SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Two cases of plasmacytoma of the testis presenting as primary testicular tumors are presented. This lesion may be confused both clinically and histologically with other more common pathologic conditions.
Extramedullary plasmacytoma arising in the kidney is rare. Only 8 cases have been reported. Recently, we noted the ninth case, the second case seen at the Mayo Clinic. Clinically, the tumor mimics a renal cell carcinoma or a transitional cell carcinoma of the renal pelvis.
An extramedullary plasmacytoma (EMP) is presented with an isolated lesion in the urinary bladder accompanying an IgG-K paraproteinemia. After a short-term oral melphalan administration, the tumor soon regressed together with the paraprotein, and has never recurred during the two-year follow-up. This is the fourth case of primary EMP of the urinary bladder reported in the literature.
A case of a plasmacytoma arising in the left ovary of a 56-year-old woman is reported. The diagnosis is supported by the unequivocal histology and the detection of a monoclonal IgG/Kappa cell population by an immunoperoxidase PAP technique.
A plasmacytoma of the ovary in a 63-year-old is described. It was associated with an IgA K paraprotein. Myelomatosis developed 2 years after excision of the tumor.
We examine the influence of the immunoglobulin locus on the expression of the translocated c-myc oncogene in mouse plasmacytomas. The level of c-myc RNA was 30- 35-fold greater in tumor cells than in normal, quiescent B cells. Mitogen stimulation of the lymphocytes with lipopolysaccharide induced a 15-fold increase in c-myc expression per cell to a level that was similar to that in the transcription of the translocated c-myc gene involved initiation from sequences in the first c-myc intron. Abundant RNA transcripts were also found from the noncoding strand of the c-myc intron in most tumor lines. S1 nuclease mapping was used to locate the intronic sequences that are used to initiate the tumor-specific c-myc RNAs. Six different initiation sites within the intron were mapped, none of which have the TATA sequence usually associated with eucaryotic RNA polymerase II promoters. The noncoding strand transcripts were also found to initiate in the c-myc intron. Transcription of the c-myc coding strand was independent of the position of the translocation breakpoint, even when the heavy chain switch and constant regions were deleted.
A novel mechanism of oncogene activation by transposition of a tissue-specific cellular enhancer is described. A rearranged c-myc oncogene was cloned from murine plasmacytoma ABPC17 in the expectation that it would reflect the t(6;15) chromosome translocation carried by this tumor. The rearrangement instead reflects an insertion 361 bp 5' to the c-myc gene on chromosome 15. The insert conveys a 2.3 kb segment of the immunoglobulin heavy (H) chain locus from chromosome 12. Since the insertion introduces the lymphoid-specific enhancer from the JH-Smu region and also disrupts a region implicated in normal c-myc control, it may account for the c-myc transcription observed in ABPC17. The structure of the transposed segment and a corresponding deletion in the JH-Smu region suggests that the transposition reflects a complex recombination between chromosomes 15 and 12. Since the t(6;15) breakpoint is not near c-myc, chromosome 15 must have undergone an independent exchange with chromosome 6.
An antiserum against a monoclonal protein of IgG/kappa type from a patient S. was produced by immunization of guinea pigs. Idiospecificity of the antiserum (anti-Id AS) was tested by immunoprecipitation and hemagglutination inhibition. About 70% mononuclear cells prepared from the bone marrow (BM) aspirate of this patient stained positive when the antiserum was used in an indirect immunofluorescence (IF) procedure detecting surface membrane structures. Commercial antisera specific for gamma, kappa and lambda immunoglobulin (Ig) chains stained only 5-17% of the cells. With mu chain and delta chain specific antisera no reactivity could be observed. The presence of idiotype cross-reacting determinants (Id-CR-D), that is idiotypes not associated with Ig isotypes could be also demonstrated by a significant increase of 3H-thymidine incorporation of the BM cells in the presence of the anti-Id AS. Phytohemagglutinin (PHA), pokeweed mitogen (PWM) and concanavalin A had no effect. In a cell sorting experiment using affinity gel chromatography it could be shown that the anti-Id AS preferentially binds to proplasmacytes. Cells of this type were enriched two-fold over plasma cells in the eluate. The analysis of peripheral blood lymphocytes (PBL) from the patient revealed about 40% positive cells without correlation to a certain subpopulation. Administration of prednisolone to the patient resulted in a significant reduction of the Id positive cells within two days. In conclusion it appears that our antiserum detects cells of an individual tumour clone within PBL and BM-cells. By the stimulating effect of the anti-Id AS a proliferative potential of plasmacytoma cells could be defined which may work also 'in vivo'. Thus, Id-CR-D may operate as a tumour growth receptor.
Mononuclear cells from a bone marrow infiltrated by plasmacytoma cells were examined by electron microscopy. An analysis was performed according to different cytoarchitectural forms of the endoplasmic reticulum (ER). Six types of plasma cells could be distinguished. The bone marrow cells were treated with an anti-idiotype antiserum from a guinea pig prepared against the patient's monoclonal serum protein and with a FITC conjugated anti-guinea pig antiserum from the rabbit as second layer. Then the cells were passed through an affinity gel column with anti-FITC antibodies. The original preparation and the cells separated on the affinity gel were analysed by electron microscopy. It was found that an ultrastructurally distinct type of plasma cell was enriched 3.5-fold over the original sample by the separation procedure.
Expression of non-rearranged and rearranged c-myc in a mouse plasmacytoma cell line S194 cultured in different serum concentration or temperature was examined. Exponentially growing S194 cells expressed a high level of rearranged c-myc and a low level of non-rearranged c-myc mRNAs. The levels of the two c-myc mRNAs were nearly the same in the cells in which growth was suppressed by lowering serum concentrations or incubation temperature in culture medium. Furthermore, even when serum-deprived S194 cells resumed growth following serum restimulation, the induction of non-rearranged c-myc mRNA, observed in a mouse T-cell lymphoma cell line BW5147, was not demonstrated. In contrast to the unchanged c-myc expression, the level of N-ras mRNA was related to changes in cell growth rate induced by changes in serum concentration in S194 cells. These results suggest that not only the rearranged c-myc but also the non-rearranged c-myc is unresponsive to serum stimulation and temperature changes, even though cell growth rate is markedly changed.
We report a large solitary plasmacytoma arising in the sternum of a 62-year-old man. On computed tomography the tumor demonstrated a multilobular appearance associated with bone destruction and expansion and absence of intrinsic calcification. Computed tomography was helpful in determining the size and extent of the tumor and in suggesting the correct diagnosis.
The transcription factor NF-kappa B appears to play an important role in immunoglobulin gene expression and lymphokine production, and may play a role in primary B cell activation. Constitutive nuclear expression of NF-kappa B has been found in all mature B cell lines with the notable exception of the murine plasmacytoma, S107. We report herein that S107 cells express cytoplasmic kappa B-binding material detected by electrophoretic mobility shift assay that by several criteria represents authentic NF-kappa B. Despite the presence of cytoplasmic NF-kappa B, several stimuli known to induce nuclear translocation of NF-kappa B failed to do so in S107 cells, including: the PKC agonist, PMA; the protein synthesis inhibitor, cycloheximide; and LPS. Transfection of S107 cells with a kappa B-CAT reporter gene construct confirmed the absence of functional activity. Importantly, a global failure of nuclear transcription factor expression was ruled out by the ability of PMA to induce nuclear expression of another trans-acting factor, AP-1. Thus, rather than lacking NF-kappa B altogether, S107 cells manifest disordered regulation of NF-kappa B in which cytoplasmic material is incapable of translocation to the nucleus. While Northern analysis failed to reveal a gross defect in the mRNA coding for the DNA binding subunit of NF-kappa B, UV-photo-cross-linking followed by denaturing gel electrophoresis demonstrated the presence of a cytoplasmic kappa B-binding protein of abnormally elevated molecular size. This finding suggests that the abnormal regulation of NF-kappa B in S107 cells is associated with the appearance of an unusual kappa B-binding molecule.
The effects of 6-hydroxydopamine (6-OHDA), N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) and anti-nerve growth factor (anti-NGF) on the development and growth of a tumor of non-neuronal origin were studied in mice. Murine LPC-1 plasmacytoma cells were grown either subcutaneously (s.c.) as solid tumors in the hindleg or intraperitoneally (i.p.) in ascitic form. Growth of s.c. tumors was monitored by caliper measurements of the hindleg at the site of tumor cell inoculation; growth of ascitic tumors was followed by electrophoretic determination in plasma of the tumor associated protein IgG2a kappa, M component. Adult mice were treated with 6-OHDA or DSP-4 six hours prior to tumor cell implantation; newborn mice were treated with anti-NGF and tumor cells were given 9 weeks later. Both chemical- and immunosympathectomy significantly altered the growth pattern of solid and ascitic tumors (P less than 0.0001). The effect of sympathectomy on the growth of solid tumors was most pronounced during the early phase of tumor growth. The data document that the effect of each drug treatment on tumor growth was not due to direct cytotoxic actions of the agents employed on tumor cells but the result of impairment of sympathetic functions. The findings of this study suggest a role of the sympathetic nervous system in tumor growth.
A murine plasmacytoma (MPC) with a reciprocal translocation between chromosomes 15 and 16 with breakpoints in 15D2/3 and 16B1 is reported. The breakpoint on chromosome 15 is identical to the breakpoint in the MPC-associated typical (12;15) and kappa variant (6;15) translocation. Therefore it probably involves the c-myc gene as well. Unlike the Burkitt lymphoma (BL) system, a lambda/myc variant translocation has not been described in the MPC system. Chromosome 16 is known to carry the lambda gene. Therefore, the 15;16 translocation probably represents the "missing" lambda/myc variant in MPC, suggesting that the lambda gene is localized at 16B1.
A polyclonal human lymphoblastoid cell line transformed in vitro with Epstein-Barr virus produced specific anti-Rhesus D antibody. It was repeatedly enriched by rosetting procedures and subsequently cloned. The cloning conditions employed a combination of mouse macrophage feeder layers, antimycoplasma agents, and low density passage. Formal evidence of monoclonality was obtained in one case which was of human IgG1 isotype and was secreted at the level of 15-20 micrograms/ml. All clones showed long-term stability in culture after 10 months of continuous passage. Both polyclonal and monoclonal cell lines possessed antigens characteristic of highly differentiated B cells, yet they also expressed Epstein-Barr virus nuclear antigen (EBNA). This study exemplifies a simple method for obtaining monoclonal antibody secreting plasmacytomas of human origin.
Twenty-four cases of solitary plasmacytoma of the mandible are reported in the literature. The criteria for the selection of cases and for their diagnosis are described. It is a rare condition, with a maximum occurrence in the fifth to seventh decades and a male to female ratio of 2:1. It predominates in the premolar and molar regions. Clinical and radiological features are non-specific. Diagnosis is by biopsy. Treatment of preference is surgery. Irradiation of greater than 5,000 Rads is also recommended. Investigations must be carried out for multiple myeloma. Long-term regular surveillance is advised, for infrequently, multiple myeloma may develop.
An anti-idiotype antibody (anti-Id Ab) was made by immunization of a rabbit with the IgG-2/lambda paraprotein from a plasmacytoma patient (Sa). The antibody was directed against determinants of heavy (H) and light (L) chains on the F(ab)2 piece of the paraprotein. Using this antibody an unusual pattern of cytoplasmic fluorescence was seen with bone marrow cells of the patient. One population (type I) showed reactivity in association with gamma and lambda chains, the other (type II) with the anti-Id Ab only. So, by immunological methods, biclonality could be demonstrated using the anti-Id Ab but not with anti-isotype antibodies. L chains of mol. wt 23.5 and 17.0 kd were observed. The H and L chains of small molecular weight were not detected in the patient's serum nor in the culture supernatant. Thus, deleted and intracellularly degraded H and L chains may cause the unusual staining pattern of the type II cells.
We report two cases of solitary plasmacytoma of the skull, a very unusual presentation and location of this tumor. There seems to be no difference in prognosis between the tumor originating from the skull (osseous form) and from the dura mater (non-osseous form), differently from the data of other parts of the body. The risk of secondary multiple myeloma appears to be low but the mean follow-up is too short for any conclusion on this point.