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J Spira

Publications and source records attributed to J Spira.

At least 37 records · Page 2Linked to original sources
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

Cytogenetic studies on abelson-virus-induced mouse leukemias.

The karyotype of Abelson-virus-induced murine leukemias was studied by G-banding. In contrast to the regular trisomy of chromosome 15 in most murine T-cell leukemias, Abelson leukemias were purely diploid, and remained diploid for up to seven consecutive passages in vivo. The hypothesis is advanced that integration into the recipient cell of the DNA copy of the large cellular insert, carried by the Abelson virus, may perform a function similar to the effects of gene duplication by trisomy in the more slowly developing murine leukemias.

Abelson murine leukemia virus↗
PubMed1980

Cytogenetic studies on IgA/lambda-producing murine plasmacytomas: regular occurrence of a T(12;15) translocation.

Seven IgA/lambda-producing murine plasmacytomas had the 12;15 translocation, previously found in IgA/kappa-producing plasmacytomas, and lacked the rcpT(6;15) translocation, also found in some kappa producers. The results suggest that the generation of the 12;15 translocation is an important, perhaps essential event during the genesis of plasmacytomas. The possibility that the distal region of chromosome 15 may contain a "supergene" area involved with the differentiation and/or normal responsiveness of various types of lymphoreticular cells, must be seriously considered on the basis of the present and previous evidence on plasmacytomas, as well as the extensive evidence now available on the role of chromosome 15-changes in the genesis of murine lymphomas. The involvement of chromosome 12 is of interest in view of the fact that it is known to carry the heavy-chain immunoglobulin determinants.

Animals↗
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

Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas.

The karyotypes of pristane-induced mouse plasmacytomas were studied by G banding. Only primary tumors or early passage generations were analyzed. In contrast to murine T cell leukemias that showed a regular trisomy of chromosome 15, all plasmacytomas showed a consistent translocation of the distal part of chromosome 15 to either chromosome 6 [rcpT(6;15)] or 12 [T(12;15)]. The specific breakpoints were at 6C, 15D3/E ro D2/3 and 12F2. Early passage generations often showed a mixed population with two different translocations, suggesting polyclonal origin. Considered together with the known karyotypic features of murine and human lymphomas, these findings support the theory that the nonrandom chromosomal changes in lymphoproliferative malignancies are associated with the type of the target cell, rather than with the etiological agent. Moreover, the involvement of the chromosomes known to carry the heavy chain (12) and the light chain (6) determinants, respectively, raises the question of whether the translocations may be related to the DNA level rearrangements known to occur during the differentiation of normal plasma cells.

Animals↗
PubMed1979

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Trypsin-Giemsa banding studies on T cell leukemias induced in Robertsonian translocation mice by dimethylbenz[a]anthracene and Moloney leukemia virus show a trisomy of chromosome 15 even in cases in which chromosome 15 has undergone centromeric fusion with chromosomes 1, 5, or 6. These results suggest that the duplication of gene(s) located on chromosome 15 is of critical importance for murine T cell leukemia development.

Animals↗
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

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

Chromosome banding, isoenzyme studies and determination of Epstein-Barr virus DNA content on human Burkitt lymphoma/mouse hybrids.

Four independently fused hybrid clones derived from a cross between the mouse mammary carcinoma TA3Ha and the human Burkitt lymphoma line Daudi were tested for the EBV-determined nuclear antigen (EBNA), EBV-DNA and the presence of human chromosomes, in the course of serial propagation in vitro. EBNA and EBV-DNA were lost in parallel with the loss of human chromosomes. It seems that the persistence of EB-viral genetic information does not require the presence of a specific human chromosome(s) in this particular hybrid combination.

Animals↗
PubMed1975

Biological effects evaluated as a function of patient thickness, beam quality, SSD,and treatment schedule.

Continuing efforts are being made by clinical radiotherapists to evaluate radiationcomplications to normal tissue and organs by specific time-dose parameters. Currently,the NSD concept of Ellis is receiving wide application in the literature in the reporting of radiation complications and normal tissue tolerances. To afford an easy and broad application of the NSD concept to the evaluation of physiological, functional, or structural changes, the authors have evolved mathematical expressions for the calculations of NSD as a function of patient thickness, beam energy, SSD, and treatment schedule involving coplanar field arrangements whether the fields are treated alternately or simultaneously. Several interesting aspects evolving form the concepts of treatment planning interms of the NSD or biological effects indicate that 1) for beam energies above 22 MeV, treatment is more ideally performed by treating only one field per day, since the depth of electronic equiliberium provides more effective sparing of superficial organs andtissues; 2) large-field therapy, such as the total nodal irradiation of Hodgkin'sdisease, can be more effectively treated in terms of tissue sparing by higher energy beamsthan cobalt-60 or 4-MeV for practically all patient dimensions; 3) a new concept ofintegral biological dose,the "gram-ret", is proposed, which represents the quantitation of total biological effect; 4) a series of tables with multiplication factors programmed on a digital computeris presented, which very quickly make available the NSD in any fractionated radiation treatment cycle to any plane of the body as a fuction of the beam energy, SSD, patient thickness, and continuous or split-course therapy schedule.

Dose-Response Relationship, Radiation↗
PubMed1975

Variation of percentage depth dose with beam area of 43 MV roentgen ray beam from a betatron.

The central axis percentage depth dose of a 43 MV roentgen ray beam from a betatron, is found to decrease with increasing beam area at depths more than the depth of maximum dose build-up. At depths less than the depth of maximum dose build-up, a reverse trend is seen. This type of variation of central axis percentage depth dose with beam area is found due to the presence of extraneous radiation originating in the field flattening filter (compensator) and the collimator of the betatron.

Radiotherapy Dosage↗