13  Complete Record


  BCL10 is not the gene inactivated by mutation in the 1p22 deletion
region in mantle 

cell lymphoma.

  Bullinger L; Leupolt E; Schaffner C; Mertens D; Bentz M; Lichter P;
Dohner H; 

Stilgenbauer S

  Abteilung Innere Medizin III, University of Ulm, Germany.

  Leukemia  (ENGLAND)  Aug 2000  14 (8) p1490-2  ISSN: 0887-6924

  Language: ENGLISH

  Document Type:   JOURNAL ARTICLE       

  Journal Announcement: 0010


  The BCL10 gene has recently been cloned from the 1p22 breakpoint of

translocation t(1 ;14)(p22;q32) observed in mucosa-associated lymphoid
tissue (MALT) 

lymphoma.  BCL10 was shown to be a proapoptotic-signaling gene encoding
a protein 

that contains an amino-terminal caspase recruitment domain (CARD). 
Mutations within 

the BCL10 coding region resulting in truncated BCL10 proteins with loss
of their 

proapoptotic function and preservation of their NF-kappaB activating
function were 

detected in MALT lymphoma.  Based on these findings it was proposed that
BCL10 might 

have tumor suppressor function.  Deletions involving 1p22 are commonly
observed in 

mantle cell lymphoma (MCL).  To investigate its role in MCL we have
analyzed a series 

of 15 MCL for deletion and mutation of BCL10.  Monoallelic 1p22
deletions were 

detected by fluorescence in situ hybridization in five of the 15 cases
and were shown 

to affect BCL10 in all cases.  BCL10 was screened for mutations by DNA
sequencing of 

RT-PCR amplified transcripts.  In none of the 15 MCL cases studied were

found in the BCL10 coding region.  A previously reported polymorphism
exhibiting a 

silent 24C > G substitution was found in eight MCL cases and in four
healthy probands.  

A missense mutation 13G >T resulting in a substitution of a serine by an
alanine was 

seen in one of the controls.  Our results strongly suggest that BCL10 is
not the 

candidate tumor suppressor gene inactivated by deletion or mutation in
band 1p22 in 


  Tags: Human; Support, Non-U.S. Gov't

  Descriptors: *Chromosome Deletion; *Chromosomes, Human, Pair 1; *Gene

*Lymphoma, Mantle-Cell--Genetics--GE; *Mutation; *Neoplasm

DNA Primers; Genes, Suppressor, Tumor

  CAS Registry No.: 0   (Bcl10 protein); 0   (DNA Primers); 0  
(Neoplasm Proteins)

  16  Complete Record


  Lymphocyte predominance Hodgkin's disease: the use of bcl-6 and CD57
in diagnosis 

and differential diagnosis.

  Kraus MD; Haley J

  The Lauren V. Ackerman Laboratory of Pathology, Washington University
School of 

Medicine, St. Louis, Missouri 63110, USA. kraus@path.wustl.edu

  American journal of surgical pathology  (UNITED STATES)  Aug 2000  24
(8) p1068-78

  ISSN: 0147-5185

  Language: ENGLISH

  Document Type:   JOURNAL ARTICLE       

  Journal Announcement: 0010


  Distinction of lymphocyte predominance Hodgkin's disease (LPHD) from
other forms of 

lymphoma often requires immunohistochemistry (IHC).  Most previously

recommended panels include markers to define the large neoplastic cells
(for example, 

CD20, J chain, CD45) as well as the non-neoplastic background cells
(CD21, CD45RO, 

CD57, TiA 1).  In the present study we examine the practical use of a
double IHC 

method designed to look simultaneously at two germinal center specific
cell types: 

bcl6+ cells and {bc16+, CD57+} co-positive cells.  All 10 nodular LPHD
had bcl6+ 

large cells and numerous CD57+ small background cells, including
{bcl6+CD57+} cells 

in rosettes.  One case of LPHD with large cell transformation contained
numerous bcl6

+ large cells both singly (in areas of typical LPHD) and in sheets (in
foci of large 

cell transformation), many CD57+ small cells but few {bcl6+CD57+}
co-positive cells 

and no rosettes.  In none of the five cases of florid progressive
transformation of 

germinal centers were true rosettes seen, although all contained
variable numbers of 

bcl6+ large cells and CD57+ cells.  Lymphocyte-rich classic Hodgkin's
disease LRCHD 

cases were notable for bcl6 reactivity in Reed-Sternberg cells in all
cases, numerous 

background small bcl6+ lymphocytes, and rare CD57+ cells.  Two
phenotypic profiles 

were associated with the 10 cases of T cell-rich B cell large cell
lymphoma (TCRBCL).  

In the first, group "A," six of six cases had bc16- large cells and few
CD57+ small 

cells, and none had significant numbers of {bcl6+, CD57+} co-positive
cells.  In the 

second, group "B," four of four cases had bcl6+ large cells with
numerous CD57+ and {

bcl6+, CD57+} co-positive cells.  These findings not only show that LPHD
can be 

distinguished from its morphologic mimics through identification of
specific germinal 

center cell types, but also identifies a second group of TCRBCL (group
"B") whose 

phenotype suggests it might be an architectural variant of nodular LPHD.

  Tags: Human

  Descriptors: *Antigens, CD57--Analysis--AN;
*B-Lymphocytes--Pathology--PA; *DNA-

Binding Proteins--Analysis--AN; *Hodgkin Disease--Diagnosis--DI;
*Hodgkin Disease--

Pathology--PA; *Proto-Oncogene Proteins--Analysis--AN;

*Transcription Factors--Analysis--AN; *Tumor Markers,

Diagnosis, Differential; Eosine Yellowish-(YS); Hematoxylin; Hodgkin

Immunology--IM; Immunohistochemistry; Immunophenotyping;

  CAS Registry No.: 0   (proto-oncogene protein bcl-6); 0   (Antigens,
CD57); 0   

(DNA-Binding Proteins); 0   (Proto-Oncogene Proteins); 0  
(Transcription Factors); 0 

  (Tumor Markers, Biological); 17372-87-1   (Eosine Yellowish-(YS));


  21  Complete Record


  BCL10 gene mutation in lymphoma.

  Du MQ; Peng H; Liu H; Hamoudi RA; Diss TC; Willis TG; Ye H; Dogan A;
Wotherspoon AC; 

Dyer MJ; Isaacson PG

  Department of Histopathology, Royal Free and University College London

School, London, United Kingdom. m.du@ucl.ac.uk

  Blood  (UNITED STATES)  Jun 15 2000  95 (12) p3885-90  ISSN: 0006-4971

  Language: ENGLISH

  Document Type:   JOURNAL ARTICLE       

  Journal Announcement: 0010


  BCL10 is directly involved in t(1;14)(p22;q32) of mucosa-associated
lymphoid tissue 

(MALT) lymphoma.  Wild-type BCL10 promoted apoptosis and suppressed

transformation in vitro, whereas truncated mutants lost the
pro-apoptotic activity 

and exhibited gain of function enhancement of transformation.  We
studied 220 

lymphomas for genomic BCL10 mutation by polymerase chain

conformational polymorphism and DNA sequencing.  Nineteen mutations were
found in 13 

lymphoma specimens, as follows: 8 of 120 (6.7%) mucosa-associated
lymphoid tissue 

(MALT) lymphomas, 4 of 42 (9.5%) follicular lymphomas, and 1 of 23
(4.3%) diffuse 

large B-cell lymphomas.  No mutations were found in 14 mantle cell
lymphomas or 21 T-

cell lymphomas.  High-grade MALT lymphoma tended to show a slightly
higher mutation 

frequency (2 of 25, 8%) than low-grade MALT tumor (6 of 95, 6.3%). 
Among low-grade 

gastric MALT lymphoma, mutations were found in 3 of 11 tumors that did
not respond to 

Helicobacter pylori eradication therapy, but none were found in 22
tumors that 

regressed completely after H pylori eradication.  All 14 potentially

mutations were distributed in the carboxyl terminal domain of BCL10. 

accounted for 10 of these mutations; 10 of 14 mutations caused truncated
forms of 

BCL10.  Western blot analysis of a mutant case confirmed the presence of

BCL10 products of anticipated size.  Our results suggest that BCL10
mutation may play 

a pathogenic role in B-cell lymphoma development, particularly in
aggressive and 

antibiotic unresponsive MALT lymphomas, and may further implicate the

importance of the carboxyl terminal of the molecule.  (Blood. 

  Tags: Female; Human; Male; Support, Non-U.S. Gov't

  Descriptors: *Lymphoma, Mucosa-Associated Lymphoid
Tissue--Genetics--GE; *Mutation; 

*Neoplasm Proteins--Genetics--GE; Aged; Base Sequence; Exons; Lymphoma,

Genetics--GE; Lymphoma, B-Cell--Pathology--PA; Lymphoma,
Mucosa-Associated Lymphoid 

Tissue--Pathology--PA; Lymphoma, T-Cell--Genetics--GE; Lymphoma,

PA; Middle Age; Polymerase Chain Reaction; Polymorphism, Single-Stranded

Conformational; Retrospective Studies; Sequence Deletion

  CAS Registry No.: 0   (Bcl10 protein); 0   (Neoplasm Proteins)

  22  Complete Record


  Molecular insights into the immunopathogenesis of follicular lymphoma.

  Stamatopoulos K; Kosmas C; Belessi C; Stavroyianni N; Kyriazopoulos P;
Papadaki T

  First Department of Medicine, Athens University School of Medicine and

General Hospital, Athens, Greece.

  Immunology today  (ENGLAND)  Jun 2000  21 (6) p298-305  ISSN:

  Language: ENGLISH


  Journal Announcement: 0010


  Follicular lymphoma is caused by the transformation of a
germinal-center-derived B 

cell with a t(14;18) chromosomal translocation.  The distribution of

mutations within immunoglobulin genes indicates that follicular-lymphoma
cells can 

interact with antigen.  In addition, nonimmunoglobulin genes such as
BCL6 seem to 

undergo somatic hypermutation.  Here, Kostas Stamatopoulos and
colleagues relate the 

molecular data about immunoglobulin genes and the protooncogenes BCL2
and BCL6 to the 

pathogenesis and evolution of follicular lymphoma.  (46 References)

  Tags: Human; Support, Non-U.S. Gov't

  Descriptors: *Genes, Immunoglobulin; *Lymphoma,
Follicular--Etiology--ET; B-

Lymphocyte Subsets--Immunology--IM; B-Lymphocyte Subsets--Pathology--PA;

Human, Pair 14--Genetics--GE; Chromosomes, Human, Pair 18--Genetics--GE;

Deletion; DNA Nucleotidyltransferases--Metabolism--ME; Gene
Rearrangement, B-

Lymphocyte; Germinal Center--Pathology--PA; Hematopoiesis--Genetics--GE;

Disease--Pathology--PA; Immunoglobulin Variable Region--Genetics--GE; 

Immunoglobulins, kappa-Chain--Genetics--GE; Immunoglobulins,

GE; Lymphoma, Follicular--Genetics--GE; Lymphoma,

Lymphoma, Follicular--Pathology--PA; Models, Immunological; Mutation;

Proteins--Genetics--GE; Neoplasm Proteins--Immunology--IM;
Reed-Sternberg Cells--

Pathology--PA; Translocation (Genetics); Tumor Stem
Cells--Immunology--IM; Tumor Stem 


  CAS Registry No.: 0   (Immunoglobulin Variable Region); 0  
(Immunoglobulins, kappa-

Chain); 0   (Immunoglobulins, Heavy-Chain); 0   (Neoplasm Proteins)

  Enzyme No.: EC 2.7.7.-   (DNA Nucleotidyltransferases); EC 2.7.7.-  


  35  Complete Record


  Lack of BCL10 mutations in Hodgkin's disease-derived cell lines.

  Re D; Benenson E; Wolf J; Diehl V; Staratschek-Jox A

  Department of Internal Medicine I, University of Cologne,

9, 50924 Cologne, Germany. daniel.re@uni-koeln.de

  British journal of haematology  (ENGLAND)  May 2000  109 (2) p420-2 
ISSN: 0007-


  Language: ENGLISH

  Document Type:   JOURNAL ARTICLE       

  Journal Announcement: 0009


  The pathogenetic events leading to the malignant transformation of

Sternberg cells are unknown.  As Hodgkin-Reed-Sternberg cells are
resistant to CD95-

mediated apoptosis and chromosomal aberrations involving the 1p22 region

the proapoptotic BCL10 gene represent a recurrent event in Hodgkin's

cell lines, analysis of the BCL10 gene and its transcripts was
performed.  As 

transcription of wild-type BCL10 was detected in all Hodgkin's
disease-derived cell 

lines analysed, alterations of the coding sequence of the BCL10 gene are
unlikely to 

contribute to the malignant transformation of the Hodgkin-Reed-Sternberg

  Tags: Human; Support, Non-U.S. Gov't

  Descriptors: *Hodgkin Disease--Genetics--GE; *Neoplasm

Alleles; Cell Line, Transformed; Chromosome Aberrations; Chromosomes,
Human, Pair 1; 

Mutation; Polymerase Chain Reaction--Methods--MT; Reverse Transcriptase

Chain Reaction--Methods--MT; Sequence Analysis, DNA

  CAS Registry No.: 0   (Bcl10 protein); 0   (Neoplasm Proteins)

  40  Complete Record


  Clinical significance of the t(14;18) and BCL2 overexpression in
follicular large 

cell lymphoma.

  Weisenburger DD; Gascoyne RD; Bierman PJ; Shenkier T; Horsman DE;
Lynch JC; Chan WC; 

Greiner TC; Connors JM; Vose JM; Armitage JO; Sanger WG

  Department of Pathology and Microbiology, University of Nebraska
Medical Center, 

Omaha 68198-3135, USA.

  Leukemia & lymphoma  (SWITZERLAND)  Feb 2000  36 (5-6) p513-23  ISSN:

  Contract/Grant No.: CA36727--CA--NCI

  Language: ENGLISH

  Document Type:   JOURNAL ARTICLE       

  Journal Announcement: 0008


  Follicular large cell lymphoma (FLCL) is an aggressive disease that
responds to 

anthracycline-containing chemotherapy much like diffuse large B-cell
lymphoma (DLBCL).  

Since the t(14;18) and/or bcl2 protein expression are less common in
FLCL than in its 

low-grade counterparts, we sought to determine whether these features
were predictive 

of survival as in DLBCL.  We studied 50 patients with FLCL who were
treated with 

curative intent.  The t(14;18) was found by cytogenetic analysis in 56%
of the 

patients and bcl2 protein was expressed by the tumor cells in 73%, but
neither was 

predictive of survival.  However, abnormalities of chromosome 17p and
the presence of 

trisomy 21 were adverse predictors of survival, as were a number of
clinical features.  

We conclude that neither the absence of the t(14;18) nor the lack of
bcl2 expression 

explain the good response of a subset of patients with FLCL to curative

  Tags: Female; Human; Male; Support, U.S. Gov't, P.H.S.

  Descriptors: *Chromosomes, Human, Pair 14; *Chromosomes, Human, Pair
18; *Genes, 

bcl-2; *Lymphoma, Large-Cell, Follicular--Genetics--GE; *Translocation

*Tumor Markers, Biological; Aged; Genetic Markers; Lymphoma, Large-Cell,

Pathology--PA; Lymphoma, Large-Cell, Follicular--Physiopathology--PP;
Middle Age; 

Prognosis; Survival Analysis

  CAS Registry No.: 0   (Genetic Markers); 0   (Tumor Markers,