Midterm 1 Flashcards

1
Q

benign

A

-grows slowly
-low mitotic index
-well-defined border
-not invasive
-doesn’t metastasize
-can be removed surgically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

malignant

A

-grows rapidly
-high mitotic index
-not defined/not encapsulated
-invasive
-spreads distantly (metastasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

solid tumors

A

-epithelia (carcinoma)
-connective tissue (sarcomas)
-nervous system (neuroectodermal tumors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

diffuse tumors

A

blood tumors
-leukemia, lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

somatic mutation theory (SMT)

A

-mutations gives cell a growth advantage
-leads to clonal expansion
-successive mutations giving greater advantages and more clonal expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cancer in the context of evolution

A
  1. mutation gives cell competitive advantage
  2. selective pressures from body prevent mutation from growing
  3. the only cells that survive are the ones that randomly mutate to be resistant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

driver mutation

A

causes/contributes to oncogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

passenger mutation

A

accumulate due to poor genome maintenance in cancer cells, but incidental to cancer phenotype
-outnumber driver mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cancer=mutation+opportunity

A

-not every cell with a mutation becomes cancer
-not every cell with an oncogenic mutation becomes cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are experimental models to study cancer?

A

-cell culture (yeast, bacteria)
-animals: genetically induce cancer or transplant human cancers into immunocompromised animals
-humans (organoids, genetics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

functional analysis of potentially cancerous mutations

A

is it necessary?
-remove a part and see if processes are turned off
is it sufficient?
-add one thing and see if process is turned on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

necessity tests-how to remove a gene or protein?

A

-gene knockouts
-interference with RNA (knockdowns)
-interference with protein (function blocking antibody, dominant-interference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

sufficiency tests-how to add a gene or protein?

A

-gene: deliver gene construct that results in gene expression
-RNA: inject X into mRNA
-protein: inject X protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

reverse transcriptase PCR (rtPCR)

A

-isolate cells, then mRNA
-reverse transcribe mRNA to cDNA
-use primers to amplify specific regions
-measure output thru gel, fluorescence, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

in situ hybridization

A

-fix whole tissue
-use a probe that is the DNA sequence reverse complement of gene being tested
-tells spatial where the gene is located

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

RNAseq

A

-isolate mRNA
-PCR to cDNA and add adapters sequence
-map result back to the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

western blot

A

-separates protein by size
-uses a fluorescent antibody to target specific protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

flow cytometry

A

cells of interest are labeled with antibodies and sorted using a laser

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

immunohisochemistry(IHC)/ immunoflurescence

A

-primary antibody binds to antigen of interest
-2nd antibody is fluoresently labeled
-can see where antigen is located

20
Q

immunnoprecipitation

A

isolation of proteins and other biomolecules from cell or tissue lysates for the purpose of subsequent detection by western blotting and other assay techniques.

21
Q

cyclin dependent kinase (CDK)

A

add a phosphate group to proteins to activate or inactivate them
-always present in a cell
-default function is inactive
-only active when bound to a specific cyclin

22
Q

cyclins

A

activate CDKs
-specific cyclins are made at specific times

23
Q

Wee1 kinase

A

inhibitory phosphorylation

24
Q

cdc25 phosphatase

A

removal of inhibitory phosphorylation

25
Q

CAK

A

activating phosphorylation

26
Q

spindle assembly checkpoint (SAC)

A

misalignment of chromosomes prevents CDK from activating APC
-alignment of chromosomes is detected by a conformational change in proteins on the chromosome caused by microtubule attachment and tension (during metaphase)
-prevents cell from going into anaphase until all chromosomes are aligned

27
Q

oncogene

A

encodes a protein that can cause cancer

28
Q

proto-oncogene

A

“normal” unmutated version of an oncogene

29
Q

Her2

A

receptor that regulates cell growth and division

30
Q

ligand

A

small protein or molecule

31
Q

receptor

A

transmembrane protein that binds to extracellular cue and initiates intracellular signals

32
Q

effector

A

generally many molecules acting in cascade can cluster by protein-protein interactions motifs

33
Q

transcription factor

A

regulate gene expression

34
Q

cell signalling

A

-transmission from outside of cell to nucleus
-fast ON and OFF
-energetically cheap

35
Q

gene expression

A

-slow ON and OFF
-stable changes
-energetically costly

36
Q

receptor tyrosine kinases (RTKs)

A

-high affinity cell surface receptors for polypeptide growth factors
-causes trans-autophosphorylation
-activate Ras/MAPK pathway
-transient phosphorylation syncs with entry into S phase

37
Q

EGF (epidermal growth factor)

A

-small protein that stimulates epithelial cell division
-binds to EGF receptor

38
Q

steps of RTK firing

A
  1. specific ligand binding (EGF binds)
  2. stable dimerization of RTK by EGF binding
  3. trans-autophosphorylation
    -triggers tyr phosphorylation of downstream effectors
39
Q

how are mitogens/RTKs linked to the cell cycle

A

-many growth factors signal through RTKs
-activating the Ras-mediated MAPK pathway to promote proliferation

40
Q

what are mutations in RTK firing that are oncogenic?

A

-mutations affecting structure: lack of ligand binding site that results in the constant dimerization and phosphorylation of the tyr kinase domain
-mutations causing overexpression: mutation in regulatory region that results in constitutive expression, results in molecular crowding and unregulated phosphorylation and unregulated cell growth

41
Q

herceptin that targets Her2

A

antibody therapy
-blocks cleavage of Her2, prevents signal transduction pathway
-blocks dimerization, prevents signal transduction pathway
-endocytosis: downregulates Her2 by bringing it inside the cell
-activation of antibody-dependent cell-mediated cytotoxicity: immune effector cell binds to herceptin, results in a immune attack and lysis of the tumor cell

42
Q

oncogene

A

gene capable of transforming a normal cell into a tumor cell

43
Q

v-onco

A

-viral oncogene
-gene carried in a virus, derived from a cellular gene, promotes proliferation in infected cell

44
Q

c-onco

A

-cellular oncogene
-gene that promotes cellular proliferation in a controlled manner under normal situations

45
Q

Rous experiment

A
  1. sarcoma in a chicken is removed
  2. grind up sarcoma with sand and pass thru fine pore filter
    -only allowed virus thru
  3. inject filtrate into chicken and observe to see if tumor grows
    Results: discovered RSV
46
Q

focus assay

A

way to measure oncogenic properties
-an immunostaining technique and a variation of the viral plaque assay