掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrep.2025.101946

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Adoptive T cell therapy, using T cell receptor-engineered T (TCR-T) cells and chimeric antigen receptor T (CAR-T) cells, is a potent immunotherapy option. Bladder cancer is a prevalent urological malignancy, particularly in cases of muscle invasion and metastasis, for which systemic therapy is crucial. Immunotherapy utilizing immune checkpoint blockade has been approved for bladder cancer treatment. The antitumor effect of an immune checkpoint blockade based on cytotoxic T cells (CTLs) and the patient's immune status is essential. The chemotherapeutic drug cisplatin (CDDP) is a key drug in bladder cancer treatment. However, it has been shown to suppress T cells, making combination therapy with CDDP and immunotherapy difficult. To address this, we developed TCR-T cells specific for bladder cancer cells. In previous studies, we found that the tumor-associated antigen CLSPN is overexpressed in CDDP-resistant bladder cancer cells and that the antigenic peptide HLA-A*02:01/CLSPN1254-1262, encoded by CLSPN, could be targeted by a CTL clone. The TCR was cloned from the HLA-A*02:01/CLSPN1254-1262 specific CTL clone yc3. We also designed a codon-optimized TCR sequence using GeneArt® GeneOptimizer® (Opt TCR) and compared the TCR-T cells using the original TCR sequence (Ori TCR-T cells) and the codon-optimized TCR sequence (Opt TCR-T cells). Opt TCR-T cells exhibited higher TCR transduction efficiency, higher TCR expression levels, higher avidity, and greater cytotoxicity than did Ori TCR-T cells. These results suggest that HLA-A*02:01/CLSPN1254-1262 specific Opt TCR-T cells are promising candidates for CDDP combination therapy.

DOI： 10.1080/21645515.2024.2414542

PubMed

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掲載種別：研究論文（学術雑誌）  

DOI： 10.1126/scitranslmed.adk8832

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掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/1346-8138.17149

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掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/1346-8138.17043

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Epidermal keratinocytes, forming the outermost layer of the human body, serve as a crucial barrier against diverse external stressors such as ultraviolet radiation. Proper keratinocyte differentiation and effective responses to external stimuli are pivotal for maintaining barrier integrity. Heat is one such stimulus that triggers the synthesis of heat shock proteins (HSPs) when cells are exposed to temperatures above 42 °C. Additionally, activation of the transient receptor potential cation channel subfamily V member 1 (TRPV1) occurs at 42 °C. Here, we explore the interplay between TRPV1 signaling and HSP induction in human keratinocytes. Both heat and capsaicin, a TRPV1 agonist, induce expression of HSP27, HSP70, and HSP90 in keratinocytes. Interestingly, pharmacological inhibition of TRPV1 attenuates heat-induced HSP27 expression, but not that of HSP70 or HSP90. Furthermore, both heat and capsaicin stimulation result in distinct phosphorylation patterns of heat shock factor 1 (HSF1), with phosphorylation at serine 326 being a common feature. Notably, genetic manipulation to mimic dephosphorylation of HSF1 at serine 326 reduces HSP27 levels. Additionally, ΔNp63, a key regulator of epidermal differentiation, negatively modulates HSP27 expression independently of HSF1 phosphorylation status. While heat stimulation has no effect on ΔNp63 expression, capsaicin reduces its levels. The precise role of TRPV1 signaling in keratinocytes warrants further investigation for a comprehensive understanding of its impact on barrier function.

DOI： 10.1016/j.bbrc.2024.149817

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記述言語：英語  

DOI： 10.1111/1346-8138.17070

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Eribulin inhibits microtubule polymerization and improves the overall survival of patients with recurrent metastatic breast cancer. A subgroup analysis revealed a low neutrophil to lymphocyte ratio (NLR) (<3) to be a prognostic factor of eribulin treatment. We thus hypothesized that eribulin might be related to the immune response for breast cancer cells and we analyzed the effects of eribulin on the immune system. Immunohistochemical staining revealed that human leukocyte antigen (HLA) class I expression was increased in clinical samples after eribulin treatment. In vitro assays revealed that eribulin treatment increased HLA class I expression in breast cancer line cells. RNA-sequencing demonstrated that eribulin treatment increased the expression of the NOD-like family CARD domain-containing 5 (NLRC5), a master regulator of HLA class I expression. Eribulin treatment increased the NY-ESO-1-specific T-cell receptor (TCR) transduced T (TCR-T) cell response for New York oesophageal squamous cell carcinoma 1 (NY-ESO-1) overexpressed breast cancer cells. The eribulin and TCR-T combined therapy model revealed that eribulin and immunotherapy using TCR-T cells has a synergistic effect. In summary, eribulin increases the expression of HLA class 1 via HLA class 1 transactivatior NLRC5 and eribulin combination with immunotherapy can be effective for the treatment of breast cancer.

DOI： 10.1111/cas.15986

PubMed

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The efficacy of combination therapy with an immune checkpoint inhibitor (ICI) and cytotoxic chemotherapeutic agents has been investigated in cancer, including melanoma. Before ICIs were introduced, dacarbazine or temozolomide (TMZ) were used to treat melanoma. Several studies using glioma or colorectal cancer cells showed that TMZ can increase the tumor mutation burden (TMB) and induce mismatch repair (MMR) deficiency associated with microsatellite instability (MSI). These could increase immunoreactivity to an ICI, but this has not been evaluated in melanoma cells. We investigated the effects of TMZ on MSI status and TMB in melanoma cells. To evaluate the TMB, we performed whole-exome sequencing using genomic DNA from the human melanoma cell lines Mel18, A375, WM266-4, G361, and TXM18 before and after TMZ treatment. Polymerase chain reaction amplification of five mononucleotide repeat markers, BAT25, BAT26, NR21, NR24, and MONO27, was performed, and we analyzed changes in the MSI status. In all cell lines, the TMB was increased after TMZ treatment (the change amount of TMB with ≤ 5% variant allele frequency [VAF] was 18.0-38.3 mutations per megabase) even in the condition without obvious cytological damage. MSI after TMZ treatment was not observed in any cells. TMZ increased TMB but did not change MSI status in melanoma cells.

DOI： 10.1111/1346-8138.16925

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記述言語：英語  

DOI： 10.1111/ijd.16771

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記述言語：日本語   出版者・発行元：(一社)日本皮膚悪性腫瘍学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Evasion from immunity is a major obstacle to the achievement of successful cancer immunotherapy. Hybrids derived from cell-cell fusion are theoretically associated with tumor heterogeneity and progression by conferring novel properties on tumor cells, including drug resistance and metastatic capacity; however, their impact on immune evasion remains unknown. Here, we investigated the potency of tumor-macrophage hybrids in immune evasion. Hybrids were established by co-culture of a melanoma cell line (A375 cells) and type 2 macrophages. The hybrids showed greater migration ability and greater tumorigenicity than the parental melanoma cells. The hybrids showed heterogeneous sensitivity to New York esophageal squamous cell carcinoma-1 (NY-ESO-1)-specific T-cell receptor-transduced T (TCR-T) cells and two out of four hybrid clones showed less sensitivity to TCR-T compared with the parental cells. An in vitro tumor heterogeneity model revealed that the TCR-T cells preferentially killed the parental cells compared with the hybrids and the survival rate of the hybrids was higher than that of the parental cells, indicating that the hybrids evade killing by TCR-T cells efficiently. Analysis of a single-cell RNA sequencing dataset of patients with melanoma revealed that a few macrophages expressed RNA encoding melanoma differentiation antigens including melan A, tyrosinase, and premelanosome protein, which indicated the presence of hybrids in primary melanoma. In addition, the number of potential hybrids was correlated with a poorer response to immune checkpoint blockade. These results provide evidence that melanoma-macrophage fusion has a role in tumor heterogeneity and immune evasion. © 2023 The Pathological Society of Great Britain and Ireland.

DOI： 10.1002/path.6083

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND/AIM: Malignant melanoma is a fatal skin cancer and is among the most immunogenic malignancies expressing melanoma-differentiation antigens and neoantigens. SRY-related HMG-box 10 (SOX10) is a transcription factor and a neural-crest differentiation marker that is used as a diagnostic marker for melanoma whilst playing a role in melanoma initiation through activation of the SOX10-MITF axis. SOX10 was shown to play a role in melanoma initiation by inducing expression of immune checkpoint molecules (e.g., HVEM and CEACAM1). In this study, we aimed to investigate the relationship between SOX10 and the expression an immune checkpoint molecule, programmed death-1 ligand 1 (PD-L1). MATERIALS AND METHODS: SOX10 overexpression and knockdown was performed using SOX10 gene transfection and SOX10 siRNA transfection into A375 melanoma cells. PD-L1 expression was assessed by flow cytometry and western blotting. T cell response was evaluated using NY-ESO-1 specific TCR-transduced T (TCR-T) cells by IFNγ ELISPOT assay. RESULTS: SOX10 overexpression increased the expression of PD-L1, whereas SOX10 knockdown, using siRNA, decreased its expression. IFNγ ELISPOT assay revealed that overexpression of SOX10 decreased the susceptibility of cells to NY-ESO-1-specific TCR-T cells. CONCLUSION: SOX10 has a role in the intrinsic immune suppressive mechanisms of melanoma through expression of PD-L1.

DOI： 10.21873/anticanres.16296

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Bladder cancer is a major and fatal urological disease. Cisplatin is a key drug for the treatment of bladder cancer, especially in muscle-invasive cases. In most cases of bladder cancer, cisplatin is effective; however, resistance to cisplatin has a significant negative impact on prognosis. Thus, a treatment strategy for cisplatin-resistant bladder cancer is essential to improve the prognosis. In this study, we established a cisplatin-resistant (CR) bladder cancer cell line using an urothelial carcinoma cell lines (UM-UC-3 and J82). We screened for potential targets in CR cells and found that claspin (CLSPN) was overexpressed. CLSPN mRNA knockdown revealed that CLSPN had a role in cisplatin resistance in CR cells. In our previous study, we identified human leukocyte antigen (HLA)-A*02:01-restricted CLSPN peptide by HLA ligandome analysis. Thus, we generated a CLSPN peptide-specific cytotoxic T lymphocyte clone that recognized CR cells at a higher level than wild-type UM-UC-3 cells. These findings indicate that CLSPN is a driver of cisplatin resistance and CLSPN peptide-specific immunotherapy may be effective for cisplatin-resistant cases.

DOI： 10.1007/s00262-023-03388-5

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: The immunohistochemical evaluation of programmed death ligand 1 (PD-L1) is important for selecting treatments. Several antibodies are available for such evaluations, but data regarding the differences in the antibodies' positivity are limited in melanoma, particularly the acral and mucosal types. We investigated the differences in melanoma tissues' PD-L1 expression among the commonly used PD-L1 antibodies and then evaluated the relationship between PD-L1+ tumor cells and tumor-infiltrating lymphocytes (TILs). PATIENTS AND METHODS: We examined 56 primary lesions and 8 metastatic lymph node samples from 56 Japanese patients with melanoma (28 acral melanoma, 8 mucosal melanoma, 18 cutaneous melanoma, 2 unknown). Immunohistochemical staining was performed using three primary antibodies against PD-L1 (E1L3N, SP142, and 28-8). PD-L1-positive staining in tumor cells was defined as ≥ 1% expression. RESULTS: The positive rates were 25.0% for 28-8, 34.0% for E1L3N, and 34.0% for SP142 in 64 samples. The positive rates of acral melanoma were 10.7% for 28-8, 21.4% for E1L3N, and 21.4% for SP142. The positive rate of mucosal melanoma for which all three antibodies reacted was 12.5%. The positive rates of cutaneous melanoma were 55.6% for 28-8, 66.7% for E1L3N, and 66.7% for SP142. Significant relationships were observed among the PD-L1+ tumor cells, CD4+ TILs, and CD8+ TILs (p < 0.001). CONCLUSION: The staining results by E1L3N, SP142, and 28-8 antibodies were within the allowable range, although the positive rates by E1L3N and P142 were slightly higher than that of 28-8. CD4+ TILs and CD8+ TILs were quantitatively correlated with PD-L1-positive tumor cells.

DOI： 10.1007/s10147-022-02189-7

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media LLC  

その他リンク： https://link.springer.com/article/10.1007/s10147-022-02189-7/fulltext.html

DOI： 10.1007/s10147-022-02189-7

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/cod.14001

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記述言語：日本語   出版者・発行元：(一社)日本アレルギー学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

A sebaceous nevus is a congenital skin hamartoma caused by postzygotic HRAS or KRAS mosaic mutations. With age, affected individuals may develop secondary tumors within a sebaceous nevus. RAS mutations are harbored from the onset of sebaceous nevus, and further mutations can be expected to be required in order to explain the initiation of secondary tumors. However, genetic analyses of the secondary tumors have not been conducted. Herein, we describe the rare coexistence of a poroma and a trichoblastoma arising in a sebaceous nevus. This is the first report of an investigation of multiple genes in a secondary tumor in an SN. First, HRAS c.37G>C, which is the common mutation in sebaceous nevus, was detected in all three lesions (sebaceous nevus, poroma, and trichoblastoma). Next, to elucidate the potential second-hit mutations in the secondary poroma and trichoblastoma, we applied a panel sequencing for skin cancers that was newly developed in our institution. Our comparison of the mutational profile of 95 skin cancer-related genes in each of the three lesions newly revealed TP53 p.R158P in the poroma and NOTCH2 p.G329S in the trichoblastoma. TP53 p.R158P has been determined as a pathogenic mutation in other tumors, and NOTCH2 p.G329S was a novel mutation. We identified two novel mutations that may have contributed to the pathogenesis of the secondary tumor's development. The roles of the mutations remain unclear.

DOI： 10.1111/1346-8138.15919

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Barrier disruption and an excessive immune response in keratinocytes are now considered to have important roles in the pathophysiology of atopic dermatitis (AD). Furthermore, disturbed keratinocyte differentiation is considered to underlie AD. ΔNp63, a p53-like transcription factor, is a major regulator of keratinocyte differentiation. However, the functional significance of ΔNp63 in AD has not been clarified. OBJECTIVE: In this study, we aimed to investigate the influence of the type 2 inflammatory environment on ΔNp63 expression and AD-associated molecules regulated by ΔNp63 in keratinocytes. METHODS: The immunohistochemical expression profiles of ΔNp63 and AD-related molecules were evaluated in human skin tissue. The function of ΔNp63 in the regulation of AD-related molecules and the influence of the type 2 inflammatory environment on ΔNp63 expression were investigated using human primary keratinocytes. Expression of ΔNp63 was manipulated using the RNA interfering method. RESULTS: In healthy skin tissue, we observed an inverse expression pattern between ∆Np63 and some barrier-related proteins including filaggrin, caspase-14, claudin-1, and claudin-4. ΔNp63 regulated expression of these genes and proteins. In addition, production of IL-1β and IL-33, pro-inflammatory cytokines, was modulated by ΔNp63. Furthermore, prolonged IL-13 exposure increased the thickness of the three-dimensional culture of keratinocytes. IL-13 interfered with ΔNp63 downregulation during calcium-induced keratinocyte differentiation. IL-13 modulated some barrier-related and inflammation-related molecules, which were regulated by ΔNp63. CONCLUSIONS: We have shown that ΔNp63 modulated AD-related barrier and inflammatory molecules. In addition, ΔNp63 expression was affected by IL-4/IL-13. IL-13-ΔNp63 axis would integrate two major factors of AD pathogenesis: dysregulated barrier and inflammation.

DOI： 10.1002/iid3.427

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1684/ejd.2021.3997

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語  

DOI： 10.1016/j.alit.2020.04.011

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Cholinergic urticaria (CholU) decreases affected individuals' quality of life because they must avoid stimuli including exercise and hot bathing. Although case reports have indicated that regular sweating activities are effective for CholU with hypohidrosis, little evidence is available. This retrospective medical record review examined CholU patients who received any form of treatment at our hospital. Twenty-seven cases (78% men; median age 22 years, range 12-70 years) were analyzed. Fourteen (52%) patients had acquired idiopathic generalized anhidrosis (AIGA). Among the 12 patients receiving sweating therapy (4 with, 8 without AIGA), improvement of symptoms was confirmed in 11 (92%; sweating therapy alone: n = 5, with H1 blocker: n = 5, with steroid pulse: n = 1) including 8 (67%) showing complete response (CR). In this sweating-therapy group, CR was achieved by six of the eight (75%) patients without AIGA and two of the four (50%) patients with AIGA. Among the 15 patients without sweating therapy, symptom improvement was observed in 9 (60%; steroid pulse: n = 7, H1 blocker: n = 2) including 1 (7%) achieving CR. Sweating therapy was safely undertaken except in one case in which the patient showed angioedema and anaphylaxis. Regular sweating activities could be a potential therapeutic option for CholU patients.

DOI： 10.1111/dth.13647

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語  

DOI： 10.1111/1346-8138.15095

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記述言語：日本語   出版者・発行元：(株)北隆館  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Some studies showed that clinical response to immune check point inhibitors is lower in acral and mucosal melanoma than in cutaneous melanoma. Although the synergistic effect of radiotherapy (RT) and ipilimumab has been reported in patients with brain metastasis, the efficacy of combined RT and anti-programmed death 1 (PD-1) therapy for acral and mucosal melanoma is unclear. The present study aimed to evaluate the efficacy of combined RT and anti-PD-1 therapy for acral and mucosal melanoma. We retrospectively analyzed patients with acral or mucosal melanoma who were treated with anti-PD-1 and RT at Sapporo Medical University Hospital. In 10 patients (acral, 3; mucosal, 7), the response rate (RR) and the disease control rate (DCR) were 40% and 60%, respectively. As regards mucosal melanoma, four of the seven patients had achieved complete response + partial response, and three had progressive disease (RR = 57.1%). Meanwhile, two of the three patients with acral melanoma had stable disease and one had progressive disease (RR and DCR were 0% and 66.6%, respectively). Except for the patients treated with palliative RT for bone metastasis in the present study, the RR was 50% (4/8 patients), and the DCR was 75% (6/8 patients). Vitiligo developed after RT in five (50%) patients at a median duration of 2 months after RT. The clinical response and the high occurrence of vitiligo suggest that the combination of RT and anti-PD-1 therapy could be effective in some patients with mucosal melanoma.

DOI： 10.1111/1346-8138.14805

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1001/jamadermatol.2018.5379

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Dermoscopy is a widely used non-invasive technique for diagnosing skin tumors. In melanocytic tumors, e.g., melanoma and basal cell carcinoma (BCC), the effectiveness of dermoscopic examination has been fully established over the past two decades. Moreover, dermoscopy has been used to diagnose non-melanocytic tumors. Here, we review novel findings from recent reports concerning dermoscopy of melanoma and non-melanoma skin cancers including BCC, sebaceous carcinoma, actinic keratosis, Bowen's disease, squamous cell carcinoma (SCC), Merkel cell carcinoma (MCC), extramammary Paget's disease (EMPD), and angiosarcoma.

DOI： 10.3389/fmed.2019.00180

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記述言語：英語  

DOI： 10.1002/cia2.12037

Web of Science

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記述言語：英語  

DOI： 10.1684/ejd.2018.3381

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記述言語：英語  

DOI： 10.1111/1346-8138.14297

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記述言語：英語  

DOI： 10.1111/ijd.14004

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記述言語：日本語   出版者・発行元：日本皮膚科学会-西部支部  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚悪性腫瘍学会  

医中誌

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記述言語：日本語   出版者・発行元：(株)医学書院  

医中誌

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記述言語：日本語   出版者・発行元：(株)医学書院  

医中誌

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記述言語：日本語   出版者・発行元：(株)医学書院  

医中誌

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総ページ数：256   記述言語：日本語  

CiNii Books

ASIN

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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J-GLOBAL

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：英語   出版者・発行元：(一社)日本癌治療学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚悪性腫瘍学会  

医中誌

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記述言語：日本語   出版者・発行元：日本皮膚科学会-西部支部  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：日本皮膚病理組織学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：日本皮膚科学会-西部支部  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道農村医学会  

内臓悪性腫瘍の臍転移は、発見者の名前からSister Mary Joseph's nodule(SMJN)と呼ばれている。今回、過去17年間に当科で病理組織学的にSMJNと診断した4例を提示し、同期間に転移性皮膚腫瘍と病理診断した46例(SMJNを含む)の臨床像について報告した。46例の原発巣は肺癌が最も多く11例、次いで、胆管癌5例、膵臓癌4例の順であり、膵臓癌のうち3例がSMJNであった。原発巣が判明してから皮膚転移出現までの期間(n=18)は、1年以内が6例、1〜2年が4例、2〜3年が4例、3〜4年が1例、皮膚転移が初発症状であったものが3例であった。

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本皮膚アレルギー・接触皮膚炎学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：(公社)日本皮膚科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道産科婦人科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道産科婦人科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道産科婦人科学会  

医中誌

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記述言語：日本語   出版者・発行元：東北連合産科婦人科学会・北日本産科婦人科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道外科学会  

医中誌

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記述言語：日本語   出版者・発行元：北海道外科学会  

医中誌

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