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PubMed1979

Cutaneous plasmacytomas. A review and presentation of an unusual case.

Recent reviews separate four types of plasma cell tumor: multiple myeloma, extramedullary plasmacytoma (without multiple myeloma), solitary myeloma of bone, and plasma cell leukemia. Cutaneous plasma cell tumors may arise from lymphatic or vascular spread of tumor (metastatic cutaneous plasmacytoma) or by direct extension from bone lesions. The former, metastatic cutaneous plasmacytomas, are quite rare. Specific malignant plasmacyte cutaneous tumors can also be seen in extramedullary plasmacytoma, solitary myeloma of bone, and plasma cell leukemia. We present a patient with multiple myeloma and lymphedema of the right arm, who developed a pathologic fracture of the right humerus and subsequently developed numerous metastatic cutaneous plasmacytomas localized to the lymphedematous arm. Direct immunofluorescence of frozen sections and enzymatically released cells from tumor nodule failed to reveal cell-associated immunoglobulins.

Female↗

PubMed1997

Characterization of C57BL/6 plasmacytomas lacking a c-myc translocation.

BALB/c peritoneal plasmacytomas induced by a variety of agents are invariably associated with a c-myc translocation. In contrast, naturally arising bone marrow plasma cell tumors in C57BL/KaLwRij mice lack this translocation. This difference has led to the suggestion that these are 2 fundamentally different plasma cell diseases. Herein, we have analyzed 2 rare C57BL/6 peritoneal plasmacytomas in terms of characteristics associated with the bone marrow-derived lines. Like the bone marrow lines, these peritoneal plasmacytomas do not exhibit c-myc translocations, indicating that c-myc translocation is not an obligatory event in the development of all murine extramedullary plasmacytomas. However, myc is dysregulated at the mRNA level, indicating that myc overexpression may be fundamental to most plasma cell diseases but that dysregulation can occur by alternative mechanisms possibly reflecting different genetic backgrounds.

Animals↗

PubMed1976

Cervical lymph node metastasis as the first manifestation of localized extramedullary plasmacytoma.

Two patients who had cervical lymph node metastases as the first symptom of a localized soft tissue extramedullary plasmacytoma of the epiglottis and nasopharynx, respectively, are described. Classical multiple myeloma was excluded by bone marrow biopsies and x-ray studies of the skeleton. In both patients, the primary tumor was diagnosed 2 years after excision of the cervical lymph node. One patient had a IgD, lambda myeloma protein in the serum and excreted lambda Bence-Jones protein into the urine. No M-component was found in the other patient. Both are living with a long survival of 8 and 4 years respectively. The presence of a cervical lymph node plasmacytoma should suggest an upper respiratory tract or oropharynx plasmacytoma rather than a primary lymph node plasmacytoma.

Aged↗

PubMed1988

Metastatic extramedullary plasmacytoma: a case report and review of the literature of a rare pseudocarcinoma.

Extramedullary plasmacytomas are unusual plasma cell tumors arising outside the bone marrow. Most extramedullary plasmacytomas are solitary, but occasionally they disseminate, usually in conjunction with systemic myelomatosis. The authors report a case of disseminated extramedullary plasmacytoma with a picture suggestive of metastatic pancreatic carcinoma. This unusual presentation reconfirms the need for tissue diagnosis in all suspected cases of pancreatic carcinoma and demonstrates that extramedullary plasmacytoma can be an aggressive cancer without any sign of osseous or systemic disease.

Aged↗

PubMed1977

Cell-mediated immunity against particulate and solubilized tumor-associated antigens of murine plasmacytomas detected by macrophage migration inhibition assays.

Cell-mediated immunity (CMI), as detected by the agarose microdroplet macrophage migration inhibition (MMI) assay, was investigated using peritoneal exudate cells (PEC) of BALB/c mice and several crude membrane (CM) and solubilized preparations of murine plasmacytomas. The MMI assay was quite sensitive and detected inhibition of macrophage migration as low as picogram quantities of CM, NP40 detergent- and papainsolubilized preparations (CS) of ADJ-PC5 and LPC-1 plasmacytomas. The data were highly reproducible from one experiment to the next with the same or different lots of the CM or solubilized extracts. Specificity studies demonstrated that ADJ-PC5 and LPC-1 plasmacytomas expressed cross-reactive tumor-associated antigens (TAA) as detected by MMI and confirmed by tumor challenge and Winn neutralization experiments. No cross-reactivity was observed with similar extracts prepared from an unrelated syngeneic simian virus 40 (SV40)-induced sarcoma. The inhibition of macrophage migration observed was mediated by culture supernatants generated from the mixture of plasmacytoma-immune spleen cells with antigens and then assayed in an indirect MMI assay on normal PEC. The agarose microdroplet MMI assay appeared to be a rapid and sensitive method to measure TAA recognition and to monitor TAA isolation and solubilization with minimum numbers of immune cells.

Animals↗

PubMed1983

Analysis of the growth characteristics of a primary BALB/c IgG plasmacytoma.

Spontaneously arising and chemically or virally induced tumors usually cannot be analyzed in the early stages of tumorigenesis. Growth characteristics of these tumors thus are not available and it is unknown whether their expansion at any stage is influenced by the immune system. We have developed the following strategy to evaluate possible deviations from exponential growth in initial stages when a tumor is not yet manifest and in order to overcome the two main objections against most experiments in tumor immunology: use of possibly selected transplantable tumors and high initial cell doses. BALB/c mice received 0.5 ml of Pristane intraperitoneally three times within 16 weeks. This treatment induces plasmacytomas in 58% of the animals within 1 year. Mice were bled twice a week beginning with the 5th week after the last injection and sera were stored. Guinea-pig anti-idiotypic antibodies were raised against the IgG myeloma protein of a plasmacytoma developing in mouse 6-15 and a radioimmunoassay was set up. Sera of mouse 6-15 were then tested in retrospect for appearance and increase of the myeloma idiotype Id 6-15. We followed this idiotype thus for 19 weeks from a concentration of about 10 micrograms/ml up to 3 mg/ml serum. Plasmacytoma 6-15 cell growth was calculated from the Id 6-15 levels. In early phases wave-like fluctuations were found, possibly due to varying ratios of secretor to total plasmacytoma 6-15 cells. This phase was followed by an exponential increase in secretor cell number. At no time was there evidence for anti-idiotypic auto-antibodies against Id 6-15. The data are discussed in connection with possibly early activation of cellular components of the immune system.

Animals↗

PubMed1983

Fusion of DNA region to murine immunoglobulin heavy chain locus corresponds to plasmacytoma-associated chromosome translocation.

Murine plasmacytomas frequently exhibit a translocation of the distal region of chromosome 15 to the end of chromosome 12, where the immunoglobulin heavy chain locus resides. A candidate for the DNA across the chromosome fusion point is a cloned region of non-immunoglobulin DNA which in most plasmacytomas has recombined near the alpha heavy chain constant region gene. That the incoming DNA, provisionally designated LyR (lymphoid rearranging) DNA, does derive from chromosome 15 is shown here by blot analysis of DNA from two panels of somatic cell hybrids: hybridomas between an AKR T-lymphoma (Tikaut) and CBA mouse cells with a cytogenetically distinctive chromosome 15, and between mouse and Chinese hamster cells. LyR DNA segregated with chromosome 15 in all lines and the results assign LyR to the distal two thirds of that chromosome. This assignment, together with the previously reported high frequency of recombination between LyR and C(alpha) in plasmacytomas and associated alteration of LyR transcription suggests that translocation activates a LyR gene involved in plasmacytoma oncogenesis. Moreover, LyR rearrangement in certain T-lymphomas, such as the Tikaut line examined here, also implicate that gene in oncogenesis of some T-lymphomas.

Animals↗

PubMed1983

Interchromosomal recombination of the cellular oncogene c-myc with the immunoglobulin heavy chain locus in murine plasmacytomas is a reciprocal exchange.

The 15:12 chromosome translocations found in most murine plasmacytomas involve the cellular gene (c-myc) homologous to the oncogene (v-myc) of avian retrovirus MC29, Translocation links the c-myc gene of chromosome 15 to the immunoglobulin heavy (H) chain locus of chromosome 12, often within the switch recombination (S) region 5' to the alpha constant region (C alpha) gene. We have investigated c-myc rearrangements in 21 BALB/c plasmacytomas and three B lymphomas by Southern blot analysis. We show that the t(15;12) is a reciprocal chromosome exchange since most tumours contain not only a c-myc gene linked to the S alpha C alpha region but also a separate structure with S mu or S alpha linked to the c-myc 5'-flanking region. Analysis of the two rearrangement products cloned from plasmacytoma J558 suggests that one type of H locus target for translocation is an S alpha region recombined with S mu; two other targets appear to be other switched heavy chain genes and an unrearranged C alpha gene. Nearly all the chromosome 15 breakpoints fall within a 1.1-kb region spanning a 5' c-myc exon; hence scission of the transcriptional unit by translocation can account for the altered c-myc transcription in plasmacytomas. The c-myc breakpoint region lacks substantial homology with S mu or S alpha, arguing against homologous recombination as the translocation mechanism.

Animals↗

PubMed1985

Variant (6;15) translocations in murine plasmacytomas involve a chromosome 15 locus at least 72 kb from the c-myc oncogene.

The variant (6;15) translocations in murine plasmacytomas join the myc oncogene-bearing band of chromosome 15 and the immunoglobulin kappa band of chromosome 6. We recently cloned a region from chromosome 15 linked to C kappa and have now used probes from that region to define the major locus of plasmacytoma variant translocations, which we denote pvt-1. In five of nine plasmacytomas we analysed, the 6;15 translocation resulted from reciprocal recombination between the C kappa locus and a 4.5-kb region of pvt-1. Moreover, nearby we located the region shown by others to have undergone a complex (15;12;6) translocation in plasmacytoma PC7183. All the chromosome 6 breakpoints fell between 1 and 3 kb 5' to C kappa but only two were near J kappa genes. Thus the J kappa -C kappa region appears to be a recombination 'hot spot' in lymphocytes, but the breaks are unlikely to be mediated via V/J recombination enzymes. Comparison of a cloned 108-kb region across pvt-1 and another of 52 kb across c-myc established that the pvt-1 breakpoints lie at least 72 kb from the c-myc promoters. Since c-myc is expressed at a substantial level, the 6;15 translocation apparently activates c-myc. Activation may occur directly, at a remarkable distance along the chromosome, or indirectly, via a putative pvt-1 gene product.

Animals↗

PubMed1975

Extramedullary plasmacytoma of the breast.

The clinical and histopathological features of a case of solitary extramedullary plasmacytoma of the breast are described. After 46 mth of follow-up, there has been no recurrence of the tumour, and no evidence of further extramedullary plasmacytomas, multiple myeloma or diffuse myelomatosis either clinically, radiologically or on biochemical and haematological investigations. She has developed diabetes mellitus. Distinction is made between the true extramedullary plasmacytoma and those which are a manifestation of multiple myeloma. The unpredictable behaviour and prognosis of extramedullary plasmacytomas is indicated.

Breast Neoplasms↗

PubMed1995

Interacisternal A-particle (IAP) genes show similar patterns of hypomethylation in established and primary mouse plasmacytomas.

Alterations in cell programming associated with neoplastic transformation may involve widespread changes in patterns of DNA methylation. Increased expression of IAP elements in plasmacytomas compared with LPS-stimulated normal B-cells is accompanied by extensive hypomethylation of IAP sequences (Mietz and Kuff 1990), subsets of which are revealed with the LS2, LS3 and T1 probes. Multiple common LS- and PC-specific IAP loci are hypomethylated in established plasmacytomas, showing that hypomethylation does not occur entirely randomly. Many of the same IAP loci are hypomethylated in primary plasmacytomas induced by two different methods, as soon as recognizable tumor tissue can be isolated. In primary tumors hypomethylation frequently appears to occur in DNA flanking the IAP elements. In the established tumors the hypomethylated sites occur primarily in the IAP LTR, suggesting that for these loci hypomethylation begins in the flanking DNA and is extended into the IAP LTRs during progression of the tumors. The newly hypomethylated IAP LTRs in primary plasmacytomas (as compared to normal B cells) may provide a set of reporter genes for chromosomal regions that are characteristically hypomethylated in these transformed cells and that may contain cellular genes whose activation is related to the transformation process.

5-Methylcytosine↗

PubMed1995

Illegitimate recombinations between c-myc and immunoglobulin loci are remodeled by deletions in mouse plasmacytomas but not in Burkitt's lymphomas.

Recombinations between c-myc and immunoglobulin loci are a hallmark of Burkitt's lymphomas and mouse plasmacytomas. Analyzing the fine structure of these illegitimate rearrangements has revealed differences between the recombinations in these two tumors. Recombinations are nearly reciprocal in Burkitt's lymphomas, whereas in most BALB/c plasmacytomas large stretches of c-myc sequences have been deleted. The recombinations detected during preneoplastic development of plasmacytomas, in contrast, have most of the c-myc sequences retained on either one of the translocated chromosomes. We conclude that initial recombination structures are subjected to secondary changes in mouse plasmacytomas. In Burkitt's lymphomas the primary recombination sequence is preserved in tumor cells.

Animals↗

PubMed1986

Specificity of the generation and expression of enhanced anti-plasmacytoma immunity by spleen cells from melphalan-treated MOPC-315 tumor bearers.

We have shown previously that low-dose melphalan (L-PAM) therapy of mice bearing a large MOPC-315 plasmacytoma enables their hitherto immunosuppressed spleen cells to exert potent anti-MOPC-315 cytotoxicity following in vitro immunization with MOPC-315 tumor cells. Here we show that, following in vitro immunization with MOPC-315 tumor cells, spleen cells from such L-PAM-treated MOPC-315 tumor bearers exhibited enhanced T-cell-mediated cytotoxicity not only against the MOPC-315 tumor, but also against another plasmacytoma (MOPC-104E) possessing surface immunoglobulin (SIg) of a different idiotype than the MOPC-315 cells, as well as against a variant of the MOPC-315 tumor which does not produce nor possess SIg (SIg- MOPC-315). The enhanced cytotoxicity was directed against target antigens which are not expressed on the surface of the syngeneic WEHI 22.1 thymoma or the natural killer-sensitive YAC-1 cells. Plasmacytoma shared antigens, other than immunoglobulins, were able to stimulate spleen cells from L-PAM-cured MOPC-315 tumor bearers to generate in vitro a secondary type anti-plasmacytoma cytotoxic response. L-PAM-cured MOPC-315 tumor bearers exhibited in vivo immunity against SIg- MOPC-315 tumor cells, which was sufficiently triggered by the SIg- cells to bring about the rejection of a challenge of at least 100-fold the minimal lethal tumor dose of the SIg- MOPC-315 cells. Thus, SIg- MOPC-315 tumor cells present among SIg+ tumor cells in the parental MOPC-315 tumor inoculum can be eradicated in the L-PAM-treated MOPC-315 tumor bearers by the immune response to SIg+ tumor cells as well as by the immune response to SIg- tumor cells themselves.

Animals↗

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↗

PubMed1998

Solitary plasmacytoma of the calvarium: a review of clinical and prognostic features.

Primary craniocerebral plasmacytomas are uncommon they represent only 0.7% of all plasmacytomas. We report one case of solitary plasmacytoma of the skull and discuss the clinical features and prognosis of this tumor. There seems to be no difference in prognosis between plasmacytomas originating from the bone (osseous form) and those originating from the dura mater (non-osseous form). In these lesions, the risk of secondary multiple myeloma appears to be low.

Adult↗

PubMed1996

Secondary plasmacytoma of the testis: report of a case.

We report a case of secondary plasmacytoma of the testis. The patient previously had had plasmacytoma of the nasal cavity, and then recurrences occurred in the right ethmoid sinus, sphenoid sinus, nasopharynx and clavicle before testicular plasmacytoma has developed. This is the 49th case of testicular plasmacytoma reported in the world literature.

Humans↗

PubMedDate not supplied

Solitary plasmacytoma: experiences from Central Anatolia.

BACKGROUND: Solitary plasmacytoma localised to bone or soft tissue without myeloma. AIM: Clinical features and survival was analysed in patients from Central Anatolia. METHODS: Twenty-three solitary plasmacytoma (18 male, 5 female) were evaluated retrospectively. Median age was 58 years (46-72). The major localisation was vertebral column. RESULTS: All patients but one (larynx) had surgical resection and 21 patients received radiotherapy postoperatively. Multiple myeloma developed in eight patients (35%) and local relapse was detected in one patient. Eight patients died, causes of death were multiple myeloma progression in six patients, local relapse of intracranial plasmacytoma in one patient and cranial trauma in one patient who was in complete remission. Three and 5 years progression free survival were 45.6% and 22.8% respectively and overall survivals were 54.4% and 27.2% respectively. CONCLUSION: Solitary plasmacytoma cases should be followed carefully regarding local relapse and progression to myeloma.

Bone Neoplasms↗

PubMed1997

[Primary renal plasmacytoma. A case report].

We describe a patient with a primary renal plasmacytoma. In the literature available, only six clinical cases have been reported. A 64-year-old patient is presented who had the clinical signs of a renal cell carcinoma. Histological examination after nephrectomy, however, revealed a plasmacytoma. Based on this case, we discuss how one should proceed in this disease. Primary renal plasmacytoma can be tentatively diagnosed preoperatively only in the presence of paraproteinemia or Bence-Jones proteinuria, as it cannot be distinguished from other renal tumors by imaging procedures. Postoperatively, further staging procedures must rule out bone involvement (solitary myeloma or multiple myeloma). Nephrectomy is required in patients with plasmacytoma only if renal complications occur.

Carcinoma, Renal Cell↗