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W D Ludwig

Publications and source records attributed to W D Ludwig.

At least 145 records · Page 8Linked to original sources
PubMed1993

The role of GM-CSF in the treatment of acute myeloid leukemia.

After a first study showed that GM-CSF following chemotherapy effectively accelerated neutrophil recovery and reduced early mortality in high risk patients with AML, a second study was begun in which GM-CSF was applied preceding chemotherapy and continuing until neutrophil recovery in the initial 5 chemotherapy courses for patients with newly diagnosed AML. The CR rate in patients of 16-75 (median 50) years was 75% in GM-CSF patients and 84% in controls. GM-CSF patients showed a trend to more frequent rapid blast clearance and fewer persistent leukemias and a significantly superior remission duration as of this update two-and-a-half years after the study started. It should be shown later by this study whether GM-CSF multiple course priming and longterm administration adds to the cure rate of patients with AML.

Adolescent↗
PubMed1993

High-dose versus intermediate dose cytosine arabinoside combined with mitoxantrone for the treatment of relapsed and refractory acute myeloid leukemia: results of an age adjusted randomized comparison.

193 patients with relapsed or refractory acute myeloid leukemia (AML) were entered into a prospective randomized comparison of high-dose versus intermediate dose cytosine arabinoside (AraC) both combined with mitoxantrone (mitox) according to the previously established sequential HD-AraC/mitox regimen (S-HAM). AraC was administered by 3 hr inf. q 12 hrs on days 1, 2, and 8, 9 at randomly assigned doses of either 3.0 versus 1.0 g/m2 in pts. < 60 years of age or 1.0 versus 0.5 g/m2 in older pts. Mitox was given to all cases at a dose of 10 mg/m2/d on days 3, 4, and 10, 11. Randomization was stratified for primary refractoriness against induction therapy and the length of first remission in relapsed cases (< 6 mths., 6-18 mths., > 18 mths.). From 151 presently evaluable cases 72 pts (48%) achieved a complete remission (CR), 38 cases (25%) were non-responders (NR) and 41 pts. (27%) died within the first 6 weeks after the start of treatment (early death = ED). No significant differences were found in CR rates being 52% and 44% for the 3.0 versus 1.0 g/m2 AraC regimens in pts. < 60 years and 48% and 45% after 1.0 versus 0.5 g/m2 AraC in older pts. No differences between the respective regimens emerged either for the time to CR (median 46 days) nor remission duration (median 4.5 mths). Analysis of treatment failures, however, demonstrated a significantly higher rate of NR after the lower dose regimens in both age groups of 41% and 32% versus 11% and 14% in pts. receiving AraC at higher doses (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Acute myeloid leukemias expressing lymphoid-associated antigens: diagnostic incidence and prognostic significance.

A portion of patients with acute myeloid leukemia also display surface antigens associated with lymphoid development (Ly+AML). The incidence of Ly+AML varies considerably between independent studies, both overall and with regard to individual antigens. On average, lymphoid-associated antigen expression is relatively low in AML. The reasons for some striking differences between conflicting reports are not clear, but are most probably due to various technical aspects including several arbitrary parameters. The data accumulated from the literature lead to the following conclusions: (i) use of different reagents against the CD surface antigens, different positive/negative cut-off levels, analysis of fresh or frozen cell material and variable sensitivities of the analytical instruments (expression of lymphoid-associated antigens was commonly weaker than myeloid-associated markers) seriously influence the results; (ii) most antigens (CD1, CD2, CD3, CD5, CD8, CD10, CD19, CD20, CD21, CD22) were expressed on less than 10% of AML cases; (iii) the CD4 and CD7 antigens, also found on normal monocytic and immature myeloid progenitor cells, were detected in 24% and 15% of AML cases, and their expression correlated with FAB M4/M5 and M1/M2 morphology, respectively; (iv) differences between pediatric and adult Ly+AML were restricted to CD4 and CD19 expression being detected more often in childhood cases; (v) there is no cytogenetic anomaly specific for Ly+AML; anomalies exclusively associated with lymphoid malignancies were not seen; aberrations involving 11q23, 14q32, and the 9;22 translocation seem to be increased; (vi) in most studies, expression of lymphoid-associated antigens (with the exception of CD7) on AML blasts lacked prognostic significance; CD7+AML appears to be a particular subset of malignant myeloid progenitors. In summary, these findings suggest that in general, Ly+AML may not represent a biologically distinct form of leukemia as these cases have similar clinical features and respond to therapy in a comparable manner.

Adult↗
PubMed1993

Terminal deoxynucleotidyl transferase (TdT) expression in acute myeloid leukemia.

Terminal deoxynucleotidyl transferase (TdT) was initially considered as a marker of immature lymphoid cells, but many studies have since provided conclusive evidence for the existence of TdT+ cases of acute myeloid leukemia (AML). The reported incidence of TdT+ AML cases varies largely (from 0% to 55%, average of combined data of the literature 18%, children 19%, and adults 21%) suggesting interlaboratory differences in the types of AML examined, the sensitivity of the method used, and the percentage of positive blasts taken as cut-off value. Significantly higher frequencies of TdT+ AML were reported in studies employing immunocytochemical staining (alkaline phosphatase anti-alkaline phosphatase or immunoperoxidase) than in series using immunofluorescence microscopy or biochemical assays. Statistical analysis of various cut-off levels demonstrates an inverse correlation between cut-off point and incidence. The combined data show that TdT-positivity is more common in the immature cell types (M0, M1), with no correlation with age or sex. Except for contested suggestions of an association with t(6;9) and t(8;21), no clear relationship between karyotype and TdT status has been documented. Although an association between T-cell receptor or immunoglobulin gene rearrangements and expression of TdT in AML was postulated, subsequent studies could not demonstrate this correlation. There was no significant relationship with other immunophenotypic markers except for CD34 positivity suggesting that the TdT+ cells represent an immature population. The percentage of positive cells was usually lower in AML than in ALL; in most cases only a subpopulation of the AML cells was TdT+. Thus, TdT could be viewed as a marker of hematopoietic immaturity. In about one-half of the studies on adults, TdT expression was reported to indicate a poor prognosis; others did not find any prognostic difference between TdT+ and TdT- AML cases. No correlation between TdT-positivity and prognosis was found in childhood AML.

Adult↗
PubMed1993

tal-1 deletions in T-cell acute lymphoblastic leukemia as PCR target for detection of minimal residual disease.

Polymerase chain reaction (PCR) techniques based on amplification and identification of leukemia-specific DNA sequences provide a sensitive diagnostic method for detection of minimal residual disease (MRD) with a detection limit of 10(-5) to 10(-6) (1-10 malignant cells in 10(6) normal cells). To date, the main leukemia-specific DNA sequences used as PCR targets in detection of MRD are breakpoint fusion regions of chromosome translocations and junctional regions of rearranged immunoglobulin (Ig) or T-cell receptor (TcR) genes. The recently identified tal-1 deletions involving the sil and tal-1 genes, provide a potential MRD-PCR target. tal-1 deletions are site-specific because they are mediated via recombination signal sequences homologous to Ig/TcR genes. In line with this homology, tal-1 deletions also show random insertion and deletion of nucleotides at their breakpoints, resulting in highly variable breakpoint fusion regions. The fusion region diversity can be applied to design patient-specific oligonucleotide probes. Our Southern blot analyses of a large series of 313 acute leukemias with a specific tal-1 deletion probe (SILDB) demonstrated that tal-1 deletions exclusively occur in T-cell acute lymphoblastic leukemia (T-ALL) and not in precursor B-ALL or acute non-lymphocytic leukemias. In addition, we did not detect tal-1 deletions in normal blood cells and normal thymocytes by PCR analysis. The diversity observed in tal-1 deletion fusion regions with an average insertion and deletion of approximately 7 and approximately 6 nucleotides, respectively, allowed us to design fusion-region-specific probes. The specificity of the fusion-region probes was proven and the detection limit of the MRD-PCR technique was tested in a series of dilution experiments. The observed detection limit of 10(-5) indicates that tal-1 deletions in T-ALL represent ideal leukemia-specific PCR targets for detection of MRD.

Base Sequence↗
PubMed1993

Expression of identical E2A/PBX1 fusion transcripts occurs in both pre-B and early pre-B immunological subtypes of childhood acute lymphoblastic leukemia.

The translocation t(1;19)(q23;p13) in pediatric patients with acute lymphoblastic leukemia (ALL) was demonstrated in early reports to result in a consistent fusion between the E2A and PBX1 gene sequences and in the expression of a uniform, chimeric E2A/PBX1 mRNA with transforming potential. More recent observations suggested that cytogenetically identical t(1;19) translocations can result in the transcription of different mRNA species and that expression of the E2A/PBX1 message may be restricted to patients with the t(1;19) who display a pre-B phenotype of ALL. To further assess the correlation between the immunologic subtypes of the disease and specific genetic alterations, we have performed cytogenetic and molecular analyses in 221 children with B-lineage ALL. Expression of the chimeric E2A/PBX1 message was detected in 21 patients. Out of 14 patients, in whom cytoplasmic immunoglobulin (cig) analyses were available, no less than four had a cig- B-cell precursor ALL, whereas 10 displayed a cig+ B-ALL immunophenotype. These findings are at variance with a recent report in which expression of the E2A/PBX1 message was linked exclusively to a subset of patients who displayed a cig+ pre-B-cell precursor phenotype of ALL. In seven cases diagnosed before 1986, cig analyses were not available, and consequently E2A/PBX1 expression could not be correlated to a particular immunological subtype of B-cell precursor ALL. Our results have important implications for the detection of residual disease in pediatric patients where expression of the typical E2A/PBX1 mRNA may occur both in cig+ (pre-B) and cig- (early pre-B) immunologic subtypes of ALL.

Child↗
PubMed1993

SIL-TAL1 deletion in T-cell acute lymphoblastic leukemia.

The TAL1 gene on chromosome 1 encodes a hematopoietic transcription factor. Disruption of TAL1 via chromosomal translocation or a site-specific deletion has been reported in up to 30% of T-cell acute lymphoblastic leukemias (T-ALL). Here we used a polymerase chain reaction (PCR) assay to identify the 90 kb SIL-TAL1 deletion in a group of 19 cutaneous T-cell lymphomas and a series of 142 T-ALL patients (76 children, 66 adults). While none of the T-cell lymphoma exhibited a SIL-TAL1 recombination, seven T-ALL cases showed a type d1 and two patients a type d2 deletion. Of pediatric T-ALL, 9% (7/76) and of adult patients only 3% (2/66) were characterized by this genomic lesion. The deletion correlated with commitment to the T-cell receptor (TCR) alpha beta lineage, but lacked association with a distinct maturation stage. Sequence analysis of SIL-TAL1 breakpoints revealed marked heterogeneity at the junctional region among the nine patients due to random deletion and insertion of N-region nucleotides or templated P-nucleotide addition mediated via illegitimate V(D)J recombinase action. Clonospecific oligomer probes in conjunction with PCR allowed the detection of minimal residual disease in one out of four patients monitored during complete hematologic remission.

Adolescent↗
PubMed1993

Translocation t(1;22) mimicking t(1;19) in a child with acute lymphoblastic leukemia as revealed by chromosome painting.

The karyotype of a boy with acute lymphoblastic leukemia (ALL) presenting with numerical and structural chromosome aberrations as determined by Giemsa-banding was further investigated using chromosome painting (CP). A translocation t(11;18)(q23;q21) was verified by this approach, and gain of chromosome 21 material due to a structural rearrangement was detected. Moreover, an unbalanced translocation of the long arm of chromosome 1, resembling the well known translocation t(1;19), was demonstrated to involve chromosome 22 instead of chromosome 19. Immunophenotyping of the leukemic blasts led to the diagnosis common ALL (CD19+, CD10+, clg-). Our case indicates that in ALL a translocation t(1;19) may be mimicked by other chromosomal rearrangements, and that CP may efficiently complement conventional cytogenetics in the exact characterization of the involved chromosomes.

Child↗
PubMed1993

Detection and clinical relevance of genetic abnormalities in pediatric acute lymphoblastic leukemia: a comparison between cytogenetic and polymerase chain reaction analyses.

The E2A/PBX1 and the BCR/ABL fusion genes result from the t(1;19)(q23;p13) and the t(9;22)(q34;q11), respectively, and encode oncoproteins which are thought to play an important role in the development of acute lymphoblastic leukemia (ALL) subtypes associated with adverse prognosis. The use of the polymerase chain reaction (PCR) for the detection of these genetic rearrangements may offer advantages over cytogenetic techniques which are often unsatisfactory in patients with ALL and, furthermore, provide a useful tool for monitoring of residual disease. However, it has not yet been evaluated whether the employment of PCR at the time of diagnosis improves the detection rate of these clinically relevant genetic anomalies. We have developed a multiprimer-PCR protocol which facilitates the detection of each of the four chimeric E2A/PBX1 and BCR/ABL mRNAs in a single reaction. This protocol was used for the evaluation of bone-marrow or blood samples from 251 children with ALL in whom cytogenetic analyses had been performed. Of the 251 patients, 221 had a B-cell precursor immunophenotype. In this group, 21 patients (9.5%) carrying the E2A/PBX1 rearrangement and three patients (1.4%) with BCR/ABL transcripts were detected by PCR. Twelve of these cases had escaped the detection by conventional cytogenetic analysis. In two of 12 patients with a typical t(1;19)(q23;p13), no E2A/PBX1 transcripts were identified by PCR, thus suggesting the presence of different molecular rearrangements. Residual leukemic cells were detected by PCR in five of eight patients who were followed during complete clinical remission. The frontline use of PCR has an important impact on the timely diagnosis, therapeutic decisions, and monitoring of high-risk patients with B-cell precursor leukemia who carry the E2A/PBX1 or BCR/ABL fusion genes.

Adolescent↗
PubMed1992

Favorable outcome of B-cell acute lymphoblastic leukemia in childhood: a report of three consecutive studies of the BFM group.

In 1981 the BFM group introduced a new treatment strategy for B-cell acute lymphoblastic leukemia (B-ALL). A cytoreductive prephase (prednisone/cyclophosphamide) was followed by eight 5-day courses of chemotherapy. Fractionated cyclophosphamide, methotrexate (MTX) 0.5 g/m2 (24-hour infusion), and MTX intrathecally were administered at each course and cytosine arabinoside (ARA-C)/teniposide (VM-26) was given alternately with doxorubicin. In study ALL-BFM-83, central nervous system (CNS) chemotherapy was intensified by adding dexamethasone, while MTX/ARA-C was administered intraventricularly. Therapy duration was reduced to six courses. In study ALL-BFM-86, MTX 0.5 g/m2 was replaced by high-dose (HD) MTX, 5 g/m2 (24-hour infusion), and MTX/ARA-C/prednisolone intrathecal therapy was introduced. Doses of ARA-C and VM-26 were increased and fractionated, cyclophosphamide was partially replaced by ifosfamide, and vincristine was added. CNS irradiation was 24 Gy for prevention and 30 Gy for overt disease in studies ALL-BFM-81 and -83, but was omitted in ALL-BFM-86. In all, 87 patients were enrolled, 22 (8 CNS-positive) in study All-BFM-81, 24 (7 CNS-positive) in study ALL-BFM-83, and 41 (0 CNS-positive) in study ALL-BFM-86. The estimated 5-year duration of event-free survival (EFS) was 43% in study ALL-BFM 81, 50% in study ALL-BFM-83, and 78% in study ALL-BFM-86 (minimal follow-up, 25 months). Nineteen of 24 relapses occurred while on therapy or shortly thereafter. In study ALL-BFM 81, the CNS was the most frequent site of failure. In ALL-BFM-83, there were no isolated CNS relapses, but more bone marrow (BM) relapses occurred. In ALL-BFM-86, localized manifestations were the predominant site of failure, no isolated BM relapses occurred, and only one CNS relapse was diagnosed. No single parameter exerted a consistent influence on outcome with one exception. The presence of residual disease after the first two courses was correlated with an increased risk of therapy failure. We conclude that an intensive, short-pulse therapy delivered within a 4-month period is highly effective in the treatment of B-ALL. In addition to fractionated cyclophosphamide/ifosfamide, a 24-hour infusion of HD MTX 5 g/m2 in conjunction with an i.th. therapy is an important component for prevention of both systemic and CNS relapses. CNS irradiation is not needed for CNS-negative patients.

Adolescent↗
PubMed1992

A switch toward demethylation is associated with the expression of myeloperoxidase in acute myeloblastic and promyelocytic leukemias.

Expression of numerous genes encoding myeloid-specific proteins is tightly regulated during normal myeloid differentiation. This heterogeneous group of genes thus offers a tool for dissection of different maturational steps of myelopoiesis. We have previously shown that the human myeloperoxidase (MPO) gene is modified at numerous CpG residues in normal myeloid cells and in myeloid cell lines in a development-specific and expression-associated manner. In the present work, we have applied this type of methylation analysis to primary leukemia myeloid cell samples. We found that expression of MPO messenger RNA (mRNA) is grossly limited to leukemias of late myeloblastic and promyelocytic stages; expression is thus associated with progressive demethylation in the 5' region of the MPO gene. This modification was not global. Low-level induction of MPO mRNA expression in very immature leukemic cells using phorbol ester was not accompanied by progressive demethylation. This type of methylation analysis of a myeloid-specific gene may yield a molecular indicator for different types of myeloid leukemias.

Blotting, Northern↗
PubMed1992

Effects of human stem cell factor (c-kit ligand) on proliferation of myeloid leukemia cells: heterogeneity in response and synergy with other hematopoietic growth factors.

A novel hematopoietic growth factor, the stem cell factor (SCF), for primitive hematopoietic progenitor cells has recently been purified and its gene has been cloned. In this study we tested the mitogenic activity of recombinant human SCF on myeloid leukemia cells as well as the expression of its receptor. We have investigated the proliferation of 31 myeloid leukemia cell lines as well as fresh myeloid leukemic blasts from 17 patients in a 72-hour 3H-thymidine uptake assay in the presence of various concentrations of recombinant human (rh) SCF alone or in combination with saturating concentrations of granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, M-CSF, interleukin-3 (IL-3), or erythropoietin (EPO). Only five of 31 lines, but fresh leukemic blasts from 12 of 17 patients with acute myeloid leukemia (AML), significantly responded to SCF. The responding cell lines were of the acute promyelocytic, chronic myeloid, megakaryoblastic, and erythroleukemia origin, the responding blast preparations of all French-American-British subtypes. Synergistic activities of SCF were found with G-CSF, GM-CSF, EPO, and IL-3. To determine the SCF binding sites on leukemic cells, we used 125I-radiolabeled SCF in Scatchard analysis and cross-linking studies. The leukemic cell lines responding to SCF expressed from 2,300 up to 29,000 binding sites per cell. The SCF receptor expression was downregulated in vitro by the presence of its ligand. Cross-linking studies demonstrated a 150-Kd SCF receptor on the surface of all responding myeloid leukemias. This study suggests that SCF may be an important factor for the growth of myeloid leukemia cells, either as a direct stimulus or as a synergistic factor for other cytokines. Furthermore, using polymerase chain reaction analysis of total RNA from the myeloid leukemia lines, we found expression of SCF-mRNA in 17 of 30 lines, suggesting autocrine mechanisms in the growth of a subgroup of leukemic cells by coexpression of SCF and its receptor.

Cell Division↗
PubMed1992

Functional expression of c-kit by acute myelogenous leukemia blasts is enhanced by tumor necrosis factor-alpha through posttranscriptional mRNA stabilization by a labile protein.

The c-kit proto-oncogene encodes a transmembrane glycoprotein identical to the receptor for the recently cloned stem cell factor (SCF). The present study examines constitutive synthesis of transcripts in primary acute myelogenous leukemia (AML) blasts and the effects of recombinant human tumor necrosis factor (TNF)-alpha on c-kit mRNA expression in these cells. The c-kit transcripts were detectable at low levels in 10 of 10 different AML samples investigated. TNF treatment of AML cells was associated with enhanced c-kit mRNA expression in all specimens. Nuclear run-on transcription assays indicated that the c-kit gene was transcriptionally active in all leukemias examined and the rate of transcription was unaffected by exposure to TNF, suggesting posttranscriptional control mechanisms of c-kit mRNA accumulation. In the absence of TNF, the half-life of c-kit transcripts was 2 to 3 hours, while in TNF-treated AML cells, c-kit half-life was found to be 5 to 9 hours. Inhibition of protein synthesis reduced TNF-induced c-kit mRNA expression by Northern blot analysis, but did not affect the rate of c-kit gene transcription. In the presence of inhibition of protein synthesis, the half-life of c-kit transcripts in TNF-induced leukemia cells decreased to 2 to 4 hours. These findings indicate that levels of c-kit mRNA are controlled by a labile protein that is involved in TNF-mediated stabilization of c-kit transcripts. The effects of TNF-alpha also extended to the protein level in that TNF-alpha treatment of primary AMLs was associated with enhanced surface expression of the SCF receptor by some of these cells. While exogenous SCF induced clonogenic growth of all primary AML samples investigated, TNF-alpha failed to stimulate leukemic cells to proliferate. However, the combination of SCF and TNF-alpha resulted in synergistic growth stimulation in seven of nine different AML specimens investigated. The finding of transmodulation of the SCF receptor through posttranscriptional modifications might further contribute to our understanding of the synergistic interplay of TNF-alpha and SCF.

Cycloheximide↗
PubMed1992

Recombinant human stem cell factor stimulates growth of a human glioblastoma cell line expressing c-kit protooncogene.

The growth of a panel of eight different human glioblastoma cell lines was examined in a human tumor cloning assay in agar, a tritiated thymidine uptake assay, and by counting cell numbers, in cultures performed in the absence or presence of increasing concentrations (1 to 100 ng/ml) of recombinant human stem cell factor (SCF). Growth of 7 of 8 cell lines was not significantly and reproducibly affected by recombinant human SCF. However, growth of the CRL 1620 cell line could be stimulated up to 5-fold by the cytokine. In contrast to the other cell lines investigated, CRL 1620 expressed the c-kit protooncogene assessed on the mRNA and protein level. Furthermore, SCF-induced proliferation of CRL 1620 cells was sensitive to the tyrosine kinase inhibitor erbstatin. Our data suggest that SCF can be operative in growth modulation of malignant cells outside the hematopoietic system, and this finding should be further studied for its possible clinical implications.

Cell Division↗
PubMed1992

Synergy of interleukin 3 and tumor necrosis factor alpha in stimulating clonal growth of acute myelogenous leukemia blasts is the result of induction of secondary hematopoietic cytokines by tumor necrosis factor alpha.

Colony growth of leukemic colony-forming units (L-CFU) obtained from patients with primary acute myelogenous leukemia stimulated with recombinant human interleukin 3 (rh IL-3) is significantly potentiated when recombinant human tumor necrosis factor alpha (rh TNF-alpha) is present in cultures. The costimulatory activity of tumor necrosis factor (TNF) alpha is dose dependent and maximum at TNF-alpha concentrations of 10 ng/ml. At high density, L-CFU proliferatively respond to TNF-alpha stimulation in the absence of exogenous rh IL-3. Studies of the mechanism of action of rh TNF-alpha on acute myelogenous leukemia L-CFU growth suggest that TNF-alpha acts by inducing release of growth stimulatory hematopoietic cytokines by the leukemic cells themselves, including IL-1 alpha, IL-1 beta, Granulocyte-macrophage colony-stimulating factor (CSF), granulocyte CSF, and IL-6. Treatment of L-CFU cultures, with neutralizing antibodies to IL-1 alpha, IL-1 beta, granulocyte-macrophage CSF, granulocyte CSF, and IL-6 to eliminate the endogenous source of these factors is associated with significant inhibition of the synergistic interplay of TNF-alpha and IL-3.

Drug Synergism↗
PubMed1992

Human Lyb-2 homolog CD72 is a marker for progenitor B-cell leukemias.

S-HCL 2 is the prototype antibody of the recently defined CD72 cluster (human Lyb-2). Under nonreducing conditions, S-HCL 2 monoclonal antibody (mAb) precipitates a glycoprotein of 80-86 kDa. Under reducing conditions, a dimer of 43 and 39 kDa, with core proteins of 40 and 36 kDa, is precipitated. CD72 expression in normal and malignant tissues is different from expression of all other previously described human B-cell antigens. In peripheral blood and bone marrow, the antigen appears to be present on all B lymphocytes, with the exception of plasma cells. In tissue, immunohistochemical staining revealed positivity for all known B-cell compartments; however, pulpa macrophages of the spleen and von Kupffer cells exhibited distinct positivity for CD72 also. Among 83 malignant non-Hodgkin's lymphomas examined by immunohistochemistry (alkaline phosphatase anti-alkaline phosphatase technique), all 54 B-cell lymphomas, including precursor B-cell lymphomas, Burkitt's lymphomas, germinal center lymphomas, chronic lymphocytic leukemias, and hairy cell leukemias, were CD72 positive, but no T-cell lymphomas were. Flow cytometry study of more than 80 mainly acute leukemias (52 B-cell leukemias) showed reactivity with S-HCL 2 mAb over the full range of B-cell differentiation. In particular, very early B cells in cytoplasmic Ig (cIg)-negative, CD19-positive pre-pre-B-cell leukemias and hybrid leukemias (mixed myeloid and B-cell type) were consistently positive for CD72 on the cell surface. Therefore, CD72 may become an important marker for progenitor B-cell leukemias.

Antibodies, Monoclonal↗