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N Haran-Ghera

Publications and source records attributed to N Haran-Ghera.

At least 55 records · Page 3Linked to original sources
PubMed1984

Age-related expression of TL antigen in AKR/J mice.

A survey of age-related expression of thymus-leukemia (TL) alloantigens (TL 1,2,4) among bone marrow, spleen and thymus cells of grossly normal and leukemic AKR/J mice is presented. The response of the stained cells to antisera directed against TL antigens was analysed by means of the fluorescence-activated cell sorter (FACS) apparatus. A transient expression of TL antigens on cells among the bone marrow population was observed in 1- to 20-day-old AKR/J mice, followed by an undetectable level up to 3 months and its reappearance thereafter. Thymocytes expressed TL from the age of 4 months onwards, reaching a transient maximal level at the age of 6 months in females and 8 months in males. Subsequently, an age-related decrease took place. In spleen cells from newborn mice TL expression was seen, followed by a rapid decrease to undetectable levels up to the age of 5-6 months. In most tests the expression of TL4 preceded the TL 1,2 phenotype. The frequency of TL+ leukemias was about 50% among the early-occurring spontaneous leukemias (in 5- to 7-month-old mice) and decreased to 20% with age increase. Leukemia development following treatment with methyl-nitrosourea (MNUA) or exposure to X-rays increased the frequency of TL+ tumors to 75-100%. These results suggest that heterogeneous target cells are involved in AKR leukemogenesis.

Aging↗
PubMed1982

Distribution of preleukemic cells in fractionated bone marrow of mice.

Separation of preleukemic cells (having the potential to develop further into overt T-cell leukemias) from bone marrow cell populations was attempted. Donor mice of preleukemic bone marrow included C57BL/6 mice inoculated intrathymically with D-RadLV or AKR/J mice carrying spontaneous preleukemic cells among their bone marrow cells. Fractionation of bone marrow cells suspended in bovine serum albumin (BSA) by equilibrium density centrifugation or by velocity sedimentation at 1 g unit gravity using discontinuous density gradient of Ficoll was applied. The leukemogenic potential of the separated bone marrow fractions was tested by evaluating leukemia development following their transfer into appropriate recipients. No enrichment of D-RadLV-induced preleukemic cells was found in any of the four bone marrow fractions obtained following separation on BSA gradient. Separation of D-RadLV-induced preleukemic cells was afforded by using the Ficoll gradients. Preleukemic cells were located mainly among four out of 21 fractions tested, consisting mostly of 10 to 14 micrometers size cells. In contrast, preleukemic cells from AKR donors were distributed among most of the separated fractions. It is suggested that these variable results may reflect homogeneity or heterogeneity of progenitor target cells undergoing transformation.

Animals↗
PubMed1982

The oncostatic effect of methyl-CCNU on various experimental lymphoreticular neoplasms.

Studies on the chemotherapeutic potential of methyl-CCNU on experimental leukemias were undertaken. A number of murine transplantable in vivo lines (chemical carcinogen-induced T and B leukemias; radiation- and viral-induced T leukemias of C57BL/6, C3H/eb and SJL/J origin; radiation-induced myeloid leukemias and spontaneous reticulum cell neoplasms of SJL/J mine) were used in these studies. The optimal dose of methyl-CCNU and optimal timing of administration were extensively investigated on two sample lines of T cell leukemias of C57BL/6 mice. Leukemic cell eradication could be achieved in almost all of the different leukemias treated, irrespective of whether induction was brought about by chemical or physical means or due to a viral leukemogenic agent. Studies undertaken to elucidate the effect of methyl-CCNU on the establishment of preleukemic cells following induction of leukemia by the radiation leukemia virus (RadLV) or by total body irradiation, indicated the oncostatic effect of methyl-CCNU on early preleukemic cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

H-21-linked control of immunological resistance to viral leukemogenesis as a response to preleukemic cells.

The mechanism of resistance to leukemogenesis by two radiation leukemia virus variants, A-RadLV and D-RadLV, was investigated. Resistance to these viruses is linked to H-21 in both B10.S and C57BL/10 mice. The resistance of virus-infected mice to transplantation of syngeneic. A- or D-RadLV-induced lymphoma cells was similar to their resistance to leukemogenesis by the same viruses. This resistance could be transferred by lymphoid cells from immune donors to normal recipients, and it was specific for RadLV lymphomas. Virus-primed (responder x sensitive)F1 hybrids rejected only resistant-type parental lymphoma cells. Hence, it appears that H-21-linked resistance to RadLV leukemogenesis is regulated by Ir genes. Resistant mice immunized by A- or D-RadLV rejected syngeneic lymphoma cells, irrespective of whether they were sensitive or resistant to the RadLV variant used for the induction of the lymphoma cells. It follows that resistant and sensitive type lymphomas are antigenically similar for the effector mechanism, and that the Ir genes may be expressed in the sensitization phase of the reaction. In virus-infected mice which are resistant to A- or D-RadLV we were able to demonstrate the presence of preleukemic lymphocytes. Normal mice could be immunized by these preleukemic cells against lymphoma challenge. These data are interpreted to suggest that mice having H-21-linked resistance to RadLV infection may be sensitized by their preleukemic cells, and that these preleukemic cells are then arrested in their development as a result of the immune response.

Animals↗
PubMed1981

Malignant cell arrest in thymus and spleen of mice bearing transplanted tumors.

The relationship between the local outgrowth of different subcutaneous transplantable tumors (plasmacytoma MOPC-315, mastocytoma P-815; Lewis lung carcinoma-3LL; fibrosarcoma; lymphomas and mammary adenocarcinoma) and tumor cell spread in different organs was evaluated. The presence of tumor cells in thymus, spleen, lung, and liver was demonstrated by using both in vivo and in vitro methods. Sequestration of tumor cells derived from the transplanted solid tumor was indicated within 3 to 7 days after tumor graft, shortly before or after early palpable outgrowth of the primary tumor was observed. Tumor cells present in thymus and spleen might affect immune responses of tumor-bearing mice.

Animals↗
PubMed1980

Non-random duplication of chromosome 15 in murine T-cell leukemias: further studies on translocation heterozygotes.

Four combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T-cell leukemia-associated duplication of chromosome 15 is a non-random or a random event. In leukemias of AKR x CBAT6T6F1 (Group 1) and C57BL x CBAT6T F1 (Group IV) crosses the duplication was non-random, affecting the AKR-derived chromosome 15 (Group 1) and CBAT6T6-derived T (14;15) 6 chromosome (Group IV), respectively. In contrast, in leukemias induced in CBA x CBA T6T6F1 combinations (Group III) - where both chromosomes 15 (normal and translocated) were CBA-derived-the duplication was random. Similarly, in the Rb6;15 x CBAT6T6F1 cross (group II) the duplication of chromosome 15 appeared to be random. The results supported the hypothesis that the genetic content of chromosome 15 rather than its translocated state is decisive for the preferential duplication of this chromosome in T-cell leukemogenesis. However, the genetic background of the strain from which chromosome 15 is derived may also influence the duplication pattern of individual tumors.

Animals↗
PubMed1980

Genetic resistance to murine leukemia induced by different radiation leukemia virus variants; a comparative study on the role of the H-2 complex.

Association of resistance to leukemogenesis with the H-2 complex was investigated. Three variants of the radiation leukemia virus: D-RadLV, RadLV and RS-RadLV were tested. Using congenic and recombinant mouse strains, the region including H-2K and I-A/B was found to be involved with resistance to all three viruses. In addition, H-2D-region linked resistance was found in leukemogenesis in two of the three passages. The phenotypic expression of resistance associated with H-2D seemed to depend on the simultaneous presence of H-2K-H-21-linked resistance alleles. The H-2 haplotypes associated with resistance or sensitivity to the different RadLV variants were different for each passage, suggesting that there is a large degree of heterogeneity both in H-2-linked resistance and between the radiation-induced leukemia viruses.

Alleles↗
PubMed1980

Expression of peanut agglutinin receptors on virus-induced preleukemic cells in mice.

Preleukemic bone marrow and spleen cells of irradiated C57BL/6 mice that were inoculated with the radiation-induced leukemia virus variant D-RadLV differ from autonomous end-stage leukemia cells in the expression of the receptor for peanut agglutinin. As a result, the preleukemic cells are agglutinated by peanut agglutinin and the end-stage cells are not. This observation provides further evidence that preleukemic cells possess surface markers similar to those of the prothymocyte. In vitro and in vivo thymocyte-virus interactions reveal that cells susceptible to D-RadLV transformation are present mainly among the peanut agglutinin-receptor-bearing thymocyte population which has previously been demonstrated to be immunologically immature.

Animals↗
PubMed1980

Potential leukemic cells among bone marrow cells of young AKR/J mice.

Potentially leukemic cells have been identified among bone marrow cells of AKR/J mice from the age of 14 days onward. Transfer of AKR/J bone marrow into irradiated hybrid mice (AKR/J X DBA/2)F1 caused a high leukemia incidence (50-100%) of AKR origin, very often within a short latent period. Similar transfer of AKR/J marrow into irradiated AKR/J recipients did not enhance spontaneous tumor development. In contrast to the leukemic AKR cells that express the T-cell surface component Thy-1.1, the potential leukemic cells among bone marrow cells of young AKR mice were shown to lack the expression of this antigen. The development of preleukemic AKR marrow into overt leukemia in hybrid mice was dependent on the presence of an intact thymus and exposure of the recipients to x-rays shortly before marrow transfer. Evidently, preleukemic AKR bone marrow undergoes sequential changes, affected by host factors, leading ultimately to development of overt leukemia.

Age Factors↗
PubMed1980

Nonrandom chromosomal changes in thy-1-positive and thy-1-negative lymphomas induced by 7,12-dimethylbenzanthracene in SJL mice.

Leukemias were induced by 7,12-dimethylbenzanthracene feeding of intact, thymectomized, or Freund's adjuvant-pretreated SJL mice. Four of six Thy-1-positive thymomas that arose in intact mice had a pseudodiploid stemline with one morphologically similar or identical marker. Banding analysis showed that the marker had arisen by the translocation of the distal part of one chromosome 15 to one X chromosome [t(X;ter 15)]. Two normal No. 15 chromosomes were also present in the same metaphase plates. These four Thy-1-positive lymphomas were thus trisomic for the distal part of chromosome 15. All 8 Thy-1-negative lymphomas, originating in the spleen or lymph nodes of thymectomized or adjuvant-pretreatment mice, had a trisomy of chromosome 12 and also a trisomy of either chromosome 3 or chromosome 18. These results further stress the importance of gene dosage effects, related to the distal part of chromosome 15, in Thy-1-positive T-cell leukemogenesis. The cytogenetic difference between the Thy-1-positive and -negative leukemias supports our hypothesis that nonrandom chromosomal changes in murine leukemias are dependent on the target cell type, rather than the inducing agent.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Non-random duplication of chromosome 15 in murine T-cell leukemias induced in mice heterozygous for translocation T(14:15)6.

Trisomy of chromosome 15 is a highly regular feature of murine T-cell leukemogenesis. We have studied the chromosomal constitution of 7,12-dimethylbenza(a)anthracene (DMBA)-induced T-cell leukemias in C57BL X CBAT6T6 F1 mice. The CBAT6T6-derived chromosome T(14:15)6 was regularly duplicated whereas the C57BL-derived normal chromosome 15 was only present in one copy. It was concluded that the gene(s) that tend to duplicate in parallel with the neoplastic transformation of the prothymocyte to an overt leukemic cell have a greater chance of duplicating and/or may have a stronger promoting effect on leukemogenesis if stronger promoting effect on leukemogenesis if located on the CBA-derived, structurally rearranged T(14:15)6 than the corresponding genes located on the C57BL-derived normal chromosome 15.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Effective tumor immunization induced by cells of elevated membrane-lipid microviscosity.

The immunogenicity of a series of mouse tumor lines propagated in vivo (T and B lymphomas and mammary adenocarcinoma) was tested after alteration of the cell membrane-lipid microviscosity. Tumor cells used for immunization were first treated to alter the lipid content, then irradiated and injected intraperitoneally into syngeneic mice. A second identical immunization was performed 14 days later. The degree of immunization in the treated mice was assessed by survival time after challenge with untreated viable tumor cells of the same origin as the immunizing cells. For all tumors tested, enrichment of the immunizing cells with cholesterol or cholesteryl hemisuccinate, which increased the membrane-lipid microviscosity significantly, afforded a marked increase in immunization, compared to that obtained with cells that were only irradiated. Furthermore, in over 90% of the mice that were pretreated with cholesteryl hemisuccinate-enriched cells, tumor growth after the challenge was not detectable. Because the lipid-modifying treatments of the immunizing cells involve no toxic substances, these results may provide the basis for a potent approach to immunotherapy of human cancer.

9,10-Dimethyl-1,2-benzanthracene↗