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PubMed1990

Transcriptional down-regulation of the rearranged C-myc expression in murine cell hybrids between a plasmacytoma and a T-cell lymphoma.

Regulation of the rearranged and non-rearranged c-myc expression was studied in murine cell hybrids (SBWI and SBWII) between plasmacytoma (S194) and T-cell lymphoma (BW5147) cells. Expression of the rearranged c-myc of heterogeneous mRNA sizes (1.8 approximately 2.4 kb) was markedly down-regulated in these hybrids regardless of retention of the gene. On the other hand, expression of the non-rearranged c-myc (2.4 kb) was not significantly affected in these hybrids. Treatment of SBWI hybrid cells with cycloheximide enhanced the non-rearranged c-myc 2- to 4-fold but did not release the down-regulation of the rearranged c-myc at all, suggesting that the down-regulation of the rearranged c-myc in the hybrid cells was mainly at a transcriptional rather than a post-transcriptional level. This was supported by the results of nuclear run-on assay: the high level of run-on transcripts in S194 cells declined in SBWI hybrid cells comparable to the level in BW5147 cells. The rearranged c-myc was hemi-methylated in S194 cells and the pattern was the same in SBWI hybrid cells. Furthermore, down-regulation of the rearranged c-myc in the hybrid was also not restored by treatment with 5-azacytidine (5-AzaC), 12-O-tetradecanoylphorbol-13-acetate (TPA) or forskolin, suggesting no causative involvement of DNA methylation or protein phosphorylation in down-regulation. Higher DNase I sensitivity of the rearranged c-myc in S194 cells decreased to a similar extent to that of the non-rearranged c-myc after cell fusion with BW5147 cells. These results suggest that expression of the rearranged c-myc is down-regulated at the level of transcription in murine cell hybrids between a plasmacytoma and a T-cell lymphoma, probably by changing chromatin configuration around the gene from the open to the closed state.

Animals↗
PubMed1991

Differential susceptibility of BALB/c and DBA/2 cells to plasmacytoma induction in reciprocal chimeras.

Reciprocal chimeras were generated between BALB/c and DBA/2 mice by inoculating newborn recipients of either strain with bone-marrow (BM) cells of the other through the periorbital vein. DBA/2 mice inoculated with the BALB/c with proven chimerism will be referred to as C----D, the reciprocal as D----C. The BALB/c cells carried a Robertsonian 6;15 (Rb6;15) chromosome marker to facilitate identification. The chimeric mice contained between 5% and 70% of donor cells when examined at 4 to 5 weeks of age. Six of 10 C----D developed plasmacytomas (MPC) after 3 x 0.5 ml monthly pristane treatment (incidence 60%) and 8 of 25 (incidence 32%) after 2 to 3 x 0.5 ml pristane followed by Abelson virus (A-MuLV) infection. Seven of 15 D----C developed MPC after pristane treatment (incidence 47%) and 4 of 17 after pristane + A-MuLV (incidence 24%). All tumors that have arisen in both reciprocal chimeras originated from BALB/c cells independently of the degree of chimerism. All tumors contained an Ig/myc translocation. Among the C----D chimeras, 5 carried t(12;15) and I t(6;15) in the pristane-treated group, while 4 carried t(12;15), I t(6;15) and 3 t(15;16) in the pristane + A-MuLV. Among the D----C chimeras 6 carried t(12;15) and I t(6;15) in the pristane-treated group, while 3 t(12;15) and I t(6;15) in the pristane + A-MuLV. No tumors developed in 18 pristane- and 22 pristane + A-MuLV-treated DBA/2 mice nor in 15 pristane- and 17 pristane + A-MuLV-treated (BALB/c x DBA/2)F1 mice. The data indicate that BALB/c and DBA/2 cells differ in their propensity to transform into plasmacytoma in identical host environments after both pristane and pristane + A-MuLV treatment. They also show that the oil granuloma can support MPC development in either type of chimeric host.

Abelson murine leukemia virus↗
PubMed1991

Re-transformation of non-transformed hybrids between c-myc-activating mouse plasmacytoma cells and normal fibroblasts by transfection with activated c-Ha-ras but not c-myc.

In a mouse plasmacytoma S194, c-myc oncogene is rearranged with Ig gene by chromosomal translocation and is consequently activated. We previously reported that transformation of phenotype and expression of rearranged c-myc were repressed in independently isolated hybrid clones, I-1 and IV-10, between S194 and normal fibroblasts. In order to investigate the relationship between transformation of phenotype and oncogene expression, transcriptionally enhanced c-myc or activated c-Ha-ras was transfected into I-1 or IV-10I, a subclone of IV-10. Transfectants expressing high levels of c-myc were found to retain the non-transformed phenotypes. On the other hand, transfectants expressing activated c-Ha-ras showed the transformed phenotypes. These results suggest that enhanced expression of c-myc is not sufficient for re-transformation of the non-transformed hybrid clones between c-myc-activating plasmacytoma cells and normal fibroblasts, but expression of activated c-Ha-ras could diminish or overcome the tumor-suppressive activity of normal fibroblasts.

Animals↗
PubMed1985

Mapping of the c-myc, pvt-1 and immunoglobulin kappa genes in relation to the mouse plasmacytoma-associated variant (6;15) translocation breakpoint.

A variant mouse plasmacytoma (MPC)-associated translocation chromosome has arisen by pericentric inversion and exchange of the distal segments of a Robertsonian 6;15 fusion chromosome in the CAK TEPC 1198 mouse plasmacytoma, as described earlier. In situ hybridization was performed on the normal and the inverted Rb chromosomes, using myc and kappa probes. On the normal Rb chromosome, myc was in the 15 D2/3 region, whereas kappa hybridized in the 6 C2 area, as expected. On the inverted Rb chromosome, myc remains on the centrometric side of the translocation breakpoint on the chromosome 15-derived portion, whereas kappa has moved to the chromosome 6-derived segment that joined the same breakpoint on the telomeric side. Taken together with our recent demonstration that the murine c-myc locus is oriented 'head up' on chromosome 15, and with the results of Cory and co-workers concerning the relationship between the kappa gene and the associated pvt-1 region in the CAK TEPC 1198 tumor, the following conclusions can be drawn: (i) in the variant translocation of the CAK TEPC 1198 MPC, the breakage occurs 3' of the c-myc gene, as in the human Burkitt lymphoma-associated variant translocations; (ii) the pvt-1 gene on chromosome 15 is distal to the myc gene; (iii) the kappa light chain locus is oriented 'head up' on mouse chromosome 6 and faces pvt-1 and, beyond it, c-myc, in a head-to-tail configuration.

Animals↗
PubMed1980

Extramedullary plasmacytoma: simulating a soft tissue sarcoma of the chest wall.

Extramedullary plasmacytoma occurs infrequently as compared to osseous myoloma. A single case of extramedullary plasmacytoma was seen during the last 10 years whose initial presentation was that of a soft tissue sarcoma of the chest wall. Clinical data along with relevent investigation and treatment results are discussed with a review of the literature.

Biopsy↗
PubMed1979

Amyloid in localised deposits and plasmacytomas of the respiratory tract.

Clinical and histological features of 25 cases with amyloid deposits in the respiratory tract are described. The false cord is the commonest single site of such "primary" amyloid involvement. Evidence of extensive involvement and replacement of seromucinous glands by amyloid was seen in each case. Fourteen cases of plasmacytoma with "secondary" amyloid deposits are also described. The nose and nasopharynx were principally involved as with respiratory tract plasmacytomas in general but a similar association of the amyloid with seromucinous glands was also seen. Electron microscopy showed early involvement of the basal lamina of the duct of a seromucinous gland by amyloid in one case. Possible reasons for the association of amyloid precursors in respiratory tract amyloid with seromucinous glands are given.

Adult↗
PubMed2007

Extramedullary plasmacytoma of the adenoids.

Extramedullary plasmacytomas are extremely rarely diagnosed in children. We report two cases of extramedullary plasmacytoma detected coincidentally in the adenoidectomy specimens of children younger than 4 years. We show that these children are disease-free after local excision as the only treatment. Surgical treatment without anti-neoplastic therapy in pediatric plasma cell dyscrasias of the pharyngeal lymphoid tissue may be a sufficient curative therapy.

Adenoidectomy↗
PubMed1993

The role of idiotype-specific, CD4+ T cells in tumor resistance against major histocompatibility complex class II molecule negative plasmacytoma cells.

It is known that immunoglobulins can be processed and that idiotypic peptides are presented on MHC class II molecules to T cells. It has also been demonstrated that T cells can recognize a complex of an Id-peptide/MHC molecule as a tumor-specific antigen on B lymphoma cells. However, plasmacytomas, an important type of B cell malignancies, most often lack class II molecules and are thus expected to be poor targets for Id-specific, CD4+ T cells. Nevertheless, we now demonstrate that cloned, MHC class II restricted T cells, specific for a lambda 2(315) idiotypic peptide, convey protection in vivo (Winn assay) against the class II molecule-negative MOPC315 (alpha, lambda 2(315)) plasmacytoma. T cells can also inhibit the growth of MOPC315 cells in vitro provided that MHC compatible (H-2d) splenocytes and extra lambda 2(315) are added. Based on these data we suggest that the myeloma protein secreted by MOPC315 cells attains such a high local concentration in vivo that it is processed and presented by neighboring host APC to the Id-specific T cells. Such activated T cells secrete lymphokines which may directly affect the growth of MOPC315 cells in the vicinity. Alternatively, lymphokines from activated T cells stimulate local host cells, like macrophages, to become tumoricidal.

Animals↗
PubMed1999

Plasmacytoma induction in specific pathogen-free (SPF) bcl-2 transgenic BALB/c mice.

Germ-free (GF) and specific pathogen free (SPF) BALB/c mice are refractory to plasmacytoma induction by pristane (McIntire and Princler, 1969, Byrd et al 1991). It was therefore suggested that MPC development may depend on antigenic stimulation. If so, it may conceivably act by preventing the apoptotic elimination of tumor precursor cells. We have tested this idea by elevating the apoptotic threshold by the introduction of a bcl-2 transgene. We have found that MPCs could be induced by pristane oil in transgene carrying SPF mice. An E mu activated bcl-2 transgene was introduced into SPF BALB/c mice. The mice were used after two backcrosses (BC-2). Pristane oil treatment was started at 4 to 6 weeks of age (3 x 0.3 ml via i.p. at monthly intervals). For each transgene carrier a transgene negative littermate was used as control. Fifteen of 24 (63%) transgene carriers developed plasmacytomas after latency periods between 67 and 146 days (mean = 112 +/- 30 days) after the first pristane injection. Five additional transgene carriers developed lymphoma (3 cases) or mixed MPC and lymphoma (2 cases). In contrast, no tumors developed in 16 transgene negative littermates that were kept > 300 days under observation. Karyotyping showed that 10/15 (66%) of the MPCs carried a T(12;15) translocation, 4/15 (27%) carried both T(12;15) and T(6;15) translocations in the same metaphase plate, and 1/15 (7%) was translocation free. A T(12;15) translocation was also detected in one of the 2 mice with mixed tumor type. Pristane treated bcl-2 transgenic C57B1/6 mice remained tumor free, although T(12;15) translocation carrying cells were found in the peritoneal fluid of 4/20 mice 176 days after pristane.

Animals↗
PubMed1995

Induction of plasmacytomas in genetically susceptible mice with silicone gels.

Silicone gels injected intraperitoneally into strains of mice related to BALB/c develop plasmacytomas in approximately the same numbers and with similar phenotypes as previously obtained with pristane. Silicone gels produce few side effects and are well tolerated for long periods. Silicone gels contain several components that are potentially biologically active: residual vinyl groups and platinum. Microscopic and histological evidence suggests the silicone gel is degraded over a long period of time. Preliminary studies with long chain liquid dimethylpolysiloxanes with viscosities of 1000 cSt and 12,500 cSt have not produced plasmacytomas as yet. The plasmacytomagenic action of the gel appears to be due to the release of liquids from the gel matrix.

Animals↗
PubMed1994

Budd-Chiari syndrome and Epstein-Barr virus (EBV) associated plasmacytoma in a patient with chronic active EBV infection.

A 42-year-old Japanese man with chronic active Epstein-Barr virus (EBV) infection initially responded to treatment with interleukin-2 (IL-2). Six months later he developed thrombosis in the hepatic veins, and Budd-Chiari syndrome associated with severe hepatic damage was diagnosed. He also developed a solitary EBV-positive plasmacytoma in the right femur. Since these rare complications occurred after long-term IL-2 therapy, the possibility that long-term IL-2 therapy might cause Budd-Chiari syndrome and liver damage as well as EBV-associated plasmacytoma is discussed.

Adult↗
PubMed1985

Comparison of patterns of hybrid resistance to the BALB/c plasmacytomas LPC-1 and MPC-11.

Patterns of genetic control of hybrid resistance to the BALB/c plasmacytoma LPC-1 were studied for comparison with those to MPC-11, a plasmacytoma investigated previously. The overall patterns of hybrid resistance to the two tumors were similar, i.e., hybrids between BALB/c and BALB congenic resistant (CR) strains, A and A CR strains, SJL and DBA/2 were as susceptible to LPC-1 as BALB/c mice themselves, whereas hybrids between BALB/c and AKR, C57BL/Ks, DBA/1, C57BL/6 (B6), C57BL/10 (B10) and B10 CR strains were resistant to LPC-1 as previously shown with MPC-11. Heterozygosity within the H-2 complex alone was insufficient for resistance to either tumor. Among hybrids between BALB/c and the B10 CR strains, however, the presence of certain H-2 haplotypes influenced the degree of resistance seen and this H-2 effect was different for the two tumors. A sex effect on resistance to LPC-1, but not to MPC-11, was seen among F1 hybrids between BALB/c and DBA/1 although not in any other F1 hybrids. Among ((B10 X BALB/c)F1 X BALB/c) and (BALB/c X (B10 X BALB/c)F1) and ((BALB/c X B10)F1 X BALB/c) and ((BALB/c X B10)F1 X BALB/c) backcross mice, however, significantly more males than females were resistant to LPC-1 and the results of this study are compatible with the idea that in F1 hybrids between BALB/c and B10, resistance to LPC-1 is controlled by two dominant autosomal genes, one of which is sex-limited and neither of which is linked to H-2. In contrast, hybrid resistance to MPC-11 in this cross is controlled by a single gene. Cross-protection experiments indicated that the two tumors share at least one tumor-associated transplantation antigen.

Animals↗
PubMed1988

Effect of low-dose cyclophosphamide therapy on specific and nonspecific T cell-dependent immune responses of spleen cells from mice bearing large MOPC-315 plasmacytomas.

Some T cell-dependent immune parameters were examined in mice bearing a large MOPC-315 plasmacytoma before and after treatment with a low dose (15 mg/kg) of CY. Prior to CY therapy, spleen cells from mice bearing a large MOPC-315 tumor were depressed in their ability to generate an in vitro cytotoxic response to the MOPC-315 tumor, to a different syngeneic plasmacytoma, MOPC-104E, and to an allogeneic thymoma, EL4. The spleen cells of these mice were also depressed in their ability to proliferate in response to the T cell mitogen PHA. Following CY therapy, the spleen cells generated an enhanced anti-MOPC-315 cytotoxic response by day 2, and the level of this response continued to increase so that by day 7, it was greatly enhanced and was much greater than the response of normal spleen cells. The recovery of the cytotoxic responsiveness to the antigenically related MOPC-104E tumor after CY therapy followed a similar pattern. In contrast, the spleen cells of these animals remained depressed in their cytotoxic response to the antigenically unrelated EL4 thymoma for at least 11 days after CY therapy. Although the anti-EL4 response recovered by day 14, the level of antitumor cytotoxicity generated did not exceed that generated by normal spleen cells. The PHA response remained greatly depressed in CY-treated MOPC-315 tumor bearers, even 14 days after the chemotherapy. Thus, at a time following low-dose CY therapy, when potent T cell-dependent antiplasmacytoma immunity had completed the eradication of a large MOPC-315 tumor burden not eliminated through the direct effect of the drug, the T cell-dependent response to an unrelated tumor and to PHA remained depressed.

Animals↗
PubMed1978

Chemotherapy in the management of extramedullary plasmacytoma.

The results of chemotherapy in 24 patients with extramedullary plasmacytoma are reported. Complete regressions, including disappearance of monoclonal paraprotein and healing of bone lesions, were seen in 12 of 20 (60%) patients with disseminated disease. Extramedullary plasmacytoma responds better to chemotherapy than myeloma, and treatment should be pursued with vigour until all signs of disease have disappeared. Sensitivity to single-agent chemotherapy may vary, and if treatment fails with one agent, others should be tried.

Adult↗
PubMed1989

Plasmacytoma of the breast. Unusual initial presentation of myeloma: report of two cases and review of the literature.

Two patients who presented initially with breast masses proven to be plasmacytomas, are described. In both cases the breast masses led to the diagnosis of multiple myeloma, which was retrospectively already present at the time of the breast biopsy. One patient with IgG lambda-type myeloma developed plasma cell leukemia and amyloidosis and failed to respond to radiochemotherapy. The second patient was in complete remission, four years after therapy, but has subsequently relapsed and died. All cases of breast plasmacytoma, described in the medical literatures are reviewed, and guidelines for future therapy are suggested.

Breast Neoplasms↗
PubMed1979

[Unusual location of extramedullary plasmacytomas (author's transl)].

Two cases of solitary extramedullary plasmacytoma, one of the nasopharynx and one of the tongue are reported. Although there was no paraprotein secretion present, we were able to demonstrate an intracytoplasmic monoclonal immunoglobulin (type IgG-kappa) by immunohistochemical methods. Twelve months following surgical treatment both patients locally and by serum controls are free of residual disease. We confirm former studies in the literature that the prognosis of solitary extramedullary plasmacytomas seems to be good after surgical or radiation therapy. Continuous individual follow-up including serum and X-ray controls are obligatory.

Female↗
PubMed1995

Immunotherapy of a plasmacytoma with attenuated salmonella.

An attenuated strain of Salmonella typhimurium, SL3235, developed as a prototypic typhoid vaccine, is shown to retard growth of a murine plasmacytoma, TEPC-183, and to prolong survival of tumor-bearing mice. Live salmonella, but not acetone-killed organisms, had antitumor activity. The immunotherapeutic effect was demonstrable when the tumor was injected intralesionally or intraperitoneally. Increased survival, longer mean time to death, and retardation of tumor growth were found when the salmonella were given intralesionally as late as the sixth day post-tumor injection. Timing of salmonella inoculation, as well as the salmonella dose, had an effect on treatment efficacy. Injection of salmonella intraperitoneally exerted a strong antitumor effect when given as late as the third day post-tumor inoculation. The highest dose (2 x 10(6)) of salmonella was less effective than doses 10- or 100-fold lower. TEPC-183 plasmacytoma is rapidly growing and highly immunosuppressive, so the ability of the salmonella to exert therapeutic activity against it is a measure of the potency of the vaccine. These observations are of interest, as they show that a genetically engineered, avirulent strain of Salmonella has immunotherapeutic properties similar to those of BCG and other biological response modifiers, and might have clinical potential as an antitumor agent.

Animals↗
PubMed1994

Autologous bone marrow transplantation for intra-abdominal extramedullary plasmacytoma.

A patient with an extramedullary plasmacytoma of the omentum and ovaries is described. In spite of the presence of a very high concentration of paraprotein (103.5 g/l IgG k), bone marrow involvement was not demonstrated either at presentation or during the course of the disease. After debulking surgery, chemotherapy (vincristine, prednisone, and cyclophosphamide) was initiated. Although this resulted in considerable improvement, the paraproteinemia persisted. After ten courses of chemotherapy there was recurrence of the tumor with involvement of the lymph nodes in the right axilla. Chemotherapy was changed to a CHOP regimen (cyclophosphamide, adriamycin, vincristine, and prednisone), followed by autologous bone marrow transplantation with the BEAM regimen (BCNU, etoposide, cytarabine, melphalan) as conditioning therapy. The patient was still in complete remission 1 year after transplantation. This case demonstrates that an extramedullary plasmacytoma may become manifest as extensive but localized disease with high levels of paraprotein, and that autologous bone marrow transplantation as a therapeutic modality can lead to prolonged complete remission of the disease.

Abdominal Neoplasms↗