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

The nitrosoureas (BCNU, CCNU, methyl CCNU) represent a new class of antineoplastic agents with a broad spectrum of antitumor activity. They are cell-cycle nonspecific cytotoxic agents. Postulated modes of action and pharmacology of these nitrosoureas are reviewed. Their therapeutic effectiveness as single agents and in combinations have been recognized in malignant lymphomas, multiple myeloma, melanoma, glioblastoma multiforme, gastric and colorectal carcionma, and small-cell carcinoma of the lung. The nitrosoureas are administered on an intermittent 6--8-week schedule because of delayed and frequently severe bone marrow toxicity which may be cumulative in nature.
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PMID:Nitrosoureas: a reappraisal of clinical trials. 39 66

Injection of isologous monoclonal antibodies (SR2, SR3) caused anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM nephritis) in WKY/NCrj rats. The antibodies were obtained from hybridoma cells derived from fusion of the spleen of a nephritic WKY/NCrj rat injected with rat solubilized renal basement membranes with adjuvant, and mouse SP2-myeloma cells. They belonged to the rat IgG2a subclass and bound to rat kidney in a linear pattern along the glomerular and tubular basement membranes. Histological changes in glomeruli were detected at day 1 after the injection; proteinuria with haematuria appeared on day 2; and proteinuria became severe and reached a plateau by day 5. These results demonstrate that anti-GBM nephritis can even be induced by an isologous monoclonal antibody and that the rat IgG2a subclass is at least nephritogenic. The experimental model of anti-GBM nephritis with isologous monoclonal antibodies makes it possible and easier to analyse further the mechanism of anti-GBM nephritis.
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PMID:Isologous monoclonal antibodies can induce anti-GBM glomerulonephritis in rats. 146 May 40

Continued monitoring of a family for new malignant tumors has revealed diverse immunological and neoplastic disorders during a 15-year period. In 1966, the proband developed lymphoma. In 1975, his antibody titers to Epstein-Barr virus (EBV) became elevated, and again, he developed a malignant lymphoma. He also had borderline hypo-immunoglobulin A, died of glioblastoma multiforme in 1977, and at autopsy, had adenomatous colonic polyps. His eldest brother has normal immunoglobulin levels, but developed immune thrombocytopenia in 1973 and had elevated EBV antibody titers in 1980. Another brother had hypo-immunoglobulin A, thymoma in 1965, and adenomas and adenocarcinoma of the colon. Two other brothers succumbed to glioblastoma in 1968 and 1969. The father of the proband had bronchiectasis in 1952, hypo-immunoglobulin M documented in 1972, and elevated EBV antibody titers 5 years preceding development of a malignant lymphoma. The latter contained 10 EBV genome equivalents/cell by EBV viral DNA/DNA reassociation kinetics analysis. The proband's grandmother had died of an immunoglobulin G-secreting myeloma in 1977, and his grandfather had borderline low immunoglobulin M, elevated EBV antibody titers, and hypopharyngeal carcinoma in 1980. Predisposition to oncogenesis in this family was probably inherited.
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PMID:Diverse familial malignant tumors and Epstein-Barr virus. 627 70

A case of IgD myeloma who developed a glioblastoma multiforme in the left temporal lobe after a partial remission is reported. The clinical and laboratory particular features of IgD myeloma are pointed out and the association of the multiple myeloma and secondary neoplasms is discussed.
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PMID:[Second neoplasm in a patient diagnosed with IgD myeloma. Presentation of a case and review of the literature]. 838 7

Recently, a novel phosphatase designated PTEN/MMAC1/TEP1 and located on chromosome 10q23.3 has been implicated as a new tumor suppressor gene in human cancer. Allelic loss and mutation of this gene has been reported in epithelial derived tumors, including breast cancer and prostate cancer, and in glioblastoma multiforme. The present study was designed to evaluate the potential involvement of PTEN in the pathogenesis of lymphoid neoplasms. We analyzed 27 hematopoietic cell lines (representing a variety of lymphoid lineages), 65 primary lymphoid tumors (including 24 lymphoblastic leukemia/lymphoma [LBL], 30 large B-cell lymphoma [LBCL], 7 Burkitt's lymphoma [BL], and 4 anaplastic large cell lymphoma [ALCL]), and 25 nonmalignant lymph node controls. Gene deletion and gross rearrangement were evaluated using Southern blot analysis, and mutations were studied by polymerase chain reaction (PCR)-single-strand conformation polymorphism (SSCP) (PCR-SSCP) and sequencing. Six of 27 cell lines (22.2%) and 3 of 65 primary lymphomas (4.6%) contained alterations of this gene. A large homozygous deletion spanning exons 2 through 5 was detected in one LBL cell line, and two insertions potentially resulting in premature termination, were detected in a second LBL cell line. Nonconservative nucleotide variations were found in two other cell lines (one LBCL and one BL) and in one primary case of LBCL. In addition, two other cell lines (one BL and one myeloma) and two primary lymphomas, both LBCL, contained small deletions within intron 7. These deletions mapped to a poly-T-rich tract just 5' to the intron 7/exon 8 spice site. Their significance is unclear, as they may represent polymorphisms. Overall, our results suggest that abnormalities of the PTEN gene can contribute to pathogenesis in a small percentage of malignant lymphomas.
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PMID:PTEN gene alterations in lymphoid neoplasms. 978 81

The authors report a case of multiple myeloma with increased accumulation of Tc-99m hexamethylpropylene amine oxime (HMPAO) on brain SPECT. Tc-99m HMPAO is a lipophilic compound that freely passes through the intact blood-brain barrier and cell membrane and is rapidly converted to a hydrophilic form by glutathione and then retained in the neuron for several hours. In general, Tc-99m HMPAO shows decreased accumulation in brain tumors. However, some reports of increased accumulation in brain tumors, such as meningioma, glioblastoma multiforme, high-grade astrocytoma, pituitary adenoma, and multiple myeloma, have been published. The Tc-99m HMPAO uptake in these tumors has been attributed to tumor blood flow or glutathione contents within the tumor. With regard to uptake to Tc-99m HMPAO in multiple myeloma, the tumor size is considered to be an additional factor.
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PMID:Multiple myeloma showing increased accumulation of Tc-99m hexamethylpropylene amine oxime on brain SPECT. 1083 12

Thalidomide caused severe malformations in babies born to mothers taking the drug for morning sickness in the late 1950s and early 1960s. It is now known that these teratogenic effects are due to potent anti-angiogenic and immunomodulatory actions. These properties have lead to the testing of thalidomide in a number of infective, inflammatory and malignant conditions. Promising activity has been reported in myeloma, AIDS-related Kaposi's sarcoma, renal cell carcinoma and glioblastoma multiforme. A review is presented of the history of thalidomide and its recent development with an emphasis on applications in malignant disease.
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PMID:Thalidomide in the treatment of cancer. 1114 86

Thalidomide is a synthetic derivative of glutamic acid with sedative-hypnotic activity, which caused devastating teratogenic effects in the 1960s. This paper reviews the possible mechanisms of its teratogenic effect, its new therapeutic indications, the proposed mechanisms for its antitumor activity and, finally, reviews published studies of its application in oncology. Current data demonstrates that thalidomide is clinically promising in multiple myeloma, glioblastoma multiforme and renal cell cancer. Furthermore, a beneficial effect of the drug has been proposed in cancer-related cachexia, which merits further investigation. Well-designed, randomized studies are warranted to establish the possible indications of thalidomide as an antitumor compound.
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PMID:Thalidomide: an old sedative-hypnotic with anticancer activity? 1171 19

In summary, use of plasmapheresis has changed in recent years given advances in medical technology that have allowed a wider clinical application in the critical care setting. Membrane filtration technology has provided an alternative to centrifugation that can be easily applied in intensive care units. Use of plasmapheresis has also changed in recent years reflecting the availability of evidence largely obtained from controlled prospective studies. However, the clinical efficacy of plasmapheresis for many acute renal conditions is still controversial. Plasmapheresis appears to be a useful adjunct to conventional therapy in the treatment of anti-GBM nephritis, severe dialysis-dependent forms of pauciimmune RPGN, cryoglobulinemia, and HUS-TTP. Reported data also suggest a possible benefit of plasmapheresis in patients with myeloma cast nephropathy, sepsis, and poisoning/overdose, but the case for plasmapheresis in these disorders is largely unproven and the reported evidence insufficient to recommend its use outside research settings. In contrast, data from controlled trials do not support a role for plasmapheresis in immune complex-mediated RPGN, such as lupus nephritis, and acute allograft rejection. The more widespread application of prospective, randomized, controlled clinical trials should help to better define the value of plasmapheresis for treatment of acute renal diseases.
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PMID:Plasmapheresis. Technical aspects and indications. 1205 39

Experimental studies have demonstrated that thalidomide (Thal), a drug developed as a sedative, has antitumoural properties. The possible antitumour mechanisms of action involve: inhibition of angiogenesis, cytokine-mediated pathways, modulation of adhesion molecules, inhibition of cyclooxygenase-2 and stimulation of immuno response. Therefore, Thal is under clinical evaluation in oncology. This paper provides an overview of the data currently available in literature regarding, in terms of activity and toxicity, the use of Thal in cancer patients. Multiple myeloma is so far the most responsive malignancy. A moderate activity has been documented in certain solid tumours: glioblastoma multiforme, renal cell carcinoma and malignant melanoma. Tolerability is generally satisfactory with peripheral neuropathy being the most relevant dose-dependent toxicity. The more frequent, but moderate side effects are: somnolence, constipation, dizziness and fatigue. More studies are needed to properly evaluate the anticancer activity of Thal alone or in combination with other anticancer treatments. Preliminary studies suggest promising results of Thal in combinations with corticosteroids and cytotoxic drugs as front-line therapy of multiple myeloma. Regarding therapy of solid tumours in the adult, combination with chemotherapy, radiation therapy and molecular-targeting compounds are under investigation.
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PMID:Thalidomide: a new anticancer drug? 1283 55


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