Plasmacytoma of the stomach.
A case of plasmacytoma of the stomach is described. The clinical presentation, diagnostic pitfalls and the treatment of this rare entity are discussed.
Adult↗
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Local recurrence of solitary plasmacytoma of the mandible.
A case of local recurrence of mandibular plasmacytoma has been presented. Review of the literature disclosed only one previous report of this phenomenon.
Adult↗
[Plasmacytoma of the testis: report of a case].
We report on a case of testicular plasmacytoma in a patient with multiple myeloma (MM), who is currently in a state of remission following chemotherapy and radiotherapy. The literature is reviewed, and testicular involvement in plasma cell neoplasms is discussed.
Adult↗
Gastric plasmacytoma with rod-shaped intracytoplasmic inclusions. Report of a case studied by light and electron microscopy and immunohistochemistry.
A 78-year-old man with primary gastric plasmacytoma showing massive rod-shaped intracytoplasmic inclusions is presented. The patient was initially diagnosed as having a benign gastric ulcer and underwent partial gastrectomy. Around the ulcer of the resected stomach specimen, diffuse proliferation of plasma cells with massive rod-shaped intracytoplasmic inclusions was noticed by light microscopy. Immunohistochemically, these cells were found to contain IgM-kappa-type immunoglobulin upon peroxidase-antiperoxidase (PAP) staining. Electron microscopy showed that the intracytoplasmic inclusions were localized in the rough endoplasmic reticulum and had a lattice structure with a periodicity of about 120 A.
Aged↗
Cimetidine reverses tumor growth enhancement of plasmacytoma tumors in mice demonstrating conditioned immunosuppression.
Mice were given repeated injections, at 21 day intervals, of cyclophosphamide paired with a novel taste (saccharin) in the drinking water. Subsequent challenge with a syngeneic plasmacytoma tumor led to elevated tumor growth and mortality only in conditioned mice that were reexposed to saccharin. This effect was abolished by conditioned exposure to a histamine type II-receptor antagonist.
Animals↗
The murine IgA-secreting plasmacytoma MOPC-315 expresses somatostatin receptors.
We have previously shown that some neuropeptides had a profound effect on in vitro Ig synthesis (especially IgA) and mitogen-driven murine lymphocyte proliferation. MOPC-315, an IgA-secreting plasmacytoma line, has been extensively used in studies of the regulation of IgA synthesis. In this report we show that the neuropeptide somatostatin (SOM) inhibits proliferation ([3H]thymidine uptake) of MOPC-315 and also inhibits IgA synthesis in vitro. MOPC-315 cells bind both fluorescent SOM and [125I]SOM specifically. On cytofluorimetric analysis, 68 +/- 6.8% (mean +/- SE, n = 7) of MOPC 315 cells labeled with fluorescent SOM and this staining was compatible by incubation with an excess of unlabeled peptide. Specific [125I]SOM binding increased linearly with cell concentration, was rapid and achieved equilibrium after 20 min at 4 degrees C. It was temperature-dependent, readily reversible, and under equilibrium conditions demonstrated a dissociation constant of 1.6 +/- 0.7 nM (mean +/- SE, n = 5). Scatchard analysis showed that MOPC-315 cells had 40,733 +/- 16,050 (mean +/- SE) binding sites for SOM per cell. The characteristics of the interactions of SOM with MOPC-315 cells suggest a specific receptor-mediated mechanism whereby this neuropeptide may modulate lymphocyte function.
Animals↗
Splenic immune effector and suppressor cells in mice bearing a growing plasmacytoma.
The occurrence of tumor immunity in mice bearing a growing plasmacytoma (PC) was studied by local adoptive transfer assay. Spleen cells from mice with a large PC but not with a nonpalpable or small PC retarded and often inhibited entirely the growth of homologous PC. They occasionally caused late regression of growing homologous and heterologous PC. The individual tumor-specific immune effector cells were found to be radiosensitive, non-adherent, Thy 1-positive T-cells. They were resistant to treatment of mice with high-dose cyclophosphamide (CTX). Their generation, however, was abrogated by low-dose CTX and irradiation at the early stage of their development. Spleen cells from PC-bearing mice treated with high-dose CTX were enhanced in their effector activity, suggesting the co-existence of CTX-sensitive suppressor cells. The suppressor cells could be demonstrated in spleens of mice bearing a heterologous PC and were found also to be radiosensitive, non-adherent, Thy 1-positive T-cells. Their generation was blocked by treatment of mice with CTX during the early stage of PC development. These findings provide evidence for the occurrence of immune effector T-cells in mice with a growing PC. This immunity appears to be down-regulated by CTX-sensitive suppressor cells.
Animals↗
Extramedullary plasmacytoma of the thyroid.
We report a patient with solitary extramedullary plasmacytoma of the thyroid gland. We describe the computed tomographic findings correlated with the radionuclide imaging and surgical findings and review the related literature.
Humans↗
Selective in-vitro activation of BALB/c T suppressor lymphocytes specific for syngeneic ADJ-PC-5 plasmacytoma cells.
T suppressor (Ts) lymphocyte activation is the first reaction of the immune system under conditions which simulate early stages of tumourigenesis. There is evidence that the Ts cell inducing antigen on ADJ-PC-5 plasmacytoma cells of BALB/c origin is a self antigen, which is also expressed on normal BALB/c spleen cells. In order to study this Ts cell inducing determinant in more detail we have developed an in vitro system which allows the selective activation of ADJ-PC-5 specific Ts cells in the absence of activation of cytotoxic T (Tc) cells. The system now allows us to study the modulation of Ts cell induction and function.
Animals↗
Formation of lipid-linked oligosaccharides by MOPC 315 plasmacytoma cells. Decreased synthesis by a nonsecretory variant.
MOPC 315 is a BALB/c plasmacytoma which secretes a trinitrophenol-binding IgA lambda 2 paraprotein. We have investigated the incorporation of [3H]mannose into lipid-linked oligosaccharide precursors in wild-type MOPC 315/J and variant nonsecretory 315/P cells. In pulse labeling experiments, no differences could be detected in the ability of the two cell types to incorporate [3H]mannose into lipid-linked oligosaccharides containing 5 or less mannose residues. In contrast, quantitation of the incorporation of [3H]mannose into larger lipid-linked oligosaccharides and proteins revealed a 49 and 40% decrease, respectively, in the 315/P cells compared to wild-type cells. Further characterization of the lipid-linked structures documented a marked decrease in glucosylated oligosaccharides isolated from 315/P cells. When membranes from the two cell lines were analyzed for their ability to transfer [3H]glucose from UDP-[3H]glucose to [3H]glucosylphosphoryldolichol, an apparent deficiency was noted in the 315/P preparations. However, if assay conditions were adjusted to include AMP in the reaction mixtures, no differences in the in vitro synthesis of [3H]glucosylphosphoryldolichol or [3H]glucose-labeled oligosaccharide-lipid could be detected. In these reactions AMP was found to prevent hydrolysis of UDP-[3H]glucose by inhibiting nucleotide pyrophosphatase (EC 3.6.1.9), the specific activity of which was determined to be more than 100 times greater in variant 315/P compared to wild-type MOPC 315/J cells. This large difference in specific activity was not accompanied by similar differences in the activity of several other enzymes analyzed. A decrease in whole cell UDP-glucose pool size was not detected in 315/P cells. Therefore, if nucleotide pyrophosphatase is important for the control of substrates for glycosylation, it must regulate nucleotide sugar levels at a site other than the cytoplasm of cells, perhaps at the location of synthesis of the larger lipid-linked oligosaccharides.
Animals↗
In vitro induction of tumor-specific immunity. III. Lack of requirement for H-2 compatibility in lysis of tumor targets by T cells activated in vitro to oncofetal and plasmacytoma antigens.
Many recent studies have demonstrated that cytotoxic T lymphocytes (CL) activated to various antigens other than those of the H-2 complex, will lyse target cells only when H-2 compatibility exists between the CL and target cell. From these observations, it has been inferred that T lymphocytes might only be capable of responding to H-2 antigen or antigens that become associated with H-2 region gene products. Our results suggest that this is not the case, and that in some situations, cytotoxic T lymphocytes can specifically lyse target cells of different H-2 types. Two in vitro systems are described where primary induction of cytotoxic T lymphocytes to oncofetal and plasmacytoma antigens results in CL capable of lysing suitable targets bearing these antigens, of either syngeneic or allogeneic derivation. Thus it is proposed that although interaction antigens involving H-2 components may preferentially activate T lymphocytes, this does not imply a restriction on the recognition potential of T lymphocytes.
Animals↗
Plasmacytoma growth factor activity of murine granulocyte-macrophage colony-stimulating factor.
Mouse plasmacytoma FLOPC21 was adapted to culture in the presence of a mouse Th cell supernatant. A stable factor-dependent cell line was derived from this culture and the factor responsible for its growth was identified as granulocyte-macrophage colony-stimulating factor.
Animals↗
Gamma-chain heavy-chain disease with primary thyroid plasmacytoma.
A case of gamma-chain heavy-chain disease was associated with primary thyroid plasmacytoma. The patient has been free of complaints for two years since the removal of the tumorous thyroid. The heavy-chain fragment (molecular weight, 32,000 daltons) has disappeared from the serum and urine, while the previously low levels of normal immunoglobulins have increased. The immunoglobulin anomaly may be correlated with the chronic antigen stimulus.
Aged↗
Restorative effects of levamisole on cell-mediated immune responses following chemotherapy with aniline mustard in mice bearing ADJ-PC5 plasmacytoma.
Restorative effects of levamisole on general and tumor-associated cell-mediated immune responses were investigated following aniline mustard (AM) chemotherapy of BALB/c mice bearing ADJ-PC5 plasmacytoma. Total eradication of tumor following AM chemotherapy resulted in severe depression of lymphoproliferative (LP) responses which recovered after a prolonged period of 4-6 weeks. During this time, spleen cells from these treated mice were shown to be generally depressed to T- and B-cell mitogens. Levamisole, an anthelmintic drug capable of enhancing depressed immune responses in mice and in man, was employed following AM chemotherapy in an attempt to restore immunocompetency. Administration of levamisole following AM had a significant effect on the ability of mice to resist rechallenge with ADJ-PC5 tumor and in tumor cell neutralization. The enhanced resistance to tumor cell challenge appeared to be associated with a faster recovery of the general T-cell immunocompetence as demonstrated in the LP assays among the mice receiving chemotherapy followed by adjuvant therapy. Levamisole, when administered alone to tumor-bearing mice, did not appear to possess a direct antitumor effect. In addition, levamisole did not potentiate cellular immunity to higher than normal levels in nonimmunodepressed mice. These results demonstrate the efficacy of levamisole as a restorative agent of the general and tumor-associated immunocompetency in the immunodepressed host.
Aniline Mustard↗
Gastric plasmacytoma: an early lesion diagnosed with the aid of immunoperoxidase and immunogold techniques.
A case of gastric plasmacytoma in a 34-yr-old woman has been presented. The demonstration of monotypic intracytoplasmic immunoglobulin of IgM-kappa type in biopsy specimens by immunoperoxidase technique contributed the confident histological diagnosis. In the resected stomach, IgM-kappa monoclonal proliferation of plasmacytic tumor cell was also demonstrated in the lamina propria and in the perivascular space of the submucosa, which was distinct from plasma cells of polyclonal nature diffusely infiltrating in the adjacent mucosa. The double immunogold staining confirmed the presence of immunoglobulin IgM-kappa type in the distended rough endoplasmic reticulum of the tumor cell.
Adult↗
Plasmacytoma and gastric amyloidosis associated with nodular pulmonary amyloidosis.
The authors report an association of gastric and pulmonary amyloidosis in a 74 year old woman. The patient had had a gastric plasmacytoma for the last 11 years. On autopsy, the stomach was found to contain intramural deposits of amyloid, and was infiltrated by plasma cells secreting monoclonal IgG lambda light chain. In the lungs, the plasma cells in the vicinity of the amyloid deposits proved to be polytypic, suggesting that these deposits originated from circulating precursor proteins.
Amyloidosis↗
[Extramedullary plasmacytoma of small intestine--a case report].
Extramedullary plasmacytoma (EMP), being different from multiple myeloma, is very rare. One case of primary EMP of small intestine and review of literature are presented. The patient, 69-year-old male, was admitted because of left lower abdominal pain and anemia. A mass, table-tennis in size, was palpated. Intestinal obstruction was found by plain X-ray film. It was diagnosed as EMP of small intestine by pathology after exploratory celiotomy. Immunohistochemical stain showed that intracytoplasmic immunoglobulin was monoclonal IgG. Lambda. The blood Bence-Jones protein and bone marrow puncture were negative. The patient received chemotherapy after operation and was followed for two years giving satisfactory result. The pathogenesis, clinical feature, diagnostic criteria and treatment are discussed.
Aged↗
Identification of an interleukin HP1-like plasmacytoma growth factor produced by L cells in response to viral infection.
We have recently purified and partially sequenced a new T cell-derived lymphokine with growth factor activity for B cell hybridomas and plasmacytomas, which we named interleukin HP1 (HP1). Here we show that, in response to viral infection or after treatment with poly(rI).poly(rC), L cells produce a factor that is capable of supporting the in vitro growth and survival of HP1-dependent cell lines. Serologic and structural evidence is presented in favor of the identity between the fibroblast factor and HP1, demonstrating that non-T cells can make HP1-related molecules.
Animals↗