Umkc Cell Bio- Exam 4

Front 1

ECM- 3 things it is? has?
TIE
- and where those things come from?

Back 1

1. Tensile Strength- Created by Collagen Fibers
2.Incompressiblity- created by Hydrated GAG Fibers
3. Elasticity- Elastin created

Front 2

Collagen Sequences:
Genereic Collagen is made up of?

Back 2

Gly-X-Y
X-=usually Proline
Y= usually HYdroxyProline

Front 3

Collagen Sequences:
Genereic Collagen forms what shape? from what and what is every 3rd AA?

Back 3

Generic Collagen forms a triple helix from simple collagen protein/polypeptide chain. Every 3rd AA is Glycine

Front 4

# 1 protein in body?

Back 4

Collagen

Front 5

What % of our mass is collagen?

Back 5

25%

Front 6

Collagen organized in helices and then bundles:
Single collagen polypeptide chain forms into => ____ =>____=> ______

Back 6

Single collagen polypeptide chain=> TRIPLE-STRANDED COLLAGEN MOLECULE=>COLLAGEN FIRBRIL=>COLLAGEN FIBERS ... repeat 335nm

Front 7

Reason Collagen fibers are so strong? (2)

Back 7

1.Made up of collagen cells
2.Tripple Helix-cross linked w/one another

Front 8

Collagen organization linked to ______ _____

Back 8

Collagen organization linked to CELL FUNCTION

Front 9

Collagen organization linked to Cell Fx:
Organization/structure in:
Skin & Bone: and fx

Back 9

PLYWOOD structure in skin and bone cells resists stress in ANY direction... 90degree right angles/perpendicular

Front 10

Collagen organization linked to Cell Fx:
Organization/structure in:
Tendons and function

Back 10

Massively PARALLEL structure in tendon yields ENORMOUS strength, primarly in 1 DIRECTION.

Front 11

Integrins & Fibronectin couple cells to collagen:
1. Collagen-fibronectin-interin-actin form a strong bridge between _____ & __ ________

Back 11

Collagen-fibronectin-interin-actin form a strong bridge between ECM & CELL CYTOSKELETON

Front 12

Integrins & Fibronectin couple cells to collagen:
2.Clusters of intergins (local adhesions sites) can both bind & release from the ECM thru tightly reg processes, allowing:

Back 12

Crawling as intergrins bind ECM at the leading edge of the cell & release at the trailing end.

Front 13

Integrins & Fibronectin couple cells to collagen:
3.Integrins bind a wide range of ECM proteins besides fibronecting including:

Back 13

Collagen (directly) & Laminins in the Basal Lamina

Front 14

Integrins & Fibronectin couple cells to collagen:
In addition to serving as "anchors", integrins are signaling molecules that sense:

Back 14

Intracellular & extracellular signaling pathways (including Src and Focal Adhesion kinases) & binding o intracellular proteins to intergirn can trigger either release or binding to the ECM

Front 15

Integrins & Fibronectin couple cells to collagen:
How many different types of intergrins in humans? each one??

Back 15

24- each specific to particular cell types and/or tissues

Front 16

Proteoglycans are a component of what?

Back 16

the ECM

Front 17

Dense, strong CT like bone and tendon and contain mostly collagen.

Back 17

PROTEOGLYCANs

Front 18

Proteoglycans-Dense, strong CT like bone& tendon& contain mostly collagen. In contrast to what in CT....a 2nd type of ECM is prevalent:PROTEOGLYCANS

Back 18

In contrast, in CT that fills space, maintains hydration & resists compression, like the eyeball & cart, a 2nd ECM is prevalent: PROTEOGLYCAN

Front 19

Higly glycosylated proteins that form giant aggregates w/ properties of gel.

Back 19

PROTEOGLYCAN STRUCTURE

Front 20

Proteogylcans have long sugars, ______, attached along the length of their linear core protein, they can also attach to an especially long ___, ________ via a link protien to form large aggreatates.

Back 20

Proteogylcans have long sugars, GLYCOSAMINOGLYCANS (GAGs), attached along the length of their linear core protein, they can also attach to an especially long GAG, HYALURONAN via a link protien to form large aggreatates.

Front 21

Proteoglycan fx:
GAGs are highly ____ charge, attract ___ (ex: Na+) & hence (pull out) ____ from ____ ______(up to___ _ ___/_ proteoglycan). The large protein/carb aggreages + high _____ content creates a ____ ____ that resists ______ ______.

Back 21

Proteoglycan fx:
GAGs are highly NEG charge, attract CATIONS (ex: Na+) & hence (pull out) WATER from SURROUNDING CELLS( up to 50G WATER/G proteoglycan). The large protein/carb aggreages + high WATER content creates a HYDRATED GEL that resists TISSUE COMPRESSION.

Front 22

Proteoglycan fx...
In highly non-compressible tissues like ____: Collagen fibrils are ____-______ to GAGs forming a sort of _____ that dramatically limits ______.

Back 22

In highly non-compressible tissues like CARTILAGE: Collagen fibrils are CROSS-LINKED to GAGs forming a sort of CAGE that dramatically limits COMPESSION.

Front 23

ECM- tissue elasticity:
examples of elastic ct?

Back 23

Skin, Lung, Small Artery

Front 24

Elastic Fibers- Elastin Structure:
Elastin synthesis is completed by? What happens after that>? ex?

Back 24

Elastin synthesis is completed by ADOLESCENCE, after that we just LOSE ELASTIN & get LESS ELASTIC- eg. wrinkles

Front 25

ECM: Production and Degradation
ECM is dynamic- Production & Degradation are critical to?

Back 25

Remoldeling during development and during tissue repair

Front 26

ECM Production: ______ synthesize & secreate ______ & other ECM _____

Back 26

ECM Production: FIBROBLAST synthesize & secreate COLLAGEN & other ECM PROTEINS

Front 27

ECM Destruction: _______ _______ synthesis & _____ _____( ), which degrade ECM (as well as other extracellular ______)

Back 27

ECM Destruction: CONVERSELY FIBRBLASTS synthesis & MATRIX METALLOPROTEASES (MMPs), which degrade ECM (as well as other extracellular PROTEINS)

Front 28

ECM: Production and Degradation
MMPs are secreted Fibroblasts, Macrophages other cell types. MMPs secreted by MACROPHAGES play a critical role in what?

Back 28

MMPs secreated by Macrophages play a critical role in TURNOVER/REPAIR of CT, ex. at Wounds.

Front 29

ECM: Production and Degradation
In Arthritis, Macrophages are ________ to secrete _____, leading to ________ of _______.

Back 29

In Arthritis, Macrophages are HYPERACTIVATED to secrete MMPs, leading to DESTRUCTION of CARTILAGE.

Front 30

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:

Back 30

1. Tight Junction
2. Adherens Junction
3.Desmosome
4.Gap Junction
5. Hemidesmosome

Front 31

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:
1. Tight Junctions- Fx?

Back 31

1.Tight Junction: FX:
-Seals neighboring cells together in an epithelia sheet to prevent leakage of molecules between them

Front 32

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:
2. Adherens Junction-Fx:

Back 32

2. Adherens Junction: FX:
Joins an actin bundle in one cell to a similar bundle in a neighbroing cell

Front 33

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:
3.Desmosomes- FX?

Back 33

3.Desmosome fx:
Join the intermediate filaments in one cell to those in a neighboring cell.

Front 34

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:
4. Gap Junction- FX?

Back 34

4. Gap Junction: FX:
- Allows the passage of small water-soluble ions and molecules in the cytosol

Front 35

CELL-CELL (mostly) Connection in Tissue
5 types of Connections:
5.Hemidesmosomes Fx:

Back 35

5.Hemidesmosomes Fx:
-Anchors intermediate filaments in a cell to the basal lamina

Front 36

CELL-CELL (mostly) Connection in Tissue
Which of the 5 Connections fx? -Seals neighboring cells together in an epithelia sheet to prevent leakage of molecules between them

Back 36

Tight Junction: FX:

Front 37

CELL-CELL (mostly) Connection in Tissue
Which of the 5 Connections fx:
- Allows the passage of small water-soluble ions and molecules in the cytosol

Back 37

Gap Junction: FX:

Front 38

CELL-CELL (mostly) Connection in Tissue
Which of the 5 Connections fx:
Joins an actin bundle in one cell to a similar bundle in a neighbroing cell

Back 38

Adherens Junction: FX:

Front 39

CELL-CELL (mostly) Connection in Tissue
Which of the 5 Connections fx:
-Anchors intermediate filaments in a cell to the basal lamina

Back 39

Hemidesmosomes Fx:

Front 40

CELL-CELL (mostly) Connection in Tissue
Which of the 5 Connections fx:
Join the intermediate filaments in one cell to those in a neighboring cell.

Back 40

Desmosome fx:

Front 41

CELL-CELL (mostly) Connection in Tissue:
-All involve proteins that some how ____ or ______ __ ____ to another & all are ________
-All junctions involve the ________

Back 41

-All involve proteins that some how SEAL or CONNECT 1 CELL to another & all are SPECIFIC
-All junctions involve the CYTOSKELETON

Front 42

CELL-CELL (mostly) Connection in Tissue:
1. Tight Junctions- are particullary important for ____ ____ layers like the ____ & ____. ( there is NO _____

Back 42

1. Tight Junctions- are particullary important for SIMPLE EPITHELIALlayers like the NEPHRON & GUT..(there is NO SPACE between them, NO LIQUID)-@ apical end of epithelial

Front 43

CELL-CELL (mostly) Connection in Tissue:
1. Tight Junctions- sealed by a network of _____ & _____ proteins. These proteins Bind along the ___ of 1 cell associate (through their EC domain) w/ the same proteins along a 2nd. These proteins also connect to __ ______, _____ the Tight Junction!

Back 43

1.Tight Junctions- sealed by a network of OCCULDIN & CLAUDIN proteins. These proteins Bind along the PM of 1 cell associate (through their EC domain) w/ the same proteins along a 2nd. These proteins also connect to ACTIN CYTOSKELETON, STRENGTHENING the Tight Junction!

Front 44

Tight junctions seal, but adherens do what? using what?

Back 44

Adherens keep the junctions sealed using protein CADHERINS.

Front 45

CELL-CELL (mostly) Connection in Tissue:
1.tight junctions- what do tight juctions do on the apicla side of the epithelium? prevent the lumen from doing?

Back 45

Prevents lumen of the gut from slipping between cells.

Front 46

CADHERINS are a protein in adherin junctions... what type of protein are they?
what do they really do?
Dependent on?
-Other side attaches to ?

Back 46

Cadherins- transmembrane protein
-Have EC part that binds Adherins on neighboring cells.
-Calcium dependent
CA2+ + Adhesion= CADHERINS
-Other side attaches to Catein= linker cell

Front 47

Desomosome junctions:
Critical to function of what kind of filaments?
Made of: ____ different from Adherins junction:

Back 47

Critical to INTERMEDIATE FILAMENTS-
Made of: CADHERINS
Different than the ones in Adherins JX- specific for same cell type

Front 48

Hemidesmosome junctions between?
Connection?? byCadherin?? is the focal adhision sites?
RESULT of DIslodging the Hemidesmome>?
What

Back 48

Junction between CELL & UNDERLYING ECM
NO Cadherin,- Instead, BASAL LAMINA is connected to EPITHELIAL SHEETS via multiple INTEGRIN-LAMINA Contacts
As focal adhesion sites:INTEGRINS ARE CLUSTERED
RESULT of DIslodging the Hemidesmome: BLISTERS

Front 49

Gap Junctions- differ structurally and functionally from most other junctions bc?

Back 49

They don't SEAL between CELLS. (Physical contact btw cells for commnication??)

Front 50

Gap Junctions found in?
Hold region of ____ _______ of 1 cell very close to neighbor,

Back 50

Found in:Epithelial cells (like all other junctions)and other tissues- like muscle cells (like desmosomes & adherins)

Front 51

Gap Junctions are regulated by what to open and close?
-Hexameric channels termed _____ on each cell pair up to allow passage of small molecules from1 cell.

Back 51

Dopamine
-Hexameric channels termed CONNEXONS on each cell pair up to allow passage of small molecules from1 cell.

Front 52

Gap junctions- Connexons allow: 2 things

Back 52

1. Passage of small molecules from 1 cell, each junction has 100s of channels packed together.
2.Osmotic and electrical coupling (ex: in the heart muscle) between cells

Front 53

Gap Juctions:
Conneons are _______: ex NT such as ______ can regulate whether connexons in neurons are ___ or ____

Back 53

Gap Juctions:
Conneons are REGULATABLE: ex NT such as DOPAMINE can regulate whether connexons in neurons are OPEN or CLOSED

Front 54

Gap junctions- made up of connexons- made of of _____

Back 54

6 proteins

Front 55

Oculodentodigtal Dysplasia:
Inheritance:
Molecular Cause:
Cellular Cause:

Back 55

Inheritance:Very Rare Autosomal Dominant Disorder
Molecular Cause:Disease Allele of GJA1 gene, which encodes a connexin protein, results in connexon stuck in closed connection
Cellular Cause:Defective connexons lead to defects in development of epithelial tissue

Front 56

Oculodentodigtal Dysplasia:
Main Features: 3

Back 56

1.Teeth- small/missing, weak enamel(yellowing), multiple cavities, tooth loss
2. Small Eyes-abnormalities leading to vision problems, thin nose
3.Webbing of 4th and 5th finger- surgically resolved

Front 57

Tissue Renewal & Repair:
Renewal:

Back 57

Renewal: In epithelial renewal, existing ECM is used to resore original organixation to tissue. (ECM intact, just tissue damage)
=> if ECM is attatched- can be renewed

Front 58

Tissue Renewal & Repair:
Repair:

Back 58

Repair: New ECM generated along with new cells but orginal organization is lost. (ECM also damaged, not just tissue)
-If ECM is really damaged- then not orginal , but repaired-not renewed. NO WAY of renewing if ECM is damaged

Front 59

Tissue Renewal:
Key part- Cells replaced from:

Back 59

Key part- Cells replaced from from STEM CELLS

Front 60

Tissue Renewal:
*-Cells replaced from Stem Cells:
ex: 1. Normal regeneration in ____, ____, ____ to replace dying or damaged cells
2.____ epidermal wounds->
3._______ cells

Back 60

1. Normal regeneration in GUT, EPIDERMIS, LIVER to replace dying or damaged cells
2.SURFACE epidermal wounds->no scaring
3.HEMATAPOIETIC cells-> renewed all the time

Front 61

Tissue Renewal
Different tissues have wide range of renewal capacity:
1. Gut Epithelial- time
2.Epidermis-
3.RBC-
4.Bone-
5.Cardiac Mucscle &Neurons-

Back 61

Tissue Renewal
Different tissues have wide range of renewal capacity:
1. Gut Epithelial-(few days)
2.Epidermis-(~60days)
3.RBC-(~120days)
4.Bone-(Avg.cell renewed/replaced every 10 years)
5.Cardiac Mucscle &Neurons- (Essentially NEVER RENEWED)

Front 62

Tissue renewal in Epidermis:
Regeneration: In our bodies... Skin and over time...

Back 62

Regeneration: Continuosusly shed top layer of dead skin cells & continuously regenerate epidermal cells near the basal lamina cells.
Over time- cells are pushed upward as new cells form beneath them

Front 63

Tissue Renewal in Epidermis
Epithilial Cells in Epidermis:
Top part=>
Lining epithelium cells come from:
how long is the epithelium sheding cyle?

Back 63

Top Part=> dead cells=> tightly packed with keratin.
Lining epithelium cells come from: STEM CELLS near Basal LAMINA- stem cells make epethilium cells 2 month cycle from begining to sheding

Front 64

Stem Cells
1.Can regenerate-
2.can differentiate to form

Back 64

Stem Cells
1.Can regenerate INDEFINIETLY (self renewal)
2.can differentiate to form OTHER CELL TYPES

Front 65

Pathway important in Stem Cell reeneration and differentiation:

Back 65

Wnt Pathway: 4th type of ST Pathway

Front 66

Wnt Pathway: 4th type of ST Pathway
- Ligand:
-Receptor:
Dsh blocks:
GSK works w/3 things
-once Gsk is inactivated:
B-cat moves to:__- and acts as

Back 66

-Ligand:Wnt
-Receptor:Frizzled (Frz)
-Once activated, released disheveled (Dsh)
Dsh blocks: GSK3 (kinase)
GSK works w/:
1. Axin
2.Adenomatous Polyposis Coli
3.These 3 act with ubiquitin ligase to target B-catenin
-once Gsk3 is inactivated: B-cat starts to accumulate (is no longer destroyed)
B-cat moves to:NUCLEUS
- and acts as TRANSCRIPTION FACTOR

Front 67

Stem Cells can produce multiple Cell Types:
Intestinal Stem Cells:
Precurosr cells- 3

Back 67

Intestinal Stem Cells:
Precurosr cells-
1. PANETH CELL
2. BRUSH BORDER CELL
3. GOBLET CELL
Intestinal Stem Cell-> precursor cells-> (one of 3 above)

Front 68

Stem Cells can produce multiple Cell Types:
Stem Cells found in Crypt of Intestinal Cells:
Make what cells and where do the migrate or do they?

Back 68

Crrypt cells
Make:
1.Paneth Cells- stay in crypt
2.Brush border & goblet cells- migrate upwards move out of crpyt & into villus

Front 69

Wnt Pathway- differentiate/proliferation:
Where does it actually act?
- WntPathway active in crypt:

Back 69

WntPathway active in crypt:
-Wnts & Frz both expressed at high levels in crypt
-Cells proliferate

Front 70

Genetic Testing_
When deciding tx for breast cancer- a mutation in BRCA1 or BRCA2 genes benefits from ______, but unnecessary for pt’s ______________

Back 70

**GENETIC TESTING====
When deciding tx for breast cancer- a mutation in BRCA1 or BRCA2 genes benefits from CHEMO, but unnecessary for pt’s W/OUT MUTATION

Front 71

The science of tailoring a specific drug treatment (including dosage)... genetic testing =

Back 71

PHARMACOGENOMICS=

Front 72

Ex of PHARMACOGENOMICS=
Prescription of abacavir to HIV patients is guided by ____ ____

Back 72

Pharmacogenomoics...
guided by GENETIC TESTINGS...

Front 73

Dscam –

Back 73

Down Syndrom Cell Adhesion molecule:

Front 74

Expressed on neurons, alternative splicing gives each neuron a specific self-recognition tag.. THIS IS CALLED?

Back 74

Dscam – Down Syndrom Cell Adhesion molecule:

Front 75

(sequence differences that do not affect function)
All of which=90% of variation (mutation within a gene or mutation within regulatory region)

Back 75

SNP – single-nucleotide polymorphism

Front 76

Variation (mutation w/in gene)
-10% -
- <0.1% -
-90%-

Back 76

-10% - gene duplication
-<0.1% - Insertions
-90%= SNP

Front 77

Mutation in p63 can be one cause of _____

Back 77

Can be 1 cause of EctD

Front 78

IRF-6 gene causes what syndrome?

Back 78

causes Van de Woude Syndrome

Front 79

Allele shown to have correlation between this allele (shown to affect taste) and lower incidence of caries

Back 79

TAS2R38-

Front 80

TAS2R38

Back 80

Allele shown to have correlation between this allele (shown to affect taste) and lower incidence of caries

Front 81

-% of patients that do not respond positively to treatment by the 4K drugs currently in use

Back 81

40%

Front 82

Humans have ___ functional P450 genes (may activate or inactivate drugs)

Back 82

Humans have _57_ functional P450 genes (may activate or inactivate drugs)

Front 83

An anti-coagulant used in variety of heart disease.

Back 83

Warfarin-

Front 84

Warfarin-Common alleles of ____ gene ______increase sensitivity to warfarin.

Back 84

Warfarin-Common alleles of _P450_ gene -CYP2C9- increase sensitivity to warfarin. Generally, interruption of warfarin therapy is NOT recommended for dental procedures (may have loss of blood control

Front 85

Generally, interruption of ____ ______ is NOT recommended for dental procedures (may have loss of blood control

Back 85

WARFARAIN THERAPY

Front 86

Intergrin (____types in humans)– inactive form is folded in on itself, active form is stretched out.

Back 86

Intergrin (_24_ types in humans)– inactive form is FOLDED ON ITSELF, active form is STRETCHED OUT.

Front 87

iNTEGRIN Can activate intracellular signaling pathways: 2

Back 87

Src and Focal adhesion kinases

Front 88

GAGs= ______ ____ _______ (________/_______)
include: 3

Back 88

GAGs= glycosaminoglycans (cartilage / proteoglycan) Include:
1. Hyaluronan,
2. Keratin Sulfate, &
3. Chondroitin Sulfate

Front 89

MMPs = –____
Degrade ________
Critical in: turnover/repair of CT

Back 89

MMPS= MATRIC METALLOPROTEASES
Degrade: ECM
Critical in: Turnover/Repair of CT

Front 90

Occludin & Claudin

Back 90

– proteins involved in sealing tight junctions

Front 91

Cadherin – (____ + ____) form ring near apical end of cells iN ___ ______, also make up ________ (give _______ to intermediate filaments), absent in __________

Back 91

Cadherin – (Ca2+ ADHESION) form ring near apical end of cells in ADHERINS JUNCTIONS, also make up DESOMESOMES (give STRENGTH to intermediate fiLaments), absent in HEMIDESMOSOMES

Front 92

linker protein that connects cadherin to actin

Back 92

Catenin –

Front 93

links basal lamina to epithelial sheet in Hemidesmosomes (clustered)

Back 93

Integrin –

Front 94

hexameric channels in gap junctions, allow passage of small molecules

Back 94

Connexons –

Front 95

Wnt Pathway (4th type of ST pathway)–
Frizzled (Frz) is the ____ _______
Disheveled (Dsh) is activated when _____ ____ _____,
3 proteins (___ ____ ____)
act with ____ ______ to target B-Cat for destruction.
Once B-Cat is stabilized it moves to nucleus and acts as ____ ____.

Back 95

Wnt Pathway (4th type of ST pathway)–
Frizzled (Frz) is the _WNT RECEPTOR
Disheveled (Dsh) is activated when _RELEASED FROM FRZ_,
3 proteins:
1.Axin, 2.APC,3. GSK3
-act with UBIQUITIN LIPASE to target B-CAT for destruction.
Once B-Cat is stabilized it moves to nucleus and acts as TRANSCRIPTION FACTOR.

Front 96

regulate differentiation and proliferation (inactive Wnt pathway = no cell proliferation, active Wnt = proliferation)

Back 96

ST pathways like Wnt –

Front 97

What cells generate Paneth cells, brush border cells, and goblet cells?

Back 97

Intestinal Stem Cells –

Front 98

Osseous Tissue: ____ +_______ (adds ______ to skeleton, stores _____ & _____)

Back 98

Osseous Tissue:
ECM + BONE CELLS
(adds STRENGTH to skeleton, stores MINERALS & GROWTH FACTORS)

Front 99

What sense changes in bone, regulate osteoclast/osteoblast activity?

Back 99

Osteocytes –

Front 100

Cart vs. Bone: Types of collagen, amt of proteoglycan
Cartilage =
Bone =

Back 100

Cartilage= Collagen type II fibrils, MORE proteoglycans
Bone = collagen type I fibrils, hydroxyapatite crystals, LESS proteoglycans

Front 101

What is a decoy receptor for RANK (blocks RANKL), stimulated by Estrogen

Back 101

OPG – osteoprotegerin-

Front 102

M-CSF

Back 102

– macrophage colony stimulating factor

Front 103

–secrete signals (M-CSF and RANKL) leads to differentiation/fusion

Back 103

Osteoblasts

Front 104

OPG – osteoprotegerin- decoy receptor for _____ (blocks _____)
- Stimulated by :

Back 104

OPG – osteoprotegerin- decoy receptor for RANK (blocks RANKL)
- Stimulated by : ESTROGEN

Front 105

What is RANKL –

Back 105

Ligand for RANK receptor

Front 106

Pathway of Oncogenesis in:
Colon Cancer

Back 106

Loss of APC gene -> oncogenic mutation of RAS gene -> loss of _P53__ gene and loss of a gene on _CHROMOSOME 18___
Stages above are from normal -> early/late benign ->MALIGNANT CARCINOMA

Front 107

Pathway of Oncogenesis in:

Back 107

Astrocytoma (glial cell cancer)
Loss of p53 gene -> loss of cluster of genes on chromosome 9 -> multiplication of genes for epidermal GF receptor and loss of one copy of chromosome 10
Stages above are from normal -> low-grade ->high grade -> most aggressive

Front 108

Pathway of Oncogenesis in:
Astrocytoma (glial cell cancer)
Loss of ___ gene -> loss of cluster of genes on ______ __ -> _________ of genes for epidermal ____ receptor and loss of one copy of ______ __
Stages above are from normal -> low-grade ->high grade ->____ _____

Back 108

Pathway of Oncogenesis in:
Astrocytoma (glial cell cancer)
Loss of _P53__ gene -> loss of cluster of genes on __CHROMOSOME 9__ -> MULTIPLICATION of genes for epidermal __GF__ receptor and loss of one copy of --CHROMOSOME 10--
Stages above are from normal -> low-grade ->high grade -> MOST AGGRESSIVE

Front 109

Cells that function in normal cells to prevent cancer

Back 109

TSGs – tumor suppressor genes –

Front 110

Cells that function in normal cells to promote growth & survival (mutations = cancer)

Back 110

Proto-oncogenes –

Front 111

less than or greater than 46 chromosomes (abnormal #)

Back 111

Aneuploidy –

Front 112

when overexpressed (v-myc) stimulates proliferation and generation of ROS, damage DNA leading to mutations... is??

Back 112

c-Myc – transcription factor –

Front 113

Examples of RTK signal transduction mutation in cancer:
What triggers epithelial proliferation, normally it is turned on via binding of epidermal growth factor (EGF) to c-ErbB receptor (proto-oncogene).

Back 113

PDGF

Front 114

Examples of RTK signal transduction mutation in cancer:
Normally, ____switches from active to inactive forms. The v-rasoncogene is always in active form (due to mutation). Rb is TSG that regulates progression by switching from E2-f bound form to unbound form. When inactivated, proliferation doesn’t require cyclin:CDK.

Back 114

c-Ras

Front 115

Examples of RTK signal transduction mutation in cancer:
In some tumors the v-ErbBdimerizes and is activated without ____(always on)

Back 115

ErbBdimerizes and is activated without EGF (always on)

Front 116

What restrains apoptosis when no damage present, in cancer cells v-Bcl-2 restrains apoptosis regardless of damage.

Back 116

c-Bcl-2 –

Front 117

Examples of RTK signal transduction mutation in cancer:
Cdi inhibitor is TSG, when inactivated via mutation, proliferation unregulated

Back 117

p27 –

Front 118

During oncogenesis, collagen broken down by ____’s. ________ also affect ECM.

Back 118

During oncogenesis, collagen broken down by MMP’s. CYTOKINESalso affect ECM.

Front 119

What is inactivated in many cancers – Adherens junctions lost, cells detach

Back 119

E-cadherin –

Front 120

Repressed during oncogenesis, allows tumor to migrate, invade, survive, proliferat, and colonize in new tissue

Back 120

Integrins –

Front 121

Wnt& cancer:
oNormal WntSignalling in ___ cells -> normal tissue
o________Wnt signaling in stem cells -> cancer
oDysregulated Wnt signaling in _____ OR _____ cells -> cancer

Back 121

Wnt& cancer:
oNormal WntSignalling in STEM cells -> normal tissue
oDYSREGULATED Wnt signaling in stem cells -> cancer
oDysregulatedWnt signaling in PROGIENTOR OR STEMcells -> cancer

Front 122

What is inactivated in many cancers – Adherens junctions lost, cells detach

Back 122

E-cadherin –

Front 123

Repressed during oncogenesis, allows tumor to migrate, invade, survive, proliferat, and colonize in new tissue

Back 123

Integrins –

Front 124

Wnt& cancer:
oNormal WntSignalling in ___ cells -> normal tissue
o________Wnt signaling in stem cells -> cancer
oDysregulated Wnt signaling in _____ OR _____ cells -> cancer

Back 124

Wnt& cancer:
oNormal WntSignalling in STEM cells -> normal tissue
oDYSREGULATED Wnt signaling in stem cells -> cancer
oDysregulatedWnt signaling in PROGIENTOR OR STEMcells -> cancer