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At least 19 recordsLinked to original sources
PubMed1977

Detection of thymus leukemia antigens on the surface membranes of murine leukemia cells resistant to thymus leukemia antibodies and guinea pig complement.

The thymus leukemia (TL) antigens of ASL-1 murine leukemia reversibly disappeared from the membranes of cells exposed to TL antisera; the cells acquired resistance to fresh TL antiserum and complement (antigenic modulation). Three independent methods, however, indicated that the acquisition of complement resistance preceded the complete disappearance of TL antigens from the cell surface. Modulated cells reduced known titers of TL antisera by absorption; they stained positively in immunofluorescence studies involving TL antibodies and fluorescence-labeled rabbit anti-mouse immunoglobulin. TL antigens labeled previously with 125I were recovered by immunoprecipitation from cellular extracts prepared with nonionic detergent. Continued exposure of the cells to TL antiserum led to virtually complete disappearance of the antigens. Similar results were obtained for RADA-1 cells, another murine leukemia that forms TL antigens, although in this instance the cells were resistant to the cytolytic effects of TL antisera and guinea pig complement (GPC) without prior exposure to TL antibodies. The density of TL antigens remaining on the surface of different TL(+) cell types failed to correlate with resistance to TL antibodies and GPC. Cells from F, hybrids of TL(+) and TL(-) mouse strains formed TL antigens and were susceptible to TL antibodies and GPC even though the density of TL antigens formed by the susceptible cells was less than the density of TL antigens formed by modulated cells. Stable somatic hybrids of RADA-1 cells and TL(-) cells formed TL antigens at lower density than did RADA-1 cells and lysed in the presence of aliquots of the TL antisera and GPC used in previous tests.

Animals↗
PubMedDate not supplied

[Does blastic crisis as revealed in chronic myeloid leukemia simulate either acute primary leukemia or acute primary leukemia with Philadelphia chromosome?].

In ten cases of apparently primary acute leukaemia, the discovery of a Philadelphia chromosome at routine examination of the caryotype led a diagnosis of blastic crisis of chronic myeloid leukemia. The clinical, cytological and cytogenetic pictures varied and only routine caryotypic examination may be used in reaching the diagnosis. The prognosis appear to be less bad than in blastic crises occurring after a long course of chronic myeloid leukaemia and closer to that of primary acute myeloid leukaemia.

Adolescent↗
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↗
PubMed1977

Clinical relevance of circulating immune complexes in human leukemia. Association in acute leukemia of the presence of immune complexes with unfavorable prognosis.

The occurrence of circulating immune complexes was investigated in 467 serum samples from 230 leukemia patients using the [(125)I]Clq-binding test. There was an increased serum [(125)I]Clq-binding activity in 40% of patients with acute myeloid leukemia, 23% with acute lymphatic leukemia, 46% in blastic crisis of chronic myeloid leukemia, 12% with chronic lymphatic leukemia, and 13% with chronic myeloid leukemia. In 48 patients, serum was also tested for soluble immune complexes by the Raji cell radioassay; the correlation between results of the two tests was significant. The Clq-binding material had properties identical with those of immune complexes. It sedimented as 14-28s material on sucrose density gradient. It contained IgG which could be dissociated at acid pH. Its Clq-binding properties could be removed after passage through anti-IgG immuno-absorbant or after a mild reduction-alkylation treatment, but were not sensitive to deoxyribonuclease treatment. Circulating immune complexes were found most commonly during the blastic stage of leukemia.Remission took place in 75.4% of patients with no detectable circulating immune complexes at the onset of acute leukemia, but in only 32.7% of those with detected complexes during this period. Median survival times of the former group of patients were more than 18 mo in acute myeloid leukemia and acute lymphatic leukemia and more than 8(1/2) mo in blastic crisis of chronic myeloid leukemia. The corresponding median survival times in the latter patient group were 64, 135, and 90 days. These findings were unrelated to prognostic features already known.

Adolescent↗
PubMed1977

In vitro induction of cell-mediated immunity to murine leukemia cells. II. cytotoxic activity in vitro and tumor-neutralizing capacity in vivo of anti-leukemia cytotoxic lymphocytes generated in macrocultures.

The main findings of the present study are: (a) highly reactive cytotoxic lymphocytes (CTL) against syngeneic and allogeneic murine leukemia cells were generated in vitro in macro 'one-way' mixed leukocyte-tumor cultures (MLTC). Cultures set up in large tissue culture flasks contained up to 400 X 10(6) normal spleen cells (responder cells) and 20--40 X (10(6) mitomycin C-treated leukemia cells (stimulator cells). Successful sensitization in macrocultures was greatly dependent upon the responder cell density and the responder/stimulator cell ratio. Cytotoxic activity, as measured by the 51Cr-release assay, peaked on day 5--7. (b) Sensitized 'memory' lymphocytes produced in primary MLTC could be restimulated with the original tumor cells to give a more rapid and stronger secondary cytotoxic response. (c) lymphocytes sensitized to allogeneic leukemia cells reacted equally well with sensitizing leukemia cells and with the corresponding normal lymphoid target cells, whereas lymphocytes sensitized to syngeneic leukemia cells did not react with the homologous normal lymphocytes. (d) Cryopreserved normal splenocytes and leukemia cells were as efficient as fresh cells in generating allogeneic and syngeneic CTL. (e) Using a Winn-type tumor neutralization assay, it was shown that both allogeneic and syngeneic splenocytes sensitized in vitro to EL4 leukemia (of C57BL/6 mice) and to YAC leukemia (of A mice) were capable of preventing tumor growth in the syngeneic host, whereas cultured normal splenocytes frequently showed a tumor-enhancing effect. Long-term survivors, remaining after inoculation of leukemia cells and sensitized lymphocytes, also became resistant to a tumor challenge that was up to 10,000 greater than the minimum lethal dose.

Animals↗
PubMed1979

Common leukemia-associated antigen of DBA/2 mouse leukemia detected by tumor rejection and complement-dependent cytotoxicity assays.

A cytotoxic antibody for L1210 leukemia cells was found in the (C57BL/6 x DBA/2)F1 (BDF1) mice immunized with L1210 leukemia cells infected with ts mutant of HVJ (HVJ-pi) and challenged several times with uninfected L1210 leukemia cells. These immune mice fell into two categories; high and low responders regarding the titer of cytotoxic antibody produced. The antigen defined by this cytotoxic antibody was present on leukemia cells originating in DBA/2 mice but not on leukemia induced by passage-A Gross virus or spontaneous mammary tumors. This serological cross-reactivity among L1210, P388, and L5178Y leukemia cells has been substantially confirmed by the observation of cross protection against challenge with DBA/2 leukemia cells in immune BDF1 mice. These findings strongly suggested the presence of a common DBA/2 leukemia-associated antigen different from known cell-surface antigens of murine leukemia. The results obtained in the present work also demonstrated the great efficacy of non-cytopathic, viable HVJ-pi-injected tumor cells as an immunogen for inducing tumor immunity.

Animals↗
PubMed1978

New leukemia in the course of therapy of acute lymphoblastic leukemia.

We have recently observed the development of second leukemia of a morphologically different type in three patients with acute lymphoblastic leukemia (ALL) while on therapy. The "second" leukemia occurred while on therapy at 23, 27, and 32 months of initial remission. All three were receiving systemic chemotherapy (CT) and prophylactic fractional irradiation to the central nervous system (CNS). The second leukemias in these three cases were one case of juvenile chronic myelogenous leukemia (JCML) and two cases of acute leukemia of the myeloblastic type by the usual morphologic criteria including the presence of Auer rods in one. In two cases a cytogenetically new clone was detected in the remission marrow 10 and 12 months preceding the overt change in clinical status. These three cases demonstrate that second leukemia occurs in patients with ALL and that some late "relapses" fall into this categpry. The possible etiologic role of modern intensive treatment regimens in the development of second leukemia is discussed.

Child, Preschool↗
PubMed1978

Destruction of circulating leukemia cells by phagocytosis in rats with myelogenous leukemia.

Acute myelogenous leukemia was induced in outbred Long-Evans rats by iv injections of leukemia cells from a subcutaneous tumor of Shay myelogenous leukemia. In rats with this leukemia the peripheral white blood cell (WBC) counts varied from 2.4 to 700 X 10(9)/liter. No differences were found in the bone marrow of the rats with the high WBC counts and that of rats with low WBC counts. This observation could explain the large variations in the number of circulating leukemia cells caused by differences in cell proliferation or delivery of cells into the circulation. Massive phagocytosis of leukemia cells occurred in animals with low WBC counts (less than 12 X 10(9)/liter) but not in animals with high WBC counts (greater than 150 X 10(9)/liter). This phagocytosis was directed against circulating leukemia cells. The main phagocytes were Kupffer's cells of the liver and macrophages of the spleen parenchyma. In addition, phagocytosis occurred in the spleens and bone marrow by intravascular macrophages, which were derived from extravascular sites. The endothelium of the postcapillary venules of the lymph nodes participated in the phagocytosis of circulating leukemia cells while continuing to be the locus of lymphocytic return from circulation to lymphatic parenchyma. The factors underlying the differences in macrophage activity between the rats with high and low WBC counts were unknown.

Animals↗
PubMed1978

Hematogenous development of rat mature granulocytic leukemia--comparison of 2,7-FAA-induced and transplanted leukemia.

The oral administration of N,'N-2,7-fluorenylenebis-acetamide (2,7-FAA) induces leukemia, especially mature granulocytic leukemia in rats. We compared the degree of infiltration of 2,7-FAA-induced mature granulocytic leukemia with that of transplanted leukemia for the purpose of proving hematogenous development of leukemia. The bone marrow, spleen and liver were examined in the cases of diffuse lesion of 2,7-FAA-induced and transplanted leukemia. The average degree of infiltration of both 2,7-FAA-induced and transplanted leukemia was high in the bone marrow, medium in the spleen, and low in the liver. Intravenous transplantation of malignant neoplasm is an example of hematogenous metastasis. The similarity of infiltration between 2,7-FAA-induced and transplanted leukemia suggests that the former is spread by hematogenous metastasis.

2-Acetylaminofluorene↗
PubMed1979

Erythroid leukemia induced by Friend lymphatic leukemia virus in T-cell-depleted mice.

BALB/c mice depleted of T-cells by thymectomy at 3 to 5 days of age and by treatment with antithymocyte serum were inoculated with the lymphatic leukemia virus derived from Friend virus. After a long latent period, these animals developed erythroid leukemia. In contrast, intact control mice inoculated with Friend virus-associated lymphatic leukemia virus developed typical thymic (T-cell) lymphomas. Cell-free virus prepared from leukemic T-cell-depleted animals induced lymphoid, myeloid, and erythroid leukemias in intact mice. The erythroid leukemia-inducing virus differed from the spleen focus-forming component of Friend virus in its long latent period (88 to 225 days) and in its inability to induce spleen foci. End-point dilution experiments suggested that a hitherto undescribed component of the Friend virus complex might be responsible for these late-appearing erythroid leukemias.

Animals↗
PubMed1978

G(RADA1): a new cell surface antigen of mouse leukemia defined by naturally occurring antibody and its relationship to murine leukemia virus.

A new cell surface antigenic system of the mouse, designated G(RADA1), is described. The antigen is defined by cytotoxic tests with the A strain X-ray-induced leukemia RADA1 and naturally occurring antibody from random-bred Swiss mice and can be distinguished from all other serologically detected cell surface antigens of the mouse. Absorption tests indicate that G(RADA1) is present in the normal lymphatic tissue and leukemias of mouse strains with high spontaneous leukemia-incidence, e.g., AKR, C58, and C3H/Figge. Low leukemia-incidence strains, e.g., C57BL/6, BALB/c, and A lack G(RADA1) in their normal tissues, but a proportion of leukemias and solid tumors arising in these strains are G(RADA1)+. The relation of G(RADA1) to MuLV is shown by G(RADA1) appearance after MuLV infection of permissive cells in vitro; four of five N-tropic MuLV isolates, one of four B-tropic MuLV, and none of four xenotropic MuLV induce G(RADA1). Two MCF MuLV, thought to represent recombinants between N-ecotropic and xenotropic MuLV, also induce G(RADA1). Serological and biochemical characterization indicates that G(RADA1) is a type-specific determinant of the gp70 component of certain MuLV. The presence of natural antibody to RADA1 in various mouse strains and the emergence of G(RADA1)+ leukemias and solid tumors in mice of G(RADA1)- phenotype suggest widespread occurrence of genetic information coding for this antigen.

Animals↗
PubMed1978

B-cell lymphosarcoma cell leukemia: dynamics of surface-membrance immunoglobulin. Value for differentiation from chronic lymphocytic leukemia.

Circulating abnormal lymphoid cells in patients with lymphosarcoma cell leukemia show intense fluorescence when stained with fluoroscein-labeled anti-immunoglobulin. The fluorescence is brighter than normal B cells in contrast with chronic lymphocytic leukemia cells, which have much weaker fluorescence than normal. Also in striking contrast with chronic lymphocytic leukemia cells, lymphosarcoma cell leukemia cells redistribute the surface immunoglobulin rapidly during incubation at 37 degrees C to form bright caps. In this respect they more closely resemble normal B cells than chronic lymphocytic leukemia cells. In addition, in sequential studies, the appearance of these characteristics among the circulating cells of patients with lymphoma has been shown at a time when the appearance of a leukemic phase was equivocal morphologically. Thus these cellular characteristics may be helpful in the early diagnosis of a leukemic phase of lymphoma as well as distinguishing these cells from those in chronic lymphocytic leukemia.

B-Lymphocytes↗
PubMed1975

Correlation of early murine leukemia virus titer and H-2 type with spontaneous leukemia in mice of the BALB/c times AKR cross: a genetic analysis.

Tissue extracts from 6-wk old mice of the AKR strain (H-K) show high levels of infectious murine leukemia virus, and these mice show a near 100% incidence of spontaneous leukemia. In F1 mice of the cross, BALB/c times AKR (H-2K/H-2K), both the occurrence of virus and the incidence of spontaneous leukemia are suppressed to very low values, due largely to the presence of the FV-1b allele inherited from the BALB/c parent. Mice of the (BALB/c times AKR) F-1 times AKR backcross generation were observed for possible correlations between virus expressions at 6 wk of age, H-2 type and leukemia incidence. H-2 type showed at most a weak influence on the occurrence of infectious virus, but there was a very strong correlation between the level of virus expression and the occurrence of leukemia and a strong correlation between H-2 type and leukemia. In addition, there was a highly significant nonrandom distribution of virus-negative mice among the backcross litters, suggesting a maternal effect on virus expression.

Animals↗
PubMed1979

In vitro studies of cell-mediated immunity to Moloney murine leukemia virus and Moloney leukemia-associated surface antigens.

Cell-mediated immunity to Moloney murine leukemia virus (M-MuLV) and to tumor-associated surface antigens of leukemia cells induced by the virus was studied with an in vitro migration inhibition factor assay. Spleen cells of C57BL/6N mice at Day 14 following inoculation with Moloney murine sarcoma virus, produced migration inhibition factor in response to M-MuLV. The Moloney murine sarcoma virus-immune spleen cells, however, did not respond to other murine type C viruses, to AKR and Rauscher viruses, or to murine mammary tumor virus. The immune spleen cells also responded specifically to purified glycoprotein with molecular weights of 69,000 and 71,000 and proteins with molecular weights of 30,000 and 12,000, but not to protein with a molecular weight of 10,000, of the homologous M-MuLV. Migration inhibition factor production was also observed in response to soluble 3 M KCl extracts of leukemia cells, MBL-2, induced by M-MuLV. Similarly, the immune spleen cells responded to membrane fractions purified from the MBL-2 cells. Comparable membrane fractions prepared from a Gross virus-induced leukemia, E male G2, and a radiation-induced leukemia, RL male 1, were not active. The tumor-associated surface antigens of MBL-2 membranes could be solubilized by the detergent, Nonident P-40. Thus, C57BL/6N mice inoculated with Moloney murine sarcoma virus developed cell-mediated immunity to envelope and some internal antigens of M-MuLV and also to tumor-associated surface antigens of a tumor induced by this leukemia virus.

Animals↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXV. Significance of the Ph1 (including unusual translocations) in various acute leukemias.

The following rare Ph1-positive chromosome constitutions, based on the cytogenetic findings in three cases with acute leukemia, are presented. 1) A hypodiploid karyotype, primarily 43, -X, -7, -8,9p+ and a Ph1, in a patient with acute lymphoblastic leukemia (ALL) in relapse, followed by a complete remission and a normal chromosomal picture and then by the appearance of cells with a 46,XX,Ph1 karyotype. The Ph1 was due to a standard translocation between chromosomes no. 9 and no. 22. 2) The first demonstration of an unusual Ph1-translocation between chromosomes no. 19 and no. 22 in a condition other than chronic myelocytic leukemia (CML), i.e., acute myeloblastic leukemia (AML). 3) The presence of a Ph1 in acute erythroleukemia (EL) due to a translocation between chromosomes no. 4 and no. 22, this apparently being the first description of such a translocation in any disease. The cytogenetic findings, particularly those in the Ph1-positive case of ALL, were evaluated in relation to the cytologic and immunologic features, clinical courses and implications, and the interrelationship between the three conditions (AML, blastic phase of CML and ALL), which have to be considered in cases of Ph1-positive acute leukemia.

Adult↗