Copyright 2003 Pearson Education, Inc.

publishing as Benjamin Cummings

1.Cancerandthecellcycle
checkpoints,reqmtstoadvance
oncogenes
tumorsuppressorgenes
2.6Traitsofcancerouscells
3.Originsofcancerouscells

DNA

Mitotic Phase (M)

DNA
DNA

DNA

Interphase

s
si
ito
M

G2

sis
Cytokine

DNA
DNA

Cell

growth
preparation for
division

Interphase

G1
Cell growth

S
DNA replication
DNA
DNA
Interphase

DNA

 Proteins within the cell control the cell cycle

Signals affecting critical checkpoints determine
whether the cell will divide (cyclins, kinases)
G1 checkpoint

Control
system

M checkpoint

G2 checkpoint

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 8.9A

Anchorage, cell density, and chemical growth

factors affect cell division
In laboratory cultures, normal cells divide only
when attached to a surface
= anchorage dependent

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Cells continue dividing until they touch one

another
= density-dependent inhibition
Cells anchor to dish surface and
divide.

When cells have formed a

complete single layer, they stop
dividing (density-dependent
inhibition).

If some cells are scraped away,

the remaining cells divide to fill
the dish with a single layer and
then stop (density-dependent
inhibition).
Figure 8.8A
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Growth factors are proteins secreted by cells

that stimulate other cells to divide

After forming a single layer, cells

have stopped dividing.

Providing an additional supply of

growth factors stimulates further
cell division.

Figure 8.8B
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Growth factors bind to specific receptors on

the plasma membrane to trigger cell division

Growth factor
Plasma membrane

Receptor
protein

Relay
proteins

Signal
transduction
pathway

Figure 8.8B
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

G1 checkpoint

Cell cycle
control
system

 Cancer cells have abnormal cell cycles

divide excessively and form tumors

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Breast cancer cell - altered morphology

Figure 8.10x1
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Traits of cancer cells

1. Independent of GROW signal from other
cells
often, oncogenes. Ex. ras
2. Ignores STOP signal
defective damage control, so problems not
corrected.
Often, tumor suppressor genes. Ex. p53

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Traits of cancer cells, continued

3. No cell suicide (apoptosis)
If this occurs, treatments which damage
dividing cells may not work.
4. No limit to cell divisions
telomeres rebuilt on ends of xsomes
new treatment target: telomerase

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Traits of cancer cells, continued

5. Angiogenesis - formation of blood vessels

6. Metastasis - ability to move to other tissues

benign: do not move from tumor site
malignant: invasive cells, can travel in
blood and lymph system

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Malignant tumors can invade other tissues and

may kill the organism

Lymph
vessels
Tumor

Glandular
tissue
Metastasis
1

A tumor grows
from a single
cancer cell.

Cancer cells invade

neighboring tissue.

Figure 8.10
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Cancer cells spread

through lymph and
blood vessels to other
parts of the body.

Howdonormalcellsbecomecancerous?

Selectionwithintumorfor
mostcancerouscells

What is the source of oncogenes?

Mutation of a normal gene = change in DNA
sequence
UV light, Xrays, natural or synthetic chemicals
Virus (ex. HPV and cervical cancer)

Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Xsomal changes can be large or small

Deletion

Homologous
chromosomes

Duplication

Inversion

Reciprocal
translocatio
n

Nonhomologous
chromosomes
Copyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 8.23A, B

Xsomaltranslocationcanactivatean
oncogene

A chromosomal translocation in the bone marrow

is associated with chronic myelogenous leukemia

Cancer
Cancerisoneofthemostcommondiseasesinthe
developedworld:
1in4deathsareduetocancer
1in17deathsareduetolungcancer
Lungcanceristhemostcommoncancerinmen
Breastcanceristhemostcommoncancerin
women
Thereareover100differentformsofcancer

Cancer
Thedivisionofnormalcellsisprecisely
controlled.Newcellsareonlyformedforgrowth
ortoreplacedeadones.
Cancerouscellsdividerepeatedlyoutofcontrol
eventhoughtheyarenotneeded,theycrowdout
othernormalcellsandfunctionabnormally.They
canalsodestroythecorrectfunctioningofmajor
organs.

Whatcausescancer?
Cancerarisesfromthemutationofanormal
gene.
Mutatedgenesthatcausecancerarecalled
oncogenes.
Itisthoughtthatseveralmutationsneedtooccur
togiverisetocancer
Cellsthatareoldornotfunctioningproperly
normallyselfdestructandarereplacedbynew
cells.
However,cancerouscellsdonotselfdestructand
continuetodividerapidlyproducingmillionsof
newcancerouscells.

 Afactorwhichbringsaboutamutationis
calledamutagen.
Amutagenismutagenic.
Anyagentthatcausescanceriscalleda
carcinogenandisdescribedascarcinogenic.
Sosomemutagensarecarcinogenic.

Carcinogens
IonisingradiationXRays,UVlight
Chemicalstarfromcigarettes
Virusinfectionpapillomaviruscanberesponsible
forcervicalcancer.
HereditarypredispositionSomefamiliesaremore
susceptibletogettingcertaincancers.Rememberyou
cantinheritcanceritsjustthatyoumaybemore
susceptibletogettingit.

Benignormalignant?
Benigntumoursdonotspreadfromtheirsiteoforigin,but
cancrowdout(squash)surroundingcellsegbraintumour,
warts.
Malignanttumourscanspreadfromtheoriginalsiteand
causesecondarytumours.Thisiscalledmetastasis.They
interferewithneighbouringcellsandcanblockblood
vessels,thegut,glands,lungsetc.
Whyaresecondarytumourssobad?
Bothtypesoftumourcantirethebodyoutastheybothneed
ahugeamountofnutrientstosustaintherapidgrowthand
divisionofthecells.

TheDevelopmentofCancer
Withineverynucleusofeveryoneofthe
humanbody's30trillioncellsexistsDNA,
thesubstancethatcontainstheinformation
neededtomakeandcontroleverycell
withinthebody.Hereisacloseupviewof
atinyfragmentofDNA.

1.DNAofanormalcell

ThispieceofDNAisanexactcopyoftheDNAfromwhich
itcame.Whentheparentcelldividedtocreatetwocells,the
cell'sDNAalsodivided,creatingtwoidenticalcopiesofthe
originalDNA.

2.MutationofDNA

HereisthesamesectionofDNAbutfromanothercell.Ifyoucan
imaginethatDNAisatwistedladder,theneachrungoftheladderisa
pairofjoinedmolecules,orabasepair.WiththissectionofDNA,
oneofthebasepairsisdifferentfromtheoriginal.
ThisDNAhassufferedamutation,eitherthroughmiscopying(when
itsparentcelldivided),orthroughthedamagingeffectsofexposureto
radiationorachemicalcarcinogen.

3.Geneticallyalteredcell

Bodycellsreplicatethroughmitosis,theyrespondtotheir
surroundingcellsandreplicateonlytoreplaceothercells.
Sometimesageneticmutationwillcauseacellandits
descendantstoreproduceeventhoughreplacementcellsare
notneeded.
TheDNAofthecellhighlightedabovehasamutationthat
causesthecelltoreplicateeventhoughthistissuedoesn't
needreplacementcellsatthistimeoratthisplace.

4.Spreadandsecondmutation

Thegeneticallyalteredcellshave,overtime,reproducedunchecked,
crowdingoutthesurroundingnormalcells.Thegrowthmaycontain
onemillioncellsandbethesizeofapinhead.Atthispointthecells
continuetolookthesameasthesurroundinghealthycells.
Afteraboutamilliondivisions,there'sagoodchancethatoneofthe
newcellswillhavemutatedfurther.Thiscell,nowcarryingtwo
mutantgenes,couldhaveanalteredappearanceandbeevenmore
pronetoreproduceunchecked.

5.Thirdmutation

Notallmutationsthatleadtocancerouscellsresultinthecells
reproducingatafaster,moreuncontrolledrate.Forexample,amutation
maysimplycauseacelltokeepfromselfdestructing.Allnormalcells
havesurveillancemechanismsthatlookfordamageorforproblemswith
theirowncontrolsystems.Ifsuchproblemsarefound,thecelldestroys
itself.
Overtimeandaftermanycelldivisions,athirdmutationmayarise.Ifthe
mutationgivesthecellsomefurtheradvantage,thatcellwillgrowmore
vigorouslythanitspredecessorsandthusspeedupthegrowthofthe
tumour.

6.Fourthmutation

Thenewtypeofcellsgrowrapidly,allowingfor
moreopportunitiesformutations.Thenextmutation
pavesthewayforthedevelopmentofanevenmore
aggressivecancer.
Atthispointthetumourisstillcontained.

7.Breakingthroughthemembrane

Thenewer,wildercellscreatedbyanothermutationareable
topushtheirwaythroughtheepithelialtissue'sbasement
membrane,whichisameshworkofproteinthatnormally
createsabarrier.Theinvasivecellsinthistumourareno
longercontained.
Atthispointthecancerisstilltoosmalltobedetected.

8.Angiogenesis

Oftenduringthedevelopmentofearlierstagesofthetumour,or
perhapsbythetimethetumourhasbrokenthroughthebasement
membrane(aspicturedabove),angiogenesistakesplace.
Angiogenesisistherecruitmentofbloodvesselsfromthenetwork
ofneighbouringvessels.
Withoutbloodandthenutrientsitcarries,atumourwouldbeunable
tocontinuegrowing.Withthenewbloodsupply,however,the
growthofthetumouraccelerates;itsooncontainsthousandmillion
cellsand,nowthesizeofasmallgrape,islargeenoughtobe
detectedasalump

9.Invasionanddispersal

Thetumourhasnowinvadedthetissuebeyondthebasement
membrane.
Individualcellsfromthetumourenterintothenetworkof
newlyformedbloodvessels,usingthesevesselsashighways
bywhichtheycanmovetootherpartsofthebody.Atumour
assmallasagramcansendoutamilliontumourcellsinto
bloodvesselsaday.

10.Tumourcells
travelmetastasis

Whatmakesmost
tumourssolethalistheir
abilitytometastasize
thatis,establishnew
tumoursitesatother
locationsthroughoutthe
body.
Secondarytumours.
Metastasisisnow
underway,astumour
cellsfromtheoriginal
cancergrowthtravel
throughoutthebody.
Mostofthesecellswill
diesoonafterentering
thebloodorlymph
circulation.

11.Metastasis

Toformasecondarytumour,atumourcellneedstoleavethe
vesselsystemandinvadetissue.Thecellmustattachitselftoa
vessel'swall.Oncethisisdone,itcanworkitswaythrough
thevesselandenterthetissue.
Althoughperhapslessthanonein10,000tumourcellswill
survivelongenoughtoestablishanewtumoursite,afew
survivorscanescapeandinitiatenewcoloniesofthecancer.

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FactsonCancer
2006,approximately564,830Americans
diedofcancer
1.4millionnewcasesdiagnosed
1/3ofcancersarerelatedtopoornutrition,
physicalinactivity,andobesity
preventablecauses

WhatIsCancer?
Canceralargegroupofdiseasescharacterizedbythe
uncontrolledgrowthandspreadofabnormalcells
Neoplasmnewgrowthoftissuethatservesno
physiologicalfunction
Tumorclumpingofneoplasmiccells
Malignantcancerous
Benignnoncancerous
Biopsymicroscopicexaminationofcelldevelopment

WhatIsCancer?cont.
Metastasismalignanttumorsthatarenot
enclosedinaprotectivecapsulehavethe
abilitytospreadtootherorgans
MutantcellsdisruptionofRNAandDNA
withinnormalcellsmayproducecellsthat
differinform,qualityandfunctionfromthe
normalcell

DisparitiesInCancerRates
AfricanAmericanshavethehighestdeathratesfrom
cancer
Thegapincancermortalityratesisgreaternowthanin
1975
AfricanAmericanswithcertaincancersaremorelikely
togounstagedandlesslikelytoreceivetreatment
Menfrompoorercensuscountieshavea22%higher
deathratefromprostatecancerthantheiraffluent
countycomparisongroups

FactorsBelievedtoContributeto
GlobalCausesofCancer

Figure 16.2

RisksForCancer
Lifetimerisktheprobabilitythatanindividual,overthe
courseofalifetime,willdevelopcancerordiefromit
Relativeriskmeasureofthestrengthoftherelationship
betweenriskfactorsandaparticularcancer
Smoking30%ofallcancerdeaths,87%oflungcancer
deaths
Obesity50%higherriskforbreastcancerin
postmenopausalwomen,40%higherriskincoloncancer
formen

Table 16.2

BiologicalFactors
Somecancerssuchasbreast,stomach,colon,
prostate,uterus,ovariesandlungappeartorunin
families
Hodgkinsdiseaseandcertainleukemia'sshow
similarpatterns
UniversityofUtahresearchsuggeststhatagenefor
breastcancerexists
Arareformofeyecancerappearstobetransmitted
geneticallyfrommothertochild

ReproductiveAndHormonal
RisksForCancer
Pregnancyandoralcontraceptivesincrease
awomanschancesofbreastcancer
Latemenarche,earlymenopause,earlyfirst
childbirth,havingmanychildrenhavebeen
showntoreduceriskofbreastcancer

OccupationalAndEnvironmental
Factors

Asbestos
Nickel
Chromate
Benzene
Arsenic
Radioactivesubstances
Cooltars
Herbicides/pesticides

SocialAndPsychologicalFactors
Stresshasbeenimplicatedinincreased
susceptibilitytoseveraltypesofcancers
Sleepdisturbances,diet,oracombination
offactorsmayweakenthebodysimmune
system

ChemicalsInFoods
Sodiumnitratewheningestedformsa
potentialcarcinogen,nitrosamine
Sodiumnitrateisstillusedbecauseitis
effectiveinpreventingbotulism
Pesticideandherbicideresidues

ViralFactors
Herpesrelatedvirusesmaybeinvolvedinthe
developmentofleukemia,Hodgkinsdisease,cervical
cancer,andBurkittslymphoma
EpsteinBarrvirus,associatedwithmononucleosis,
maycontributetocancer
Humanpapillomavirus(HPV),virusthatcausesgenital
warts,hasbeenlinkedtocervicalcancer
Helicobacterpyloricausesulcerswhichareamajor
factorinthedevelopmentofstomachcancer

MedicalFactors
Somemedicaltreatmentsactuallyincreasea
personsriskforcancer
Diethylstilbestrol(DES)used1940to1960to
controlbleedingduringpregnancy,thedaughtersof
mothersthatusedDESwerefoundtohavean
increasedriskforcancersofthereproductiveorgans
Estrogensupplementation
Chemotherapyusedtotreatoneformofcancermay
increaseriskforanothertypeofcancer

TypesOfCancers
Classificationofcancers

Carcinomas
Sarcomas
Lymphomas
Leukemias

ColonAndRectalCancers
Thirdmostcommoncancerinmenandwomenwithover
148,610newcasesdiagnosedin2006
Riskfactors:over50yearsold,obese,familyhistoryof
colonorrectumcancerorpolyps,dietshighinfats,lowin
fiber,smoking,highalcoholconsumption,lackofexercise
90%ofcolorectalcancersarepreventable
Treatment:radiation,surgery,andpossiblechemotherapy
Prevention:regularexercise,adietheavyinfruitsand
plantoriginfoods,ahealthweight,andmoderationin
alcoholconsumption

ProstateCancer

MostcommoncancerinAmericanmen,excludingskincancer
In2006,234,460newcasesdiagnosed
1in3menwillbediagnosedintheirlifetime
Prostateisamuscular,walnutsizedglandthesurroundspartof
theurethra.Itsprimaryfunctionistoproduceseminalfluid.
Symptoms:nonspecific,weakorinterruptedurineflow,
difficultystartingorstoppingurination
Riskfactors:age,race,nationality,familyhistory,diet,
lifestyle,andvasectomy
Prevention:diethighinlycopenes,vitaminE

SkinCancer
Longtermeffectsofsunexposurecanresultinskincancer
Malignantmelanoma,deadliestformofskincancer
Sungiveoff3typesofharmfulrays:
UVA
UVB
UVC

Prevention:limitexposuretoharmfulUVrays,drinkmore
fluidsthanusual,applycoolcompressestoskin,moisturize
skin

SkinCancercont.
WhattolookforTheABCDrule
Asymmetryhalfofmoledoesnotlooklike
theotherhalf
Borderirregularitytheedgesareuneven
Colorpigmentationisnotuniform
Diametergreaterthan6mm

TypesofUltravioletRays

Figure 16.7

TesticularCancer
Affectsnearly8,250youngmenin2006
Menbetweentheages1535areatthe
greatestrisk
Importanttopracticeregulartesticularself
exams
LanceArmstrongFoundationLiveStrong
campaigntoraiseawareness

OvarianCancer
Fifthleadingcauseofcancerdeathforwomen,20,180
newcasesdiagnosedreportedin2006
Mostcommonsymptomisenlargementoftheabdomen
Riskfactorsinclude:familyhistory,age,childbearing,
cancerhistory,fertilitydrugs,talcuseingenitalarea,
geneticpredisposition
Prevention:diethighinvegetablesandlowinfat,
exercise,sleep,stressmanagement,andweightcontrol

CervicalandEndometrial
(Uterine)Cancer

9,710newcasesofcervicalcancer,41,200cases
ofendometrialcancerinU.S.in2006
Paptestcellsaretakenfromthecervicalregion
Riskfactors:
Cervicalcancer:earlyageatfirstintercourse,multiple
sexpartners,cigarettesmoking,andcertainSTIs
Endometrialcancer:age,endometrialhyperplasia,
overweight,diabetes,andhighbloodpressure

OtherCancers
Pancreaticcancersilent4%5year
survivalrate
Leukemiacancerofbloodformingtissues

DetectingCancer
Theearlierthediagnosisthebetterthe
prospectforsurvival
Magneticresonanceimaging(MRI)
Computerizedaxialtomographyscan(CAT
scan)
Prostaticultrasound
Regularselfexams,andcheckups

NewHopeInCancerTreatments
Removelesssurroundingtissueduringsurgery
Combinesurgerywithradiationor
chemotherapy
Immunotherapy
Cancerfightingvaccines
Genetherapy
Stemcellresearch