Terms etc Cytochemistry

g ranules
1 Myeloperoxidase Stains inprimarygranulesandAiertist
primary
PeroxidaseFound

AML Mpot ALL MPOG

Proto
oncogene 8 that Futation Oncogene DarkBrown Blackgranules Shouldbe it
doneonfreshspecimensince deteriorates
2 Sudan Black Stainslipids on Granulocytes Monocytes
Oncogene A dominantdisorder
Onlyonemutatedcopy AML Mpot fMaturityFstaining ALL Mpoc
isrequiredto contribute to Levkenogenesis DarkPurpleBlackgranules Canbedoneonstoredspecimen airdriedBMsmear
cells
other also
Specificesterase w L
cel's may
Causes constitutive
regulatedandoverexpression
dy 3 Esterases Nonspecificesterase showstaining
NASDA NaphtholAsDChloroacetate ANBE GifEsterase ANBE EFFIE's't
granulesBoth MonocyticcellsCt Granulocyte

SuppresorGene
Detects damaged
DNA umor
gtintiocyticegetteftp.rcyafccepjimgy
ANAEonly Megakaryocytic lineageCt
DNArepairor Apoptosis Brightredgranules in cytoplasm Inhibition
bySodiumfluoride Nat
Leukemogenicwheninactivated ordeleted AM w minimaldiff Mo
A recessivedisorder both

to
alleles

Inability preventcells w damagedDNA

fromprogressingthroughthecellcycle
so
be
must Moe
Éim
SBBC DAG
NAS

i shiithhhimdarnels
Aight mBY it's
AMol M5 80 blastsare feta c
Is
Eheight

Loss offunction mutation AML w o Maturation M1 p Guglielmosyndrome Mb Pure

ErythremicMyelosis
Mpo t SBBH NASDA t Leukem
Erythroid

AML w Maturation Mz
wedon'tcareaboutCytochem tC8 21 RUNX1 RUNX1T1 willsuffice
Acute Promyelocytic Leukemia M3 Most buthasbest
aggressiveleukemia p rognosis iftreated
acid arit a
ATRACA
transRetinoic
wedon'tcareaboutCytochem t 1517 PML RARAwilldifferentiation
suffice
Blockspromyelocyte

4 Periodic Acid Schaff Stains Glycogen GlycoproteinsMucoprotein AMWCar

C AML ALL 13 Ct AML MSMGMT ALLL1 L2
leukemia
Erythro DiGuglielmoSyndrome
5 Acid Phosphatase Stains ACPpresentin Lymphocytes ALLCt
 Leukemias
CML AML ALL CLL
Acquired disease ofHsc
ntro characterized
by
Leukocytess immatureleukocytes
WBC
Batophilight

Splenomegaly Hallmark
c ofCML
Philadelphia chromosome
t 922 ABLBCRTranslocatio

Age 40 60yo Oldage

Patho

ii g
Chromosomes

genesis

Is
ABLBCRfusiongene
Forms an abnormalTyrosinekinase
whichcauses
Uncontrolled Mitosis
Factors
evenwithout
mayouth

AgainAgain AProtooncogene
ABLgene normalwhen in 9 Chromosome

It istranslocatedto 22
chromosome

It fuseswithBCR Breakpointclustergene
ABL
Forms
Berhybridgene Philadelphiachromosome
Thishybrid ispotentandcausesabnormal
signaltransductioneven wo Growth
factors
Uncontrolled Mitosis 6 CM
 Leukemias
CML AML ALL CLL
Taken
oraldaily
Treatment Imanifib till death
Tyrosinekinaseinhibitor

Classi Phase of CMLCAB

Chronic Phase AcceleratedPhaser Blastphase
Ication 10Blastsin m 10.19 blastsin s
Blastasinmyelokast
20Blastsinm
20 Basophilsinsideextra
medullary blast
ci
Eia.int ABl thrombocytopenia s
Leukocytes
splenomegaly
proliferation

areunrelatedtotreatment
mat

SC Mutation
linical
TWBCT
eatures RBI
Mattes
t thrombocytopenia butimmature
Amenia Tete Yeding Infections

PalilethargyJiji
4 Hypermetabolism
Because
ofuncontrolledmitosis thecancercells
areutilizingalltheAtpfromwhatweeat
Weightlosslassitude anorexia silents

D 5 Splenomegaly is MASSIVE
normAnemia
pair 1 BloodPicture Ianb s normalatakin
zoo.com
ab are tare
immature mature
Garden
phases
PartyAppearance
to
ttrercenularity and.IE
try eunseie ertmatewBc.rac.elatelet

2 BoneMarrowExam
level
Molecular chromosomestcaizaazcr.am

99h05is 3 Cytogenetics EM Ye by
chromosomes length
Arrange

Xx a icing
4 Cytochemistry
Commonquestion atratielphisingate

scorecar Leukemoid Ranus cmc i

is
I C Eetscore
5
successful
therapy
to
OtherintjjestigationmeruricemiaDue
eurine
c atabolism

maycausenot
 Leukemias
CML AML ALL CLL
 Leukemias
CML AML ALL CLL