Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.
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PMID:Furosemide, mithramycin, and salmon calcitonin in hypercalcemia. 13 Feb 39

An unusual and extensive calcification of islets of Langerhans was found at autopsy in a man, 58 years old, who developed myeloma and, subsequently, hypercalcemia and diabetes. Although the islet cell calcification appears to be related to the hypercalcemia, the pathogenesis of the calcification is not clear, as primary metastatic calcification of pancreatic islets due to hypercalcemia does not occur. In support of this, a retrospective study of pancreatic tissue from 52 hypercalcemic patients with parathyroid adenoma and 34 patients with multiple myeloma, who frequently have hypercalcemia, did not reveal islet calcification. The islet calcification is ascribed to primary islet cell degeneration and necrosis, with hypercalcemia playing an augmenting but crucial role. It is considered that the combination of islet degeneration and calcification resulted in the diabetic state.
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PMID:Selective calcification of pancreatic islets of Langerhans. An unusual association with hypercalcemia and diabetes mellitus. 35 Jun 76

A 62-year-old woman presenting with intracranial lesion eroding the sella with compression of optic chiasma was found to have plasmacytoma of the pituitary area. At the time of initial surgery, the patient had no biochemical, immunologic or marrow findings of multiple myeloma. The intracranial tumor was interpreted initially as chromophobe adenoma on light microscopy, but the diagnosis of plasmacytoma was established by electron microscopic examination of the tumor. The case illustrates the usefulness of electron microscopy as a diagnostic tool.
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PMID:Multiple myeloma masquerading as chromophobe adenoma. 44 46

PRAD1 (parathyroid adenoma 1) gene at chromosome 11q13 has been cloned from parathyroid adenomas as a putative oncogene, activated by translocation with the parathyroid hormone gene. 4.5 kb and 1.7 kb mRNA are transcribed and both have the same open reading frame of 885 bp encoding 34 kd protein of a cyclin gene family, cyclin D1. Recently, overexpression of PRAD1 gene has been reported to be correlated closely with the rearrangement of bcl-1 locus, particularly in centrocytic lymphoma. In our study, overexpression of PRAD1 gene was shown in five B cell lines with t(11;14)(q13;q32) including one centrocytic lymphoma line and 4 myeloma lines, when compared with other hematopoietic cell lines without translocation. One of the cell lines, SP-49, demonstrated a truncated mRNA of 3.4 kb, in addition to 1.7 kb of normal size. Southern blot analysis demonstrated a rearrangement with PRAD1 cDNA probe, suggesting that the gene is altered in this particular cell line. By cloning analysis, we confirmed that 1.8 kb deletion in 3' region of PRAD1 gene eliminating the destabilizing signal of PRAD1 mRNA, gave rise to the aberrant mRNA of 3.4 kb. These findings suggest that PRAD1 gene is most likely the candidate oncogene for bcl-1 activated by t(11; 14)(q13;q32) translocation. The gene alteration found in one cell line, SP-49, might also play an important role for deregulation of the gene.
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PMID:[Overexpression of PRAD1 gene in B-cell malignancy with t(11;14)(q13;q32) translocation]. 151 59

A total of 87 human specimens with 10 histological types of primary neoplasm were studied immunohistochemically with monoclonal antibodies specific for beta-hexosaminidase (Hex). High levels of Hex were found in malignant neoplasms of the skin, cervix, colorectum and in benign as well as neoplastic plasma cells, while no activity was detected in normal epidermis, normal colorectal epithelium or benign naevi. The strongest immunohistochemical reaction was revealed in tumor cells of malignant melanoma. Adenomas and adenocarcinomas of the colorectum showed high levels of Hex with a basal pattern of immunoreactivity more frequent in the tumor cells of adenocarcinomas than adenomas. Fibroblasts and macrophages in the tumors often disclosed immunoreactivity. In most of the sections (including those from plasma cell neoplasms), 7E4 antibody showed low immunoreactivity compared to 2E3, except for non-neoplastic plasma cells, which were as a rule positive with 7E4 and largely negative with 2E3 antibody. This result probably indicated different isoenzymes in benign and neoplastic plasma cells.
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PMID:Immunohistochemical studies of beta-hexosaminidase in neoplastic and normal tissues with monoclonal antibodies. 153 74

The proto-oncogene PRAD1 (parathyroid adenoma 1) on chromosome 11q13 was found to be overexpressed in all five B-cell lines with t(11;14)(q13;q32) translocation tested. One B-cell lymphoma and four myeloma cell lines with this translocation demonstrated more than 10-fold overexpression as determined by Northern blot analysis, when compared with normal lymphoid tissues such as thymus, spleen and lymph node. Hematopoietic cell lines without the translocation were also examined, but none of these demonstrated the overexpression, confirming that overexpression of the PRAD1 gene is associated with t(11;14) translocation. A truncated form of mRNA was seen in one of five cell lines with the translocation, SP-49. Hybridization with different regions of the PRAD1 cDNA revealed that the truncated form of mRNA retained the coding region but had lost the 3' untranslated region. Southern blot analysis demonstrated a gene rearrangement in this SP-49 cell line. To study the genetic alteration responsible for the truncated form of mRNA in this cell line, the rearranged allele as well as the germline allele were cloned. The restriction map revealed that the rearranged portion was at the 3' end of the PRAD1 gene, eliminating the mRNA-destabilizing signal AUUUA. Human-rodent hybrid cell analysis demonstrated that the region introduced 3' of PRAD1 was derived from chromosome 11, suggesting that the PRAD1 gene region is deleted at the 3' end. Over-expression of the PRAD1 gene in association with t(11;14)(q13;q32) translocation suggested that in these cases the regulation of PRAD1 was altered by the juxtaposed gene, most likely the immunoglobulin heavy-chain gene from chromosome 14.
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PMID:Gene rearrangement and overexpression of PRAD1 in lymphoid malignancy with t(11;14)(q13;q32) translocation. 153 1

In a chance observation, a 74-year-old woman was found to have hypercalcaemia (3.0 mmol/l) and multiple skeletal osteolyses. A diagnosis of multiple myeloma was made after the demonstration of paraproteins in serum (IgG-kappa) and a 10% proportion of plasma cells in a pelvic crest biopsy. Oral chemotherapy with melphalan and prednisone failed to alter the calcium level. Simultaneous increase in alkaline phosphatase and reduction in serum phosphate concentration led to further tests: determination of peripheral venous parathormone concentration, ultrasound examination of the neck, thallium-technetium subtraction scintigraphy and selective venous parathormone measurements. The results demonstrated the coexistence of primary hyperparathyroidism. The calcium level became normal after surgical removal of a parathyroid adenoma.
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PMID:[Hypercalcemia in coexistent parathyroid adenoma and multiple myeloma. Problems of differential diagnosis]. 266 81

A patient with primary hyperparathyroidism and multiple myeloma did not have roentgenographic evidence of either disease, yet there was biochemical evidence for both diseases. Hyperparathyroidism was diagnosed by hypercalcemia and increased parathyroid hormone values. Multiple myeloma was diagnosed by serum gamma-globulin component of 2.74 g/dL with a monoclonal spike and bone marrow plasmacytosis of 31%. The serum IgA level was 2.22 g/dL and the IgG and IgM levels were normal. Serum and urine immunoelectrophoresis showed abnormal IgA and lambda arcs. Computed tomography of the neck localized a parathyroid adenoma that was found and removed at surgery.
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PMID:Primary hyperparathyroidism complicated by multiple myeloma. 648 91

A case of multiple myeloma in which hypercalcaemia persisted despite an otherwise good response to conventional treatment is described. The hypercalcaemia was eventually found to be due to a parathyroid adenoma. Despite the frequent association of hypercalcaemia and malignant disease, and the relative frequency of primary hyperparathyroidism as a cause of hypercalcaemia, there are very few reports of multiple myeloma and parathyroid adenoma occurring together. This case emphasizes the need to be aware that there may be more than one cause of hypercalcaemia in a patient with multiple myeloma.
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PMID:Refractory hypercalcaemia. Parathyroid adenoma or multiple myeloma? 669 88

A clinical diagnosis of myeloma was made in a 44-year-old woman with anaemia, a markedly raised erythrocyte sedimentation rate, osteolytic lesions in the pelvis, and a pathological fracture of the femur. Confirmatory trephine biopsy showed, instead of plasma cell infiltration, destruction of the normal micro-anatomy of the marrow with bridging fibrosis, gross osteoclastic proliferation, and areas of new bone formation. These are the features of hyperparathyroidism. Subsequently, a solitary adenoma of the parathyroid glands was demonstrated and resected. This case illustrates the value of examination of the trabeculae in trephine biopsy specimens in the diagnosis of bone disease.
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PMID:Diagnostic value of trephine biopsy in bone disease. 686 77


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