Exam 1 Materials Flashcards
1
Q
What is cancer in epithelial cells called?
A
Carcinomas
1
Q
What is cancer in connective tissues called?
A
Sarcomas
2
Q
What is cancer in the blood called?
A
Leukemias
3
Q
What is cancer in lymphatic systems called?
A
Lymphomas
4
Q
What is cancer?
A
An aberration of normal development.
5
Q
Cancer cells behave dependently. True or False
A
False.
Cancer cells behave independently
6
Q
What is tumor?
A
Abnormal growth of solid tissue.
7
Q
What is the earliest stage of tumor called?
A
Benign tumor
8
Q
What is the invasive tumor called?
A
Malignant tumor
9
Q
Which factors drive cells into senescence?
A
Telomere sequence in DNA.
The telomere sequence gets shorten each time the cell devides.
10
Q
Stem cells can divide indefinitely without control. True or False
A
False.
Stem cells can divide indefinitely under tight control.
11
Q
Since cancer cells behave like stem cells. Cancer cells can differentiate. True or False
A
False.
Cancer cells cannot differentiate.
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.
13
Q
Provide an example when normal cells can be invasive.
A
Neutrophils chasing down pathogens using chemotaxis.
14
Q
What are the four major properties of cancer cells?
A
- Immortalized
- Do not form differentiated tissues
- Escape apoptosis
- Invasive
15
Q
What is the molecular basis of cancer?
A
Mutation
16
Q
Which gene tells the cell to stop proliferating?
A
Tumor supressor gene.
17
Q
What are the four causes of cancer?
A
- Random mutations
- Inherited mutations
- Viral infections
- Environmental factors (chemical; physical)
18
Q
Which job was the first to be found associated with cancer?
A
Chimney sweeps
19
Q
What did Yamagiwa find in his experiment?
A
- Chemicals can induce cancer
- Cancer can be studied in the lab
20
Q
What are Carcinogens?
A
Agents that contribute to the formation of a tumor
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.
22
Q
Virus cannot cause cancer in animals. True or False
A
False.
Virus can cause cancer in animal.
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.
24
What did they find when they cultivate RSV (Respiratory syncytial virus) with normal cells.
RSV can transform cells in culture. (from normal cells to cancer cells)
25
Cancer is a disease of abnormally developing tissues. **True** or **False**
False.
Cancer is a disease of malfunctioning cells rather than abnormally developing tissues.
26
What is contact inhibition?
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.
27
What type of virus is RSV? What is its genomic material?
retrovirus.
RNA
28
All RNA viruses are retroviruses. **True** or **False**
False.
Not all RNA viruses are retroviruses
29
Which genomic sequence of RSV confers tumorigenicity of the chicken cells?
src sequence
30
What is c-src classied as? Proto-oncogene or Oncogene?
Proto-oncogene
c-src (cellular src)
31
What is v-src classified as? Proto-oncogene or Oncogene?
Oncogene
v-src (viral src)
32
What is src protein classified as?
Src is tyrosine kinase
33
What does kinase protein do?
Phosphorylation.
Add phosphate group to protein.
34
Which part of the protein guides the protein to integrate into the cell membrane?
Myr
35
What is Myr? What is its function?
Myr is a lipid modification.
Myr promotes their binding to cell membranes for a variety of biological functions.
36
What is the function of SH2?
Binds any peptides that have phosphorylated Tyrosine
37
What is the function of SH3?
Binds polyproline motifs.
38
What inactivates the src protein in mice?
Phosphorylated Tyr 527 inactivates src protein
39
What is missing in the v-src protein comparing to normal src protein in mice?
Tyrosine at position 527
40
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?
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
How does proto-oncogene **c-src** turn into oncogene **v-src**?
1. Retrovirus 'kidnapped' normal proto-oncogene (c-src) and turn into oncogene (provirus + c-src = v-src).
42
All retroviruses can cause cancer. **True** or **False**
False. (only some exceptions)
43
Walk through the procedures in this picture.
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
In this experiment, if the result shows that there is no formation of transformed cells. What does this tell us?
The targeted oncogene is not successfully obtained.
45
What could be the reasons explaining why there are some untransformed fibroblast in this picture? **(2 reasons discussed in class)**
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
In this experiment, the result shows that the transformation (into cancer cells) rates are low. What does this suggest?
It suggests that we are possibly dealing with only one single oncogene.
47
How can we distinguish human genomes from other eukaryotic genomes (i.e mice)?
Repetitive sequences. (Alu sequence is human-specific repetitive sequence)
48
During the process of generating a bacteriophage genomic library, what do these white holes contain?
Virions
49
[Western blotting with anti-phosphotyrosine antibodies]
Which band shows the target of Src? Why?
band at ~120.
There is no band shown at 120 under non-myristylated v-Src transfected cells column.
50
What is the function of **p120 catenin**?
Modulates cell-cell adhesion
51
What is the role of **focal adhesion kinase**?
Involved in cell-matrix interactions.
52
What is **focal adhesion**?
Cluster of integrins at the site of contact with the ECM.
53
What is the special ECM that epithelial cells secrete called?
Basal lamina
54
What recruit FAK to the membrane?
Integrins.
55
What phosphorylate FAK at first when integrins recruit it?
FAK phosphorylate itself (autophosphorylated)
56
What happens to the cell when Src-FAK is more active?
Less adhesion, more migration
57
What do Src-FAK signals regulate?
Adhesion turnover
58
Cell-matrix interactions only occur in **one way** from the ECM to Cell. **True** or **False**
False
It occurs both way. "outside-in" and "inside-out"
59
What else does Src-FAK promote in cell beside cell migration?
Cell survival and growth
60
What would be the result of this southern blot?
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
In the experiment of identifying the human oncogen, what did they find?
**Ras** is the transforming human oncogene, **not src** -> huge finding
62
What are the **three factors** that can transform proto-oncogene to oncogene?
1. Viruses
2. Carcinogen
3. Random mutations
63
Ras is a kinase. **True** or **False**
FALSE!
64
What is the role of Ras?
It acts as a molecular switch.
65
Ras is **activated** when bound to which molecule?
GTP
66
Ras is **INactivated** when bound to which molecule?
GDP
67
How do you **inactivate** Ras-GTP?
Hydrolyze GTP to GDP
68
Which molecule helps to speed up the hydrolysis process of Ras-GTP?
GAP (GTPase activating protein)
69
GAP helps Ras-GTP to remove the phosphate group from GTP. **True** or **False**
False.
GAP helps Ras works better by changing Ras configuration
70
Which molecule helps to activate Ras-GDP?
GEF (guanosine exchange factor).
71
Assuming we have a great amount of GTP and GDP. What would be the factor determine activation state of Ras?
The amount of GAPs and GEFs.
More GAPs => More inactivated Ras
More GEFs => More activated Ras
72
What makes Ras oncogenic?
Mutated Ras cannot bind to GAP which make Ras cannot hydrolyze GTP -> GDP. Therefore, Ras is constitutively active (Ras-GTP)
73
Mutation in Ras is frameshift mutation. **True** or **False**
False.
It is point mutation (glycine - valine)
74
What are the main key players involved in forming vulva in C.elegans?
1 gonadal anchor cell (AC)
6 vulval precursor cells (VPCs)
75
What does the anchor cell do to the vulval precursor cells?
The AC signals the VPCs to adapt vulval fates
76
Why are the other VPCs (here in yellow) called VPCs, if they do not actually form the vulva?
They are capable of forming vulva if they received signals from the AC.
77
What are the three states of vulval formation in *C.elegans*?
1. Cell migration
2. Cell fusion
3. Ring formation (AC fuse with the surround cells to create a hole)
78
What is reverse genetics?
Knockout a specific candidate gene and test the consequences.
79
What is forward genetics?
Mutagenize animals randomly and select for mutation that affect a certain phenotype (i.e vulva formation)
80
What are the two reasons that normal cells may undergo apoptosis?
1. Part of a developmental program
2. When cells become "dangerous"
81
What are the two ways that Src can normally be activated?
1. Dephosphorylation of Tyr527
2. Configuration changes (e.g. SH2 bind to other proteins)
82
What acts as a substrate for migrating cell?
Extracellular Matric (ECM)
