Current Issue : October - December Volume : 2017 Issue Number : 4 Articles : 8 Articles
Background: The study aims to investigate the clinicopathological features and surgical outcomes of neuroendocrine\ntumors of ampulla of Vater (NETAoVs) patients who underwent pancreaticoduodenectomy.\nMethods: From January 2007 to December 2014, 45 patients underwent pancreaticoduodenectomy for malignant\ndisease of the ampulla of Vater in our institution. Of those, 5 patients were diagnosed as neuroendocrine tumors. The\ndata included age, sex, presenting symptoms, preoperative imaging, preoperative type of biopsy results, type of\noperation, pathologic findings and survival status.\nResults: The patientââ?¬â?¢s mean age was 55.2 Ã?± 9.7 years. Endoscopic ultrasound guided biopsy was performed in 4\npatients and gastroduodenoscopic biopsy was performed in one patient. All showed neuroendocrine tumor without\nmitosis. Mean tumor size was 1.9 Ã?± 0.56 cm (range, 1.2ââ?¬â??2.0 cm). Lymph node metastases were detected in two\npatients. All patients were synaptophysin-positive. Median periods of follow-up were 45 months (range, 43ââ?¬â??78 months).\nRecurrence after operation occurred in two patients. 4 patients were alive at the last follow-up.\nConclusions: Radical resection for NETAoVs can provide the information of status of lymph node metastasis after\nsurgery. However, correlation between lymph node metastasis and overall survival is uncertain to date....
Posttransplant lymphoproliferative disorders (PTLDs) are a diverse group of lymphoid or plasmacytic proliferations frequently\ndriven by Epstein-Barr virus (EBV). EBV-negative PTLDs appear to represent a distinct entity. This report describes an unusual\ncase of a 33-year-old woman that developed a monomorphic EBV-negative PTLD consistent with diffuse large B-cell lymphoma\n(DLBCL) 13 years after heart-lung transplant. Histological examination revealed marked pleomorphism of the malignant cells\nincluding nodular areas reminiscent of classical Hodgkin lymphoma (cHL) with abundant large, bizarre Hodgkin-like cells. By\nimmunostaining, themalignant cellswere immunoreactive for CD45, CD20, CD79a, PAX5, BCL6,MUM1, and p53 and negative for\nCD15, CD30, latentmembrane protein 1 (LMP1), and EBV-encodedRNA(EBER). Flowcytometry demonstrated lambda light chain\nrestricted CD5 and CD10 negative B-cells. Fluorescence in situ hybridization studies (FISH) were negative for cMYC, BCL2, and\nBCL6 rearrangements but showed deletion of TP53 and monosomy of chromosome 17. Next-generation sequencing studies (NGS)\nrevealed numerous genetic alterations including 6 pathogenicmutations in ASXL1, BCOR, CDKN2A, NF1, and TP53(x2) genes and\n30 variants of unknown significance (VOUS) in ABL1, ASXL1, ATM, BCOR, BCORL1, BRNIP3, CDH2, CDKN2A, DNMT3A, ETV6,\nEZH2, FBXW7, KIT, NF1, RUNX1, SETPB1, SF1, SMC1A, STAG2, TET2, TP53, and U2AF2....
Background: As the major subfamily of receptor tyrosine, erythropoietin-producing hepatocellular (Eph) receptor\nhas been related to progression and prognosis in different types of tumors. However, the role and mechanism of\nEPHA3 in gastric cancer is still not well understood.\nMethods: Specimen were collected from 202 patients who underwent gastric resection for gastric adenocarcinoma.\nThe expression of EphA3 was studied using immunohistochemistry. We analyzed the clinicopathological factors and\nprognostic relevance of EphA3 expression in gastric cancer.\nResults: High expression of EphA3 was associated with male predominance (p = 0.031), differentiated histology\n(p < 0.001), depth of tumor (p = 0.002), lymph node metastasis (p = 0.001), distant metastasis (p = 0.021), liver\nmetastasis (p = 0.024), advanced stage (p < 0.001), and high HER2 [removed]p = 0.017). Relapse-free survival (RFS)\nwas significantly worse in patients with high expression of EphA3 than in those with low expression of EphA3\n(p = 0.014). Multivariate analysis for RFS showed that depth of tumor [hazard ratio (HR) 9.333, 95% confidence\ninterval (CI) 2.183ââ?¬â??39.911, p = 0.003] and lymph node metastasis [hazard ratio (HR) 5.734, 95% confidence interval\n(CI) 2.349ââ?¬â??13.997, p < 0.001] were independent prognostic factors.Conclusions: These findings suggest that high expression EphA3 may participate in metastasis and worse survival....
Background: The osteoconductive properties of collagen containing xenogeneic bone blocks (CCXBB) remain\nunclear. The aim of this prospective single-arm clinical study was to assess the histological outcomes of CCXBB\nblocks used as bone replacement grafts for lateral bone augmentation procedures.\nMethods: In 15 patients with severe horizontal alveolar ridge resorption, lateral augmentation procedures were\nperformed using CCXBB as bone replacement grafts. Twenty-six weeks postoperatively, a re-entry procedure was\nperformed to evaluate the bone width for adequate implant placement and two histological specimens were\nretrieved from each patient, one being processed for ground sectioning and the other for decalcified paraffinincluded\nsections. In non-decalcified sections, the relative proportions occupied by bone, biomaterials, and\nconnective tissue present in the biopsies were identified. In de-calcified sections, structures and cells positive for\nosteopontin (OPN), tartrate-resistant acid phosphatase activity (TRAP), osteocalcin (OSC), and alkaline phosphatase\n(ALP) were assessed.\nResults: Soft tissue dehiscence occurred during the follow-up in 5 out of 15 patients (33.3%). The mean crest width\nat baseline was 2.78 mm (SD 0.57) and the mean crest width at re-entry was 6.90 mm (SD 1.22), with a mean ridge\nwidth increase of 4.12 mm (SD 1.32). Twenty-six bone biopsies were obtained from 13 patients. Histomorphometric\nanalysis showed a mean of 26.90% (SD 12.21) of mineralized vital bone (MVB), 21.37% (SD 7.36) of residual CCXBB,\n47.13% (SD 19.15) of non-mineralized tissue, and 0.92% of DBBM. The immunohistochemical analysis revealed a\nlarge number of OPN-positive cells 8.12% (SD 4.73), a lower proportion of TRAP positive multinuclear cells 5.09%\n(SD 4.91), OSC-positive cells 4.09% (SD 4.34), and a limited amount of ALP positive cells 1.63% (SD 2).\nConclusions: CCXBB achieved significant horizontal crestal width allowing for staged implant placement in most of\nthe patients. In light of the histological outcomes and implant failures, special attention must be placed to prevent\nsoft tissue dehiscence when CCXBB is used in severe atrophic alveolar crests....
Background: Among the many challenges in cancer diagnosis is the early distinction between metastatic cancer\nand a secondary tumor. This difficulty stems from the lack of markers that offer high sensitivity and specificity and\ncan be easily applied in routine laboratory work. An example of this challenge is distinguishing gastric metastases\noriginating from breast cancer from a gastric primary tumor. Hepatocyte nuclear factor 4 alpha (HNF4A) has been\nsuggested as a potential marker in these cases.\nThe aim of this study was to analyze the expression of HNF4A, estrogen receptor (ER), progesterone receptor (PR)\nand gross cystic disease fluid protein 15 (GCDFP-15) in a Brazilian cohort.\nMethods: We performed immunohistochemistry analysis of HNF4A, ER, PR and GCDFP-15 in 126 patients divided\ninto three cohorts: primary breast cancer, primary gastric cancer and both types of tumors.\nResults: Our data confirmed the sensitivity and specificity of the HNF4A marker compared to other currently used\nclinical markers.\nConclusion: HNF4A alone could be a gold standard marker for distinguishing primary gastric cancer from breast\nmetastasis, thus validating its potential clinical use, especially in populations with high genetic diversity....
Background: Microsatellite instability (MSI) operates as the second major pathway in the colorectal carcinogenesis.\nAlthough genetic testing remains the gold standard for the detection of MSI, the College of American Pathologists\n(CAP) recommends an initial immunohistochemical workup with a four-antibody panel (MLH1, PMS2, MSH2, and\nMSH6) to screen for a defective mismatch repair system. An increased trend towards young age colorectal\ncarcinoma (CRC) has been noticed in our population over recent years; however, neither screening for MSI by\nimmunohistochemistry (IHC)/genetic testing was done nor were its morphological features studied. We aimed to\ndetermine the frequency of mismatch repair deficiency (dMMR) by loss of IHC expression of the aforementioned\nenzymes in CRC patients and its correlatation with clinicopathologic parameters.\nMethods: This was a retrospective study conducted at Liaquat National Hospital, Karachi, between 2012 and\n2015. A total of 100 cases of CRC were included in the study that underwent surgical resection. IHC stains using\nantibodies MLH1, PMS2, MSH2, and MSH6 were performed by DAKO EnVision method on representative tissue\nblocks. The results were interpreted by senior histopathologists and correlated with clinico-pathological parameters.\nResults: A total of 100 cases of CRC were studied that included 51 males and 49 females. Thirty-four percent\n(n = 34) of the patients showed loss of IHC staining for MMR markers. Combined loss of expression for MLH1/PMS2\nwere observed in 16% (n = 16) of the cases. Loss of MSH2/MSH6 were seen in 6% (n = 6) of the cases. Loss of\nexpression for all markers were noted in 7% (n = 7) of the cases. There were 5% (n = 5) of the cases that showed\nisolated loss of MLH1 only. The tumors with dMMR status were significantly associated with right-sided location\n(p = 0.013), exhibited intra-tumoral lymphocytosis (p = 0.007), and lymphovascular invasion (p = 0.043). No significant\nassociation was seen with gender, age, tumor stage, grade, or other morphological features.\nConclusion: The frequency of mismatch repair deficiency in CRC patients was found to be 34% in Pakistani\npopulation which warrants further genetic testing to exclude Lynch syndrome. Moreover, right-sided location and\nintra-tumoral lymphocyte count may be used to identify patients who may need further workup....
Clear cell papillary renal cell carcinoma (CCPRCC) is a newly recognized entity in the 2016WHOclassification and usually presents\nas a small, circumscribed, solitary mass of indolent nature. CCPRCCs could seldom occur in conjunction with other synchronous\nor metachronous kidney tumors and even less frequently as bilateral masses. To our knowledge, multiple bilateral CCPRCCs have\nnever been described with the existence of a synchronous well-differentiated neuroendocrine tumor of the kidney and hence\nreported here as a unique case. This case report highlights the importance in considering this entity and its unusual presentation\nin the differential diagnosis as a possible mimicker of Von Hippel-Lindau syndrome....
Background: Survivin, a member of the inhibitor of apoptosis protein (IAP) family, regulates mitosis and chromosome\nsegregation. The expression of survivin proceeds during embryonic development and in addition has already been\ndemonstrated in cancer cells. However, there is also evidence of survivin expression in differentiated tissues, including\nthe gastro-intestinal tract of adult rats. A study with human colon specimens exhibited survivin in most basal crypt\nepithelial cells of normal mucosa. There is rather limited information on survivin expression in the small intestine. In\norder to paint a more detailed and thus complete picture of survivin expression patterns in the gastrointestinal tract,\nwe used an immunohistochemical approach in normal adult rat small intestinal and ascending colonic tissue.\nMoreover, to get deeper insights in the regulation of survivin expression after tissue damage, we also studied its\nexpression in mesenteric ischemia-reperfusion (I/R) injury.\nMethods: Mesenteric ischemia-reperfusion injury was induced in male Wistar rats (six animals/group) by occlusion of\nthe superior mesenteric artery for 90 min and subsequent reperfusion for 120 min. Paraffin sections of untreated or\nischemically treated tissue were assessed immunohistochemically by survivin and Ki-67 staining.\nResults: Survivin could be detected in the small intestine and ascending colon of the normoxia group. It was expressed\nmainly in the epithelial cells of the crypts and only marginally in the villi. The individual small intestinal segments studied\nrevealed comparable staining intensities. Likewise, expression of survivin was detected in the ischemically damaged small\nintestine and ascending colon. The expression pattern corresponded to the normoxic animals, as far as verifiable due to\nthe existing tissue damage. Comparison of the expression pattern of Ki-67, a protein that acts as a cellular marker for\nproliferation, and survivin demonstrated a coincidental localization of the two proteins in the small intestinal and\nascending colonic tissue.\nConclusions: Survivin was expressed strongly in epithelial cells of small intestinal as well as ascending colonic tissue. Its\nexpression was located in cells with a high proliferation rate and regenerative capacity. This further supports the decisive\nrole of survivin in cell division. Surprisingly, the ischemically damaged small intestinal and ascending colonic tissue\nshowed a comparably high expression level. These results suggest that there is already a maximal survivin expression\nunder normal conditions. However, the intestine is able to maintain the regenerative capacity even in spite of an\nischemic injury. These findings reflect the important relevance of an intact intestinal barrier....
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