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PubMed2002

Clinical impact of the differentiation profile assessed by immunophenotyping in patients with diffuse large B-cell lymphoma.

To analyze the relationship between immunophenotyping profile and main clinicopathological features and outcome in diffuse large B-cell lymphoma (DLBCL), we studied 128 patients (59 men, 69 women; median age 65 years) consecutively diagnosed with de novo DLBCL in a single institution. Cells from each patient were immunostained with CD20, CD79a, CD5, CD10, bcl-6, MUM1, CD138, bcl-2, p53, p27, and Ki-67 antibodies. Four immunophenotyping profiles were distinguished according to the pattern of differentiation: germinal center-CD10(+) (GC-CD10(+); CD10(+)/Bcl-6(+)/MUM1(-)/CD138(-)), germinal center-CD10(-) (GC-CD10(-); CD10(-)/Bcl-6(+)/ MUM1(-)/CD138(-)), post-germinal center (pGC; CD10(-)/bcl-6(+/-)/ MUM1(+)/CD138(-)), and plasmablastic (CD10(-)/bcl-6(-)/MUM1(+)/CD138(+)). Rearrangement of bcl-2 was studied by polymerase chain reaction (PCR) in 57 patients. Single-antigen expression was as follows: CD5, 2%; CD10, 21%; bcl-6, 72%; MUM1, 54%; CD138, 2%; bcl-2, 59%; p53, 28%; p27, 40%. Distribution according to differentiation profiles was as follows: GC-CD10(+), 24 patients, GC-CD10-, 30 patients; pGC, 60 patients; plasmablastic, 2 patients; other patterns, 12 patients. The pGC profile was associated with primary nodal presentation and immunoblastic morphology, whereas GC-CD10(+) tumors showed disseminated disease, centroblastic morphology, bcl-2 rearrangement, and lower Ki-67 proliferative index. GC-CD10(-) patients more often presented with primary extranodal origin, early stage, normal lactic acid dehydrogenase (LDH) levels, and low or low/intermediate International Prognostic Index (IPI) scores than the others. However, no significant difference was found in terms of response or overall survival (OS) according to these profiles. Expression of bcl-2 was associated with advanced stage, high or high-intermediate IPI, and poor OS. Expression of bcl-2 maintained predictive value in multivariate analysis, with stage and LDH. In conclusion, differentiation profile was associated with particular clinicopathological features but was not essential to predicting outcome in DLBCL patients.

Adult↗
PubMed2000

Immunophenotypic and genotypic markers of follicular center cell neoplasia in diffuse large B-cell lymphomas.

Diffuse large B-cell lymphomas (DLBCL) are a biologically and clinically heterogeneous entity. Although some DLBCL represent transformation of follicular lymphomas (FL), the proportion that is of follicular center cell (FCC) origin remains uncertain. Immunophenotypic and genotypic markers used to suggest a FCC origin for a lymphoma (bcl-6 and CD10 expression, lack of CD138 expression, bcl-2 rearrangements [R]) or to subdivide DLBCL (bcl-2 expression, bcl-6 R) were therefore investigated in 22 FL and 44 DLBCL using paraffin section immunostains and Southern blot/polymerase chain reaction analysis. All FL tested were bcl-6+ (19) and CD138- (22) with 16/19 also bcl-2 and CD10+ (classic phenotype), one bcl2+, CD10- (grade III) and two bcl2-, CD10+ (grade II or III). Bcl-2R was identified in 4/5 FL-GrI, 3/6 FL-GrII, and 1/3 FL-GrIII. Bcl-6R was found in 0/5, 2/4, and 0/3 FL, respectively. All but 3/41 DLBCL were bcl-6+ with 17/37 also bcl-2+ and CD10+. Three of these cases were also CD138+. Twelve bcl-6+ cases were bcl-2+, CD10-, six bcl-2-, CD10+, and two bcl-2-, CD10-. The three bcl-6- cases were bcl-2+, CD138- and two were CD10+. Bcl-2R was identified in 5/27 DLBCL with 4/5 bcl-2+, 3/4 tested CD10+ and 4/4 bcl-6+. Bcl-6R was identified in 7/26 including three with a classic FL phenotype. The vast majority of DLBCL in this study have an immunophenotype that supports a FCC origin. Although the proportion of DLBCL that co-expressed bcl-6, CD10 and bcl-2 was lower than for the FL, absence of bcl-2 or CD10 may be associated with higher grade FL It is also possible that bcl-6 expression is not completely specific for a FCC origin. Only a minority of cases suggested postfollicular differentiation. Only a minority of DLBCL show bcl-2R, suggesting that many have a different molecular pathogenesis than most low-grade FL. Bcl-6R did not exclude a FCC origin.

B-Lymphocytes↗
PubMed1990

Maturation-dependent adhesion of human B cell precursors to the bone marrow microenvironment.

Murine B cell precursors can be induced to proliferate in culture if allowed to bind to bone marrow derived adherent cells prepared under specific conditions. We studied the binding of human B cell precursor subpopulations to various in vitro microenvironments to determine which conditions may potentially be suitable models for human B precursor differentiation. Using the markers CD10, CD34, and CD20, B lineage populations of increasing maturation were quantitated: CD10+/CD34+, CD10+/CD20-, CD10+/CD20+, and CD10-/CD20+ cells in marrow, and CD10-/CD20+ mature B cells in peripheral blood. The adhesion of subpopulations of blood and marrow-derived light density cells to adherent cell layers or matrix was studied following a 2-h incubation in 24-well plates. The absolute number of bound B lineage cells was determined by cell counts and flow cytometry analysis. The adherence of B lineage cells to passaged human marrow fibroblasts (BM-FB) was highest in the most immature CD10+/CD34+ cells (34.3 +/- 4.2%), decreasing steadily with each stage of maturation to the peripheral blood B cells (11.2 +/- 2.4%). Increased adhesion of CD10+ B cell precursors relative to CD10-/CD20+ marrow B cells was confirmed by adhesion studies using sorted cells. The two most immature B lineage cells (CD10+CD34+ and CD10+/CD20-) showed more adherence to BM-FB than any other cell type tested, except for monocytes. Only B lineage precursor cells, erythroid precursors and CD10-/CD34+ cells showed significantly greater binding to BM-FB than to plastic. B lineage precursors bound equally well to primary and passaged human marrow fibroblasts, but bound significantly less well to passaged human foreskin fibroblasts, primary human marrow stroma, extracellular matrix of marrow fibroblasts, or fibronectin. These results suggest that specific binding to marrow fibroblasts is part of the differentiation program of early B lineage precursors. This binding activity gradually and predictably decreases during B lineage differentiation, in contrast to expression of other binding receptors, such as LFA-1 and CD44, which increase during B lineage maturation.

Antigens, Differentiation, B-Lymphocyte↗
PubMed2006

Prognostic significance of clinical and immunological parameters in diffuse large B-cell lymphomas.

The aim of the study was to evaluate influence of CD10 expression on overall survival with risk factors according of the IPI. CD10 expression was evaluated in 45 patients with diagnosis of Diffuse large B-cell lymphomas. Unfavorable parameters of the International prognostic index (IPI) were compared in the CD10 positive and CD10 negative groups, number of unfavorable clinical findings in CD10 positive and CD10 negative cases were similar at diagnosis. The study revealed that the CD10 antigen expression is an unfavorable prognostic factor in the high and high-intermediate risk groups regarding to the IPI, overall survival is shorter in the CD10 positive cases and was 14,1 month compared with 23,5 month in CD10 negative group(p<0,01). CD10 antigen expression may have importance as one of the prognostic factors in patients with diagnosis of diffuse large B-cell lymphomas. Interestingly, that influence of CD10 expression on overall survival in the low and low-intermediate risk groups (IPI) wasn't revealed (p>0,05).

Adult↗
PubMed1988

Immunobiologic differences between normal and leukemic human B-cell precursors.

The early stages of normal human B-cell differentiation were studied by flow cytometry and cell sorting based on expression of CD10 (CALLA) and CD19 antigens in fetal liver. Both CD10+ CD19+ and CD10+ CD19- precursor populations proliferated in vitro to form B-cell precursor colonies under stimulation from low molecular weight B-cell growth factor (L-BCGF) or recombinant interleukin 3 but did not respond to high molecular weight B-cell growth factor (H-BCGF). The colonies derived from the CD10+ CD19- fraction showed induction of CD19 expression in 10-50% of growing cells, suggesting that CD10 expression precedes CD19 expression in B-cell ontogeny. This hypothesis was corroborated by less-differentiated marker profiles of the progeny of CD10+ CD19- B-cell precursors as compared to CD10+ CD19+ B-cell precursors in BCGF-stimulated cultures and by higher percentages of CD10+CD19- versus CD10-CD19+ B-cell precursors. CD19 crosslinking on normal fetal liver or bone marrow B-cell precursors was associated with an increase in cytoplasmic calcium concentration, but was inhibitory for colony formation. Leukemic B-cell precursors from acute lymphoblastic leukemias (ALLs) differed from normal B-cell precursors in their in vitro proliferative responses, since (i) they responded not only to L-BCGF and rIL-3 but also to H-BCGF and (ii) their proliferation was stimulated rather than inhibited by CD19 crosslinking. A clonogenic leukemic counterpart for the CD10+CD19- normal B-cell precursor population does not exist among malignant cells from B-cell precursor ALL patients, suggesting that the CD19 receptor may be involved in leukemogenesis of human B-cell precursor ALL.

Antibodies, Monoclonal↗
PubMed2002

Immunohistochemical profile of common epithelial neoplasms arising in the kidney.

To distinguish common epithelial tumors arising in the kidney may have significant implications, in terms of molecular ontogeny and prognosis. It is important to investigate the distribution of immunoexpression of commonly used markers among renal neoplasms and to develop a useful panel as an adjunct to histologic examination, which could lead to the accurate diagnosis of both primary and metastatic tumors. Immunohistochemical stains for CD10, vimentin (VIM), E-cadherin (E-CD), cytokeratins (CK) 7, 8, 19, and 20, high molecular weight keratin (HCK), and peanut lectin agglutinin (PL) (Arachis hypogaea) were performed on 45 (96 for CK7, CK20) conventional (CC), 20 papillary (PC), and 6 (24 for CK7, CK20) chromophobe renal carcinomas (CPC); 12 oncocytomas (OC); 5 collecting duct carcinomas (CDC), and 25 urothelial carcinomas of the renal pelvis (UC). Reactivity for CD10 was evaluated on the basis of the presence of cell surface staining; that for all CKs, cytoplasmic/membranous staining; and that for PL, luminal staining. Both CD10 and VIM were predominantly expressed in CC and PC; E-CD in CPC, OC, and UC; CK7 in PC, CPC, and UC; CK8 and CK19 in CDC and UC; CK20 in UC; HCK in CDC and UC; and PL in CDC. CC and OC were predominantly CK7-/CK20-; PC, CK7+/20-; CPC, CK7+/CK20- or CK7-/CK20-; and UC, CK7+/CK20- or CK7+/CK20+. CDC showed slight predominance of CK7-/20- over CK7+/CK20-. CC was most frequently CD10+/CK7-/HCK-/PL-; PC, CD10+/CK7+/HCK-/PL-; CPC, CD10-/CK7+/HCK-/PL-; OC, CD10-/CK7-/HCK-/ PL-; CDC, CD10-/CK7+/HCK-/PL+ or CD10-/CK7-/ HCK+/PL+; and UC, CD10-/CK7+/HCK+/PL-. Discriminant analysis suggested that CD10/CK7/HCK/PL may be a useful primary immunopanel for distinguishing among CC, PC, CDC, and UC.

Adenoma, Oxyphilic↗
PubMed2005

Comparison of genome profiles for identification of distinct subgroups of diffuse large B-cell lymphoma.

Diffuse large B-cell lymphoma (DLBCL) comprises molecularly distinct subgroups such as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) DLBCLs. We previously reported that CD5(+) and CD5(-)CD10(+) DLBCL constitute clinically relevant subgroups. To determine whether these 2 subgroups are related to ABC and GCB DLBCLs, we analyzed the genomic imbalance of 99 cases (36 CD5(+), 19 CD5(-)CD10(+), and 44 CD5(-)CD10(-)) using array-based comparative genomic hybridization (CGH). Forty-six of these cases (22 CD5(+), 7 CD5(-)CD10(+), and 17 CD5(-)CD10(-)) were subsequently subjected to gene-expression profiling, resulting in their division into 28 ABC (19 CD5(+) and 9 CD5(-)CD10(-)) and 18 GCB (3 CD5(+), 7 CD5(-)CD10(+), and 8 CD5(-)CD10(-)) types. A comparison of genome profiles of distinct subgroups of DLBCL demonstrated that (1) ABC DLBCL is characterized by gain of 3q, 18q, and 19q and loss of 6q and 9p21, and GCB DLBCL is characterized by gain of 1q, 2p, 7q, and 12q; (2) the genomic imbalances characteristic of the CD5(+) and CD5(-)CD10(+) groups were similar to those of the ABC and GCB types, respectively. These findings suggest that CD5(+) and CD5(-)CD10(+) subgroups are included, respectively, in the ABC and GCB types. Finally, when searching for genomic imbalances that affect patients' prognosis, we found that 9p21 loss (p16(INK4a) locus) marks the most aggressive type of DLBCL.

Adult↗
PubMed2004

[CXCR4 expression in B-lineage acute lymphocyte leukemia and its significance].

The study was aimed to explore the chemokine receptor CXCR4 expression on the B-lineage acute lymphocyte leukemia (B-ALL) cells of various differentiation stages and its relationship with myeloid antigen expression. Flow cytometry was used to detect the CXCR4 expression by means of double-fluorescence labeling with CD19/SCC gating. The results demonstrated that 92.9% B-ALL patients were positively expressed CXCR4. The CD10, CD34 antigens were differently expressed in differentiation stages of B-ALL. The immunotypes of (1) CD10(-)/CD34(+), (2) CD10(+)/CD34(+), (3) CD10(+)/CD34(-), (4) CD10(-)/CD34(-) presented at various differential stages from premature to mature. The positive rate of CXCR4 were (27.60 +/- 15.25)%, (30.95 +/- 15.50)%, (55.62 +/- 18.37)% and (77.25 +/- 10.86)% from (1) to (4) respectively. The median fluorescence intensity (MFI) of CXCR4 expression were 46.69 +/- 15.06, 47.43 +/- 12.39, 79.28 +/- 24.71 and 132.92 +/- 88.09. CXCR4 expressions were not significantly different between the premature stages of CD10(-)/CD34(+) and CD10(+)/CD34(+) subtypes, but both were lower than the CXCR4 expression in CD10(+)/CD34(-) and CD10(-)/CD34(-) subtypes. The highest incidence of CXCR4 expression was found in CD10(-)/CD34(-) B-ALL. The average level of CXCR4 expression on B-ALL cell with positive myeloid antigen CD13 or/and CD33 (my(+)B-ALL) was (12.56 +/- 3.88)% of positive rate and 39.82 +/- 11.58 of MFI, both of which were less than the positive rate (37.57 +/- 11.59)% and the MFI (50.72 +/- 13.34) on B-ALL cells with negative myeloid antigen expression (mye(-)B-ALL). In conclusion, the CXCR4 expression is associated with differentiation level of B-ALL cells and down-regulated when co-expressed with myeloid antigens.

Adolescent↗
PubMed1997

B-lineage acute lymphoblastic leukemia of childhood. An institutional experience.

A total of 119 children (1990-95) with acute lymphoblastic leukemia (ALL) B-lineage either CD10+ or CD10- were registered into a single non-randomized chemotherapy protocol. Only untreated patients with standard risk were included in the study. Their ages ranged from 1.8-10 years with a mean of 5.1 years. There were 82 (68%) children with early pre B-All, 35 (29%) with pre B-ALL and 2(1.6%) with transitional pre B-ALL (p < 0.00001). The patients were divided according to CD10 reactivity, either + (94 children) or -(25 patients). The event-free survival (EFS) at 60 months for the CD10+ children was of 78% (alive 73/94), while for the CD10- was 71% (alive 18/25) (p = 0.6) and 74% for both groups. The factors that influenced favorably the survival in the CD10+ group were the age between 3 to 5.99 years (p < 0.00001), sex (either male or female), leukocyte count between 10-24.9 x 10(9)/l (p < 0.00001), LDH under 300 U/I (p < 0.00001) and L1 bone marrow cytomorphology (p < 0.00001). In the CD10- patients, the EFS was favorably influenced by the female sex (p = 0.04), leukocyte count under 10 x 10(9)/l (p = 0.05) and LDH < 300 U/l (p = 0.02). CNS infiltration was documented in 4.2% (5/119). Mortality secondary to chemotherapy was seen in 7%. In conclusion, this is the first large series in Mexican children with B-lineage ALL published. Because of the relatively small number of patients in each group (pre B and transitional pre B), all the patients in the current series were treated alike. When the 119 patients were divided only on the basis of CD10 reactivity, the EFS for both groups (CD10+ and-) was similar; therefore, the reactivity to CD10 has no prognostic value in this type of ALL.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

Regeneration pattern of precursor-B-cells in bone marrow of acute lymphoblastic leukemia patients depends on the type of preceding chemotherapy.

Immunofluorescence stainings for the CD10 antigen and terminal deoxynucleotidyl transferase (TdT) can be used for the detection of leukemic blasts in CD10+ precursor-B-acute lymphoblastic leukemia (precursor-B-ALL) patients, but can also provide insight into the regeneration of normal precursor-B-cells in bone marrow (BM). Over a period of 15 years, we studied the regeneration of CD10+, TdT+, and CD10+/TdT+ cells in BM of children with (CD10+) precursor-B-ALL during and after treatment according to three different treatment protocols of the Dutch Childhood Leukemia Study Group (DCLSG) which differed both in medication and time schedule. This study included a total of 634 BM samples from 46 patients who remained in continuous complete remission (CCR) after treatment according to DCLSG protocols VI (1984-1988; n = 8), VII (1988-1991; n = 10) and VIII (1991-1997; n = 28). After the cytomorphologically defined state of complete remission with CD10+ and CD10+/TdT+ frequencies generally below 1% of total BM cells, a 10-fold increase in precursor-B-cells was observed in protocol VII and protocol VIII, but not in protocol VI. At first sight this precursor-B-cell regeneration during treatment resembled the massive regeneration of the precursor-B-cell compartment after maintenance treatment, and appeared to be related to the post-induction or post-central nervous system (CNS) therapy stops in protocols VII and VIII. However, careful evaluation of the distribution between the 'more mature' (CD10+/TdT-) and the 'immature' (CD10+/TdT+) precursor-B-cells revealed major differences between the post-induction/post-re-induction precursor-B-cell regeneration (low 'mature/immature' ratio: generally <1.0), the post-CNS treatment regeneration (moderate 'mature/immature' ratio: 1.2-2.8), and the post-maintenance regeneration (high 'mature/ immature' ratio: 5.7-7.6). We conclude that a therapy stop of approximately 2 weeks is already sufficient to induce significant precursor-B-cell regeneration even from aplastic BM after induction treatment. Moreover, differences in precursor-B-cell regeneration patterns are related to the intensity of the preceding treatment block, with lower 'mature/immature' ratios after the highly intensive treatment blocks. This information is essential for a correct interpretation of flow cytometric immunophenotyping results of BM samples during follow-up of leukemia patients. Particularly in precursor-B-ALL patients, regeneration of normal precursor-B-cells should not be mistaken for a relapse.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2003

[Analysis of immunophenotype of B-lineage acute lymphoblastic leukemia cells by 4-color flow cytometry].

To investigate the characteristics of immunophenotype of B-lineage acute lymphoblastic leukemia (B-ALL) cells in Chinese cases, B-ALL cells from 181 patients were analyzed by 4-color flow cytometry with CD45/SSC gating. The results demonstrated that the antigen expression frequencies were as follows: CD19 (100%), HLA-DR (98.9%), CD38 (88.5%), CD10 (76.8%) and CD34 (76.8%). CD117 and T antigens (CD2 and CD7) were rarely expressed. Childhood group ( or= 19 years) had a higher expression rate of myeloid antigens (CD13 and/or CD33). Subtype CD10(+)/CD34(+) took the highest percentage in three age groups. Percentages of CD10(-)/CD34(+) group increased by age. Subtype CD10(-)/CD34(+) had the highest myeloid antigen co-expression. Comparing with CD45-positive cases, those with CD45-negative or CD45(+/-) always had higher CD10 expression. Bcr/abl mRNA was evaluated in 43 samples from patients with B-ALL. Myeloid antigen co-expression was not different in bcr/abl(+) and bcr/abl(-) groups, and m-bcr/abl(+) was mainly observed in subtype CD10(+)/CD34(+). In conclusion, typical B-ALL cells expressed CD19(+), HLA-DR(+), and CD117(-). CD34, CD10 and CD45 expression varied in different maturation stages. The immunophenotypic subtype of B-ALL in adolescents was similar to that in the adults. Blasts with CD45(+) were mostly seen in CD10(-) cases. CD13 and/or CD33 co-expression was fewer in children patients. m-bcr/abl(+) was mainly seen in subtype CD10(+)/CD34(+).

Adolescent↗
PubMed2003

[Immunophenotypic features of bcr/abl fusion transcript-positive B-lineage acute lymphoblast leukemia].

To investigate the biological features of leukemic cells in bcr/abl fusion transcript-positive B-lineage acute lymphoblastic leukemia (B-ALL), 3- or 4-color flow cytometry with directly conjugated monoclonal antibodies was used to detect the immunophenotype of the cells in 26 patients with bcr/able-positive B-ALL and 32 patients with bcr/abl-negative B-ALL. bcr/abl fusion transcript was detected by RT-PCR. Immunoglobulin heavy chain (IgH) gene rearrangement was detected by PCR. The results showed that all of the B-ALL patients were positive for CD19. There was significant difference in expression of CD34 (96.2% vs 65.6%), CD10 (96.2% vs 71.8%) and CD38 (43.8% vs 95.4%) between bcr/abl-positive and -negative groups. In bcr/abl-positive B-ALL group, the co-expression rates of CD10(+)/CD19(+)/CD34(+), CD10(+)/CD34(+)/HLA-DR(+) and CD10(+)/CD34(+)/CD38(-) were 92.3% (24/26), 73.1% (19/26) and 56.2% (9/16), respectively. In bcr/abl-negative group, co-expression of CD10(+)/CD19(+)/CD34(+) and CD10(+)/CD34(+)/HLA-DR(+) were 43.8% (14/32) and 37.5% (12/32), respectively, there were significant differences (P < 0.05) between bcr/abl-positive and -negative groups, but none of the cases co-expressed CD10(+)/CD34(+)/CD38(-). The detection rate of monoclonal IgH gene rearrangement (58.8%, 10/17) was lower in bcr/abl-positive group than that (85.7%, 12/14) in bcr/able-negative group. It is concluded that the expression rates of CD34 and CD10 are higher, and CD38 and IgH gene rearrangement are lower in bcr/abl-positive B-ALL cases, CD10(+)/CD34(+)/CD38(-) is a unique feature of immunophenotype, and this phenotype of leukemia cells is closer to that of early B-lineage progenitor cells.

Adolescent↗
PubMed1991

Expression of 5'-nucleotidase (CD73) related to other differentiation antigens in leukemias of B-cell lineage.

Ecto-5'nucleotidase (5'NT; CD73) expression was studied with a monoclonal antibody (7G2) and a radiochemical assay and compared with the expression of other antigens in B-cell-lineage leukemias on cells from 100 leukemic patients and two cell lines. A B-cell origin was confirmed by the expression of CD19 and HLA-DR. Four stages of B-cell leukemias were defined: stage I (pro-B) as CD10-, cytoplasmic mu- (c mu-), surface Ig- (sIg-); stage II (cALL) as CD10+/c mu-/sIg-; stage III (pre-B) as CD10+ or -/c mu+/sIg-; and stage IV (B) as CD10-/c mu-/sIg+. A linear correlation was found between immunohistochemical and radiochemical determination of 5'NT (r = .86). 5'NT expression was low in T-cell leukemias and stage I, high in stages II and III, and low again in stage IV of B-cell leukemias. 5'NT expression was not related to c mu, CD20, CD21, CD22, CD34, and terminal deoxynucleotidyl transferase (TdT) expression, but was significantly related to CD10 and inversely related to kappa/lambda expression. However, the 5'NT activity in CD10+ leukemias (stages II and III) shows a very wide range. Within the group of CD10+ leukemias no differences were detected between 5'NT+ and 5'NT- cells in their expression of other B-cell antigens. We conclude that the place of 5'NT in leukemias corresponding to early stages of B-cell development has been characterized. 5'NT is expressed in CD10+ stages and decreases before the expression of sIgs. Future studies should make clear whether a high expression of this enzyme in CD10+ stages is a normal maturation phenomenon or a malignant phenomenon.

5'-Nucleotidase↗
PubMed2005

Abnormal patterns of antigenic expression in follicular lymphoma: a flow cytometric study.

In order to distinguish follicular lymphoma (FL) from reactive hyperplasia (RH), flow cytometric (FC) immunophenotypic studies have been used primarily to look for monotypic CD5- CD10(+) B cells with much more limited use of bcl-2 stains. We studied what additional diagnostic information could be extracted from routine FC studies in a retrospective study of 90 FL and 91 RH cases. The following significant differences were identified: dimmer CD19 on CD10+ B cells in FL (P < .0001), brighter CD10 and more numerous CD10(+) B cells in FL (P < .0001), and brighter CD20 on neoplastic B cells than on other B cells in FL (P = .002) or in RH (P = .05). In the FL cases, no correlations could be documented between any phenotypic findings. Grade 3 FL had significantly dimmer CD10 expression than lower grades (P = .05). Visual analysis of CD10(+) vs CD10(-) smaller B cells showed dimmer CD19 on the CD10(+) cells in 28 (44%) of 64 evaluable FL cases and 0 of 87 evaluable RH cases. These findings expand the ways in which FC studies can be used to help diagnose FL and suggest that the phenotypic aberrations identified do not represent normal developmental pathways.

Antigens, CD↗
PubMed2004

Ectopeptidases are differentially expressed in hepatocellular carcinomas.

We investigated the expression pattern of neprilysin (CD10), aminopeptidase N (CD13) and angiotensin-I converting enzyme (CD143) in hepatocellular carcinomas (HCC), and their putative roles in hepatocarcinogenesis. Tissue samples were obtained from 31 patients with HCC. Tissue samples obtained from non-neoplastic liver, fetal livers and focal nodular hyperplasias (FNH) were used by comparison. Transcription and expression of CD10, CD13, and CD143 were studied by quantitative RT-PCR, Western blotting, and immunohistochemistry. Cell proliferation assays were performed with the C3A hepatoma cell line. The mRNA and protein of each of CD10, CD13 and CD143 were differentially expressed in HCCs. CD10 was decreased in HCCs as compared to non-neoplastic liver tissue, while CD13 and CD143 were mildly increased. In fetal liver and FNHs, the expression of CD10 was less intense than in the surrounding non-tumorous liver. The expression patterns of CD13 and CD143 in fetal livers and FNHs were similar to HCCs and were predominantly localized in bile canaliculi (CD13) and endothelial cells (CD143). CD10 and CD13 mRNAs were expressed by C3A cells and blocking either CD10 or CD13 ectopeptidase activity retarded cell growth significantly in vitro. We demonstrate that ectopeptidases are differentially expressed in HCCs and may have influence on tumor biology. Overall, expression of CD10 in non-neoplastic and neoplastic hepatocytes appears to correlate inversely with their state of proliferation or differentiation. CD13 shows a characteristic canalicular distribution pattern and may be important for cell polarization and bile compartmentalization in HCCs, while CD143 may influence angiogenesis.

Adult↗
PubMed1987

Phenotypic similarities and differences between CALLA-positive acute lymphoblastic leukemia cells and normal marrow CALLA-positive B cell precursors.

Expression of differentiation markers in common acute lymphoblastic leukemia (cALL) cells from 25 patients was compared with subpopulations of normal common ALL antigen (CALLA) (CD10)-positive bone marrow lymphoid cells (cBMLs). In cBML, CD10 intensity is positively correlated with CD34 (MY10) and terminal transferase (TdT) expression and inversely correlated with common leukocyte antigen (CLA), CD20 (B1), and ctyoplasmic mu chain (Cmu) expression. In cALL, CD10 density was inversely correlated with CLA and Cmu expression and strongly correlated with CD34 expression as in cBML. In contrast to cBML, TdT and CD20 expression were not related to CD10 density in cALL. Furthermore, cALL TdT intensity measured by enzyme immunoassay was not related to expression of CD10, CLA, or CD34, but was positively correlated with CD20 expression. Cmu expression in cALL was inversely correlated with expression of CD34 and positively correlated with CLA as in cBML, but showed no association with TdT intensity or CD20 expression in contrast to the relationship found in cBMLs. Analysis of TdT intensity and Cmu expression in sorted subpopulations of cells from individual patients that were positive or negative for CD34, CD20, or CD10 was consistent with the data obtained by comparison of cells from different patients. These results indicate that from patient to patient and within individual patients, cALL cells express the markers CD34, CLA, CD10, and Cmu in a coordinated fashion similar to cBMLs, but demonstrate differences in expression of TdT and CD20 with respect to the marrow cells considered their normal counterparts. The cALL cells that are CD34 positive show increased expression of CD10 and are less likely to be CLA or Cmu positive, suggesting that they may represent a phenotypically less differentiated form of cALL than does CD34-negative cALL.

Acute Disease↗
PubMed2002

Induction of apoptosis and CD10/neutral endopeptidase expression by jaspamide in HL-60 line cells.

Jaspamide (asplakinolide) is a natural peptide isolated from marine sponges of Jaspis species and has fungicidal and growth-inhibiting activities. We characterized the jasplakinolide-induced loss of viability by programmed cell death in the HL-60 human promyelocytic leukemia cell line and found that this process was accompanied by neutral endopeptidase (NEP)/CD10 expression on the surface of the apoptotic cells. HL-60 cells do not normally express detectable amounts of NEP/CD10 on their surface or intracytoplasmically, but upon jaspamide treatment, CD10 was synthesized de novo, its expression being inhibited by cycloheximide pretreatment. Once synthesized, NEP/CD10 interfered with the jasplakinolide signal delivered to HL-60 cells. Inhibition of NEP/CD10 by the NEP inhibitor phosphoramidon or by an anti-CD10 monoclonal antibody significantly increased apoptosis induction. The appearance of CD10 on the cell surface was blocked by preincubation of the cells with the monocytic/macrophage-differentiating agents vitamin D3 and phorbol 12-myristate 13-acetate, but not by the granulocytic differentiating agents retinoic acid or dimethyl sulfoxide. Moreover, in the promonocytic U937 and mature monocytic THP-1 cell lines, jaspamide induced apoptosis but not CD10 expression. In HL-60 cells, CD10 expression was partially but not totally blocked by the broad-spectrum caspase inhibitor benzyloxacarbonyl-Val-Ala-Asp-fluoromethylketone, indicating a connection between apoptosis induction and CD10 synthesis. Our findings suggest that the CD10 expression is related to the programmed cell death induction by jaspamide, and also with the process of granulocytic differentiation in HL-60 cells.

Apoptosis↗
PubMed2001

cDNA arrays and immunohistochemistry identification of CD10/CALLA expression in hepatocellular carcinoma.

The histological diagnosis of hepatocellular carcinoma (HCC) can be complicated by difficulty in differentiation from cholangiocarcinoma and metastatic carcinoma. Immunohistochemical stains currently in use are suboptimal in terms of specificity and sensitivity. Using cDNA array analysis for differential gene expression, we demonstrated a significant increase in mRNA expression level of CD10/CALLA, a type 2 cell-surface metalloproteinase, in HCC, which was subsequently confirmed by reverse transcriptase-polymerase chain reaction and Western blotting analysis. To test the possibility of using CD10/CALLA as a diagnostic marker for HCC, various intrahepatic tumors were studied immunohistochemically using a monoclonal antibody for CD10. A characteristic canalicular-staining pattern was observed in normal hepatocytes and at the apical surface of bile duct epithelial cells. The canalicular expression of CD10 was identified in 9 of 15 HCCs examined (60%), whereas 10 cholangiocarcinomas and 8 of 9 metastatic carcinomas lacked this staining. In three of the six HCCs negative for CD10, the surrounding nonneoplastic liver tissue was also negative, suggesting fixation-associated loss of immunoreactivity. Six HCCs had stronger CD10 staining in tumor cells when compared to the surrounding nonneoplastic tissue. Three cases of benign bile duct adenomas also expressed CD10 at the luminal aspect. One of the MCs showed a diffuse, cytoplasmic staining for CD10, a pattern readily distinguishable from that of HCC. A panel of other immunohistochemical markers were also studied for comparison, including polyclonal anti-carcinoembryonic antigen, cytokeratin (CK) 7, CK20, and alpha-fetoprotein. Our results demonstrate that cDNA arrays can be effectively used to identify new diagnostic markers, and that CD10 is a reliable marker for identifying HCC, particularly when used in conjunction with a panel of immunohistochemical markers (polyclonal anti-carcinoembryonic antigen, CK7, CK20, and alpha-fetoprotein) and in the distinction from cholangiocarcinoma.

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