyrosine residues in several different proteins.

gene expression

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15
Q

v-erb-B codes ________.

A

codes for a protein that is similar in structure to the cell surface receptor for epidermal growth factor (EGFR).
This raises the possibility that this protein has growth stimulating properties like EGFR.

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16
Q

EGFR receptor is a member of a family of related proteins that _______

A

(like pp60v-src) exhibit tyrosine-specific protein kinase activity

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17
Q

v-abl codes for a _______.

A

protein kinase that phosphorylates tyrosine residues on other proteins

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18
Q

v-able is similar to the human cellular gene (c-ABL) that is found in the______

A

BCR-ABL translocation in the Philadelphia chromosome and is overexpressed in BCR-ABL CML

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19
Q

Many of the products of oncogenes mimic _______

A

hormones or growth stimulating factors either by resembling natural hormones or by affecting the structure of the cell surface receptors for these hormones

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20
Q

oncogene altered receptors then send signals to the ________

A

cell nucleus in an unregulated manner to affect growth.

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21
Q

c-onc genes

A

Proto-oncogenes

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22
Q

Cellular prototypes of the v-onc genes exist in_______ .

A

all normal eukaryotic cells

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23
Q

The proto-onc or c-onc genes are involved in _______

A

spontaneous malignancies that have nothing to do with a retrovirus.

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24
Q

a change in gene regulation or gene structure due to a cellular mutation could _______

A

activate these genes to cause a malignancy.

quantitative changes (too much protein) or qualitative changes (overactive or unregulated protein) in the proto-oncogene are responsible for these effects.

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25
Q

quantitative changes

A

too much protein

26
Q

qualitative changes

A

overactive or unregulated protein

27
Q

c-src has a differences from v-src

A

different carboxy-terminal amino acid sequence

and c-src has numerous introns that do not exist in v-src.

28
Q

c-myc differences than v-myc

A

c-myc also has many introns not present in v-myc, although the coding sequences are nearly identical (7 amino acid changes)

29
Q

if v-onc genes originated from c-onc genes, substantial rearrangements occurred _____

A

during or after the capture (at least with many such oncogenes).

30
Q

A few c-onc genes ligated to retroviral promoters can _________

A

transform normal cells when introduced via DNA mediated transformation (examples: c-ras). Other c-onc genes do not directly transform normal cells.

31
Q

c-ras genes have been ______,

A

point mutated

Mutations are found in either codon 12 or codon 61 of the ras gene product.

32
Q

c-ras point mutations produce a _____

A

ras protein that is unregulated and is always “on”. Detection of these ras mutations indicates a poor prognosis.

33
Q

Gene amplification of c-onc genes has also been detected in some ______.

A

cancers and is very useful for prognosis.

34
Q

N-myc, a member of the______, and is found ______.

A

c-myc family of oncogenes

amplified in neuroblastoma

35
Q

The HER2/neu oncogene (also called erbB2), which encodes a ________.

A

integral membrane protein kinase (see v-erb-B) is amplified in about 20% of breast cancers.

Higher levels of amplification correlate with a poor prognosis.

36
Q

support for the quantitative model

A

HER2/neu being amplified in breast cancer

37
Q

support for qualitative model:

A

c-ras genes being point mutated and always on

38
Q

Translocations of c-onc genes have been observed in certain human cancers, and also indicate ______.

A

a poor prognosis

39
Q

The translocation results in

A

inappropriate and high level expression of the oncogene (See Burkitt lymphoma and the Philadelphia chromosome (BCR- ABL translocation)

40
Q

several genes must _________. to transform a normal cell to a malignant one

A

simultaneously be changed to transform a normal cell to a malignant one.

Mutations in both tumor suppressors and oncogenes are needed.

The best evidence for this idea has been found in colon cancer.

41
Q

loss of _____ and an increased ______ coupled to loss of _____ can be particularly deadly.

A

growth regulation

mutation rate

programmed cell death (apoptosis)

42
Q

In theory, tumor cells may have some of their properties reversed by either _________. This can be accomplished either __________

A

blocking the action of oncogenes and/or adding back any missing tumor suppressors.

at the gene level (gene therapy) or by using drugs or antibodies.

43
Q

monoclonal antibodies specific for the protein product of the HER2/neu/erbB2 oncogene can ______. These antibodies are called _____

A

HER2/neu/erbB2 oncogene can reverse the transformed phenotype of the cancer cell

V

44
Q

drugs that inhibit HER2/neu/erbB2 are being used to ______

A

extend the life of breast cancer patients. More drugs of this type are currently in clinical trials for both breast and lung cancer.

45
Q

Injection of the RB gene into a RB-negative small cell lung cancer line will inhibit _____.

A

tumorigenesis.

46
Q

E1B mutant adenoviruses:

A

which cannot inactivate p53 and thereby cannot kill wild-type cells, will kill p53- cancer cells preferentially

47
Q

A drug has been used to correct the mutant conformation of dominant-negative p53 mutations . This drug blocks the _______

A

production of tumors by these p53 mutant cells in a mouse model system.

48
Q

In patients with BCR-ABL translocation, the ABL tyrosine kinase can be inhibited by

A

Gleevac, an ATP analogue. Clinical trials have shown that

Gleevac is effective in 95% of these patients

49
Q

“Molecularly targeted therapy” or “rationally designed drug therapy.”

A

identifying the defect in the tumor from the patient and then targeting the therapy to fit it.

50
Q

Why do drugs that inhibit “normal” cellular proteins (c-myc, c-abl, etc.) kill only the cancer cells?

A

One idea is that cancer cells but not normal cells have become dependent or “addicted” to the overexpressed oncogene.

This referred to as “oncogene addiction”

51
Q

oncogenes and tumor suppressor genes are being used as “molecular markers” in both ____

A

cancer diagnosis and prognosis.

52
Q

The elucidation of the function of these genes also will be useful for therapies, either at the gene and/or protein levels and forms the basis of _______

A

“Personalized Medicine”.

53
Q

_________ is being used for targeted therapy and for “personalized medicine” in cancer.

A

Molecular knowledge of the genome in cancer cells (Bioinformatics)

54
Q

“heat map” is created in which changes in gene copy number are _____. The “heat map” is created by ___________.

A

correlated with tumor grade

hybridization of the tumor DNA to “gene chip” containing all human genomic DNA sequences as molecular probes

55
Q

Heat map, red color indicates:

green indicates:

A

Red color indicates increases and

green indicates decreases.

56
Q

The Breast cancer Xpress ChipTM measures the expression of _____.

A

123 genes known to be altered in breast cancers

This includes tumor suppressors such as BRCA1 and p53 and oncogenes such as estrogen receptor (ER) and erbB2. The information is then used for diagnosis, prognosis and therapy.

57
Q

patients with high erbB2 are treated with _____ and those with high ER levels are treated with ______

A

Herceptin

tamoxifen (estrogen antagonist).

58
Q

With the advent of whole genome sequencing, cancer therapy is being designed _____

A

on a personal basis depending on the type of mutations (oncogene, tumor suppressor, etc.) in the tumor and the known therapeutic responses to these lesions

59
Q

the env gene codes for

A

for virus membrane glycoproteins,

60
Q

pol gene codes for

A

a virus polymerase

M2M exam 3 wk 1 (15 decks)

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