Home About us Contact
|
Home About us Contact | ||
|
|
||
Epithelial Markers (epithelial + marker)
Selected AbstractsEpithelial markers in primary sinonasal mucosal melanomaHISTOPATHOLOGY, Issue 1 2004C Feeley No abstract is available for this article. [source] Expression of c-MET, low-molecular-weight cytokeratin, matrix metalloproteinases-1 and -2 in spinal chordomaHISTOPATHOLOGY, Issue 5 2009Takahiko Naka Aims:, In skull base chordoma, c-MET expression has been reported to correlate with younger patient age and favourable prognosis; however, it also contributes to tumour invasiveness, especially in recurrent lesions, suggesting variable roles for c-MET according to clinical status. The aim of this study was to investigate the significance of c-MET expression in spinal chordoma, which affects patients who are 10,20 years older than those with skull base chordoma. Methods and results:, Using immunohistochemical techniques, the expression of c-MET and its ligand, hepatocyte growth factor (HGF) was investigated in 34 primary spinal chordomas and compared with other clinicopathological parameters. Expression of c-MET and HGF was observed in 85.3 and 21.7% of lesions, respectively. c-MET expression correlated with the expression of an epithelial marker, low-molecular-weight cytokeratin (CAM5.2). Lesions with higher c-MET expression showed significantly stronger expression of proteinases, including matrix metalloproteinase (MMP)-1 and MMP-2. However, c-MET expression was not associated with patient age, proliferative ability estimated by MIB-1 labelling index, or prognosis. Conclusions:, c-MET expression was observed in most spinal chordomas and correlated with the expression of CAM5.2, suggesting a relationship to an epithelial phenotype. [source] Small cell carcinoma of the prostate expressing prostate-specific antigen and showing syndrome of inappropriate secretion of antidiuretic hormone: An autopsy case reportPATHOLOGY INTERNATIONAL, Issue 12 2003Shigeo Kawai An autopsy case of primary small cell carcinoma (SCC) of the prostate in a 68-year-old man is reported. The patient was admitted to hospital because of a bloody stool and suspected rectal cancer. However, a diagnosis of prostate cancer was made on the basis of a digital rectal examination, the serum level of prostate-specific antigen, and a needle biopsy of the prostate. The patient also experienced a syndrome of inappropriate secretion of antidiuretic hormone. He died 29 days after admission. At autopsy, the tumor had invaded the rectum, bladder and pelvic peritoneum. Metastases to the heart, vertebrae and lymph nodes were observed. Microscopically, the tumor was composed of small round cells that showed a solid growth pattern. Rosette formations were observed. Immunohistochemically, the tumor cells were positive for a prostatic epithelial marker and neuroendocrine markers. A high level of antidiuretic hormone was detected in the tumor tissue. To our knowledge, this is the first reported case of SCC of the prostate in which both a prostatic epithelial marker and neuroendocrine markers have been found in the same tumor. This finding supports the hypothesis that SCC of the prostate originates from a multipotential stem cell of the prostatic epithelium. [source] Cytopathological diagnosis of adult retinoblastoma in a vitrectomy specimen,DIAGNOSTIC CYTOPATHOLOGY, Issue 1 2010Maria E. Orellana M.D. Abstract Retinoblastoma (RB) is extremely rare in adults. We describe a case of RB diagnosed by cytology in a vitrectomy specimen of a 23-year-old patient who presented with diminished visual acuity and retinal detachment in the absence of a clinically-visible mass. Cytological examination of the vitreous fluid showed clusters of loosely cohesive atypical cells with high nuclear to cytoplasmic ratio and "salt and pepper" chromatin pattern in a background of normal neuronal retinal cells. Nuclear molding was present as well as numerous apoptotic bodies. The cells were focally positive for epithelial markers and showed strong and diffuse positivity for neuroendocrine markers. Ki-67 stained 90% of the "atypical cells" nuclei, in contrast to nonneoplastic retinal neuronal cells, which were negative for the marker. A diagnosis of RB was rendered, and subsequently was confirmed in the enucleation specimen. The cytological differential diagnosis is discussed as well as the role that cytology and immunohistochemistry can play in differentiating neoplastic cells from normal retinal cellular elements in vitreous fluid specimens. Diagn. Cytopathol. 2010. © 2009 Wiley-Liss, Inc. [source] Characterization of t(6;11)(p21;q12) in a renal-cell carcinoma of an adult patientGENES, CHROMOSOMES AND CANCER, Issue 5 2007Lorenza Pecciarini Renal-cell carcinoma (RCC) constitutes a heterogeneous group of tumors with specific chromosome aberrations. Recently, a new small group of RCC, occurring in children and young adults, has been described as characterized by t(6;11)(p21;q12). It has been shown that this translocation results in the fusion of the 5, portion of the ALPHA gene (11q12) with the transcription factor gene TFEB (6p21). Herewith, we report the first complete cytogenetic and molecular characterization of a t(6;11)-positive RCC of an adult patient, a 54-year-old woman. The tumor was histologically defined as RCC with peculiar features and it was negative for epithelial markers and positive for melanocytic markers. Chromosome QFQ banding analysis of short-term cultured cells from the RCC showed t(6;11)(p21;q12) as the sole cytogenetic abnormality. The translocation was confirmed by FISH analysis. RT-PCR analysis, performed on total RNA isolated from both neoplastic and normal tissue samples, revealed an ALPHA,TFEB chimeric transcript in the tumor sample; sequencing of the RT-PCR product defined a novel TFEB gene breakpoint cluster region, broader than the one reported thus far. Western blot analysis showed a band at the expected size of wild-type TFEB in the neoplastic tissue compared to the normal sample, supporting that the fusion gene does not encode for a chimeric protein but it causes an upregulation of the wild-type TFEB. Our data contribute to define better this rare RCC type, which is typical not only of childhood but can also be found in adulthood. © 2007 Wiley-Liss, Inc. [source] Derivation, characterization, and phenotypic variation of hepatic progenitor cell lines isolated from adult ratsHEPATOLOGY, Issue 2 2002Li Yin Liver progenitor cells (LPCs) cloned from adult rat livers following allyl alcohol injury express hematopoietic stem cell and early hepatic lineage markers when cultured on feeder layers; under these conditions, neither mature hepatocyte nor bile duct, Ito, stellate, Kupffer cell, or macrophage markers are detected. These phenotypes have remained stable without aneuploidy or morphological transformation after more than 100 population doublings. When cultured without feeder layers, the early lineage markers disappear, and mature hepatocyte markers are expressed; mature hepatocytic differentiation and cell size are also augmented by polypeptide and steroidal growth factors. In contrast to hepatocytic potential, duct-like structures and biliary epithelial markers are expressed on Matrigel. Because they were derived without carcinogens or mutagens, these bipotential LPC lines provide novel tools for models of cellular plasticity and hepatocarcinogenesis, as well as lines for use in cellular transplantation, gene therapy, and bioreactor construction. [source] Isolation and characterization of epithelial progenitor cells from human fetal liverHEPATOLOGY RESEARCH, Issue 1 2008Yi-Nan Liu Aim:, Hepatic progenitor cells can serve as an alternative source of hepatocytes for the treatment of liver diseases. Methods:, We isolated and expanded the epithelial progenitor cells (EPC) from the human fetal liver and investigated the differentiation of EPC into hepatic cells by fluorescence-activated cell sorter (FACS), real-time polymerase chain reaction (PCR), immunofluorescence assay, western blotting, and periodic acid,Schiff staining. Results:, Isolated EPC possessed highly proliferative ability and subpassaged for more than 25 passages. Real-time PCR showed that EPC expressed liver epithelial markers (cytokeratin [CK]8 and CK18) and biliary-specific markers (CK7 and CK19). FACS analysis indicated that these cells were positive for CD117, CD147, CD90, CD44, human leucocyte antigen class I and CD71, but negative for CD34 and CD45. The EPCpossessed multipotential indicated by differentiating into osteoblasts and adipocytes; when subjected to the hepatic differentiation condition, EPC could be induced to hepatocyte-like cells, which expressed albumin, alpha-fetoprotein, and CK18 proteins. Two months after EPC transplantation, we observed that the grafted cells differentiated into hepatocyte-like cells and there was no observable tumor mass. Conclusion:, We have isolated and characterized the human fetal liver-derived EPC and these cells may serve as an ideal cell source for cell-replacement therapy of diseased livers. [source] Nicotine induces cell proliferation, invasion and epithelial-mesenchymal transition in a variety of human cancer cell linesINTERNATIONAL JOURNAL OF CANCER, Issue 1 2009Piyali Dasgupta Abstract Cigarette smoking is strongly correlated with the onset of nonsmall cell lung cancer (NSCLC). Nicotine, an active component of cigarettes, has been found to induce proliferation of lung cancer cell lines. In addition, nicotine can induce angiogenesis and confer resistance to apoptosis. All these events are mediated through the nicotinic acetylcholine receptors (nAChRs) on lung cancer cells. In this study, we demonstrate that nicotine can promote anchorage-independent growth in NSCLCs. In addition, nicotine also induces morphological changes characteristic of a migratory, invasive phenotype in NSCLCs on collagen gel. These morphological changes were similar to those induced by the promigratory growth factor VEGF. The proinvasive effects of nicotine were mediated by ,7-nAChRs on NSCLCs. RT-PCR analysis showed that the ,7-nAChRs were also expressed on human breast cancer and pancreatic cancer cell lines. Nicotine was found to promote proliferation and invasion in human breast cancer. The proinvasive effects of nicotine were mediated via a nAChR, Src and calcium-dependent signaling pathway in breast cancer cells. In a similar fashion, nicotine could also induce proliferation and invasion of Aspc1 pancreatic cancer cells. Most importantly, nicotine could induce changes in gene expression consistent with epithelial to mesenchymal transition (EMT), characterized by reduction of epithelial markers like E-cadherin expression, ZO-1 staining and concomitant increase in levels of mesenchymal proteins like vimentin and fibronectin in human breast and lung cancer cells. Therefore, it is probable that the ability of nicotine to induce invasion and EMT may contribute to the progression of breast and lung cancers. © 2008 Wiley-Liss, Inc. [source] Periostin, secreted from stromal cells, has biphasic effect on cell migration and correlates with the epithelial to mesenchymal transition of human pancreatic cancer cellsINTERNATIONAL JOURNAL OF CANCER, Issue 12 2008Atsushi Kanno Abstract Periostin is a secretory protein that has been suggested to function as a cell adhesion molecule and promote the invasiveness or growth rate of tumors. However, little is known about the association of its expression and epithelial to mesenchymal transition (EMT), which is considered to play a crucial role in cancer cell metastasis. Thus, the authors investigated whether periostin could be involved in the process of EMT and the role of this gene in pancreatic cancer development. The expression of periostin was observed mainly in stromal cells but very little in cancer cells by immunohistochemistry and real-time RT-PCR. In vitro, pancreatic stellate cells (PSCs) exhibited a much higher basal expression of periostin compared with cancer cells. Periostin secreted in the supernatant from 293T cells that expressed periostin (approximately 150 ng/ml) inhibited the migration of pancreatic cancer cells. Coculture assay revealed that periostin expression in PSC was induced by pancreatic cancer cells. To assess the direct role of periostin in pancreatic cancer cells, the authors generated pancreatic cancer cell lines that stably express periostin. The induced expression of periostin (to 150 ng/ml) altered the morphology of cancer cells, changing them from mesenchymal to epithelial phenotypes with the induction of epithelial markers and a reduction of mesenchymal markers, and showed reduced cell migration in vitro and formed smaller tumors as well as suppressed metastasis in vivo. On the other hand, high concentration of recombinant periostin (1 ,g/ml) promoted cell migration with AKT activation. The findings suggest that periostin has biphasic effect on the development of pancreatic cancer. © 2008 Wiley-Liss, Inc. [source] Relevance of a new rat model of osteoblastic metastases from prostate carcinoma for preclinical studies using zoledronic acidINTERNATIONAL JOURNAL OF CANCER, Issue 4 2008François Lamoureux Abstract Animal models that mimic osteoblastic metastases associated with prostate carcinoma are required to improve the therapeutic options in humans. A new model was then developed and characterized in immunocompetent rats. The bisphosphonate zoledronic acid (ZOL) was tested to validate this model as a therapeutic application. Rat AT6-1 prostate tumor cells were characterized in vitro at the transcriptional (bone and epithelial markers) and functional (induction of mineralized nodules) levels. The bone lesions induced after their direct injection into the femur bone marrow were characterized by radiography, microscanner and histology analyses. ZOL effects were studied in vivo on bone lesion development and in vitro on AT6-1 cell proliferation, apoptosis and cell cycle analysis. Apart from epithelial markers, AT6-1 cells express an osteoblast phenotype as they express osteoblastic markers and are able to induce mineralized nodule formation in vitro. A disorganization of the trabecular bone at the growth zone level was observed in vivo after intraosseous AT6-1 cell injection as well as cortical erosion. The tumor itself is associated with bone formation as revealed by SEM analysis and polarized light microscopy. ZOL prevents the development of such osteoblastic lesions, related to a direct inhibitory effect on tumor cell proliferation independent of caspase 3 activation, but associated with cell cycle arrest. A new rat model of osteoblastic bone metastases was validated in immunocompetent rats and used to show the relevance of using ZOL in such lesions, as this compound shows bifunctional effects on both bone remodelling and tumor cell proliferation. © 2007 Wiley-Liss, Inc. [source] Acral lentiginous melanoma: an immunohistochemical study of 20 casesINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2003You Chan Kim MD Background Though acral lentiginous melanoma (ALM) is a major type of malignant melanoma, no immunohistochemical study on this type of melanoma has been reported. Objective The purpose of this study is to analysis the immunohistochemical findings of ALM using routinely used immune markers. Methods An immunohistochemical study was performed on paraffin sections of 20 ALMs using S-100 protein, HMB-45, MART-1, vimentin, epithelial membrane antigen (EMA) and CAM 5.2. Results S-100 protein (95%) was found to be a more sensitive marker than either HMB-45 (80%) or MART-1 (70%) for recognizing ALM. Melanin bleaching was useful for recognizing heavily pigmented ALM using both S-100 protein and HMB-45. The intensity of HMB-45 correlated well with the melanin content. However, there was no significant correlation between the intensity of S-100 protein and the melanin content. One and two out of 20 cases stained focally with EMA and CAM5.2, respectively, but these cases stained also with HMB-45 and/or S-100 protein. Conclusions S-100 protein and HMB-45 were relatively sensitive markers for recognizing ALM. Despite the occasional positivity for the epithelial markers in ALM, all epithelial marker-positive cases stained also with HMB-45 and/or S-100 protein. Therefore, we recommend that the panel of antibodies used for recognizing ALM should contain at least S-100 protein and HMB-45. [source] In vitro and in vivo cytokeratin patterns of expression in bioengineered human periodontal mucosaJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2009I. Garzón Background and Objective:, Development of human oral mucosa substitutes by tissue engineering may provide new therapeutic tools for the management of periodontal diseases. In this study we evaluated a fibrin,agarose human oral mucosa substitute both in vitro and in vivo. Material and Methods:,In vitro bioengineered oral mucosa substitutes were developed from irrelevant biopsy samples of human oral gingiva. In vivo evaluation of the constructed tissues was performed by implantation into athymic nude mice. The expression of several epithelial markers was assessed by microarray analysis and immunohistochemistry. Results:, Bioengineered oral mucosa samples kept in vitro developed a multilayered epithelium that expressed several cytokeratins, including some markers of simple epithelia (cytokeratins 7, 8 and 18), along with markers of stratified epithelia (cytokeratins 5 and 13) and of cell proliferation (proliferating cell nuclear antigen). Bioengineered tissues grafted in vivo onto nude mice exhibited very good biointegration with the host, showing a cytokeratin expression pattern that was very similar to that of normal native oral mucosa controls. Histological analysis of the artificial tissues demonstrated that oral mucosa substitutes evaluated in vivo were structurally mature, showing some typical structures of human native oral mucosa such as rete ridges and chorial papillae, along with numerous blood vessels at the fibrin,agarose stromal substitute. These structures were absent in samples evaluated in vitro. Conclusion:, The results indicate that this model of human oral mucosa, constructed using fibrin,agarose scaffolds, shows similarities to native oral mucosa controls and imply that bioengineered oral mucosa substitutes could eventually be used clinically. [source] Primary synovial sarcoma of the kidney: Report of a case confirmed by molecular detection of the SYT-SSX2 fusion transcriptsPATHOLOGY INTERNATIONAL, Issue 5 2001Shune Koyama We describe an unusual case of primary synovial sarcoma of the kidney. A 47-year-old woman had a tumor massively replacing the right kidney. There were no primary extrarenal neoplastic lesions. Microscopically, the tumor was composed of a cellular proliferation of relatively uniform spindle-shaped cells having atypical spindle or oval nuclei arranged in fascicles with tumor necrosis, without epithelial areas. Immunohistochemically, a small number of the tumor cells were positive for epithelial markers such as cytokeratin and epithelial membrane antigen. The SYT-SSX2 fusion transcripts were detected by a reverse transcription,polymerase chain reaction (RT,PCR) using RNA extracted from formalin-fixed, paraffin-embedded tissue. ETV6-NTRK3 fusion gene transcripts that result from t(12; 15)(p13;q25), which is characteristic of cellular congenital mesoblastic nephroma, were not demonstrated. To our knowledge, this is the ninth case of primary renal synovial sarcoma. This case report indicates that synovial sarcoma should be taken into account for the differential diagnosis of renal spindle cell tumors and the molecular assay detecting the SYT-SSX fusion transcripts is useful for the final diagnosis of synovial sarcoma arising in an unusual location. [source] Immunohistochemical detection of cytokeratin and epithelial membrane antigen in leiomyosarcoma: A systematic study of 100 casesPATHOLOGY INTERNATIONAL, Issue 1 2000Jun Iwata Although ,aberrant' expression of the epithelial markers, cytokeratin (CK) and epithelial membrane antigen (EMA), in leiomyosarcoma has been described previously, there has not been a study of this phenomenon with clinicopathological correlation in a large series of lesions at different anatomical sites. We investigated systematically the immunohistochemical reactivity for CK and EMA in 100 cases of leiomyosarcoma. CK and EMA were positive in 38% and 44% of the cases, respectively. Although staining was usually focal, extensive immunoreactivity was observed in 11% with CK and 6% with EMA. There was no correlation between immunoreactivity for CK and EMA in leiomyosarcomas and non-neoplastic smooth muscle at the same location. Immunoreactivity for CK and EMA was not correlated with the location, age, sex, histological grade, or histological features, except for more frequent EMA positivity in vascular and uterine tumors than in soft tissue cases. These results indicate that CK and/or EMA-positive leiomyosarcomas do not have distinctive clinicopathological features differing from those of negative cases. However, the considerable frequency of immunoreactivity for these epithelial markers in leiomyosarcoma, occasionally with diffuse and strong immunopositivity, should be recognized as a potentially serious diagnostic pitfall in the differential diagnosis of other malignant spindle cell neoplasms. [source] Evidence of Temporary Airway Epithelial Repopulation and Rare Clonal Formation by BM-derived Cells Following Naphthalene Injury in MiceTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 9 2007Vladimir B. Serikov Abstract The goal of the study was to investigate participation of bone marrow (BM) cells in the process of airway epithelial restoration after naphthalene-induced injury. We transplanted sex-mismatched green fluorescent protein (GFP) -tagged BM-derived cultured plastic-adherent mesenchymal stem cells into 5Gy-irradiated C57BL/6 recipients. After 1 month of recovery, experimental animals were subjected to 250 mg/kg naphthalene IP. Animals were killed at 2,30 days after naphthalene. By immunofluorescence, immunohistochemistry, and by in situ hybridization for the Y-chromosome, we observed patches of donor-derived cells in the large and small conducting airways, mostly at 2,6 days after injury. GFP+ cells in the epithelium of airways were positive for pancytokeratin and some other epithelial markers. Although rare, GFP+ cells formed clear isolated patches of the bronchial epithelium, consistent with clonal formation; as some cells were also positive for proliferating cell nuclear antigen, a marker of proliferating cells. After day 12, only occasional GFP+ cells were present in the epithelium. These data confirm that bone marrow-derived cultured mesenchymal cells can participate in the recovery of the injured airway epithelium after naphthalene-induced injury with minimal long-term engraftment. Anat Rec, 2007. © 2007 Wiley-Liss, Inc. [source] Epithelial to Mesenchymal Transition During Late Deterioration of Human Kidney Transplants: The Role of Tubular Cells in FibrogenesisAMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2005Attapong Vongwiwatana The hallmark of failing renal transplants is tubular atrophy and interstitial fibrosis (TA/IF). Injury to tubular epithelial cells (TEC) could contribute to fibrogenesis via epithelial,mesenchymal transition (EMT). We examined the features of EMT in renal transplants that developed TA/IF. Biopsies from 10 allograft kidneys with impaired function and TA/IF and 10 biopsies from transplants with stable function were compared to their implantation biopsies. Relative to implantation biopsies, TEC in TA/IF kidneys showed loss of epithelial markers (E-cadherin, cytokeratin) with altered distribution. Some TEC also showed new cytoplasmic expression of mesenchymal markers vimentin, S100A4, and alpha smooth muscle actin (,-SMA) and collagen synthesis marker heat shock protein (HSP-47), both in deteriorating and atrophic tubules. Double immunostaining showed coexpression of cytokeratin and vimentin, S100A4 and HSP-47, indicating intermediate stages of EMT in TA/IF. These changes were absent or much less in transplants with stable function. EMT features in the TA/IF group correlated with serum creatinine (vimentin, S100A4, HSP-47), history of T-cell-mediated rejection (cytokeratin, S100A4) and proteinuria (cytokeratin). These findings support a model in which the TEC damage induces loss of epithelial features and expression of fibroblast features, as a common pathway of deterioration by either immunologic or nonimmunologic processes. [source] Primary hepatic clear cell myomelanocytic tumor,APMIS, Issue 12 2007Case report, review of the literature A case of hepatic clear cell myomelanocytic tumor in a 31-year-old woman presenting clinically with abdominal pain is reported. Histopathologic examination showed a lesion characterized by a population of large epithelioid cells with clear or eosinophilic granular cytoplasm, rich in glycogen. Immunohistochemically, the tumor cells were positive for HMB-45, Melan-A and muscle-specific actin, but negative for epithelial markers, desmin, S-100 protein, and neuroendocrine markers. Ultrastructurally, the tumor cells had abundant glycogen, well-developed rough endoplasmic reticulum, microtubules and aberrant melanosomes. Clinical and pathologic features with a brief review of the relevant literature for hepatic CCMMT as a variant of perivascular epithelioid cell tumor (PEComa) are discussed. [source] Epithelial marker expression in Salzmann nodular degeneration shows characteristics of limbal transient amplifying cells and alludes to an involvement of the epithelium in its pathogenesisACTA OPHTHALMOLOGICA, Issue 5 2010Philipp Eberwein Abstract. Purpose:, To look at the epithelial nature of Salzmann nodular degeneration (SND) and its possible relation with the aetiology of the subepithelial collagen deposition. Methods:, Histological slides of 28 patients with SND were analysed for limbal and central corneal epithelial markers. Expression pattern of these markers in the basal layer of the epithelium was analysed and compared to the expression pattern in central corneal and limbal epithelium. Statistical analysis was performed by means of analysis of variance. Results:, Expression of the epithelial stem cell marker ABCG2 and p63 was low in SND. Expression of CK12, a marker for terminally differentiated epithelium, was low, as well. But, CK19 and Enolase-alpha expressions were significantly increased and resembled the expression pattern of transient amplifying cells (TAC) of the limbus. Conclusion:, The epithelium in SND shows similar characteristics as TAC of the limbus and seems to be metabolically more active than the differentiated central corneal epithelium. This could be related to the deposition of subepithelial collagen fibrils seen in SND and points out a possible involvement of the corneal epithelium in the aetiology of Salzmann nodular degeneration. [source] | |||||||||||||||||||||||||