A Case of Pulmonary Amyloidosis Associated with Multiple Myeloma Successfully Treated with Dimethyl Sulfoxide

Iwasaki, Tsuyoshi; Hamano, Teruaki; Aizawa, Kaori; Kobayashi, Kumiko; Kakishita, Eizo

doi:10.1159/000204262

Cited by 28 publications

(16 citation statements)

References 8 publications

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“…DMSO, an industrial solvent, caused partial or total disappearance of experimentally induced amyloid deposits in mice (Hanai et al, 1979), and therapeutic trials on patients with amyloidosis indicated that prolonged treatment with DMSO may be effective in certain types of systemic amyloidosis (Isobe et al, 1976;Iwasaki et al, 1994). DMSO treatment induced a dramatic reduction in pulmonary infiltration in a patient with IgG multiple myeloma and no serious side-effect of DMSO was encountered (Iwasaki et al, 1994).…”

Section: Gel Mobility Shift Assaymentioning

confidence: 99%

“…DMSO treatment induced a dramatic reduction in pulmonary infiltration in a patient with IgG multiple myeloma and no serious side-effect of DMSO was encountered (Iwasaki et al, 1994). Therapy of HMBA, another polar compound that is more potent than DMSO in inducing differentiation of murine erythroleukaemia cells (Reuben et al, 1976), had some success in clinical trials against certain cancers (Young et al, 1988).…”

Section: Gel Mobility Shift Assaymentioning

confidence: 99%

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Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents

Goto

Yamamoto‐Yamaguchi²,

Honma³

1996

Br J Cancer

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Summary A low concentration of differentiation inducers such as dimethylsulphoxide (DMSO), sodium butyrate, hexamethylene bisacetamide and sodium phenylacetate greatly enhanced the antiproliferative effect in vitro and in vivo of interferon a (IFN-a) to several human lung adenocarcinoma cells. The agents induced morphological changes in the adenocarcinoma cells and the agents together with IFN-a-induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. To understand the mechanism of the DMSO-enhanced interferon sensitivity, we examined the effect of DMSO on high-affinity IFN-a receptor and interferon-stimulated promoter-binding factors. The lung adenocarcinoma cells were not impaired in IFN-a receptor and interferon-stimulated gene transactivation factor 3 (ISGF-3). Our data suggest that the enhancement of interferon sensitivity in the lung adenocarcinoma cells acts downstream of the activation of ISGF-3.Keywords: interferon; lung carcinoma; differentiation inducer; biological response modifier Lung cancer survival remains poor, with approximately 13% a 5 year survival in 1993 (Ginsberg et al., 1993). The most active drugs so far have been cis-platinum (II) diamine dichloride (CDDP) (Loether and Einhorn, 1984), vindesine (Klastersky et al., 1983), vinblastin, mitomycin C and ifosphamide (Worrall, 1982) in the chemotherapy of nonsmall-cell lung cancer. The overall response rate is in the range 20-30% with 3-5% complete responses (Donnadieu et al., 1991). The current treatment results from non-smallcell lung cancer clearly call for improved therapy.The degree of differentiation is an important prognostic factor in many tumours. Induction of differentiation is closely linked to loss of tumorigenicity, and differentiation inducers can block the phenotypic expression of malignant cells. The use of all-trans retinoic acid in the treatment of patients with acute promyelocytic leukaemia has shown that differentiation therapy can lead to a predictable clinical remission (Huang et al., 1988;Degos, 1990;Ohno et al., 1993). However, administration of differentiation inducer alone in experimental therapy of solid tumours has produced only low remission rates. Furthermore, differentiation induction of solid tumours is not always an irreversible process. These b findings call for other strategies, such as combination of differentiation induction with chemotherapy, radiotherapy and/or immunotherapy. Induction of differentiation alters the properties of leukaemia and embryonal carcinoma cells, such as sensitivities to chemotherapeutic drugs (Okabe-Kado et al., 1986;Honma et al., 1991;Okabe-Kado et al., 1991;Guchelaar et al., 1993). We previously reported that treatment with haemin, an inducer of erythroid differentiation, greatly increased the sensitivity of human myeloid leukaemia K562 cells to 1-fl-D-arabinofuranosyl cytosine (Honma et al., 1991;Okabe-Kado et al., 1986), and that erythroid differentiation factor (activin A) enhanced the sensitivity of multidrug-resistant leukaemia cells...

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Section: Gel Mobility Shift Assaymentioning

confidence: 99%

Section: Gel Mobility Shift Assaymentioning

confidence: 99%

Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents

Goto

Yamamoto‐Yamaguchi²,

Honma³

1996

Br J Cancer

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“…DMSO has a number of important properties that make it useful clinically. DMSO has been used successfully to treat urinary (McCammon et al, 1998), pulmonary (Iwasaki et al, 1994), rheumatic (Morassi et al, 1989) and dermatological disorders (Burgess et al, 1998). Because of its anti-inflammatory and antioxidant properties, DMSO has also been used with some success to treat gastrointestinal disorders (Salim, 1992a;Salim, 1992b).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic effects of dimethyl sulphoxide (DMSO) on cochlear organotypic cultures

2008

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The amphipathic molecule dimethyl sulphoxide (DMSO) is a solvent often used to dissolve compounds applied to the inner ear; however, little is known about its potential cytotoxic side effects. To address this question, we applied 0.1 to 6% DMSO for 24 h to cochlear organotypic cultures from postnatal day 3 rats and examined its cytotoxic effects. DMSO concentrations of 0.1% and 0.25% caused little or no damage. However, concentrations between 0.5 and 6% resulted in stereocilia damage, hair cell swelling and a dose-dependent loss of hair cells. Hair cell damage began in the basal turn of the cochlea and spread towards the apex with increasing concentration. Surprisingly, DMSO-induced damage was greater for inner hair cells than outer hair cell whereas nearby supporting cells were largely unaffected. Most hair cell death was associated with nuclear shrinkage and fragmentation, morphological features consistent with apoptosis. DMSO treatment induced TUNEL positive staining in many hair cells and activated both initiator caspase-9 and caspase-8 and executioner caspase-3; this suggests that apoptosis is initiated by both intrinsic mitochondrial and extrinsic membrane cell death signaling pathways.

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“…1 In this context, peak plasma concentrations reach values as high as 20 mmol/L. DMSO is also used as a solvent for chemotherapeutic drugs and, due to its antiinflammatory properties, has been successfully used in humans for treating rheumatic, 2 pulmonary, 3 gastrointestinal, 4,5 neurological, 6,7 urinary, 8 and dermatological 9,10 disorders. DMSO further exhibits protective effects in animal models of middle cerebral artery occlusion, 11 cerebral hypoperfusion-related neuronal death, 12 mercuric chloride-induced kidney injury, 13 and chemical liver injury.…”

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confidence: 99%

Dimethyl Sulfoxide Inhibits Tissue Factor Expression, Thrombus Formation, and Vascular Smooth Muscle Cell Activation

et al. 2006

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Background-Subacute stent thrombosis is a major clinical concern, and the search for new molecules to cover stents remains important. Dimethyl sulfoxide (DMSO) is used for preservation of hematopoietic progenitor cells and is infused into patients undergoing bone marrow transplantation. Despite its intravenous application, the impact of DMSO on vascular cells has not been assessed. Methods and Results-In human endothelial cells, monocytes, and vascular smooth muscle cells (VSMC), DMSO inhibited tissue factor (TF) expression and activity in response to tumor necrosis factor-␣ or thrombin in a concentration-dependent manner. DMSO did not exert any toxic effects as assessed by phase-contrast microscopy, trypan blue exclusion, and lactate dehydrogenase release. Real-time polymerase chain reaction revealed that inhibition of TF expression occurred at the mRNA level. This effect was mediated by reduced activation of the mitogen-activated protein kinases c-Jun terminal NH 2 kinase (51Ϯ6%; Pϭ0.0005) and p38 (50Ϯ3%; PϽ0.0001) but not p44/42 (PϭNS). In contrast to TF, DMSO did not affect expression of TF pathway inhibitor or plasminogen activator inhibitor-1. In vivo, DMSO treatment suppressed TF activity (41%; PϽ0.002) and prevented thrombotic occlusion in a mouse carotid artery photochemical injury model. DMSO also inhibited VSMC proliferation (70%; Pϭ0.005) and migration (77%; Pϭ0.0001) in a concentration-dependent manner; moreover, it prevented rapamycin and paclitaxel-induced upregulation of TF expression. Conclusions-DMSO suppresses TF expression and activity, as well as thrombus formation; in addition, it inhibits VSMC proliferation and migration. Given its routine use in modern clinical practice, we propose DMSO as a novel strategy for coating drug-eluting stents and treating acute coronary syndromes.

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A Case of Pulmonary Amyloidosis Associated with Multiple Myeloma Successfully Treated with Dimethyl Sulfoxide

Cited by 28 publications

References 8 publications

Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents

Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents

Cytotoxic effects of dimethyl sulphoxide (DMSO) on cochlear organotypic cultures

Dimethyl Sulfoxide Inhibits Tissue Factor Expression, Thrombus Formation, and Vascular Smooth Muscle Cell Activation

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