chronic lymphocytic leukemia report
TRANSCRIPT
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[CHRONIC LYMPHOCYTIC LEUKEMIA, BLOOD]. B-cell chronicl!"hoc#ic le$%e!i& i' #he !o'# co!!on chronic le$%e!i& in
&($l#' in )e'#ern co$n#rie'. Mo'# c&'e' in*ol*e +loo( &n( +one!&rro i#h or i#ho$# in*ol*e!en# o l!"h no(e', '"leen, li*er,&n( o#her or&n'. The neo"l&'#ic l!"hoc#e' &re '!&ll +$# 'lih#ll&rer #h&n nor!&l '!&ll l!"hoc#e' &n( 'ho 'c&n# c#o"l&'! &n(ro$n( #o 'lih#l irre$l&r n$clei con#&inin cl$!"e( chro!in/#hree &rro'0. N$cleoli &re '!&ll #o in(i'#inc#. A ch&r&c#eri'#ic!or"holoic e$re i' #he "re'ence o 1'!$(e2 or 1+&'%e#2 cell'/#o &rrohe&('0 hich &re e''en#i&ll neo"l&'#ic cell' #h o#1'!$(e(2 ($rin 'li(e "re"&rion +ec&$'e o #he r&ile n$re o#he'e cell'. Co!"&re #he cell 'i3e o CLL cell' i#h & 'inle l&rer&n$l&r l!"hoc#e /c$r*e( &rro0.
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[CHRONIC LYMPHOCYTIC LEUKEMIA, BLOOD]. Thi' '!e&r 'ho' #he"re'ence o o$r '!&ll neo"l&'#ic l!"hoc#e' &n( #hree '!$(e
cell' /&rrohe&('0. The (i&no'i' on +loo( '!e&r i' '$'"ec#e( +&'e(on ch&r&c#eri'#ic !or"holo &n( con4r!e( $'in 5o c#o!e#ric&n&l'i' o +loo( &n(6or +one !&rro hich $'$&ll 'ho' &ch&r&c#eri'#ic i!!$no"heno#"e. The neo"l&'#ic cell' ener&ll'ho e7"re''ion o CD89, (i! CD:;, !onoclon&l i!!$nolo+$lin%&""& or l&!+(& lih# ch&in, &n( co-e7"re''ion o CD< &n( CD:=.
The cell' (o no# e7"re'' CD8; or +cl->. The (i! e7"re''ion o CD:;&n( '$r&ce i!!$nolo+$lin' i' *er co!!on.
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[CHRONIC LYMPHOCYTIC LEUKEMIA, BLOOD]. Co!"&re #he 'i3e o#hi' neo"l&'#ic l!"hoc#e i#h re( +loo( cell'. A CLL cell i' onl
'lih#l l&rer #h&n & re( +loo( cell &n( 'ho' cl$!"e( chro!in,'o!e#i!e' li%ene( #o & 1'occer +&ll.2 Hoe*er, "ic&l CLL cell'!& no# 'ho #hi' chro!in cl$!"in &n( (i&no'i' c&n onl +e!&(e $'in i!!$no"heno#"in.
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[CHRONIC LYMPHOCYTIC LEUKEMIA, BLOOD]. A#"ic&l !or"holo!& !&nie'# + irre$l&r n$clei 'hoin cle#' &n( (ee" roo*e'
'i!il&r #o cell' o ollicle cen#er cell l!"ho!& &n( !&n#le cellle$%e!i&. The CLL cell' i#h n$cle&r cle#', in(en#ion', &n( (ee"roo*e' &re #er!e( 1Rie(er cell'.2 Di&no'i' !$'# +e e'#&+li'he($'in i!!$no"heno#"in 'hoin e7"re''ion o CD:;, CD89, CD
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[CHRONIC LYMPHOCYTIC LEUKEMIA, BLOOD]. No#e #hree 1Rie(er2CLL cell' i#h n$cle&r in(en#ion' &n( no#che'. The'e cell' &re
l&rer #h&n #"ic&l CLL cell'. A+o$# ?;@ o &ll CLL c&'e' 'ho(e#ec#&+le chro!o'o!&l &+nor!&li#ie' !o'# co!!onl (ele#ion o8=8.= &n( le'' co!!onl #ri'o! 8:, &n( (ele#ion' o 88::-:=,8"8=, &n( >:8 reion'. A+o$# ;-
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Histologic patterns of trephine biopsies from bone marrow reveal patterns that
can be useful in assessing patient risk.
Nodular patterns are made up of mature lymphocytes. The nodules arelarger-than-normal lymphoid follicles and lack clear centers. There is no
interstitial infiltration. Fat cells are preserved. Nodular patterns are
associated with low-risk disease.
Interstitial patterns show some degree of replacement of normal
hematopoietic tissue by mature lymphocytes, but fat cells and bone
marrow structure are preserved. Interstitial patterns are also associated
with low-risk disease.
iffuse patterns show diffuse lymphoid infiltration with massive
replacement of normal hematopoietic tissue as well as replacement of
fat cells. iffuse patterns are associated with high-risk disease.
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"ntil recently, !-#$$ cells were differentiated from other !-cell
lymphoproliferative diseases by immunophenotyping with % cell membrane
protein markers& 'mIg ('urface )embrane-bound Immunoglobulin*, #% (T+antigen*, # (The Fc eceptor for Ig/*, F)#0 (a specific conformation of
#1, possibly multimeric and possibly associated with membrane
cholesterol*, and # (gp+%2 a !-cell adhesion molecule*.
#03b (a signal transduction molecule that associates with 'mIg* is now
preferred to #,
a change that has significantly increased the ability to discriminate between !-
#$$ and other
!-cell disorders.
4n immunophenotyping scoring system was developed that gives a value of +
or 1 according
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!ecause of the limitations of the ai and !inet systems in predicting the progression of
#$$, other prognostic criteria are being considered2 for instance, advanced disease
stage, male gender, #5 e6pression 718, and atypical morphology predict relatively
poor outcomes in #$$. 4dditionally, karyotyping and molecular biology techni9ues reveal
that the behavior of certain genetic markers in #$$ may offer insights into the molecular
mechanism of the disease and predict treatment outcome.
In a study of 1% patients with #$$, :38 were found to have an abnormal karyotype.
;enetic abnormalities included&structural abnormality of chromosome +9+