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BIOL445-Cancer Biology > Exam 1 Materials > Flashcards

Exam 1 Materials Flashcards

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1
Q

What is cancer in epithelial cells called?

A

Carcinomas

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1
Q

What is cancer in connective tissues called?

A

Sarcomas

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2
Q

What is cancer in the blood called?

A

Leukemias

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3
Q

What is cancer in lymphatic systems called?

A

Lymphomas

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4
Q

What is cancer?

A

An aberration of normal development.

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5
Q

Cancer cells behave dependently. True or False

A

False.

Cancer cells behave independently

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6
Q

What is tumor?

A

Abnormal growth of solid tissue.

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7
Q

What is the earliest stage of tumor called?

A

Benign tumor

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8
Q

What is the invasive tumor called?

A

Malignant tumor

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9
Q

Which factors drive cells into senescence?

A

Telomere sequence in DNA.
The telomere sequence gets shorten each time the cell devides.

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10
Q

Stem cells can divide indefinitely without control. True or False

A

False.

Stem cells can divide indefinitely under tight control.

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11
Q

Since cancer cells behave like stem cells. Cancer cells can differentiate. True or False

A

False.

Cancer cells cannot differentiate.

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12
Q

Normal cells cannot be invasive like cancer cells. True or False

A

False.

Normal cells can be invasive at the right time and place.

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13
Q

Provide an example when normal cells can be invasive.

A

Neutrophils chasing down pathogens using chemotaxis.

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14
Q

What are the four major properties of cancer cells?

A
  1. Immortalized
  2. Do not form differentiated tissues
  3. Escape apoptosis
  4. Invasive
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15
Q

What is the molecular basis of cancer?

A

Mutation

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16
Q

Which gene tells the cell to stop proliferating?

A

Tumor supressor gene.

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17
Q

What are the four causes of cancer?

A
  1. Random mutations
  2. Inherited mutations
  3. Viral infections
  4. Environmental factors (chemical; physical)
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18
Q

Which job was the first to be found associated with cancer?

A

Chimney sweeps

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19
Q

What did Yamagiwa find in his experiment?

A
  1. Chemicals can induce cancer
  2. Cancer can be studied in the lab
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20
Q

What are Carcinogens?

A

Agents that contribute to the formation of a tumor

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21
Q

Why is it hard to link a specific environmental factor as a potential contributor to cancer?

A

Cancer is a long term process (accumulation of mutations).
It would take years to study the impact of a potential risk that causes cancer.

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22
Q

Virus cannot cause cancer in animals. True or False

A

False.

Virus can cause cancer in animal.

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23
Q

How can we collect infectious agents in the infected tissues?

A

Grinding the tissues into tiny pieces, mix with some fluid and let it run through the filter => Collect filtrate which might contain the infectious agents.

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24
Q

What did they find when they cultivate RSV (Respiratory syncytial virus) with normal cells.

A

RSV can transform cells in culture. (from normal cells to cancer cells)

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25
Q

Cancer is a disease of abnormally developing tissues. True or False

A

False.

Cancer is a disease of malfunctioning cells rather than abnormally developing tissues.

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26
Q

What is contact inhibition?

A

A process of inhibiting cell growth when cells come into contact with each other, and thus form a monolayer of normal cells in culture dish.

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27
Q

What type of virus is RSV? What is its genomic material?

A

retrovirus.
RNA

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28
Q

All RNA viruses are retroviruses. True or False

A

False.

Not all RNA viruses are retroviruses

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29
Q

Which genomic sequence of RSV confers tumorigenicity of the chicken cells?

A

src sequence

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30
Q

What is c-src classied as? Proto-oncogene or Oncogene?

A

Proto-oncogene
c-src (cellular src)

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31
Q

What is v-src classified as? Proto-oncogene or Oncogene?

A

Oncogene
v-src (viral src)

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32
Q

What is src protein classified as?

A

Src is tyrosine kinase

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33
Q

What does kinase protein do?

A

Phosphorylation.
Add phosphate group to protein.

34
Q

Which part of the protein guides the protein to integrate into the cell membrane?

A

Myr

35
Q

What is Myr? What is its function?

A

Myr is a lipid modification.
Myr promotes their binding to cell membranes for a variety of biological functions.

36
Q

What is the function of SH2?

A

Binds any peptides that have phosphorylated Tyrosine

37
Q

What is the function of SH3?

A

Binds polyproline motifs.

38
Q

What inactivates the src protein in mice?

A

Phosphorylated Tyr 527 inactivates src protein

39
Q

What is missing in the v-src protein comparing to normal src protein in mice?

A

Tyrosine at position 527

40
Q

From Src paper, in figure 3D we could see that pancreatic cell line PaTu 8988t has a high IC50 when treated with herbymycin (inhibitor) compare to other cell lines, however, from figure 2 (not shown in here) PaTu 8988t has a low level of Src expression and low activity of Src. What does it us from this finding?

A

Herbimycin has low specificity to Src protein which explaining the reason why IC50 of PaTu 8988t has a much higher IC50 compare to other cell lines.

This cell line is Src independent; but Herbimycin is still effective treating this cell line which suggests that Src could be one of the major contributors to cancer

41
Q

How does proto-oncogene c-src turn into oncogene v-src?

A
  1. Retrovirus ‘kidnapped’ normal proto-oncogene (c-src) and turn into oncogene (provirus + c-src = v-src).
42
Q

All retroviruses can cause cancer. True or False

A

False. (only some exceptions)

43
Q

Walk through the procedures in this picture.

A
  1. DNA is extracted from the host cells (virus in this case)
  2. DNA isbroken into many pieces using restriction enzyme
  3. DNA pieces are mixed in calcium phosphate solution.
  4. DNA-Calcium phosphate solution is transferred to the new tissues.
44
Q

In this experiment, if the result shows that there is no formation of transformed cells. What does this tell us?

A

The targeted oncogene is not successfully obtained.

45
Q

What could be the reasons explaining why there are some untransformed fibroblast in this picture? (2 reasons discussed in class)

A
  1. They might contain human DNA but not a human oncogene
  2. They might contain a human oncogene that was cut in the middle
46
Q

In this experiment, the result shows that the transformation (into cancer cells) rates are low. What does this suggest?

A

It suggests that we are possibly dealing with only one single oncogene.

47
Q

How can we distinguish human genomes from other eukaryotic genomes (i.e mice)?

A

Repetitive sequences. (Alu sequence is human-specific repetitive sequence)

48
Q

During the process of generating a bacteriophage genomic library, what do these white holes contain?

A

Virions

49
Q

[Western blotting with anti-phosphotyrosine antibodies]
Which band shows the target of Src? Why?

A

band at ~120.
There is no band shown at 120 under non-myristylated v-Src transfected cells column.

50
Q

What is the function of p120 catenin?

A

Modulates cell-cell adhesion

51
Q

What is the role of focal adhesion kinase?

A

Involved in cell-matrix interactions.

52
Q

What is focal adhesion?

A

Cluster of integrins at the site of contact with the ECM.

53
Q

What is the special ECM that epithelial cells secrete called?

A

Basal lamina

54
Q

What recruit FAK to the membrane?

A

Integrins.

55
Q

What phosphorylate FAK at first when integrins recruit it?

A

FAK phosphorylate itself (autophosphorylated)

56
Q

What happens to the cell when Src-FAK is more active?

A

Less adhesion, more migration

57
Q

What do Src-FAK signals regulate?

A

Adhesion turnover

58
Q

Cell-matrix interactions only occur in one way from the ECM to Cell. True or False

A

False

It occurs both way. “outside-in” and “inside-out”

59
Q

What else does Src-FAK promote in cell beside cell migration?

A

Cell survival and growth

60
Q

What would be the result of this southern blot?

A

Human and Mouse have different restriction sites.

Mouse: 1 band at 3.3
Human: 1 band at 9.4 (3.3+6.1)
Transfected mouse: 2 bands -> 1 band at 3.3 and 1 band at 9.4 (because transfected mouse contains both src sequences; one is mouse-src and other one is oncogenic human-src)

61
Q

In the experiment of identifying the human oncogen, what did they find?

A

Ras is the transforming human oncogene, not src -> huge finding

62
Q

What are the three factors that can transform proto-oncogene to oncogene?

A
  1. Viruses
  2. Carcinogen
  3. Random mutations
63
Q

Ras is a kinase. True or False

A

FALSE!

64
Q

What is the role of Ras?

A

It acts as a molecular switch.

65
Q

Ras is activated when bound to which molecule?

A

GTP

66
Q

Ras is INactivated when bound to which molecule?

A

GDP

67
Q

How do you inactivate Ras-GTP?

A

Hydrolyze GTP to GDP

68
Q

Which molecule helps to speed up the hydrolysis process of Ras-GTP?

A

GAP (GTPase activating protein)

69
Q

GAP helps Ras-GTP to remove the phosphate group from GTP. True or False

A

False.

GAP helps Ras works better by changing Ras configuration

70
Q

Which molecule helps to activate Ras-GDP?

A

GEF (guanosine exchange factor).

71
Q

Assuming we have a great amount of GTP and GDP. What would be the factor determine activation state of Ras?

A

The amount of GAPs and GEFs.
More GAPs => More inactivated Ras
More GEFs => More activated Ras

72
Q

What makes Ras oncogenic?

A

Mutated Ras cannot bind to GAP which make Ras cannot hydrolyze GTP -> GDP. Therefore, Ras is constitutively active (Ras-GTP)

73
Q

Mutation in Ras is frameshift mutation. True or False

A

False.
It is point mutation (glycine - valine)

74
Q

What are the main key players involved in forming vulva in C.elegans?

A

1 gonadal anchor cell (AC)
6 vulval precursor cells (VPCs)

75
Q

What does the anchor cell do to the vulval precursor cells?

A

The AC signals the VPCs to adapt vulval fates

76
Q

Why are the other VPCs (here in yellow) called VPCs, if they do not actually form the vulva?

A

They are capable of forming vulva if they received signals from the AC.

77
Q

What are the three states of vulval formation in C.elegans?

A
  1. Cell migration
  2. Cell fusion
  3. Ring formation (AC fuse with the surround cells to create a hole)
78
Q

What is reverse genetics?

A

Knockout a specific candidate gene and test the consequences.

79
Q

What is forward genetics?

A

Mutagenize animals randomly and select for mutation that affect a certain phenotype (i.e vulva formation)

80
Q

What are the two reasons that normal cells may undergo apoptosis?

A
  1. Part of a developmental program
  2. When cells become “dangerous”
81
Q

What are the two ways that Src can normally be activated?

A
  1. Dephosphorylation of Tyr527
  2. Configuration changes (e.g. SH2 bind to other proteins)
82
Q

What acts as a substrate for migrating cell?

A

Extracellular Matric (ECM)

BIOL445-Cancer Biology (3 decks)

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