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  • 1
    Language: English
    In: Histopathology, 2013-03, Vol.62 (4), p.617-631
    Description: Aims Lipid droplets (LDs) are dynamic storage compartments for energy‐rich fats that are nearly ubiquitously present in eukaryotic cells, exerting tissue‐specific functions in metabolically active cell types, and are increased in conditions following cellular damage or lipid overload. The LD–cytoplasm interface is stabilized by amphiphilic proteins of the PAT/perilipin family (perilipin/perilipin‐1, adipophilin/perilipin‐2, and TIP47/perilipin‐3). We evaluated the value of adipophilin immunohistochemistry for the diagnosis of diseases associated with LD accumulation. Methods and results In human tissues, adipophilin‐positive LDs were especially prominent in steroidogenic cells of the adrenal gland, testis, and ovary, in hepatocytes and hepatic stellate cells, in cardiac, striated and smooth myocytes, in lactating mammary gland epithelial cells, and in plurivacuolar adipocytes. Variable amounts of adipophilin‐positive LDs were also detected almost ubiquitously in epithelial cells of the gastrointestinal tract and skin. In diseases associated with lipid storage, adipophilin was strongly expressed in lipid‐laden macrophages in atherosclerosis, in cardiomyopathies, kidney diseases, hepatocyte steatosis, colon ischaemia, and at the border of organ infarcts. Conclusions Adipophilin immunohistochemistry visualizes small LDs in tissues under physiological and disease conditions that are not visible by conventional light microscopy. Immunohistology for adipophilin may facilitate histomorphological diagnosis of diseases and definition of the extent of metabolic dysregulation, such as in organ infarcts, cardiomyopathies, kidney diseases, and microvesicular steatosis.
    Subject(s): perilipin ; metabolism ; steatosis ; adipophilin ; PAT proteins ; Immunohistochemistry ; Testis - metabolism ; Lactation ; Fatty Liver - pathology ; Humans ; Hepatic Stellate Cells - metabolism ; Male ; Hepatocytes - metabolism ; Lipids - biosynthesis ; Mammary Glands, Human - metabolism ; Lipids - chemistry ; Female ; Membrane Proteins - metabolism ; Foam Cells - pathology ; Foam Cells - metabolism ; Infarction - metabolism ; Infarction - pathology ; Kidney Diseases - metabolism ; Ovary - metabolism ; Biomarkers - metabolism ; Fatty Liver - metabolism ; Kidney Diseases - pathology ; Muscle Cells - metabolism ; Cardiomyopathies - pathology ; Lipid Metabolism ; Adrenal Glands - metabolism ; Adipocytes - metabolism ; Cardiomyopathies - metabolism ; Perilipin-2 ; Proteins ; Physiological aspects ; Gastrointestinal system ; Atherosclerosis ; Ovarian cancer ; Index Medicus
    ISSN: 0309-0167
    E-ISSN: 1365-2559
    Source: Academic Search Ultimate
    Source: Wiley Online Library All Backfiles
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: International journal of cancer, 2017-10-15, Vol.141 (8), p.1643-1653
    Description: Cyclin K plays a critical role in transcriptional regulation as well as cell development. However, the role of Cyclin K in prostate cancer is unknown. Here, we describe the impact of Cyclin K on prostate cancer cells and examine the clinical relevance of Cyclin K as a biomarker for patients with prostate cancer. We show that Cyclin K depletion in prostate cancer cells induces apoptosis and inhibits proliferation accompanied by an accumulation of cells in the G2/M phase. Moreover, knockdown of Cyclin K causes mitotic catastrophe displayed by multinucleation and spindle multipolarity. Furthermore, we demonstrate a Cyclin K dependent regulation of the mitotic kinase Aurora B and provide evidence for an Aurora B dependent induction of mitotic catastrophe. In addition, we show that Cyclin K expression is associated with poor biochemical recurrence‐free survival in patients with prostate cancer treated with an adjuvant therapy. In conclusion, targeting Cyclin K represents a novel, promising anti‐cancer strategy to induce cell cycle arrest and apoptotic cell death through induction of mitotic catastrophe in prostate cancer cells. Moreover, our results indicate that Cyclin K is a putative predictive biomarker for clinical outcome and therapy response for patients with prostate cancer. What's new? Cell cycle progression genes represent a promising source for biomarker discovery in prostate cancer, though little is known about their role in the disease. This study shows in prostate cancer cells that depletion of Cyclin K, a cell cycle regulator, is associated with apoptosis and inhibition of proliferation. The effects of Cyclin K downregulation were linked to Cyclin K dependent and Aurora B‐mediated induction of mitotic catastrophe. In patients treated with adjuvant therapy, Cyclin K expression was associated with reduced biochemical recurrence‐free survival. The results warrant further investigation of Cyclin K as predictive biomarker in prostate cancer.
    Subject(s): apoptosis ; prostate cancer ; mitotic catastrophe ; cyclin K ; aurora B ; Aurora Kinase B - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Aurora Kinase B - metabolism ; Aurora Kinase B - biosynthesis ; Humans ; Cell Proliferation - physiology ; Cyclins - genetics ; Male ; Cyclins - deficiency ; Prostatic Neoplasms - genetics ; Cyclins - metabolism ; Mitosis - physiology ; Cell Cycle - physiology ; Cell Line, Tumor ; Apoptosis - physiology ; Prostate cancer ; Adjuvant treatment ; Cancer ; Apoptosis ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: BMC cancer, 2010-10-04, Vol.10 (1), p.524-524
    Description: The enhancer of zeste homolog 2 (EZH2) gene exerts oncogene-like activities and its (over)expression has been linked to several human malignancies. Here, we studied a possible association between EZH2 expression and prognosis in patients with renal cell carcinoma (RCC). EZH2 protein expression in RCC specimens was analyzed by immunohistochemistry using a tissue microarray (TMA) containing RCC tumor tissue and corresponding normal tissue samples of 520 patients. For immunohistochemical assessment of EZH2 expression, nuclear staining quantity was evaluated using a semiquantitative score. The effect of EZH2 expression on cancer specific survival (CSS) was assessed by univariate and multivariate Cox regression analyses. During follow-up, 147 patients (28%) had died of their disease, median follow-up of patients still alive was 6.0 years (range 0-16.1 years). EZH2 nuclear staining was present in tumor cores of 411 (79%) patients. A multivariate Cox regression analysis revealed that high nuclear EZH2 expression was an independent predictor of poor CSS (〉 25-50% vs. 0%: HR 2.72, p = 0.025) in patients suffering from non-metastatic RCC. Apart from high nuclear EZH2 expression, tumor stage and Fuhrman's grading emerged as significant prognostic markers. In metastatic disease, nuclear EZH2 expression and histopathological subtype were independent predictive parameters of poor CSS (EZH2: 1-5%: HR 2.63, p = 0.043, 〉5-25%: HR 3.35, p = 0.013, 〉25%-50%: HR 4.92, p = 0.003, all compared to 0%: HR 0.36, p = 0.025, respectively). This study defines EZH2 as a powerful independent unfavourable prognostic marker of CSS in patients with metastatic and non-metastatic RCC.
    Subject(s): Prognosis ; Humans ; Middle Aged ; Risk Factors ; Gene Expression Regulation, Neoplastic ; Male ; Treatment Outcome ; Kidney Neoplasms - metabolism ; Biomarkers, Tumor ; Kidney Neoplasms - diagnosis ; Immunohistochemistry - methods ; Carcinoma, Renal Cell - metabolism ; Neoplasm Metastasis ; Carcinoma, Renal Cell - diagnosis ; Female ; Aged ; Gene silencing ; Transcription factors ; Physiological aspects ; Genetic aspects ; Carcinoma, Renal cell ; Research ; Index Medicus
    ISSN: 1471-2407
    E-ISSN: 1471-2407
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: The Journal of pathology, 2015-12, Vol.237 (4), p.460-471
    Description: About 40% of clear‐cell renal cell carcinomas (ccRCC) harbour mutations in Polybromo‐1 (PBRM1), encoding the BAF180 subunit of a SWI/SNF chromatin remodelling complex. This qualifies PBRM1 as a major cancer gene in ccRCC. The PBRM1 protein alters chromatin structure and its known functions include transcriptional regulation by controlling the accessibility of DNA and influencing p53 transcriptional activity. Since little is known about the regulation of PBRM1, we studied possible mechanisms and interaction partners involved in the regulation of PBRM1 expression. Activation of p53 in RCC cells resulted in a marked decrease of PBRM1 protein levels. This effect was abolished by siRNA‐mediated down‐regulation of p53, and transcriptional activity was not crucial for p53‐dependent PBRM1 regulation. Pulse‐chase experiments determined post‐translational protein degradation to be the underlying mechanism for p53‐dependent PBRM1 regulation, which was accordingly inhibited by proteasome inhibitors. The effects of p53 activation on PBRM1 expression were confirmed in RCC tissue ex vivo. Our results demonstrate that PBRM1 is a target of p53‐induced proteasomal protein degradation and provide further evidence for the influence of PBRM1 on p53 function in RCC tumour cells. Considering the paramount role of p53 in carcinogenesis and the presumptive impact of PBRM1 in RCC development, this novel regulation mechanism might be therapeutically exploited in the future. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): kidney ; renal cell carcinoma ; PBRM1 ; TP53 ; protein degradation ; Immunohistochemistry ; Carcinoma, Renal Cell - pathology ; Tissue Array Analysis ; Humans ; Kaplan-Meier Estimate ; Proportional Hazards Models ; Tumor Suppressor Protein p53 - metabolism ; Immunoblotting ; Transcription Factors - biosynthesis ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - mortality ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - mortality ; Transfection ; Nuclear Proteins - biosynthesis ; Polymerase Chain Reaction ; Cell Line, Tumor ; Kidney Neoplasms - pathology ; RNA, Small Interfering ; Gene Expression Regulation, Neoplastic - physiology ; Tumor proteins ; Proteolysis ; Analysis ; Cancer
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
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  • 5
    Language: English
    In: Transplant international, 2012-05, Vol.25 (5), p.506-517
    Description: Summary Living donor kidney transplantation in crossmatch‐positive patients is a challenge that requires specific measures. Ten patients with positive crossmatch results (n = 9) or negative crossmatch results but strong donor‐specific antibodies (DSA; n = 1) were desensitized using immunoadsorption (IA) and anti‐CD20 antibody induction. IA was continued after transplantation and accompanied by HLA antibody monitoring and protocol biopsies. After a median of 10 IA treatments, all patients were desensitized successfully and transplanted. Median levels of mean fluorescence intensity (MFI) of Luminex‐DSA before desensitization were 6203 and decreased after desensitization and immediately before transplantation to 891. Patients received a median of seven post‐transplant IA treatments. At last visit, after a median follow‐up of 19 months, 9 of 10 patients had a functioning allograft and a median Luminex‐DSA of 149 MFI; serum creatinine was 1.6 mg/dl, and protein to creatinine ratio 0.1. Reversible acute antibody‐mediated rejection was diagnosed in three patients. One allograft was lost after the second post‐transplant year in a patient with catastrophic antiphospholipid syndrome. We describe a treatment algorithm for desensitization of living donor kidney transplant recipients that allows the rapid elimination of DSA with a low rate of side effects and results in good graft outcome.
    Subject(s): living donor ; positive crossmatch ; immunoadsorption ; antibody‐mediated rejection ; kidney transplantation ; Histocompatibility Testing ; Immunosuppression - methods ; Humans ; Middle Aged ; Blood Component Removal - methods ; Rituximab ; Graft Survival ; Male ; Treatment Outcome ; Living Donors ; Graft Rejection - diagnosis ; Kidney Transplantation - methods ; Immunosorbent Techniques ; Algorithms ; Adult ; Female ; Kidney Transplantation - immunology ; Antibodies, Monoclonal, Murine-Derived - therapeutic use ; Desensitization, Immunologic - methods ; Kidney Transplantation - adverse effects ; Viral antibodies ; Care and treatment ; Kidneys ; Organ transplant recipients ; Antibodies ; Fluorescence ; Transplantation of organs, tissues, etc ; Transplantation ; Donation of organs, tissues, etc ; Index Medicus
    ISSN: 0934-0874
    E-ISSN: 1432-2277
    Source: Wiley Online Library All Backfiles
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Human pathology, 2010, Vol.41 (2), p.293-296
    Description: Summary Invasive carcinomas arising within fibroepithelial tumors represent an uncommon manifestation of breast cancer. We report the case of a 70-year-old woman who underwent mastectomy for a malignant phyllodes tumor measuring 6 cm. Histological workup of the specimen revealed a high-grade invasive ductal carcinoma 2.5 cm in diameter within the phyllodes tumor. DNA was isolated from microdissected epithelial and stromal components of the phyllodes tumor as well as from the invasive ductal carcinoma cells. Using multiplex polymerase chain reaction, a comparative allelotyping was performed with a panel of 11 microsatellite markers. The malignant stroma of the phyllodes tumor showed loss of heterozygosity at chromosome 16q23, 17q12, 17q25, and 22q13; the epithelial tumor component shared the loss of 16q23; whereas the invasive carcinoma had lost divergent alleles at 16q23, 17q12, and 17q25, indicating a lack of clonality between phyllodes tumor and invasive ductal carcinoma. Although our data are compatible with a previously postulated common origin of epithelial and stromal components of phyllodes tumors, the coexisting invasive ductal carcinoma appears to represent a true collision tumor.
    Subject(s): Pathology ; Clonality ; Phyllodes tumor ; Breast cancer ; Loss of heterozygosity ; Gynecology. Andrology. Obstetrics ; Mammary gland diseases ; Investigative techniques, diagnostic techniques (general aspects) ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Biological and medical sciences ; Medical sciences ; Tumors ; Carcinoma, Ductal, Breast - genetics ; Immunohistochemistry ; Neoplasms, Multiple Primary - surgery ; Breast Neoplasms - surgery ; Carcinoma, Ductal, Breast - surgery ; Neoplasms, Multiple Primary - genetics ; Phyllodes Tumor - genetics ; Humans ; Neoplasms, Multiple Primary - pathology ; Loss of Heterozygosity - genetics ; Phyllodes Tumor - surgery ; Phyllodes Tumor - pathology ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Polymerase Chain Reaction ; Carcinoma, Ductal, Breast - pathology ; Female ; Aged ; Analysis ; Index Medicus
    ISSN: 0046-8177
    E-ISSN: 1532-8392
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: ProQuest Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: Modern pathology, 2012-02, Vol.25 (2), p.308-315
    Description: Renal cell carcinomas associated with Xp11.2 translocations have recently been identified as a distinct biological entity. The translocation results in the fusion of the transcription factor TFE3 to one of several different fusion partners including PRCC, PSF, NONO, ASPL or CTLC with consecutive overexpression of the chimeric protein. As the true frequency of these neoplasms as well as the biological properties of TFE3 activation in renal cell carcinomas are largely unknown, we have examined TFE3 expression as well as the underlying genetic alterations in a large, hospital-based series of renal cell carcinomas with long-term follow-up information. Out of a total of 876 tumours, TFE3 translocations were detected in five cases (0.6%). Three additional cases were identified in a second series of cases comprising of renal cell carcinomas developing in patients before the age of 50. However, using immunohistochemistry, 9% of all renal cell carcinomas showed some degree of TFE3 reactivity. Interestingly, these cases were associated with high nuclear grade, greater tumour extent and metastatic disease as well as an unfavourable patient outcome on uni- and multivariate analysis. Fluorescence in situ hybridisation (FISH) revealed TFE3 amplifications as an additional, novel mechanism leading to increased TFE3 expression levels. In conclusion, our data show that Xp11 translocation renal cell carcinomas are uncommon tumours accounting for 〈1% of adult renal cell carcinomas and that the diagnosis of Xp11 translocation renal cell carcinomas needs to be verified using molecular techniques. In turn, TFE3 overexpressing tumours show an aggressive behaviour and Xp11 translocation is only one of several possible underlying genomic alterations.
    Subject(s): Translocation, Genetic ; Kidney Neoplasms - genetics ; Prognosis ; Tissue Array Analysis ; Humans ; Middle Aged ; Carcinoma, Renal Cell - genetics ; Male ; Kidney Neoplasms - metabolism ; Young Adult ; Neoplasm Grading ; Aged, 80 and over ; Adult ; Female ; Carcinoma, Renal Cell - pathology ; Kaplan-Meier Estimate ; Proportional Hazards Models ; Reverse Transcriptase Polymerase Chain Reaction ; Carcinoma, Renal Cell - metabolism ; Adolescent ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism ; Kidney Neoplasms - pathology ; Aged ; Neoplasm Staging ; Index Medicus
    ISSN: 0893-3952
    E-ISSN: 1530-0285
    Source: Nature Open Access
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: The Journal of pathology, 2009-07, Vol.218 (3), p.370-379
    Description: β‐Catenin is a pivotal molecule of the Wnt‐signalling pathway, involved in regulation of developmental and oncogenic processes as well as in intercellular adhesion. So far, β‐catenin has been thought to be regulated mainly at the protein level. Here, we provide evidence for a transcriptional mechanism of β‐catenin regulation at the invasion front of colorectal liver metastases. In a nude mouse/LS174T cell xenograft model of colorectal liver metastases, we observed β‐catenin up‐regulation at the mRNA and protein levels and a 13.7‐fold increase of β‐catenin promoter activity in the cancer cells of the invasion front. In addition, the promoter activity was five‐fold higher in the interior of the tumour than in cells growing in cell culture. In vitro studies revealed binding of TCF‐4 to the β‐catenin promoter and reduced promoter activity by over‐expression of dominant negative TCF‐4, or β‐catenin knock‐down and increased activity by β‐catenin over‐expression, indicating that β‐catenin acts as co‐transcription factor of its own promoter. In 55% (7/13) of clinical specimens, β‐catenin mRNA was markedly elevated in the cancer cells of the invasion front. Elevation of mRNA was paralleled by increased nuclear and cytoplasmic β‐catenin protein concentrations. These data indicate that transcriptional regulation contributes to the dynamic changes of β‐catenin levels upon the confrontation of tumour cells with the host microenvironment. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): invasion front ; liver metastases ; β‐catenin promoter ; Gastroenterology. Liver. Pancreas. Abdomen ; Investigative techniques, diagnostic techniques (general aspects) ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Biological and medical sciences ; Medical sciences ; Tumors ; Neoplasm Transplantation ; Up-Regulation ; Adenocarcinoma - pathology ; Humans ; Transcriptional Activation ; Gene Expression Regulation, Neoplastic ; Transplantation, Heterologous ; Neoplasm Proteins - metabolism ; Adenocarcinoma - metabolism ; Female ; Liver Neoplasms - pathology ; Liver Neoplasms - secondary ; Neoplasm Proteins - genetics ; Disease Models, Animal ; Promoter Regions, Genetic ; Signal Transduction ; Neoplasm Invasiveness ; RNA, Messenger - genetics ; beta Catenin - metabolism ; Adenocarcinoma - secondary ; beta Catenin - genetics ; Animals ; Mice, Nude ; Liver Neoplasms - metabolism ; RNA, Neoplasm - genetics ; Mice ; Colorectal Neoplasms - pathology ; Index Medicus
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Scientific reports, 2016-02-19, Vol.6 (1), p.21344-21344
    Description: The peritoneum plays an essential role in preventing abdominal frictions and adhesions and can be utilized as a dialysis membrane. Its physiological ultrastructure, however, has not yet been studied systematically. 106 standardized peritoneal and 69 omental specimens were obtained from 107 patients (0.1-60 years) undergoing surgery for disease not affecting the peritoneum for automated quantitative histomorphometry and immunohistochemistry. The mesothelial cell layer morphology and protein expression pattern is similar across all age groups. Infants below one year have a thinner submesothelium; inflammation, profibrotic activity and mesothelial cell translocation is largely absent in all age groups. Peritoneal blood capillaries, lymphatics and nerve fibers locate in three distinct submesothelial layers. Blood vessel density and endothelial surface area follow a U-shaped curve with highest values in infants below one year and lowest values in children aged 7-12 years. Lymphatic vessel density is much lower, and again highest in infants. Omental blood capillary density correlates with parietal peritoneal findings, whereas only few lymphatic vessels are present. The healthy peritoneum exhibits major thus far unknown particularities, pertaining to functionally relevant structures, and subject to substantial changes with age. The reference ranges established here provide a framework for future histomorphometric analyses and peritoneal transport modeling approaches.
    Subject(s): Epithelium - blood supply ; Lymphatic Vessels - cytology ; Membrane Glycoproteins - metabolism ; Humans ; Middle Aged ; Child, Preschool ; Infant ; Male ; Young Adult ; Peritoneum - cytology ; Adolescent ; Adult ; Female ; Child ; Peritoneum - metabolism ; Peritoneum - blood supply ; Immunohistochemistry ; Lymphatic system ; Ultrastructure ; Surgery ; Cytology ; Infants ; Children ; Histomorphometry ; Capillaries ; Age ; Peritoneum ; Index Medicus
    ISSN: 2045-2322
    E-ISSN: 2045-2322
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Modern pathology, 2010-03, Vol.23 (3), p.480-492
    Description: In many human cancers, lipogenic pathways are activated; in some tumors, such as hepatocellular carcinoma, this is reflected by the presence of visible lipid droplets. Yet, the biology of steatogenesis in malignant tumors is largely unknown. We have recently shown that lipid droplet-associated proteins of the PAT-family, named after their constituents perilipin (perilipin 1), adipophilin (perilipin 2), and TIP47 (perilipin 3) are differentially expressed in hepatic steatogenesis. We have comprehensively investigated PAT-expression in neoplastic steatogenesis as well as in respective normal tissues with immunohistology and electron microscopy as well as protein biochemical and molecular biological methods. By staining for PAT-proteins, we found lipid droplet accumulation to be a frequent phenomenon of carcinoma cells. Although adipophilin and TIP47 stained almost ubiquitously the rim of lipid droplets in various tumor types, especially those with clear cell phenotype, perilipin was restricted to lipid droplets of hepatocellular adenoma and carcinoma, sebaceous adenoma and carcinoma, and lipomatous tumors. In hepatocellular carcinoma, perilipin, adipophilin, and TIP47 were coexpressed, and showed regional heterogeneity with a predominantly mutually exclusive localization pattern. In step-wise carcinogenesis, adipophilin expression correlated with the proliferation rate and was upregulated during early tumorigenesis, whereas perilipin was often lost during hepatocarcinogenesis. In conclusion, expression analysis of PAT-proteins showed that by far more carcinomas contain (PAT-positive) lipid droplets than expected by conventional light microscopy. PAT-proteins, such as perilipin, are differentially expressed in different tumor types and thus may support diagnostic considerations. Because inhibition of lipogenesis has been shown to exert antineoplastic effects, PAT-proteins may represent targets for interventive strategies.
    Subject(s): Neoplasms - metabolism ; Cell Proliferation ; Fatty Liver - pathology ; Tissue Array Analysis ; Humans ; Middle Aged ; Male ; Intracellular Signaling Peptides and Proteins - metabolism ; Pregnancy Proteins - metabolism ; Phosphoproteins - metabolism ; DNA-Binding Proteins - metabolism ; Adipose Tissue - metabolism ; Biomarkers, Tumor - metabolism ; Adult ; Female ; Liver Neoplasms - pathology ; Membrane Proteins - metabolism ; Carrier Proteins ; Vesicular Transport Proteins ; Fatty Liver - metabolism ; Adipose Tissue - pathology ; Lipid Metabolism ; Carcinoma, Hepatocellular - pathology ; Liver Neoplasms - metabolism ; Neoplasms - pathology ; Perilipin-3 ; Perilipin-2 ; Carcinoma, Hepatocellular - metabolism ; Perilipin-1
    ISSN: 0893-3952
    E-ISSN: 1530-0285
    Source: Nature Open Access
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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