Biomedical subjects

J Minowada

Publications and source records attributed to J Minowada.

At least 127 records · Page 7Linked to original sources

PubMed1986

Rearrangement and expression of the alpha, beta, and gamma chain T cell receptor genes in human thymic leukemia cells and functional T cells.

Using cDNA and genomic probes representing the alpha, beta, and gamma chain of the human T cell receptor genes, we have examined the structure and expression of these genes in 14 human leukemic T cell lines, representing different stages of thymic differentiation, and 15 functional human T cell clones. Rearrangement of the gamma and beta chain genes was found in all of the functional T cell clones and all but one (P30/OKUBO) thymic leukemia cell line; all of the lines that had rearrangement of the beta chain expressed beta mRNA. Expression of the alpha chain was found in all of the functional T cell clones examined, while rearrangement of the alpha chain gene, using currently available probes to the J region, could be shown in 10 of 13 functional clones. In contrast, expression of the alpha chain was found in 6 of 10 leukemic T cell lines, while rearrangement was found in six of these nine cell lines. Of the 14 leukemic cell lines studied for rearrangement of the alpha chain, rearrangement was found in six cases. The data obtained with the cell lines are consistent with an ordered rearrangement and expression of the gamma, beta, and alpha chains of the T cell antigen receptor (TcR) genes. The leukemic cell lines used in the present study have previously been characterized with regard to cell surface antigens and intracellular enzymes. Based on those results a scheme of thymic development was proposed. The developmental stages identified by those studies are not in complete agreement with stages of T cell development, as determined in the present study using molecular probes.

Cell Line↗

PubMed1986

Deregulation of c-myc by translocation of the alpha-locus of the T-cell receptor in T-cell leukemias.

Two human T-cell leukemias carrying a t(8;14)(q24;q11) chromosome translocation were studied for rearrangements and expression of the c-myc oncogene. For one leukemia, rearrangement was detected in a region immediately distal (3') to the c-myc locus; no rearrangements of c-myc were observed in the second case (DeF). However, studies with hybrids between human and mouse leukemic T cells indicated that in the leukemic cells of DeF, the breakpoint in chromosome 14 occurred between genes for the variable (V alpha) and the constant (C alpha) regions for the alpha chain of the T-cell receptor. The C alpha locus had translocated to a region more than 38 kilobases 3' to the involved c-myc oncogene. Since human c-myc transcripts were expressed only in hybrids carrying the 8q+ chromosome but not in hybrids containing the normal chromosome 8, it is concluded that the translocation of the C alpha locus 3' to the c-myc oncogene can result in its transcriptional deregulation.

Animals↗

PubMed1986

Occurrence of particular isoenzymes in fresh and cultured leukemia-lymphoma cells. I. Tartrate-resistant acid phosphatase isoenzyme.

The cells from 87 leukemia-lymphoma cell lines, 14 B-lymphoblastoid cell lines, 459 cases of leukemia-lymphoma, normal specimens, 22 leukemia-lymphoma cell lines treated with 12-O-tetradecanoylphorbol 13-acetate (TPA) and 14 cases of chronic lymphocytic leukemia (CLL) and chronic myelocytic leukemia (CML) treated with TPA were analyzed for the expression of tartrate-resistant acid phosphatase (TracP) isoenzyme separated by isoelectric focusing. The TracP isoenzyme was seen in the following leukemia-lymphoma cell lines: 4 of 30 T-cell, 2 of 35 B-cell, 1 of 6 non-T/non-B-cell, 1 of 8 myelomonocytic, 3 of 4 erythroleukemia, and 3 of 4 Hodgkin's disease-derived cell lines. The expression of the TracP band could be induced by treatment with TPA in 3 myelomonocytic leukemia cell lines. Among the different types of leukemia-lymphoma cells freshly obtained from patients, the TracP isoenzyme was detected at a high incidence in cases of B-CLL, hairy cell leukemia (HCL), and B-lymphoma. Of the myeloid leukemias, 10% to 20% displayed the TracP isoenzyme. TracP positivity was detected in the peripheral blood, tonsil, bone marrow, spleen, and liver obtained from healthy donors, but not in the thymus. The expression of the TracP band could be newly induced by TPA in cases of CLL and in cases of CML. It is concluded that TracP activity is not specific for HCL, but is found at high incidences in cases of HCL, B-CLL and B-lymphoma. The TracP isoenzyme is not expressed by very immature lymphoid leukemia cells, but by cells arrested at later stages of differentiation of the T- or B-cell lineage, and by some myeloid cells.

Acid Phosphatase↗

PubMed1986

Induction of differentiation in the human leukemia cell line SPI-802: morphological, immunological, and isoenzymatic changes.

The phorbolester 12-0-tetradecanoylphorbol 13-acetate (TPA) was used for the induction of differentiation in cells of the human leukemia cell line SPI-802. The cellular morphology, surface marker antigen expression, and isoenzyme profiles of four enzymes (carboxylic esterase, acid phosphatase, hexosaminidase, and lactate dehydrogenase) served as parameters for monitoring the induced phenotypical changes. TPA led to distinct alterations of the morphology and significantly affected the growth rate with cessation of cell proliferation. No major increase in the number of nitro blue tetrazolium-positive cells or aggregation of cells, phagocytosis of latex beads, adherence to plastic surface, or development of pseudopodia were observed. As TPA-treated SPI-802 cells remained negative for these markers of the monocyte-macrophage complex, it can be concluded that the cells did not differentiate into monocytes and macrophages. The immunological marker profile based on testing of 55 monoclonal antibodies, terminal deoxynucleotidyl transferase and two erythrocyte rosette tests indicated a differentiation of SPI-802 cells along the granulocytic cell lineage. This was confirmed by isoenzyme analysis, especially that of carboxylic esterase. An isoenzyme specific for monocytes and macrophages was not detected. In earlier studies it was found that SPI-802 cells produce hemoglobin upon exposure to TPA or hemin. This latter observation and the present results suggested a comparison with the two erythroleukemia cell lines K-562 and HEL. SPI-802 cells appear to have the potential to differentiate along several cell lineages.

Antibodies, Monoclonal↗

PubMed1986

Reactivity patterns of monoclonal antibodies positive on myelomonocytic leukemia cells as defined by esterase isoenzyme analysis.

The reactivity with monoclonal antibodies (MoAbs) specific for myelomonocytic cells and the expression of a particular esterase isoenzyme were analyzed in 159 cases of acute myeloid leukemias. The incidence of positivity of 16 MoAbs (MCS-2, MCS-1, OKM1, My-1, Leu-M1, Leu-M3, CA-2-38, MY4, MY7, MY8, MY9, VIM-D2, VIM-D5, Mo1, Mo2, 63D3) was studied using the indirect immunofluorescence technique. A carboxylic esterase isoenzyme which can be inhibited completely and selectively by sodium fluoride (NaF) was demonstrated by isoelectric focusing on horizontal polyacrylamide gels. This NaF-sensitive isoenzyme indicated the monocytic origin of the blast cells as it is specific for this cell lineage. Prior to the immunological-isoenzymatic analysis all cases were categorized into two subtypes according to morphological criteria of the FAB classification system: 147 cases of AML (FAB M1-3) and 12 cases of AMMoL/AMoL (FAB M4/5). However, 15 out of 147 cases of AML expressed the NaF-sensitive isoenzyme and were therefore assigned to the group AMMoL/AMoL. Likewise, 1 case, diagnosed morphologically as AMMoL, was negative for this marker isoenzyme and was assigned to the other leukemia subtype. The incidence of reactivity varied widely for the MoAbs tested regarding the overall results on all cases and the positivity of cases of either AML or AM-MoL/AMoL. The MoAbs were grouped into four classes depending on the pattern of reactivity with myeloblastic or monoblastic or both subtypes of acute myeloid leukemia. The MoAbs MCS-2, MY7, Leu-M1, and MY9 detected the vast majority of cases with either myelocytic or monocytic involvement (group-I: "pan-myelomonocytic" reactivity). The MoAbs MCS-1, OKM1, VIM-D5, and Mo1 showed a predominance in their staining pattern for monocytic variants, but were also positive on a substantial percentage of nonmonocytic cases (group-II: predominantly reactive with monocytic, but also myelocytic cases). The MoAbs Leu-M3, MY4, VIM-D2, Mo2, and MY8 reacted with the large majority of AMMoL/AMoL cases and with a small number of AML cases (group-III: monocyte-"specific" reactivity). The MoAbs of group-I are useful in differentiating acute lymphoid from acute myeloid leukemias. The MoAbs of group-III, and to a lower extent those of group-II, will be of considerable value in the subtyping of acute myeloid leukemias. The results show that accuracy of leukemia classification might not always be achieved by morphology alone, but that immunological and biochemical aspects should be included as well, and several MoAbs are very useful tools for classification and subtyping of acute myeloid leukemias.

Antibodies, Monoclonal↗

PubMed1986

The use of monoclonal antibodies for the identification and classification of acute myeloid leukemias.

We reviewed a library of monoclonal antibodies (MoAbs) detecting antigens on myelomonocytic cells and analysed their reactivity patterns as reported in the literature. On the basis of the frequency of positivity with the myelocytic variants (FAB M1-3) or monocytic variants (FAB M4/5) of acute myeloid leukemias, the MoAbs were assigned to one of four groups. MoAbs of Group I identified most cases of both the myelocytic and the monocytic cell lineages ('pan-myelomonocytic' reactivity) and can be used to identify acute myeloid leukemias regardless of the subtype. Group II comprised MoAbs which reacted with the majority of FAB M1-3 cases, but showed a preference in reactivity with AMMoL/AMoL cases (reactivity: myelocytic partly, monocytic predominantly). MoAbs of Group III stained most cases with monocytic phenotypes, but labelled only a small percentage of non-monocytic cases. These MoAbs are valuable tools for the detection of cases with monocytic features. Group IV MoAbs reacted with a small to intermediate percentage of myelocytic and/or monocytic cases. Besides their diagnostic application MoAbs might be used in new therapeutic approaches such as in-vivo serotherapy with MoAbs and purging of autologous bone marrow for transplantation. None of the described MoAbs appear to be leukemia-specific. Many MoAbs have been produced against non-myelomonocytic cells and were reactive with cells outside the myelomonocytic cell lineages and the hematopoietic system. Other MoAbs with apparent cell lineage-restricted reactivity regarding normal cells stained leukemic cells of other cell lineages. This phenomenon of translineage reactivity of leukemic cells with mutually exclusive markers indicating a biphenotypic marker profile might be the result of abnormal, disregulated gene expression. New classification systems of acute myeloid leukemias based on immunological marker profiles have been proposed. The analysis of reactivity of normal and malignant myelomonocytic cells with MoAbs has led to refined differentiation schemes of the normal hematopoiesis.

Antibodies, Monoclonal↗

PubMed1986

The reproducibility of acute lymphoblastic leukemia phenotype determinations: evaluation of monoclonal antibody and conventional hematopoietic markers.

Peripheral blood and/or bone marrow lymphoblasts from 25 patients with acute lymphoblastic leukemia (ALL) were tested with a panel of monoclonal antibodies (MoAbs) and conventional hematopoietic markers by three different laboratories. The results were analysed to evaluate the reproducibility of ALL phenotype determinations. Specimens were transported between laboratories by 24-h courier service and were classified on the basis of indirect immunofluorescence MoAb reactivities as follows: B-lineage ALL (BA-1+T-MCS-2-); T-lineage ALL (T+BA-1-MCS-2-); myeloid antigen ALL (MCS-2+BA-1-CALLA-T-) and unclassified ALL (BA-1-MCS-2-CALLA-T-). Conventional marker studies for surface immunoglobulin (sIg), cytoplasmic immunoglobulin (cIg), sheep erythrocyte rosette formation (E) and nuclear terminal deoxynucleotidyl transferase (TdT) were also performed. In the cases with sufficient marker data to permit classification, 90% (18/20) were identically classified by different laboratories and this concordance was statistically significant (p less than 0.05). The agreement between laboratories for individual MoAb and conventional marker analyses was statistically significant (p less than 0.05) for all markers with the exception of BA-2, cIg and TdT determinations. Six of 7 discordant BA-2 cases represented BA-2+ evaluations which had subsequent BA-2- results following specimen transportation. These findings suggest instability of the BA-2 antigen to transport conditions. A similar pattern of positive to negative evaluations following transportation was observed in 5/5 discordant results involving other MoAbs. Disagreement between laboratories for cIg and TdT determinations implies that the detection of cytoplasmic or nuclear antigens may be more prone to subjective interpretation than cell surface antigen marker analyses. Our findings suggest that immunofluorescence marker studies employing MoAbs to cell surface antigens are in general highly reproducible. Our results also indicate that specimen storage conditions and the cellular location of target antigens are important variables which may affect the reproducibility of ALL phenotype determinations.

Antibodies, Monoclonal↗

PubMed1986

Hodgkin's disease derived cell lines HDLM-2 and L-428: comparison of morphology, immunological and isoenzyme profiles.

The cell lines HDLM-2 and L-428 were established from the pleural effusions of two patients with Hodgkin's disease. We studied and compared phenotypic characteristics of HDLM-2 and L-428 cells before and during induction of differentiation with 12-O-tetradecanoylphorbol 13-acetate (TPA) using a number of parameters. TPA-treated HDLM-2 and L-428 cultures did not show adhesion to plastic surface or aggregation of cells; the cells did not develop pseudopodia and were not phagocytic. Only a slight increase in the percentage of NBT-positive cells was observed for L-428 cells. TPA led to a cessation of cell proliferation and to a dose-dependent decrease in the number of viable cells in both cell lines. In HDLM-2 and L-428, treatment with TPA induced distinct morphological changes indicative of a partial differentiation along the myeloid cell lineage. In addition, the production and expellation of benzidine-positive, unnucleated particles were observed in HDLM-2 and L-428 cells. The induced isoenzyme profiles of carboxylic esterase and acid phosphatase resembled those found in myelomonocytic leukemia cell lines. Both cell lines were negative for immunological markers of the T- and B-cell lineages, but reacted with several markers associated with the myelomonocytic cell lineages. HDLM-2 cells produced a factor which could induce differentiation in 12 leukemia cell lines. The overall results suggest that Hodgkin and Sternberg-Reed cells constitute a unique cell type and might be derived from cells of the myelomonocytic cell lineage.

Acid Phosphatase↗

PubMed1986

Reactivity pattern of 'myeloid monoclonal antibodies' with emphasis on MCS-2.

The reactivity pattern of the murine monoclonal antibody (MoAb) MCS-2 was tested on a panel of 724 cases of leukemia-lymphoma. MCS-2 was positive in 178/185 (96%) cases of AML (FAB M1-3), 10/10 cases of AMMol/AMoL (FAB M4/5), 42/45 (93%) cases of CML, 1/1 case of CMoL, 37/38 (97%) cases of CML-myeloid blast crisis, 0/9 cases of CML-lymphoid blast crisis. No positive staining was seen in 238 cases of T-CLL, mycosis fungoides, Sèzary-syndrome, B-CLL, hairy cell leukemia, multiple myeloma and T- and B-lymphoma nor in 32 cases of B-ALL, Burkitt-lymphoma, Null-ALL and immature T-lymphoma. A positive expression was found in 8/110 cases of cALL, 1/6 cases of pre B-ALL and 1/35 cases of T-ALL. Fifteen other MoAbs (MCS-1, OKM1, My-1, Leu-M1, Leu-M3, CA-2-38, MY4, MY7, MY8, MY9, VIM-D2, VIM-D5, Mol, Mo2, 63D3) which are associated with the myelomonocytic cell lineages were tested by indirect immunofluorescence on 60 or more patients (62-149 cases). A wide variability in the frequency of positivity was seen for the panel of cases studied and for the blast cell populations per individual samples: 21-96% of the AML cases (FAB M1-3) and 31-100% of the AMMoL/AMoL cases (FAB M4/5) were positive for the various MoAbs. None of the analysed MoAbs stained only myelocytic or only monocytic leukemias, but a certain degree of preference for the monocytic variants was noted for Leu-M3, CA-2-38, MY4, VIM-D2, Mo2 and 63D3. The detection of MCS-2 on immature ALL blast cells might indicate a coexpression of lymphoid and myeloid markers on very immature cells, or an abnormal gene expression by malignant cells, or the identification of a so far undetected subclass of acute leukemias.

Adult↗

PubMed1986

Heterogeneity of marker expression in B-cell leukemias and its diagnostic significance.

Lymphoproliferative disorders of B-cell origin are identified by surface immunoglobulin markers. Clinically, these include several types of leukemias and lymphomas. We have attempted to further characterize B-cell leukemias immunologically using monoclonal antibodies Leu-1 and FMC-7. While cases of classical B-CLL have been shown to react with Leu-1 monoclonal, most other B-cell leukemias often do not react with Leu-1. Our results show that use of an additional monoclonal FMC-7 does not contribute towards diagnostic reliability.

Antibodies, Monoclonal↗

PubMed1986

Morphological and isoenzymatic differentiation of B-chronic lymphocytic leukaemia cells induced by phorbolester.

Fresh leukaemia cells from the peripheral blood of 6 patients with B-chronic lymphocytic leukaemia (CLL) were cultured in the continuous presence of the phorbolester 12-O-tetradecanoylphorbol 13-acetate (TPA) for in vitro induction of differentiation. Upon treatment with TPA the cells showed distinct morphological changes consisting of cytoplasmic and nuclear enlargement, vacuolisation and protrusion of cytoplasm, eccentric location of nuclei with perinuclear clear zones, and oval to elongated cell forms. Isoenzyme profiles of the enzymes carboxylic esterase, acid phosphatase, hexosaminidase and lactate dehydrogenase (LDH) were analysed by isoelectric focusing on polyacrylamide gels. An increase in the number and in the staining intensity of isoenzymes were observed for all 4 enzymes in the TPA-exposed cells indicating a maturation along the B cell pathway. TPA triggered the new expression of the tartrate-resistant acid phosphatase isoenzyme, a marker of hairy cell leukaemia (HCL) cells, and of the hexosaminidase I isoenzyme, a marker of multiple myeloma cells. The induced phenotypic changes are suggestive of differentiation to stages corresponding to those of HCL cells or 'pre-plasma cells'.

Acid Phosphatase↗

PubMed1986

Gene encoding the alpha chain of the T-cell receptor is moved immediately downstream of c-myc in a chromosomal 8;14 translocation in a cell line from a human T-cell leukemia.

The SKW-3 cell line, which was established from the malignant cells of a patient with T-cell chronic lymphocytic leukemia, is characterized by a translocation involving chromosome 8 (band q24) and chromosome 14 (band q11) [t(8;14)(q24;q11)]. To determine the position of the gene encoding the alpha chain of the T-cell receptor and of the human protooncogene myc (c-myc) in relation to the breakpoint junctions and to evaluate their possible role in the pathogenesis of T-cell neoplasia, we applied the techniques of in situ chromosomal hybridization and Southern blot analysis to SKW-3 cells. Our results indicate that the breakpoint on chromosome 14 at band q11 occurs close to a joining sequence of the gene encoding the alpha chain of the T-cell receptor. Additional rearrangements within the alpha-chain locus appear to split the variable region cluster. As a result of the rearrangements, the constant region of this gene, as well as some variable region segments, are translocated to chromosome 8, to the 3' side of the c-myc-coding exons. The identification of a breakpoint to the 3' side of c-myc suggests that this translocation is analogous to the variant (2;8) and t(8;22) translocations observed in the B-cell malignancies.

Chromosome Mapping↗

PubMed1986

Molecular cloning of the breakpoint junction of a human chromosomal 8;14 translocation involving the T-cell receptor alpha-chain gene and sequences on the 3' side of MYC.

The MOLT-16 cell line, which was established from the malignant cells of a patient with T-cell acute lymphoblastic leukemia, is characterized by a translocation involving chromosome 8 (band q24) and chromosome 14 (band q11) [t(8;14)(q24;q11)]. To determine the position of the gene encoding the alpha chain of the T-cell receptor and of the protooncogene MYC (formerly c-myc) in relation to the breakpoint junction and to evaluate their possible role in the pathogenesis of T-cell neoplasia, we applied the techniques of in situ chromosomal hybridization, Southern blot analysis, and molecular cloning to MOLT-16 cells. Our results indicate that the breakpoint on chromosome 14 at band q11 occurs close to a joining sequence of the gene encoding the alpha chain of the T-cell receptor. The constant region and part of the joining region of this gene are translocated to the 3' side of the MYC exons. The breakpoints on chromosomes 8 and 14 are close to, but distinct from, those found in SKW-3, another T-cell leukemia cell line, which has a t(8;14). The identification of a breakpoint to the 3' side of MYC suggests that this recurring translocation is analogous to the variant t(2;8) and t(8;22) translocations observed in the B-cell malignancies.

Cell Line↗

PubMed1986

A case of TdT-positive B-cell acute lymphoblastic leukemia.

The phenotypic marker profile of a patient with B-cell acute lymphoblastic leukemia (B-ALL) is described. The blast cells showed typical FAB L3 morphology, had the characteristic t(8;14) chromosomal abnormality, and were monoclonal in the expression of surface immunoglobulins. The clinical course of this patient is consistent with the poor prognosis described for B-ALL cases. Surface marker analysis identified cells positive for surface immunoglobulins, Ia-like antigen, common ALL-antigen, and terminal deoxynucleotidyl transferase. This marker profile shows immunologic characteristics of the two B-cell leukemia subtypes, pre-B-ALL and B-ALL. This "intermediate" immunologic phenotype might either be the result of an uncoupling of the sequential immunologic maturation processes or of an arrest of the cells at an intermediate stage between the two otherwise clearly defined leukemia subtypes, but closer to the typical B-ALL stage. This latter observation is supported by isoenzyme marker analysis, as the cells were negative for the hexosaminidase I isoenzyme, which is positive in pre-B-ALL but negative in B-ALL.

Acute Disease↗

PubMed1986

Monocyte-associated acid phosphatase isoenzyme profiles as determined in acute myeloid leukaemia cells.

The acid phosphatase (acP) isoenzymes from the blast cells of 102 cases of acute myeloid leukaemia were separated by isoelectric focusing on horizontal polyacrylamide gels. The cases were classified on the basis of the FAB cooperative group criteria. Several single bands were combined into groups (I-IV). An increase in the number of acP isoenzymes was noted which paralleled the assumed maturation along the granulocytic cell lineage from FAB M1 to FAB M3 and along the monocytic cell lineage from FAB M4 to FAB M5. One isoenzyme which was resistant to tartrate inhibition was found in 40% of the monocytic variants FAB M4 and M5, but not in the nonmonocytic cases FAB M1-M3 and M6. This particular isoenzyme, which has been described as being characteristic for hairy cell leukaemia, also appears to be a marker of the monocyte/macrophage system and the respective neoplastic counterparts. The FAB M4 and M5 patients expressed a characteristic profile of group I isoenzymes which allows for the discrimination between monocytic and nonmonocytic cells.

Acid Phosphatase↗

PubMed1986

Diagnostic value of immunological leukemia phenotyping.

The diagnostic value of immunological leukemia phenotyping using a panel of reagents in immunofluorescence assays was assessed in 309 consecutive patients. The cells from 307 patients could be clearly phenotyped and assigned to one of the subgroups with a definite immunophenotype. Each phenotype was characterized by a distinct marker profile. A simplified classification scheme based on surface antigen expression is presented. A combination of complementary reagents ('first panel') was used for the first-line screening. The application of selected reagents from the 'second panel' allowed for further subtyping and confirmation of the primary diagnosis. The contribution of different key reagents to the identification of distinct immunophenotypes is discussed. Multiple marker analysis, i.e. the combination of information from several disciplines, is a necessary and very useful tool in the routine investigation of patients with hematopoietic malignancies.

Antigens, Neoplasm↗

PubMed1986

Incidence of TdT positivity in cases of leukemia and lymphoma.

The expression of the enzyme marker terminal deoxynucleotidyl transferase (TdT) was examined by immunofluorescence assay in the cells from 333 cases with various types and subtypes of leukemia or lymphoma. More than 90% of cALL and T-ALL, 70% of Null-ALL and 80% of pre-B-ALL were TdT-positive. One case in the commonly TdT-negative group of B-ALL showed TdT-positive cells. All cases of mature B-cell malignancies (B-CLL, hairy cell leukemia, B-cell lymphoma) have been TdT-negative. In the group of mature T-cell malignancies, T-CLL and mycosis fungoides were negative and 2 out of 6 mature T-cell lymphomas were TdT-positive. 13% of acute myeloid leukemias and 36% of CML in blast crisis expressed TdT. Therefore, these TdT-positive cases of CML in blast crisis also carrying the common ALL-antigen belong to the lymphoid subtype. CML and erythroleukemia were invariably TdT-negative. TdT has become an indispensable indicator of immature lymphoid leukemia cells and is particularly valuable as part of the panel of markers used in leukemia phenotyping.

B-Lymphocytes↗

PubMed1986

Establishment of a hairy cell leukemia cell line carrying Tac antigen and phagocytic activity with B-cell characteristics.

A hairy cell leukemia cell line designated "Hair-M" was established in a suspension culture derived from the peripheral blood of an 86-year-old Japanese male with a diagnosis of hairy cell leukemia. The Hair-M cells were identified as having prominent hair-like cytoplasmic projections by examination with phase-contrast and scanning electron microscopy. These cells displayed ruffled membranes and stublike microvilli similar to those observed on the surfaces of cells in the peripheral blood of the patient. Immunologic and cytochemical studies on the Hair-M cells confirmed derivation from the clone of the patient's leukemia cells. Although the cultured Hair-M cells had definite B-cell characteristics, such as IgG kappa-chains on the surface and in cytoplasm, they also demonstrated Tac antigen, which is usually expressed on activated T-cells, and myelomonocyte antigens determined by OKM-1 and MCS-1 monoclonal antibodies. Other cell surface markers, including E(-), IgGFc(-), IgMFc(-), C3R(+), Ia-like antigen(+), OKT9(+), OKT10(+), and terminal deoxynucleotidyl transferase(-), were detected; no Epstein-Barr virus-determined nuclear antigen was detected. The karyotype of the Hair-M cells was determined to be 46XY with -11, -14, and two marker chromosomes. The Hair-M cells also had phagocytic activity to rabbit anti-human IgG serum-coated polyacrylamide gel particles.

Aged↗