chronic lymphocytic leukemia report

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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+