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N Haran-Ghera

Publications and source records attributed to N Haran-Ghera.

At least 73 records · Page 4Linked to original sources
PubMed1978

Chromosome changes (trisomy 15) in murine T-cell leukemia induced by 1,12-dimethylbenz(a)anthracene (DMBA).

The banding pattern of DMBA-induced leukemias in C57BL/6 mice revealed a very constant chromosome pattern: the presence of trisomy 15 in almost all leukemic cells. This finding strongly suggests that chromosome 15 trisomy is the first detectable specific chromosome change associated with the development of DMBA-induced T-cell lymphomas. A similar association was previously shown with regard to development of radiation-leukemia-virus-induced T-cell lymphoma. It is conceivable that in tumors of diverse etiologies common cytogenetic changes may appear in the same common target-cell precursor, by a process of the "convergent microevolution" type.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Spontaneous and induced preleukemia cells in C57BL/6 mice:brief communication.

A transplantation bioassay method was used to verify the presence of preleukemia cells in C57BL/6 mice shortly after leukemogenic treatment or in relation to age increase. Preleukemia cells were identified mainly among bone marrow cells of old C57BL/6 mice or within 10 to 30 days after leukemogenic treatment of young mice with radiation-induced leukemia virus variants, fractionated doses of irradiation, or 7,12-dimethylbenz[a]anthracene (DMBA), although the overt disease did not occur until many months later. Mice could carry preleukemia cells without necessarily developing overt leukemia. Since the leukemogenic agents used in the present studies induced T-leukemias, the role of the thymus in the induction of preleukemia cells was tested. Thymectomy affected viral transformation but did not diminish the number of preleukemia cells induced by DMBA or X-ray.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Chromosome changes (trisomies #15 and 17) associated with tumor progression in leukemias induced by radiation leukemia virus.

An experimental system was developed that permitted nonrandom chromosome changes that occur in radiation leukemia virus (RadLV)-induced lymphomas to be followed during tumor progression. RadLV variant-induced preleukemia and leukemia cells originating from female inbred C57BL/6 mice were injected into male animals of the same strain. Since all donors were females and all recipients were males, the sex chromosome complements (XX and XY) were used to distinguish the preleukemia and leukemia cells from those of host origin. The G-banding analysis revealed that more than 50% of animals that were inoculated with preleukemia cells and that developed leukemia possessed tumor stem-lines of 41 chromosomes with a tristomy of chromosome #15. In animals inoculated with overt leukemia cells and in which tumor progression occurred, the G-banding an additional trisomy of chromosome #17. The cytogenic data strongly suggested that the trisomy of chromosome #15 was the first specific tumor-associated chromosome change that occurred in the process of conversion of RadLV-induced preleukemia cells to fully autonomous tumor cells.

Animals↗
PubMed1977

Resistance genes to murine leukemia in the I immune response gene region of the H-2 complex.

A resistance locus to leukemogenesis in mice by A-RadLV (a variant of the radiation leukemia virus) is described. This locus, Rrv-1, was mapped to subregions I-A, I-B, and I-J of the H-2 complex. It is suggested that Rrv-1 may be in complementation with a second locus to the right of it, between Rrv-1 and H-2D. This localization and the complementation of the two loci for resistance are characteristics similar to Ir genes, and indicate a possible relationship between the genetic regulation of immune responsiveness and susceptibility to leukemia.

Animals↗
PubMed1977

Cell surface components of carcinogen-induced lymphoid tumors in SJL/J mice.

Preleukemic cells could be detected in the bone marrow cell population of SJL/J mice within several days after induction of leukemia by repeated feedings with a chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Bone marrow cells collected 7, 30 or 60 days following carcinogenic treatment, developed lymphoid tumors upon transplantation into syngeneic irradiated recipients. The incidence of these tumors varied between 40--45% when the bone marrow cells were collected and transferred 7--30 days after feeding with DMBA, and raised to an incidence of 80% when transferred 60 days after carcinogen administration (compared to 50% incidence in the DMBA-treated bone marrow donors). A survey of several cell surface components on the lymphoid tumor cells, obtained after transplantation of preleukemic cells, indicated that most of the tumor lines bore both the Thy-1.2 antigen (weak) and the Fc receptor, whereas the rest were positive only for the Fc receptor. None of these tumor cell lines would yield a significant amount of cell-bound immunoglobulin.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Role of host endocrine status in murine leukaemogenesis.

Permanent changes in the endocrine status of female SJL/J and CR mice were induced by masculinization, ablation of endocrine glands, inoculation of hormones, or feeding of the chemical carcinogen DMBA. All these procedures resulted in modification of the host hormonal milieu, as shown by blood hormone determination. Masculinization reduced drastically the onset of lymphosarcoma and increased the incidence of systemic neoplasms respectively in DMBA-treated female SJL/J and CR mice. Continued administration of gonadotrophins increased the incidence of systemic neoplasia in CR mice. A direct correlation is suggested between onset of lymphosarcoma or other tumours in mice and a specific shift to an abnormal hormonal environment.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression.

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.

Animals↗
PubMed1977

Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. II. Analysis of the immune response.

Comparative analysis of immune responses induced by two variants of the radiation leukemia virus having high (A-RadLV) or low (D-RadLV) leukemogenic potential was performed. Effective immunization could be induced only with RadLV variants having low leukemogenic potential when injected into adult mice of specific strains, (D-RadLV in C57BL/6 mice and A-RadLV in (BALB/c X C57BL/6)F1 mice). Immunologic cross-reactivity among the RadLV variants and the leukemic cells induced by them was demonstrated in several systems. Transplantation resistance could be induced in certain strains against challenge of leukemic cells induced by both RadLV variants. Isoantisera, raised in the suitable strains, could neutralize effectively the leukemogenic activity of both A-RadLV and D-RadLV. Leukemic cells induced by each of the variants shared cell-surface antigens. Circulating anti-tumor antibodies, induced by both variants in the appropriate strains, lysed efficiently the target leukemic cells.

Animals↗
PubMed1975

Pathways in thymus- and bone marrow-derived lymphatic leukemia in mice.

The radiation- and radiation leukemia virus-induced leukemias in C57BL/6 strain mice were found to be of the thymus-derived (T) lymphocyte origin. Experimental evidence indicated that the interaction of the radiation leukemia virus with thymus-derived lymphoid cells and specifically with the thymus subpopulation bearing high levels of H-2 alloantigens were prerequisites for the development of high leukemia incidence in these test systems. In radiation leukemogenesis in C57BL/6 mice it was shown that within several days following the radiation treatment a "released" leukemogenic agent was found in the irradiated bone marrow; whereas, several days following chemical carcinogen leukemogenesis in SJL/J mice, established preleukemic or leukemic cells could be detected in the bone marrow. The analysis concerned with the lymphoid origin of chemical carcinogen-induced lymphatic leukemias in SJL/J mice indicated clearly that the carcinogen could affect different lymphoid populations. The majority of the chemical-induced leukemias were of the bone marrow-derived (B) lymphocyte origin, although some leukemias were of T lymphocyte origin, and some tumors could not be classified as either T or B leukemias, perhaps representing stem cells which do not carry the characteristic surface antigens for mature T and B cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Enhancement and retardation of spontaneous reticulum cell neoplasm development in SJL/J mice.

The enhancement or delay in the appearance of spontaneous reticulum cell neoplasms (RCN-B) in SJL/J mice was tested. Immunosuppressive treatment with antithymocyte serum and prolonged antigenic stimulation by repeated injections of sheep erythrocytes, leukemogenic cell-free centrifugates, and multichain synthetic polypeptides had no effect on the incidence or latency of spontaneous tumor appearance. Treatment with mineral oil or incomplete Freund adjuvant markedly enhanced tumor appearance (though the abundance of plasma cells induced by these treatments did not evoke the development of plasmacytomas, nor did it affect the incidence of serum paraproteinemia among mice with spontaneous tumors). Treatment with cortisone acetate, however, markedly retarded spontaneous tumor development. Tumors occurring early due to mineral oil and adjuvant treatment all had the characteristics of "RCN-B plasma cell type," and tumors occurring late due to cortisone treatment were all of the "RCN-B reticulum cell type." The possible involvement of the stem cell pool size in the enhancement or delay of spontaneous tumor development was discussed.

Animals↗