Junichi Furuta

University of Tsukuba, Tsukuba, Ibaraki-ken, Japan

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Publications (38)118.45 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Tumor lysis syndrome (TLS) is rare in the treatment of solid tumors, but it may occur in myelolymphoproliferative diseases. A 58-year-old man with bulky metastatic melanoma of the liver was treated with transcatheter arterial infusion of cisplatin and embolization therapy. The patient developed classic signs of TLS within 24 h of chemotherapy, including acute renal failure. The patient was treated with aggressive hydration, allopurinol, and repeated hemodialysis. He gradually improved and his biochemical markers returned to normal. TLS is an uncommon, but potentially life-threatening, complication in melanoma and other solid tumors. It is important for oncologists to recognize this complication and prevent its development if bulky metastatic disease and several pre-existing risk factors, such as multiple and bulky liver metastases, elevated lactate dehydrogenase, and hyperuricemia, are present.
    International journal of dermatology 08/2009; 48(7):763-7. · 1.18 Impact Factor
  • European journal of dermatology: EJD 08/2009; 19(5):525-6. · 1.95 Impact Factor
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    ABSTRACT: Common acquired skin diseases with a polygenic background, such as lichen planus, may show linear or segmental manifestations of underlying systemic skin disease. The linear arrangement in such cases is usually consistent with the lines of Blaschko. Happle summarized the various types of segmental arrangement of common polygenic diseases and proposed a novel designation of superimposed segmental dermatosis. Here, we report a unilateral linear dermatitis distributed along the lines of Blaschko on the leg, which was not self-healing and persisted for at least 6 years without complete remission, and was accompanied by preceding chronic prurigo on the extremities. Histological examination showed subacute spongiotic dermatitis and epidermal infiltration of CD4-positive cells. This case report presents a superimposed segmental dermatitis that arose based on systemic eczematous conditions, such as chronic prurigo.
    European journal of dermatology: EJD 06/2009; 19(4):337-40. · 1.95 Impact Factor
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    ABSTRACT: UV radiation is an important environmental factor in the pathogenesis of skin aging and cancer. Many harmful effects of UV radiation are associated with generation of reactive oxygen species. Cellular antioxidants prevent the occurrence and reduce the severity of UV-induced photoaging and diseases of the skin. The transcription factor Nrf2 (NF-E2-related factor 2) and its negative regulator protein, Keap1 (Kelch-like-ECH-associated protein 1), are central regulators of cellular antioxidant responses. We used nrf2-null mice to investigate the roles of the Nrf2-Keap1 system in protection of skin from harmful effects of UVB irradiation. A single irradiation with UVB induced stronger and longer lasting sunburn reaction in nrf2-null mice. Histological changes, including epidermal necrosis, dermal edema, inflammatory cell infiltration, sunburn cell formation, TUNEL-positive apoptotic cell formation, and accumulation of oxidative DNA products such as 8-hydroxy-2'-deoxyguanosine after UVB irradiation, were more prominent in nrf2-null mice. These findings indicate that the Nrf2-Keap1 pathway plays an important role in protection of the skin against acute UVB reactions, including cutaneous cell apoptosis and oxidative damage. However, there were no significant differences in skin carcinogenesis between nrf2-null and wild-type mice exposed to chronic UVB irradiation, suggesting that there is a complex and subtle balance between factors promoting and preventing photocarcinogenesis. Journal of Investigative Dermatology (2008) 128, 1773-1779; doi:10.1038/sj.jid.5701245; published online 17 January 2008.
    Journal of Investigative Dermatology 08/2008; 128(7):1773-9. · 6.19 Impact Factor
  • Journal of the European Academy of Dermatology and Venereology 05/2008; 23(2):181-3. · 2.69 Impact Factor
  • Journal of the European Academy of Dermatology and Venereology 03/2008; 22(2):241-2. · 2.69 Impact Factor
  • European journal of dermatology: EJD 01/2008; 18(2):195-6. · 1.95 Impact Factor
  • British Journal of Dermatology 12/2007; 157(5):1053-6. · 3.76 Impact Factor
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    ABSTRACT: To identify tumor-suppressor genes inactivated by aberrant methylation of promoter CpG islands (CGIs) in human malignant melanomas, genes upregulated by treatment of cells with a demethylating agent, 5-aza-2'-deoxycytidine (5-aza-dC), were searched for using oligonucleotide microarrays in melanoma cell lines, HMV-I, MeWo and WM-115. Seventy-nine known genes with CGIs were identified as being upregulated (>or=16-fold), and 18 of them had methylation of their putative promoter CGIs in 1 or more of 8 melanoma cell lines. Among the 18 genes, TFPI-2, which is involved in repression of the invasive potential of malignant melanomas, was further analyzed. Its expression was repressed in a melanoma cell line with its complete methylation, and was restored by 5-aza-dC treatment. It was unmethylated in cultured neonatal normal epidermal melanocyte, and was induced by ultraviolet B. In surgical melanoma specimens, TFPI-2 methylation was detected in 5 of 17 metastatic site specimens (29%), while it was not detected in 20 primary site specimens (0%) (p=0.009). By immunohistochemistry, the 5 specimens with promoter methylation lacked immunoreactivity for TFPI-2. The results showed that TFPI-2 is silenced in human malignant melanomas by methylation of its promoter CGI and suggested that its silencing is involved in melanoma metastasis.
    International Journal of Cancer 08/2007; 121(2):301-7. · 6.20 Impact Factor
  • European journal of dermatology: EJD 01/2007; 17(1):94-5. · 1.95 Impact Factor
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    ABSTRACT: Aberrant methylation of promoter CpG islands (CGI) is involved in silencing of tumor suppressor genes and is also a potential cancer biomarker. Here, to identify CGIs aberrantly methylated in human melanomas, we did a genome-wide search using methylation-sensitive representational difference analysis. CGIs in putative promoter regions of 34 genes (ABHD9, BARHL1, CLIC5, CNNM1, COL2A1, CPT1C, DDIT4L, DERL3, DHRS3, DPYS, EFEMP2, FAM62C, FAM78A, FLJ33790, GBX2, GPR10, GPRASP1, HOXA9, HOXD11, HOXD12, HOXD13, p14ARF, PAX6, PRDX2, PTPRG, RASD1, RAX, REC8L1, SLC27A3, TGFB2, TLX2, TMEM22, TMEM30B, and UNC5C) were found to be methylated in at least 1 of 13 melanoma cell lines but not in two cultured normal melanocytes. Among these genes, Peroxiredoxin 2 (PRDX2) was expressed in normal melanocytes, and its expression was lost in melanomas with methylation. The loss of expression was restored by treatment of melanomas with a demethylating agent 5-aza-2'-deoxycytidine. In surgical melanoma specimens, methylation of PRDX2 was detected in 3 of 36 (8%). Furthermore, immunohistochemical analysis of PRDX2 showed that disappearance of immunoreactivity tends to associate with its methylation. PRDX2 was recently reported to be a negative regulator of platelet-derived growth factor signaling, and its silencing was suggested to be involved in melanomas. On the other hand, 12 CGIs were methylated in >or=9 of the 13 melanoma cell lines and are considered as candidate melanoma biomarkers.
    Cancer Research 06/2006; 66(12):6080-6. · 8.65 Impact Factor
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    ABSTRACT: The loss of thrombomodulin (TM) expression is associated with tumour growth, infiltration and lymph node metastasis in human tumours. In melanoma cell lines, TM is reported to mediate cell adhesion, and its introduction into TM-negative melanoma cell lines suppresses their growth. In this study, we analysed TM expression in surgical melanoma specimens and the role of its promoter methylation in the loss of its expression. In 15 (75%) of the 20 specimens (five from a primary site and 15 from metastatic sites), melanoma cells lacked TM immunoreactivity. Methylation of the TM promoter region was detected in 10 (67%) of the 15 TM-negative specimens by methylation-specific polymerase chain reaction, whereas methylation was detected in two (40%) of the five TM-positive specimens. In cell lines, complete methylation of the TM promoter CpG island was detected in six (46%) of 13 melanoma cell lines, whereas no methylation was detected in two cultured normal melanocytes. There was a good correlation between the methylated status of the CpG island and the loss of TM messenger RNA (mRNA) expression. Treatment of melanoma cell lines with a demethylating agent, 5-aza-2'-deoxycytidine, induced demethylation of the promoter CpG island and the restoration of mRNA and protein expression. These findings suggest that most human melanomas lack TM expression, and that methylation of the promoter CpG island is one of the mechanisms responsible.
    Melanoma Research 03/2005; 15(1):15-20. · 2.52 Impact Factor
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    ABSTRACT: Aberrant methylation and demethylation of promoter CpG islands lead to silencing of tumor-suppressor genes and abnormal expression of normally methylated genes, respectively. Here, we analyzed human melanomas for their methylation and demethylation profiles. Methylation status of core regions in promoter CpG islands was examined for 20 (candidate) tumor-suppressor genes, 4 genes that are not considered as tumor-suppressors, but are frequently silenced in human cancers, and 6 normally methylated melanoma antigen genes (MAGEs). Analysis of 13 melanoma cell lines and 2 cultured normal human epidermal melanocytes (HEMs) showed that 9 tumor-suppressor genes and all 4 non-tumor-suppressor genes were methylated in at least 1 cell line, but never in HEMs, and that all 6 MAGE genes were demethylated in 3 to 13 cell lines. Interestingly, we detected no methylation of MGMT, PTEN, MTAP and p27, which were previously reported as silenced in melanomas. Furthermore, 3 genes that were frequently methylated in the cell lines and 6 MAGE genes were analyzed in 25 surgical melanoma samples. RARB, RASSF1A and 3-OST-2 were methylated in 5 (20%), 9 (36%) and 14 (56%) samples, respectively. MAGE-A1, A2, A3, B2, C1 and C2 were demethylated in 9 (36%), 22 (88%), 20 (80%), 7 (28%), 21 (84%) and 16 (64%) samples, respectively. At least 1 gene was methylated in 18 (72%) samples and at least 1 was demethylated in 24 (96%) samples. No correlation between frequent methylation and frequent demethylation was observed. These profiles showed that both aberrant methylation and demethylation occur widely in human melanomas.
    Cancer Science 01/2005; 95(12):962-8. · 3.48 Impact Factor
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    ABSTRACT: Aberrantly methylated DNA fragments were searched for in human pancreatic cancers, using the genome scanning technique: methylation-sensitive-representational difference analysis (MS-RDA). MS-RDA isolated 111 DNA fragments derived from CpG islands (CGIs), and 35 of them were from CGIs in the 5' regions of known genes. Methylation-specific PCR (MSP) of the CGIs in seven pancreatic cancer cell lines and two pancreatic ductal epithelial cell lines showed that 27 CGIs in the 5' regions were aberrantly methylated in at least one of the cancer cell lines. Quantitative reverse-transcription-PCR analysis showed that downstream genes of all the CGIs were either not expressed or only very weakly expressed in cancer cell lines with the aberrant methylation. In the pancreatic ductal epithelial cell lines, 18 genes were expressed at various levels, and nine genes were not expressed at all. Treatment of a cancer cell line with a demethylating agent, 5-aza-2'-deoxycytidine, restored the expression of 13 genes, RASGRF2, ADAM23, NEF3, NKX2-8, HAND1, EGR4, PRG2, FBN2, CDH2, TLL1, NPTX1, NTSR1 and THBD, showing their silencing by methylation of their 5' CGIs. MSP of 24 primary pancreatic cancers showed that all these genes, except for THBD, were methylated in at least one cancer. Some of those were suggested to be potentially involved in pancreatic cancer development and progression.
    Oncogene 12/2004; 23(53):8705-10. · 8.56 Impact Factor
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    ABSTRACT: An 88-year-old Japanese female visited our department with an asymptomatic nodule on the right cheek. Other than treatment for hypertension for 15 years, the patient had been healthy. She had noticed the nodule one year earlier, and it had slowly enlarged to 25 × 25 × 5 mm, with redness, an irregular-surface with ulcer formation, and was bony-hard with no tenderness ( Fig. 1). There were no regional lymphadenopathies. These clinical features suggested a soft tissue tumor or basal cell carcinoma. Histopathological examinations revealed that the tumor was visible from the upper dermis beneath the flattered and partly eroded epidermis, and showed atypical and pleomorphic tumor cells with large, irregularly shaped nuclei, and variable amounts of cytoplasm ( Fig. 2). Some had bizarre nuclei, and occasional mitotic figures. These histopathological findings were suggestive of malignant fibrous histiocytoma. Magnetic resonance imaging showed that the tumor extended from the upper dermis to the subcutaneous tissue, was attached to the right maxillary bone, and involved the right orbit inferior margin. Apparent invasion to the bone was not seen. The tumor was resected and included skin, subcutaneous tissue, lower orbital adipose tissue, and fascia. A skin graft was taken from the thigh to cover the tumor resection. The resected tumor specimen measured 28 × 28 × 15 mm. Although the histopathological examination results were similar to the biopsy results, the tumor cells were arranged in irregular, intertwining bands, known as a storiform pattern in some areas, and focal necrosis was also seen. The tumor cells were markedly atypical with bizarre nuclei. Subcutaneous fat tissue was widely involved, and the tumor extended into the muscle tissue. In addition, the margin was positive for tumor cells in the deeper area of the tumor. Two weeks after the first operation, the patient had developed a small, firm nodule in the center of the skin graft that rapidly enlarged to form a 10-mm tumor, which was likely the regrowth of the remaining tumor cells. A wide excision was considered, but because of her age and the extensiveness of the excision, containing maxillary bone, alternative treatment was pursued. Radiation therapy was performed five times per week, with a total dose of 60 gray. During the radiation therapy, the tumor enlargement stopped, and a skin ulcer on the grafted skin was made. The tumor started to decrease in size 1 month after the radiation therapy, and it continued to reduce in size until no tumor mass was seen by magnetic resonance imaging. No recurrence and no metastasis have occurred during the 3 years since cessation of the radiation therapy ( Fig. 3).
    International Journal of Dermatology 01/2004; 42(12):952-4. · 1.34 Impact Factor
  • Yoshihiro Umebayashi, Junichi Furuta
    The Journal of Dermatology 10/2003; 30(9):701-2. · 2.35 Impact Factor
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    ABSTRACT: A 28-year-old Japanese woman with hereditary complement (C9) deficiency and dermatomyositis is reported. She had a 3-year history of facial erythema and a 1-month history of progressive muscle weakness. Clinical and laboratory findings were suggestive of dermatomyositis; muscle biopsy confirmed an inflammatory myopathy. An unexpected finding, however, was the low titre of serum haemolytic complement (CH50). Treatment with prednisolone resulted in marked clinical improvement but did not affect the CH50 titre. Further investigation revealed a selective and total absence of the ninth complement component (C9), with direct DNA sequence analysis revealing a non-sense mutation at Arg95 of the C9 gene. This case demonstrates that the muscle lesions of dermatomyositis can occur in the presence of a complement defect that would prevent the formation of the C5b-9 membrane attack complex.
    British Journal of Dermatology 06/2001; 144(5):1080-3. · 3.76 Impact Factor
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    ABSTRACT: Severe local skin reactions to subcutaneous injection of interferon beta-1b in multiple sclerosis are rare, and only 12 cases of severe skin reaction due to interferon beta-1b have been reported to date. We report two cases of severe skin reactions in multiple sclerosis patients following the injection of subcutaneous interferon beta-1b. In case 1, after five years of treatment, a painful indurated erythematous lesion appeared at the injection site on the left buttock. On histological analysis, the lesion showed septal and lobular panniculitis with lymphocytic infiltration. In case 2, cutaneous ulceration was surrounded by painful induration, which developed at the injection site on the right thigh after four years of treatment. The lesions resolved rapidly after discontinuation of interferon beta-1b treatment in both cases. Here, we review cases of similar lesions caused by interferon beta-1b reported in the literature, and discuss the characteristics, mechanism, treatment, and prevention of such lesions.
    European journal of dermatology: EJD 18(5):579-82. · 1.95 Impact Factor

Publication Stats

311 Citations
118.45 Total Impact Points

Institutions

  • 2001–2013
    • University of Tsukuba
      • Institute of Clinical Medicine
      Tsukuba, Ibaraki-ken, Japan
  • 2005
    • National Cancer Center, Japan
      Edo, Tōkyō, Japan