Soft Tissue Myoepithelioma of the Shoulder

Soft tissue myoepitheliomas are often misdiagnosed due to their rarity. Herein, we describe a case of soft tissue myoepithelioma of the shoulder. A 72-year-old woman had a suspected sarcoma on her shoulder and under-went open biopsy. She was referred to our hospital, where the tumor was widely resected and the diagnosis of myoepithelioma was histologically confirmed. No recurrence has been observed in the 3 years since the sur-gery. Careful and prompt planning is necessary for the effective treatment of myoepithelioma

Agreement on endoscopic ultrasonography-guided tissue specimens: Comparing a 20-G fine-needle biopsy to a 25-G fine-needle aspiration needle among academic and non-academic pathologists

Background and Aim: A recently carried out randomized controlled trial showed the benefit of a novel 20-G fine-needle biopsy (FNB) over a 25-G fine-needle aspiration (FNA) needle. The current study evaluated the reproducibility of these findings among expert academic and non-academic pathologists. Methods: This study was a side-study of the ASPRO (ASpiration versus PROcore) study. Five centers retrieved 74 (59%) consecutive FNB and 51 (41%) FNA samples from the ASPRO study according to randomization; 64 (51%) pancreatic and 61 (49%) lymph node specimens. Samples were re-reviewed by five expert academic and five non-academic pathologists and rated in terms of sample quality and diagnosis. Ratings were compared between needles, expert academic and

Kimura’s disease affecting the axillary lymph nodes: a case report

Abstract Background Kimura’s disease (KD; eosinophilic granuloma of soft tissue) is an inflammatory granulomatous disorder of unknown cause with eosinophilic infiltration that occurs mainly in soft tissue. KD occurs mainly in the head and neck, but development in the axillary region is very rare. Case presentation A 74-year-old Japanese woman was evaluated for a mass that she noted in the left axillary region. On physical examination, there was a palpable, thumb-sized, hard, elastic, freely movable mass in the left axilla. Blood tests showed elevated soluble interleukin-2 receptor (sIL-2R), normal serum immunoglobulin (Ig) G4, and elevated serum IgE. Ultrasonography of the left axilla showed multiple lymph nodes (LNs) with irregular margins in which central hyperechogenicity was lost. A systemic search by computed tomography (CT) showed no systemic lymphadenopathy or other mass-like lesions suspicious for a primary tumour other than in the left axillary LNs. Biopsy of an excised LN was performed under local anaesthesia for a definitive diagnosis. Histopathology showed various-sized lymphoid follicles, large nodular lesions with an enlarged mantle zone, multiple various-sized germinal centres in single nodules, and eosinophilic infiltration between the nodes. Immunohistochemical (IHC) staining of the germinal centres was positive for cluster of differentiation (CD) 10, positive for B-cell lymphoma (bcl)-6, and negative for bcl-2. These findings led to a diagnosis of KD. Ultrasound after 3 months of follow-up showed disappearance of the axillary lymphadenopathy. Conclusions A very rare case of KD in the axillary LNs was described. KD has the potential to occur in any region

Inflammatory myofibroblastic tumor of the prostate

Introduction Inflammatory myofibroblastic tumors are borderline malignant soft tissue tumors primarily affecting the lungs and pelvic organs. This report presents a rare case of an inflammatory myofibroblastic tumor originating from the prostate gland in a young male. Case presentation A 20‐year‐old man developed gross hematuria and dysuria, revealing a prostatic mass. Pathological examination of a biopsy displayed spindle‐shaped myofibroblast proliferation and an infiltrate of inflammatory cells, leading to a diagnosis of inflammatory myofibroblastic tumor. Following fertility preservation measures, the patient underwent a robot‐assisted laparoscopic total prostatectomy with bilateral nerve sparing, resulting in a postoperative diagnosis of inflammatory myofibroblastic tumor. No recurrence was observed in subsequent imaging, and urinary continence was maintained. Conclusion Surgical resection appears effective in managing inflammatory myofibroblastic tumors of the prostate. This case underscores the importance of complete tumor resection due to the significant recurrence risk associated with inflammatory myofibroblastic tumors. Radical total prostatectomy emerges as a potential treatment strategy for prostate originating inflammatory myofibroblastic tumors

Performance of Ultra-Rapid Idylla™ EGFR Mutation Test in Non-Small-Cell Lung Cancer and Its Potential at Clinical Molecular Screening

Background: The Idylla™ EGFR Mutation Test is an ultra-rapid single-gene test that detects epidermal growth factor receptor (EGFR) mutations using formalin-fixed paraffin-embedded specimens. Here, we compared the performance of the Idylla EGFR Mutation Test with the Cobas® EGFR Mutation Test v2. Methods: Surgically resected NSCLC specimens obtained at two Japanese institutions (N = 170) were examined. The Idylla EGFR Mutation Test and the Cobas EGFR Mutation Test v2 were performed independently and the results were compared. For discordant cases, the Ion AmpliSeq Colon and Lung Cancer Research Panel V2 was performed. Results: After the exclusion of five inadequate/invalid samples, 165 cases were evaluated. EGFR mutation analysis revealed 52 were positive and 107 were negative for EGFR mutation in both assays (overall concordance rate: 96.4%). Analyses of the six discordant cases revealed that the Idylla EGFR Mutation Test was correct in four and the Cobas EGFR Mutation Test v2 was correct in two. In a trial calculation, the combination of the Idylla EGFR Mutation Test followed by a multi-gene panel test will reduce molecular screening expenses if applied to a cohort with EGFR mutation frequency >17.9%. Conclusions: We demonstrated the accuracy and potential clinical utility of the Idylla EGFR Mutation Test as a molecular screening platform in terms of turnaround time and molecular testing cost if applied to a cohort with a high EGFR mutation incidence (>17.9%)

Increased ectodomain shedding of CADM1 in T2DM pancreata.

<p>(<b>a</b>) Western blot analysis of CADM1 expression in control and T2DM pancreata. Cases are numbered as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0100988#pone.0100988.s005" target="_blank">Table S1</a>. Arrowheads indicate bands corresponding to the full-length, αCTF, and βCTF forms of CADM1. The blot was reprobed with an anti-β-actin antibody to show protein loading. (<b>b</b>) CADM1 expression per islet cell in each patient sample. For each lane in <b>a</b>, the intensities of the full-length CADM1, αCTF, βCTF, and β-actin bands were quantified, and CADM1 levels were expressed relative to β-actin and the islet cell count (/cm² of tissue). Statistical significance was analyzed with the Mann-Whitney <i>U</i>-test. <i>P</i>-values are shown. (<b>c</b>) CADM1 ectodomain shedding rates (relative amounts of CTFs to the full-length CADM1). Statistical significance was analyzed with the Mann-Whitney <i>U</i>-test. <i>P</i>-values are shown. (<b>d</b>) Correlation of HbA1c levels with full-length CADM1 expression per islet cell (left) or the CADM1 shedding rate (αCTF/full-length; right). In each graph, the dot distribution approximated a linear function (dotted lines). Correlations and statistical significance were analyzed with Spearman’s rank test. <i>R²</i> and <i>P</i>-values are shown.</p

Increased Ectodomain Shedding of Cell Adhesion Molecule 1 from Pancreatic Islets in Type 2 Diabetic Pancreata: Correlation with Hemoglobin A1c Levels

<div><p>Pulmonary emphysema and type 2 diabetes mellitus (T2DM), both caused by lifestyle factors, frequently concur. Respectively, the diseases affect lung alveolar and pancreatic islet cells, which express cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member. Protease-mediated ectodomain shedding of full-length CADM1 produces C-terminal fragments (CTFs) with proapoptotic activity. In emphysematous lungs, the CADM1 shedding rate and thus the level of CTFs in alveolar cells increase. In this study, CADM1 expression in islet cells was examined by western blotting. Protein was extracted from formalin-fixed, paraffin-embedded sections of pancreata isolated from patients with T2DM (n = 12) or from patients without pancreatic disease (n = 8) at autopsy. After adjusting for the number of islet cells present in the adjacent section, we found that full-length CADM1 decreased in T2DM islets, while ectodomain shedding increased. Hemoglobin A1c levels, measured when patients were alive, correlated inversely with full-length CADM1 levels (<i>P</i> = 0.041) and positively with ectodomain shedding rates (<i>P</i> = 0.001). In immunofluorescence images of T2DM islet cells, CADM1 was detected in the cytoplasm, but not on the cell membrane. Consistently, when MIN6-m9 mouse beta cells were treated with phorbol ester and trypsin to induce shedding, CADM1 immunostaining was diffuse in the cytoplasm. When a form of CTFs was exogenously expressed in MIN6-m9 cells, it localized diffusely in the cytoplasm and increased the number of apoptotic cells. These results suggest that increased CADM1 ectodomain shedding contributes to blood glucose dysregulation in T2DM by decreasing full-length CADM1 and producing CTFs that accumulate in the cytoplasm and promote apoptosis of beta cells. Thus, this study has identified a molecular alteration shared by pulmonary emphysema and T2DM.</p></div

Subcellular localization of endogenous and exogenous αCTF in MIN6-m9 cells.

<p>MIN6-m9 cells were untreated (−), treated with PMA (200 nM) and trypsin (0.025% w/v), or transfected with pCX4bsr-SP-αCTF. After 45 min of treatment and 2 days of transfection, CADM1 levels were assessed in western blot (<b>a</b>) and immunofluorescence (<b>b</b>) analyses using a CADM1 antibody. In <b>a</b>, arrowheads indicate full-length CADM and αCTF. The blot was reprobed with an anti-β-actin antibody to show the protein loading. In <b>b</b>, cells were double stained with CADM1 antibody (green; top) and MitoTracker (red; middle). Merged images are also shown (bottom). Data are representative of three independent experiments. Bar  = 10 µm.</p