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At least 91 records · Page 5Linked to original sources
PubMed1983

Monoclonal antibody against a differentiation antigen on human leukemia cells: cross-reactivity with rat leukemia and suppression of rat leukemia in vivo.

We produced a McAb against a normal differentiation antigen on human ANLL that cross-reacts with a rat ANLL. The McAb reacted with all ANLL cells tested as well as normal undifferentiated myelomonocytic cells. This McAb, of the IgM isotype, in the presence of C mediated lysis of human and rat leukemic cells in vitro. In addition, it mediated complete tumor suppression in rats engrafted with 10(2) to 10(3) rat leukemic cells in vivo. No significant side effects were observed in McAb-treated rats. McAb of this type may be useful in the treatment of human ANLL after conventional therapy, which often eliminates most leukemic cells, leaving a small number of residual cells. The ultimate utility of this McAb for human therapy or McAb directed against the same or other differentiation antigens remains to be determined.

Acute Disease↗
PubMed1986

Inflammatory bowel disease and leukemia. A report of seven cases of leukemia in ulcerative colitis and Crohn's disease and review of the literature.

In a review of a large number of patients with inflammatory bowel disease, leukemia was observed in five patients with chronic ulcerative colitis and in two patients with Crohn's disease. In ulcerative colitis patients, there were three cases of acute myelocytic leukemia and one case each of acute lymphoblastic leukemia and chronic granulocytic leukemia. In Crohn's disease patients, there was one case each of chronic granulocytic leukemia and chronic lymphocytic leukemia associated with thrombocythemia. Sixteen other cases of leukemia have been reported to date in inflammatory bowel disease. All types of leukemia, but particularly acute myelocytic leukemia, have been described. There has been no single common feature as to type (whether ulcerative colitis or Crohn's disease), extent and course, or medical and surgical treatment of the bowel disease. The relative risk of leukemia in patients with ulcerative colitis was 5.3 [95% confidence interval 1.7 to 12.3 (P less than 0.01)] and of acute myelocytic leukemia 11.4 [95% confidence interval 2.3 to 24.9 (P less than 0.01)]. Our data on patients with Crohn's disease were not sufficient to assess the statistical significance of leukemia in this disease. This study suggests that there may be an increased risk of leukemia, particularly acute myelocytic leukemia, in ulcerative colitis. The causal relationship, if any, remains undetermined.

Adult↗
PubMed1991

Glycolipid changes in murine myelogenous leukemias: neutral glycolipids as markers for specific populations of leukemias.

We have studied the glycolipid composition of six different murine myelogenous leukemias as well as that of T-cell leukemias and normal spleen cells. Neutral and acidic lipid fractions were isolated by column chromatography on DEAE-Sephadex and analyzed by high-performance thin-layer chromatography (HPTLC) and an HPTLC overlay method. Murine myelogenous leukemias were found to contain globo- and ganglio-series neutral glycolipids, e.g., glucosylceramide (Glc-cer), lactosylceramide (Lac-cer), globotriaosylceramide (Gb3), globoside (Gb4), Forssman glycolipid (Gb5), and asialo-GM1 (GA1). Monoblastic leukemia cells contained increased proportions of Gb3, Gb4, Gb5, and GA1. Monocytic and myelomonocytic leukemia cells contained increased proportions of Glc-cer and Lac-cer. Especially, Glc-cer accounted for approximately 60% of the total neutral glycolipids in monocytic leukemia cells. Gb3 was the major neutral glycolipid in reticulum cell neoplasm type A, and it accounted for approximately 75% of the neutral glycolipids. GA1 was the major neutral glycolipid in myeloblastic and granulocytic leukemia cells as well as T-cell leukemias. Especially, granulocytic leukemia cells contained predominantly GA1, and it accounted for approximately 80% of the total neutral glycolipids. The pattern of gangliosides in myelogenous leukemias was more complex when compared with that of the neutral glycolipids; murine myelogenous leukemias contained at least 13 gangliosides, including such major gangliosides as GM1, GM1b containing N-acetyl neuraminic acid and N-glycolyl neuraminic acid, and Ga1NAc-GM1b. Alterations of glycolipid composition in murine myeloid leukemias may be associated with cellular differentiation and maturation, and therefore these characteristic glycolipid species may be regarded as markers for specific populations of leukemia cells.

Animals↗
PubMed1993

Leukemia-associated marker combinations in acute leukemia suitable for detection of minimal residual disease.

In the absence of truly leukemia-specific antigen, antigen combinations were identified in leukemia cells that are absent or extremely rare among normal hemopoietic cells. Some of the studied combinations related to the simultaneous surface and cytoplasmic marker expression, others, expressed mainly on cell surface membrane, represented atypical or aberrant combinations. Comparing membrane (m) and cytoplasmic (c) antigen expression (followed in 23 acute leukemia cases), we observed that CD3 could be detected in cytoplasm in the majority of T-ALL cells, while was absent on cell surface membrane where simultaneous expression of more immature T cell markers, such as CD7 and CD5, could be detected. Combination of mCD7/cCD3 could be regarded as a suitable marker of individual T-ALL cells. In cases of B-precursors of acute leukemia cells, leukemia-related combination of mCD19/cCD22 was found, which could characterize a single leukemia cell. The cells in one of 11 AML followed cases were positive for CD13 in cytoplasm, but not on cell surface membrane, where CD33 and other myeloid antigens were expressed. The cells in another two AML cases were positive for CD11 in cytoplasm but not on cell surface membrane, where CD13 or CD33 were expressed. Again, marker combinations of mCD33/cCD13 and mCD13 or mCD33/cCD11, respectively, represent a leukemia-related feature, suitable for tracing single leukemia cells in double immunofluorescence. Acute leukemia defined by the coexpression on most blast cells of antigens classically attributed to different lineages (referred as atypical/aberrant marker combinations) remains a rare event. We isolated a series of 27 (12%) such cases of 225 acute leukemia patients whose cells were immunophenotyped at diagnosis. Myeloid markers were present in T-ALL of two cases, T and B markers were coexpressed in 13 cases, markers of B and myeloid lineage were associated in one case, and T cell and myeloid antigens were found in 10 AML cases; in one AML case (M3 according to FAB classification) an aberrant nuclear coexpression of TdT was observed. In one case of the last group an interesting antigen combination of CD4/CD34 present in AML with monocytic differentiation was observed. When 5 patients with leukemia-associated (aberrant) markers were again analyzed at relapse, the relevant antigen combinations were retained in all of them. In summary, 44 of 50 cases (88%) from our acute leukemia series studied for leukemia-associated antigen combination, both with surface membrane and cytoplasmic marker combinations and those with aberrant markers coexpression allow the detection of minimal residual disease.

Adult↗
PubMed1982

Natural antibodies to the structural core protein (p24) of the human T-cell leukemia (lymphoma) retrovirus found in sera of leukemia patients in Japan.

In Japan, adult T-cell leukemias and lymphomas are more common than in the United States and Europe, and in the southwest part of Japan these T-cell malignancy cases appear in clusters. Therefore, we investigated the involvement in these leukemias and lymphomas of the human T-cell leukemia virus (HTLV) that was previously isolated in one of our laboratories from cultured T cells of some patients in the United States with leukemias and lymphomas involving relatively mature T cells. High titers of antibodies capable of quantitative precipitation of (125)I-labeled p24, a well characterized core protein of HTLV, were detected in 12 of 12 patients with untreated adult T-cell leukemia (ATL). (One negative was a patient on chemotherapy.) Ten of the 12 positive samples were from an area where the disease is endemic. Strong precipitating antibodies were also detected in five of seven cases of T-cell malignant lymphoma (TML) which differs from ATL by having fewer leukemic cells in the peripheral blood. High antibody titers were also observed in one of five cases of acute monoblastic leukemia and one of eight cases of chronic myelogenous leukemia in the blast phase of the disease. Low to moderate titers of antibodies were detected in several categories of leukemia (two cases of blast-phase chronic myelogenous leukemia, two cases of acute lymphoblastic leukemia of the null-cell type, and one case of acute myelogenous leukemia). Among all categories of leukemias, except ATL and TML, more cases were negative than positive for anti-p24 activity. All of 79 sera from normal Japanese, including 39 collected from the endemic ATL area of southwest Japan, were negative for antibodies to HTLV p24. All the positive reactivities observed were highly specific to HTLV. The only competition observed in the precipitation of HTLV p24 was with HTLV or with cell lines expressing HTLV and not with various animal retroviruses or a large number of human and subhuman primate cell lines, not known to be producing HTLV. The data strongly indicate an association of HTLV with the increased incidence of ATL in parts of Japan, probably with other forms of leukemias in Japan, and, less commonly, with certain T-cell malignancies in the United States.

Antigens, Viral↗
PubMed1985

Vaccination of adult and newborn mice of a resistant strain (C57BL/6J) against challenge with leukemias induced by Moloney murine leukemia virus.

Adult or newborn C57BL/6J mice were immunized with isogenic Moloney strain MuLV-induced leukemia cells irradiated with 10,000 rads or treated with low concentrations of formalin. Groups of immunized and control mice were challenged with a range of doses of viable leukemia cells, and tumor deaths were recorded for 90 days after challenge. Then, the doses of challenge cells which produced 50% tumor deaths were calculated for immunized and control mice. The logarithm of their ratio quantified the degree of protection provided by immunization. For adult C57BL/6J mice, a single immunization with MuLV-induced leukemia cells was not effective; either cells plus Bacillus Calmette-Guérin or Corynebacterium parvum, or else two immunizations with irradiated leukemia cells were needed to produce statistically significant increases in the values of the doses of challenge cells which produced 50% tumor deaths. Cross-protection was obtained by immunization with other isogenic MuLV-induced leukemias, but not by immunization with isogenic carcinogen-induced tumors or with an isogenic spontaneous leukemia. For newborn mice, a single injection of irradiated leukemia cells provided 1.3 to 1.5 logs of protection, and admixture of B. Calmette-Guérin or C. parvum increased this protection to 2.4 to 2.7 logs. Since irradiated and frozen-thawed MuLV-induced leukemia cells contained viable MuLV, leukemia cells treated with 0.5 or 1.0% formalin were tested as an alternative. A single injection of formalin-treated isogenic leukemia cells admixed with C. parvum provided between 1.7 and 2.8 logs of protection. These results demonstrate that a single vaccination of newborn animals against a highly antigenic virally induced leukemia produces strong protection against a subsequent challenge with viable leukemia cells.

Aging↗
PubMed1990

[Human acute leukemia. II. Acute lymphoblastic leukemia. Complex classification of acute leukemia].

Acute lymphoblastic leukaemias originate from cells committed either to T-lineage (T-ALL) or B-lineage (nonT-ALL). Leukaemic cells are classified into these lines according to the expression of lineage specific differentiation markers, which are T-cell receptors, associated with CD3 antigenic complex, for the T-line and immunoglobulins for the B-line. T-ALL seem to be one type of disease, in the B-lineage it is possible to distinguish several types of diseases according to clinical findings and immunoglobulin expression. Monoclonal antibodies directed against various surface antigens are used for diagnosis of ALL and their significance in various types of ALL is evaluated. Specificity of diagnostic markers is discussed especially from the point of the so called "mixed acute leukaemias", cells of which should differentiate in myeloid and lymphoid lines. The existence of a single one "mixed acute leukaemia" has not yet been reliably proved with the use of lineage specific differentiation markers. Present knowledge of karyotype findings in acute leukaemias classified according to specific differentiation markers is reviewed and the necessity to introduce a complex classification on this basis is stressed.

Burkitt Lymphoma↗
PubMed1989

[Acute leukemias in humans. I. Definition, etiology, and pathogenesis of acute leukemias. Classification of acute myeloid leukemia].

The present knowledge of acute leukaemias is critically reviewed. Acute leukaemias are clonal malignant neoplastic diseases which do not originate from transformation of totipotent haematopoietic stem cells, but of progenitors committed to myeloid, T-lymphatic or B-lymphatic differentiation lines. The transforming event seems to be associated with a nonrandom aberrant DNA rearrangement. Although leukaemic population is clonal, originating from a single cell, it exhibits phenotypic, and sometimes even karyotype heterogeneity. In the proposed human acute leukaemias classification leukaemic cells are allocated to a particular differentiation cell line on the basis of a positive finding of the lineage specific differentiation marker. Criteria for common types of acute myeloid leukaemias are described and possible existence of several other types is discussed.

Humans↗
PubMed1977

[Immunity in leukemia: reason for onset of leukemia, agent for successful therapy of leukemia].

Authors present the facts which indicate that in human medicine there is immunity against malignant tumors and leukaemia through T lymphocytes immunological control. The appearance of leukaemia in a certain number of persons is due to reduced immunity in the patient or weak antigen immunogenicity of leukaemic cells. Authors also present evidence for the existance of tumor antigens same as in leukaemic leukocytes in human pathology. These antigens belong either to still undiscovered viruses of human leukaemia, as is the case of reverse transcriptase of RNK virus, found in leukocytes of 95 percent of patients with acute leukaemia, or they are new antigens formed by combination of cell genoma and virus genoma, or by depression of the gene which were active only during the foetal life under the influence of oncogenic chemical substances or viruses. The evidence is given too, concerning the existence of immune response in human medicine, in the form of cytotoxic antibodies or sensitized T lymphocytes to tumor antigens which can be demonstrated in vitro by the test of colonial growth inhibition of tumor cells. As the immunity does not operate against tumor or leukaemic cells, the reason for it must be sought in the disorder of the afferent part (weak immunogenicity of tumor antigens, tolerance of tumor antigens, etc.), or of the efferent part of the immune response (the presence of blocking factors in the patient's plasma). At the end, the authors also discuss about the attempts of immunological treatment of acute leukaemia, and the results to this date are encouraging.

Acute Disease↗