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Endometrial stromal tumor (EST) is an uncommon and unusual mesenchymal tumor of the uterus characterized by multicolored histopathological, immunohistochemical, and molecular features. The morphology of ESTs is similar to normal endometrial stromal cells during the proliferative phase of the menstrual cycle. ESTs were first classified into benign and malignant based on the number of mitotic cells. However, recently WHO has divided ESTs into four categories: endometrial stromal nodules (ESN), undifferentiated uterine sarcoma (UUS), low-grade endometrial stromal sarcoma (LG-ESS), and high-grade endometrial stromal sarcoma (HG-ESS). HG-ESS is the most malignant of these categories, with poor clinical outcomes compared to other types. With advances in molecular biology, ESTs have been further classified with morphological identification. ESTs, including HG-ESS, is a relatively rare type of cancer, and the therapeutics are not being developed compared to other cancers. However, considering the tumor microenvironment of usual stromal cancers, the advance of immunotherapy shows auspicious outcomes reported in many different stromal tumors and non-identified uterine cancers. These studies show the high possibility of successful immunotherapy in HG-ESS patients in the future. In this review, we are discussing the background of ESTs and the BCOR and the development of HG-ESS by mutations of BCOR or other related genes. Among the gene mutations of HG-ESSs, BCOR shows the most common mutations in different ways. In current tumor therapies, immunotherapy is one of the most effective therapeutic approaches. In order to connect immunotherapy with HG-ESS, the understanding of tumor microenvironment (TME) is required. The TME of HG-ESS shows the mixture of tumor cells, vessels, immune cells and non-malignant stromal cells. Macrophages, neutrophils, dendritic cells and natural killer cells lose their expected functions, but rather show pro-tumoral functions by the matricellular proteins, extracellular matrix and other complicated environment in TME. In order to overcome the current therapeutic limitations of HG-ESS, immunotherapies should be considered in addition to the current surgical strategies. Checkpoint inhibitors, cytokine-based immunotherapies, immune cell therapies are good candidates to be considered as they show promising results in other stromal cancers and uterine cancers, while less studied because of the rarity of ESTs. Based on the advance of knowledge of immune therapies in HG-ESS, the new strategies can also be applied to the current therapies and also in other ESTs.

Secretory carcinoma of the salivary gland (SC) is a newly introduced rare salivary gland tumor that shares histological, immunohistochemical, and genetic characteristics with secretory carcinoma of the breast. Here, we report the cytologic features of two cases of SC confirmed by surgical resection. In these two cases, SC was incidentally detected in a 64-year-old female and a 56-yearold male. Fine needle aspiration cytology revealed nests of tumor cells with a papillary or glandular structure floating in mucinous secretions. The tumor cells demonstrated uniform, round, smooth nuclear contours and distinct nucleoli. Multiple characteristic cytoplasmic vacuoles were revealed. Singly scattered tumor cells frequently showed variable sized cytoplasmic vacuoles. The cytopathologic diagnosis of SC should be considered when characteristic cytological findings are revealed. Further immunohistochemistry and gene analyses are helpful to diagnose SC.

Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects in the epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, as well as an immune disorder mediated by an imbalance toward T-helper-2 response. Melittin, a major component of bee venom, has been studied in various inflammatory diseases. However, the beneficial effects of melittin on mouse with AD-like symptoms have not been explored. Therefore, we investigated the anti-allergic effects of melittin. AD was induced by ovalbumin (OVA) patch. After agent treatment, skin tissues and sera were extracted from the sacrificed mice were used to demonstrate the effects of melittin through various molecular biological methods. The results showed that OVA-induced skin thickening and inflammatory infiltration were decreased in the melittin-treated group. Melittin prevented OVA-induced filaggrin deficiency and imbalanced inflammatory mediators. Furthermore, melittin inhibited IL-4/IL-13-induced filaggrin downregulation through the blockade of STAT3 activation in human keratinocytes. In summary, this study has shown that melittin ameliorated OVA-induced AD-like symptoms from various perspectives. The findings of this study may be the first evidence of the anti-inflammatory effects of melittin on OVA-induced AD.

Pancreatic ductal adenocarcinomas (PDACs) are highly lethal tumors characterized by a dense desmoplastic stroma comprised of cancer associated fibroblasts (CAFs) and fibrotic scar tissue. While stromal CAFs act as a barrier to therapy and release signals promoting tumor growth and invasion, the stroma restricts tumor growth in mouse models. The High Mobility Group A1 (HMGA1) protein is an oncofetal protein and epigenetic regulator that amplifies signals from the microenvironment to foster stem cell properties within intestinal epithelium. Although HMGA1 is highly expressed in embryonic and adult stem cells, it is silenced postnatally in most differentiated cells. HMGA1 becomes aberrantly re-expressed in diverse tumors where high levels predict adverse clinical outcomes. In PDAC, HMGA1 is detected only in late-stage precursor lesions or invasive tumors, but not in normal pancreas nor in early precursor lesions. Moreover, high HMGA1 nuclear staining associates with poor differentiation status and decreased patient survival. Here, we discovered a novel epigenetic program whereby HMGA1 recruits stromal CAFs and drives tumor progression by inducing FGF19. Silencing HMGA1 in PDAC cell lines slows proliferation, disrupts oncogenic properties in vitro (migration, invasion, clonogenicity, 3D sphere formation), and depletes tumor initiator cells in xenograft assays. RNA sequencing revealed transcriptional networks up-regulated by HMGA1 that function in cell signaling and proliferation; we focused on FGF19 as a potential mediator of tumor-stromal crosstalk. HMGA1 binds directly to the FGF19 promoter and recruits active histone marks (H3K4me2, H3K27Aac) to induce gene expression and protein secretion from PDAC cells. Silencing FGF19 recapitulates effects of HMGA1 silencing, disrupting oncogenic and cancer stem cell properties in vitro while depleting tumor initiator cells in vivo. In co-culture experiments, FGF19 is required for CAF migration across a membrane towards PDAC cells. Silencing HMGA1, FGF19, or treatment with FGF19 inhibitors disrupts CAF recruitment. Silencing HMGA1 or FGF19 in PDAC cells also decreases both the desmoplastic stroma and tumor growth in mouse xenografts. In primary tumors, co-expression of HMGA1 and FGF19 predict decreased survival. Together, our results reveal a novel paradigm whereby tumor cells collaborate with CAFs via HMGA1 and FGF19 to drive progression, thus illuminating FGF19 as a rational therapeutic target for PDACs overexpressing HMGA1 and FGF19. Citation Format: Lionel Chia, Shuai Shuai, Jung-Hyun Kim, Woo Jung Sung, Ruitao Zhang, Tait Huso, Leslie Cope, Karen Reddy, Linda M. Resar. HMGA1 induces FGF19 to drive tumor progression and recruit cancer associated fibroblasts in pancreatic adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2414.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial proliferation and inflammation. Intra-articular corticosteroid injections are commonly used for the treatment of arthritis affecting one or two joints. Although corticosteroid injections are fast-acting, repeated usage can result in severe adverse events. Recently, intra-articular pulsed radiofrequency (PRF) stimulation has been proposed to treat arthritis. The aim of the present study was to compare the effectiveness of intra-articular PRF with corticosteroid injection based on histopathological and motion analysis of an ovalbumin (OVA)-induced RA rabbit model. RA was induced in the right knee joint of 18 rabbits via OVA injection. The rabbits were randomly allocated into a PRF, an intra-articular corticosteroid injection or a sham PRF stimulation group. Movement was assessed in the rabbits before treatment, then at 2, 4 and 8 weeks after treatment using walking distance, fast walking time and mean walking speed. Histopathological evaluation of the distal femur and synovium was conducted 2, 4 and 8 weeks after treatment. Motion analysis demonstrated that changes in all movement variables showed significant group and time interaction as well as group effect among the three groups. The semiquantitative score based on the histopathological findings for the distal femoral condyle decreased 2 and 4 weeks after both the PRF and steroid groups, compared with the sham PRF group. Moreover, in the synovium, the semiquantitative histological score in the PRF and steroid groups tended to be lower compared with the sham PRF group, although this result was not statistically significant. Thus, intra-articular PRF stimulation may delay cartilage destruction and improve functional motion in RA.

Background: PD-L1 expression, as determined by immunohistochemistry (IHC), is the most commonly use predictive biomarker for anti-PD-1 and anti-PD-L1 agents in currently available in clinical practice. However, multiple antibodies have been utilized in IHC assays and interpretation of their results has not been standardized. Recently, several studies have compared different antibodies and IHC systems for PD-L1 tests. We aimed to evaluate the similarity and concordance between three validated, commercially available PD-L1 IHC assays for non-small cell lung cancer (Dako 22C3, Ventana SP263, and Ventana SP142). Methods: We evaluated 219 samples from patients with non-small cell lung cancer at the Daegu Catholic University Medical Center between June 2017 and July 2018. Each tumor sample was stained with PD-L1 IHC 22C3, SP263, and SP142. PD-L1 expression was scored at different cut-off levels for each IHC antibodies (22C3 assay: Results: Among the 219 samples, three different antibodies showed well correlation for PD-L1 expression (22C3 vs. SP263; r=0.896, p Conclusions: 22C3, SP263, and SP142 IHC assays showed good correlation for PD-L1 expression. 22C3 IHC assay showed good concordance with SP263, but SP142. Citation Format: Chi Young Jung, Eun Jin Kim, Woo Jung Sung. Assessment of concordance among 22C3, SP263, and SP142 immunohistochemistry assay for PD-L1 expression in non-small cell lung cancer [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology and Immunotherapy; 2018 Nov 27-30; Miami Beach, FL. Philadelphia (PA): AACR; Cancer Immunol Res 2020;8(4 Suppl):Abstract nr A07.

Alcoholic liver disease (ALD) is a worldwide health problem and hepatocyte apoptosis has been associated with the development/progression of ALD. However, no definite effective pharmacotherapy for ALD is currently available. Cilostazol, a selective type III phosphodiesterase inhibitor has been shown to protect hepatocytes from ethanol-induced apoptosis. In the present study, the underlying mechanisms for the protective effects of cilostazol were examined. Primary rat hepatocytes were treated with ethanol in the presence or absence of cilostazol. Cell viability and intracellular cAMP were measured. Apoptosis was detected by Hoechst staining, TUNEL assay, and caspase-3 activity assay. The roles of cAMP and AMP-activated protein kinase (AMPK) pathways in the action of CTZ were explored using pharmacological inhibitors and siRNAs. Liver from mice received ethanol (5 g/kg body weight) by oral gavage following cilostazol treatment intraperitoneally was obtained for measurement of apoptosis and activation of AMPK pathway. Cilostazol inhibited ethanol-induced hepatocyte apoptosis and potentiated the increases in cAMP level induced by forskolin. However, the anti-apoptotic effect of cilostazol was not reversed by an inhibitor of adenylyl cyclase. Interestingly, cilostazol activated AMPK and increased the level of LC3-II, a marker of autophagy. The inhibition of AMPK abolished the effects of cilostazol on LC3-II expression and apoptosis. Moreover, the inhibition of LKB1 and CaMKK2, upstream kinases of AMPK, dampened cilostazol-inhibited apoptosis as well as AMPK activation. In conclusion, cilostazol protected hepatocytes from apoptosis induced by ethanol mainly via AMPK pathway which is regulated by both LKB1 and CaMKK2. Our results suggest that cilostazol may have potential as a promising therapeutic drug for treatment of ALD.

581 Copyrightc 2015 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Received: 2014. 11. 28 Revised: 2015. 3. 4 Accepted: 2015. 4. 29

An oval-shaped mass with a smooth surface was found in the ear canal of a 22-month-old male infant. Although the mass appeared to be almost entirely blocking the ear canal, it was successfully removed under a surgical microscope without general anesthesia at the outpatient department. Under an optical microscope with hematoxylin and eosin staining, the specimen was observed to have a cuticle with a serrated surface and a pore canal, as well as parts of the capitulum, salivary glands, muscles, midgut, and the legs. The specimen was identified as a hard tick of the family Ixodidae, based on gross and histological findings. This paper is the first report in Korea on the diagnosis and treatment of a tick bite in the ear canal.

Periodontitis is a chronic inflammatory disease that leads to destruction of tooth supporting tissues. Porphyromonas gingivalis (P. gingivalis), especially its lipopolysaccharides (LPS), is one of major pathogens that cause periodontitis. Bee venom (BV) has been widely used as a traditional medicine for various diseases. Previous studies have demonstrated the anti-inflammatory, anti-bacterial effects of BV. However, a direct role and cellular mechanism of BV on periodontitis-like human keratinocytes have not been explored. Therefore, we investigated the anti-inflammatory mechanism of BV against P. gingivalis LPS (PgLPS)-induced HaCaT human keratinocyte cell line. The anti-inflammatory effect of BV was demonstrated by various molecular biological methods. The results showed that PgLPS increased the expression of Toll-like receptor (TLR)-4 and pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, and interferon (IFN)-γ. In addition, PgLPS induced activation of the signaling pathways of inflammatory cytokines-related transcription factors, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein 1 (AP-1). BV effectively inhibited those pro-inflammatory cytokines through suppression of NF-κB and AP-1 signaling pathways. These results suggest that administration of BV attenuates PgLPS-induced inflammatory responses. Furthermore, BV may be a useful treatment to anti-inflammatory therapy for periodontitis.

Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells gradually transform into mesenchymal-like cells losing their epithelial functionality and characteristics. EMT is thought to be involved in the pathogenesis of numerous lung diseases ranging from developmental disorders and fibrotic tissue remodeling to lung cancer. Lung cancer is the most lethal form of cancer worldwide, and despite significant therapeutic improvements, the patient survival rate still remains low. Activation of EMT endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The present review provides a brief insight into the mechanism and biological assessment methods of EMT in lung cancer and summarizes the recent literature highlighting the controversial experimental data and conclusions.

Adenocarcinoma is the most common histologic type of non-small cell lung carcinomas. The existence of lung cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT) in human tissue is controversy. The aim of this study is to investigate the expression and clinical significance of CSCs and EMT markers and evaluate the correlation between the two in lung adenocarcinoma. A total of 97 cases comprise the tissue microarray from surgical resection for primary lung adenocarcinoma. Immunohistochemistry for ALDH1 and CD44 as CSC markers and E-cadherin, vimentin, fibronectin, SMA as EMT markers was performed. High ALDH1A1 expression was statistically associated with female gender (P=0.001), smoker (P=0.012), and high pT stages (P=0.046). High CD44 expression was statistically associated with female gender (P=0.008), non-smoker (P=0.000), and no pleural invasion (P=0.039). High expression of ALDH1 was associated with good overall survival (P=0.021). High expression of CD44 was correlated with both good overall survival (P=0.024) and disease-free survival (P=0.000). Vimentin expression was associated with pT stage (P=0.001) and pleural invasion (P=0.028). E-cadherin, fibronectin and SMA were not associated with clinicopathologic correlation and all EMT markers were not correlated with survival of lung adenocarcinoma. CSC markers expression was not related to EMT. Our results showed that the expression of CSCs was associated with a good prognosis in lung adenocarcinoma. The prognostic significance of EMT markers was skeptical in this study. There is a need for more research about CSC, EMT, and the relation between these two in human lung adenocarcinoma.

The tumor microenvironment has many roles involving tumor progression, invasion and metastasis. The tumor cells at the tumor border loose epithelial properties and acquire mesenchymal features. This, epithelial-to-mesenchymal transition (EMT) has been suggested to be an important process for tissue and lymphovascular invasion. Pulmonary tissue samples from 15 patients with primary adenocarcinoma were evaluated with using immunofluorescence multi-staining the EMT-associated markers including E-cadherin and alpha-smooth muscle actin (α-SMA), and transcription factors including E-SNAIL and SLUG, and ZEB1. The data were analyzed in specific area, such as tumor center and tumor border. In this study we show that the invasive adenocarcinoma differentially expressed SNAIL and SLUG, and Zeb1 and it was associated with the loss of epithelial marker (E-cadherin) and gaining of mesenchymal marker (α-SMA) at the invasive border of lung carcinoma. The positive rates of SNAIL and ZEB1 were 26.7% and 0% in the tumor center and 40% and 20% in tumor margin, respectively. In addition, the expression of both SNAIL and ZEB1 at the border of tumor was observed in two cases (2/10). These two cases were associated with lymph node metastasis and advanced stage. The process of EMT has been suggested to be of prime importance for tissue and lymphovascular invasion. The process of EMT may be activated in the tumor border of lung adenocarcinoma. Related transcription factors, such as SNAIL and SLUG, and ZEB1, might be induced by paracrine effects of surrounded inflammatory cells and fibroblasts.

Gastrointestinal stromal tumors (GISTs) present as a spectrum, from clinically benign to malignant. Metastases usually become clinically apparent within 18–24 months of diagnosis, though they can develop as many as 30 years after primary tumor removal. The most common metastatic sites are the peritoneal surface and the liver. Pulmonary metastases are less common (approximately 7% of all metastises). Here, we report a case of pulmonary metastasis of a GIST of the rectum. A 50 year-old-woman, having received a Miles' operation for GIST of the rectum 10 years previous, was found to have a tumor in the right lung during a follow-up examination. A 2.5 cm sized well-demarcated mass presented in her lung parenchyma. The tumor was composed of spindle and epithelioid cells showing diffuse and strong cytoplasmic positivity for CD 117. These histologic and immunohistochemical findings proved that the tumor may have been the result of metastasis from the GIST of the rectum. This case suggests that GIST can metastasize after a long disease-free interval and that such cases should be carefully and regularly followed up indefinitely.

Epithelial-to-mesenchymal transition (EMT) is a process for fully differentiated epithelial cells to undergo a phenotypic change to fibroblasts via diverse intracellular signaling pathways. While the pivotal role of fibroblasts in renal fibrosis is widely accepted, their origin remains undefined. In addition, although a large number of studies have provided evidence of EMT in human kidney diseases, specific signaling pathways leading to EMT have not yet been discovered in humans. To evaluate the origin of interstitial fibroblasts and signaling pathways involved in the EMT process, we analyzed the differential expression of EMT-related molecules in paraffin-fixed sections from 19 human fibrotic kidneys and 4 control kidneys. In human fibrotic kidneys, tubular epithelial cells (TECs) with intact tubular basement membrane (TBM) showed loss or down-regulation of an epithelial marker (E-cadherin), de novo expression of mesenchymal markers (vimentin and fibronectin), and significant up-regulation of inducers and mediators controlling the EMT process (transforming growth factor-β1 (TGF-β1), p-Smad2/3, β1-integrin, p38 mitogen-activated protein kinase (MAPK), WNT5B and β-catenin) in the areas of interstitial inflammation and fibrosis, compared with their expression in control kidneys. In conclusion, the type II EMT process in humans is thought to be an adaptive response of TECs to chronic injury and is regulated by interconnections of TGF-β/Smad, integrin/integrin-linked kinase (ILK) and wnt/β-catenin signaling pathways.

Background: C4d has been used as an evaluation marker for antibody-mediated rejection for solid organ transplantation. Although some studies have proposed that complement activation is involved in renal diseases, very little information is available on pathogenesis. This study was conducted to investigate C4d deposition in IgA nephropathy and to find its relations with histopathology and albuminuria. Methods: This retrospective study included 23 patients who underwent renal biopsy at our medical center. The WHO grade of IgA nephropathy, interstitial inflammation and fibrosis, C4d staining and medical records including sex, age, and urine albumin were reviewed. Results: Thirteen patients (56.5%) were positive for C4d staining in the glomerulus and eleven patients (47.8%) were positive in the tubular epithelium. Glomerular C4d deposition was associated with albuminuria (p=0.044), and tubular C4d deposition was associated with a higher grade of IgA nephropathy (p=0.014). Conclusions: Activation of the complement system was involved in renal damage and was identified through deposition of C4d in the glomerulus and tubules. Positive C4d staining in the glomerulus and the tubules may be associated with functional damage related to glomerular filtration and poor renal outcome.

Renal tubulointerstitial fibrosis is considered to be a common final pathway related to the progressive loss of renal function in chronic kidney disease. It is characterized by the excessive accumulation of extracellular matrix through the pivotal role of epithelial-mesenchymal transition. Transforming growth factor-β1 is postulated to play a central role in renal fibrosis via a downstream pathway such as Smad. Specificity protein 1 (Sp1), which is another transcription factor, is also involved in the basal expression of extracellular matrix. In this study, we investigate the effect of Smad decoy oligodeoxynucleotides (ODN) and Sp1 decoy ODN in unilateral ureteral obstruction induced renal fibrosis in mice. Furthermore, the effectiveness of the newly designed chimeric decoy ODN, which contains both Smad and Sp1 binding sequences in one decoy molecule (Smad/Sp1 chi decoy ODN), was demonstrated. The expression of fibrosis and inflammatory related cytokines and products of fibrosis were ameliorated in the Smad, Sp1 and chimeric decoy ODN treated groups compared with the scrambled decoy ODN treated group. Epithelial-mesenchymal transition was suppressed by the Smad, Sp1 and Smad/Sp1 chi decoy ODN. Immunohistochemistry and Western-blot analysis revealed that Smad/Sp1 chi decoy ODN showed a more significant inhibitory effect on fibrosis and EMT compared with Smad and Sp1 decoy ODNs. These results support the efficacy of Smad/Sp1 chi decoy compared with a single Smad or Sp1 decoy ODNs in preventing renal fibrosis induced by unilateral ureteral obstruction.

In recent years, natural polymers such as cellulose, alginate and chitosan have been used worldwide as biomedical materials and devices, as they offer more advantages over synthetic polymers. The aim of this study was to clarify the usefulness of microbial cellulose (MC) for use as a dressing and scaffold material. For evaluating the biodegradability and toxicity of MC, we divided the rats (n = 12) into two groups (the implanted group and the non-implanted group). In the implanted group, we implanted the film type of MC in the backs of six rats. In the non-implanted group, however, we did not implant the film type of MC in the backs of the six rats. Four weeks later, we compared two groups by the gross, histological and biochemical characteristics by using blood and tissue samples. To evaluate the wound healing effects of MC, three full-thickness skin defects were made on the backs of each rat (n = 20). Three wounds on the backs of the same rats were treated with other dressing materials, namely, Vaseline gauze (group Con), Algisite M(®) (group Alg) and MC (group MC). We analysed the gross, histological and biochemical characteristics by western blotting. MC was found to be biodegradable and non-toxic. On day 3, the MC film was visible under the subcutaneous tissue; however, after 4 weeks, no remnants of the film were visible under the subcutaneous tissue. Furthermore, there was no evidence of MC-induced toxicity. Moreover, group MC showed more rapid wound healing compared with group Con. On day 14 after skin excision, group MC showed greater decrease in wound size compared with group Con (33% versus 7·2%). The wound healing effects were also substantiated by the histological findings (greater reduction in inflammation and rapid collagen deposition as well as neovascularisation) and western blotting (decreased expression of vascular endothelial growth factor and transforming growth factor-β1 in group MC on day 14 after skin excision, unlike group Con). This study showed that, in addition to having wound healing effects, MC is biodegradable and non-toxic and can, therefore, be used as a dressing and scaffold material.

Epithelioid trophoblastic tumor is an unusual type of trophoblastic tumor. Here we report on the clinicopathologic and immunohistochemical features of three cases of epithelioid trophoblastic tumor. All three patients were of reproductive age and presented with vaginal bleeding and mild elevation of human chorionic gonadotropin (hCG). All patients underwent a hysterectomy. The tumors consisted of epithelioid intermediate trophoblastic cells that were mononucleated and eosinophilic, or showed clear cytoplasm on microscopic examination. One case presented with a focal choriocarcinoma component. Immunohistochemically, the tumors displayed diffuse positivity for cytokeratin 18, E-cadherin, epidermal growth factor receptor, and p53 and focal positivity for p63 and hCG. However, expression of α-inhibin and placental alkaline phosphatase was almost negative. Tests for human placental lactogen and epithelial membrane antigen were also negative in all cases.

Mucosa-associated lymphoid tissue (MALT) lymphomas are characterized by lymphoepithelial lesions pathologically. Colonic MALT lymphomas are relatively rarer than lymphomas of the stomach or small intestine. Endoscopically, colonic MALT lymphoma frequently appears as a nonpedunculated protruding polypoid mass and/or an ulceration in the cecum and/or rectum. We report a unique case of a colonic MALT lymphoma presenting as a semipedunculated polyp. A 54-year-old man was found to have a 2-cm semipedunculated polyp in the sigmoid colon during screening colonoscopy. The polyp was removed by endoscopic mucosal resection. Histologic examination of the resected polyp revealed diffuse epithelial infiltration by discrete aggregates of lymphoma cells. We diagnosed the tumor as low-grade B-cell MALT lymphoma by immunohistochemical staining.

Extramedullary plasmacytoma (EMP) is a rare disease that occurs in 3% to 5% of patients with plasma cell disorder. It occurs most commonly in the upper respiratory tract and the oral cavity. Very few EMP cases have been reported in the central nervous system (CNS). We report herein an unusual case of EMP in the nasal cavity that recurred in the CNS without systemic involvement. A 67-year-old man visited our hospital due to a month-long bout with exophthalmos. He was diagnosed with EMP in the nasal cavity, paranasal sinus, and orbital cavity. He received radiotherapy to which he had complete responses. After 2 years, he visited our hospital because of a month-long headache. He was diagnosed with EMP recurrence in the CNS via brain magnetic resonance imaging and cerebrospinal fluid analysis. He was treated with whole brain radiotherapy and intrathecal chemotherapy with methotrexate, but he expired due to pneumonia.

Although pleomorphic adenoma commonly occurs in the salivary glands of the head and neck, tracheobronchial pleomorphic adenoma is extremely rare. 1 In this report, we report a case of pleomorphic adenoma of the trachea with active pulmonary tuberculosis. We performed surgical resection of pleomorphic adenoma of the trachea after management of pulmonary tuberculosis.

Accessory ovaries are rare entities defined as small portions of ovarian tissue situated near, and connected to, the normally placed ovary. Tumors arising in accessory ovaries are extremely rare. In particular, a fibroma arising from an accessory ovary has not been reported in the literature. We describe such a case with a fibroma developing in an accessory ovary. A 53-year-old multiparous woman presented with abdominal pain for 2 months. Pelvic computed tomography revealed 11.0 × 8.0 × 6.0 cm sized cystic mass with a thick septal wall in right adnexa. The preoperative diag- nosis was a borderline ovarian tumor. Furthermore, a laparotomy showed a cystic mass connect- ed to the right ovary by stalk. The bilateral eutopic ovaries were completely normal. Histologically, an accessory ovary was replaced by a fibroma accompanied by extensive cystic change.

Sparganosis of the breast is an uncommon disease. Cytological granulomatous inflammation is a common feature of sparganosis. The presence of larval fragments is necessary for a definitive di ­ agnosis of sparganosis in a cytological specimen. However, calcareous corpuscles entrapped in necrotic debris can be very diagnostic for sparganosis in endemic areas. We experienced three cases of mammary sparganosis diagnosed by fine needle aspiration cytology before surgical ex ­ cision. Two cases showed numerous calcareous corpuscles associated with necrotic debris thou­ ght to be degenerated parasitic bodies. The remaining case revealed a few degenerative calcare­ ous corpuscles and parasitic bodies. The presence of calcareous corpuscles and/or degenerative parasitic bodies can be an aid in the differential diagnosis between sparganosis and other forms of granulomatous mastitis, particularly in endemic areas of sparganosis.

Mature cystic teratomas of the fallopian tube are unusual, being almost incidentally identified. Here we describe a case of mature cystic teratoma arising in the fallopian tube, in a 44-year-old female. The mass was found during a regular checkup without complication. Microscopically, components from each germ layer were identified.

Background : At present, adequate prognostic markers for prostate cancer progression are still lacking, in spite of intensive investigation. Accordingly, our study examined the relationship between expression of candidate biomarkers and metastasis in prostate cancer patients. Correlation of molecular markers with prostate-specific antigen (PSA) level, Gleason sum score and tumor stage were also evaluated. Methods : A total of 105 prostate tumor specimens and specimens from 19 cases of nodular hyperplasia were obtained through Yeungnam University Hospital from 2007 to 2008. Immunohistochemical analyses for p16, phosphatase and tensin homolog (PTEN), E-cadherin, Ki-67 and Bcl-2 were performed. Results : Overexpression of Bcl-2 was significantly related to bone (p = 0.006) and nodal metastases (p = 0.017). Other biomarkers were not related to metastatic potential. There were statistically significant relationships between increased PSA level and loss of expression of PTEN (p = 0.019) and E-cadherin (p = 0.001). High Ki-67 index was significantly correlated with nodal metastasis (p = 0.029) as well as with loss of p16 expression (p = 0.002) and high Gleason score (p = 0.011). Conclusions : High Gleason score, Bcl-2 overexpression and increased Ki-67 labeling have significant predictive value in assessing the potential for prostate cancer metastasis. In addition, a high Ki-67 index is related to high Gleason score and loss of p16 expression.