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[PMID]: 26732302
[Au] Autor:Schneider N; Fisher C; Thway K
[Ad] Address:Sarcoma Unit, Royal Marsden Hospital, London, United Kingdom.
[Ti] Title:Ossifying fibromyxoid tumor: morphology, genetics, and differential diagnosis.
[So] Source:Ann Diagn Pathol;20:52-8, 2016 Feb.
[Is] ISSN:1532-8198
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ossifying fibromyxoid tumor (OFMT) is a soft tissue neoplasm of uncertain differentiation and intermediate (rarely metastasizing) biologic potential, with typical morphologic features, of an encapsulated, lobulated tumor comprising uniform polygonal cells within fibromyxoid stroma, which is surrounded by or contains metaplastic bone, classically as a peripheral rim of lamellar bone. Ossifying fibromyxoid tumor can arise at almost any site, although most frequently occurs within the extremities and trunk. Although most behave in a benign fashion, tumors can rarely show atypical or malignant features. It is now established that OFMTs represent translocation-associated tumors, with up to 85% associated with recurrent gene rearrangements, mostly involving the PHF1 gene (including in typical, atypical, and malignant neoplasms), with EP400-PHF1 in approximately 40% of tumors, and ZC3H7B-BCOR, MEAF6-PHF1, and EPC1-PHF1 fusions also described. Correct diagnosis is clinically important to ensure correct treatment and prognostication, both to avoid overdiagnosing OFMT as a malignant neoplasm such as osteosarcoma and also because of the propensity for aggressive behavior in a small number of OFMT. We review OFMT, with emphasis on the morphologic spectrum, recent molecular genetic findings, and the differential diagnosis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 2037601 MEDLINE  
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[PMID]: 26626208
[Au] Autor:Ud Din N; Ahmad Z; Ahmed A
[Ad] Address:Department of Pathology and Laboratory Medicine, Aga Khan University Hospital, Karachi Pakistan. Electronic address: nasir.uddin@aku.edu.
[Ti] Title:Schwannomas with pseudoglandular elements: clinicopathologic study of 61 cases.
[So] Source:Ann Diagn Pathol;20:24-8, 2016 Feb.
[Is] ISSN:1532-8198
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Schwannomas are benign neoplasms of peripheral nerve sheath. A number of morphologic variants of schwannoma have been described. The pseudoglandular variant is very rare. We retrieved and reviewed hematoxylin and eosin slides of all cases of schwannoma reported between 2007 and 2014 to look for pseudoglandular elements. Pseudoglandular cystic spaces were seen in 61 (6.3%) of 971 schwannomas diagnosed during the study period. Of these 61 cases, 56 (91.8%) were located in the spinal nerve roots. The majority (60.6%) were male. Mean age in these 61 cases was 41 years. Mean tumor size was 3.5 cm. All 61 cases showed typical Antoni A and Antoni B areas with multiple pseudoglandular cystic spaces scattered throughout. These areas were lined by flat to cuboidal cells which showed positivity for immunohistochemical stain S-100 and were negative for epithelial membrane antigen. An average of 7 pseudoglandular cystic spaces was noted per case. In conclusion, pseudoglandular cystic spaces are lined by Schwann cells and most likely represent degenerative changes in schwannoma probably degenerated Verocay bodies. They are rare albeit well-defined features seen in a significant though small number of schwannomas. It is important not to mistake them for other neoplasms. Larger studies are required to determine predilection of these changes in spinal nerve root schwannomas as seen in our series.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  3 / 2037601 MEDLINE  
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[PMID]: 26616722
[Au] Autor:Yigit N; Çelik E; Yavan I; Günal A; Kurt B; Karslioglu Y; Öngürü Ö; Özcan A
[Ad] Address:Department of Pathology, Gülhane Military Medical Academy and School of Medicine, Ankara, Turkey. Electronic address: nyigit@gata.edu.tr....
[Ti] Title:Distinctive immunostaining of claudin-4 in spiradenomas.
[So] Source:Ann Diagn Pathol;20:44-7, 2016 Feb.
[Is] ISSN:1532-8198
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The intercellular bridges are essential structures in maintaining the histologic organization of the epithelium, while providing a very efficient way to exchange molecules between cells and transduction of the cell-to-cell and matrix-to-cell signals. Derangement in those important structures' physical integrity and/or function, which can be assessed by the presence or absence of several intercellular bridge proteins including claudin-4, E-cadherin, and ß-catenin, was found to be related to several phenomena in the path to the neoplastic transformation. However, these proteins have not been studied in the wide variety of the skin neoplasms, in detail. Herein, we immunohistochemically assessed the expression patterns of these 3 intercellular bridge proteins on a total of 86 epidermal and eccrine adnexal tumors including basal cell carcinoma, squamous cell carcinoma, poroma, spiradenoma, syringoma, and hidradenoma. We observed a selective and distinct claudin-4 expression in the ductal-type cells of all cases of spiradenomas. Similarly, in the poromas, syringomas, and hidradenomas, claudin-4 was only positive in the luminal cells of microcystic structures, although not as conspicuous as in the spiradenomas. On the other hand, E-cadherin and ß-catenin were positive in almost all types of the tumors, in a way which was not contributory to differentiate from each other. In conclusion, we think that claudin-4 can be helpful at least in making a reliable differential diagnosis of spiradenoma when overlapping morphologic features do not allow to further subclassification in the overwhelming variety of the adnexal tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 2037601 MEDLINE  
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[PMID]: 26450632
[Au] Autor:Kamada M; Koshikawa N; Minegishi T; Kawada C; Karashima T; Shuin T; Seiki M
[Ad] Address:Department of Urology, Kochi Medical School, Kochi, Japan....
[Ti] Title:Urinary laminin-γ2 is a novel biomarker of non-muscle invasive urothelial carcinoma.
[So] Source:Cancer Sci;106(12):1730-7, 2015 Dec.
[Is] ISSN:1349-7006
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Lack of appropriate biomarkers has hampered early detection of urothelial cancer (UC), therefore, development of biomarkers for its diagnosis at earlier stages is of importance. Laminin-332 (Ln-332, formerly Ln-5), a component of basement membranes, consists of Ln-α3, Ln-ß3, and Ln-γ2 polypeptides. However, monomeric Ln-γ2 alone is frequently expressed in malignant neoplasms. If Ln-γ2 is also expressed in UC and secreted into the urine, its detection could be useful for UC diagnosis. Here, we evaluated Ln-γ2 levels from 60 patients with urinary diseases (including UC) by Western blotting, and detected it in approximately 53% of UC cases. Using immunohistochemistry, we confirmed Ln-γ2 expression in UC tissues that were positive for Ln-γ2, whereas Ln-α3 expression was absent. We next developed a sandwich enzyme-linked immunosorbent assay and applied it for screening 39 patients with non-muscle invasive UC and 61 patients with benign urologic diseases. The Ln-γ2 levels were higher in UC patients than in those with benign urologic diseases. Ln-γ2 was detected even in patients with earlier stages of UC, such as Ta, T1, or carcinoma in situ. The sensitivity of Ln-γ2 testing for UC was 97.4%, and the specificity was 45.9%, using a cut-off of 0.5 µg/g∙crn. Ln-γ2 had greater diagnostic value for detecting non-muscle invasive UC compared to conventional urine cytology and available biomarkers for UC, and may be useful as a urine biomarker for the diagnosis and monitoring of UC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/cas.12832

  5 / 2037601 MEDLINE  
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[PMID]: 26541605
[Au] Autor:Yun J; Mullarky E; Lu C; Bosch KN; Kavalier A; Rivera K; Roper J; Chio II; Giannopoulou EG; Rago C; Muley A; Asara JM; Paik J; Elemento O; Chen Z; Pappin DJ; Dow LE; Papadopoulos N; Gross SS; Cantley LC
[Ad] Address:Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA....
[Ti] Title:Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH.
[So] Source:Science;350(6266):1391-6, 2015 Dec 11.
[Is] ISSN:1095-9203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:More than half of human colorectal cancers (CRCs) carry either KRAS or BRAF mutations and are often refractory to approved targeted therapies. We found that cultured human CRC cells harboring KRAS or BRAF mutations are selectively killed when exposed to high levels of vitamin C. This effect is due to increased uptake of the oxidized form of vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter. Increased DHA uptake causes oxidative stress as intracellular DHA is reduced to vitamin C, depleting glutathione. Thus, reactive oxygen species accumulate and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Inhibition of GAPDH in highly glycolytic KRAS or BRAF mutant cells leads to an energetic crisis and cell death not seen in KRAS and BRAF wild-type cells. High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice. These results provide a mechanistic rationale for exploring the therapeutic use of vitamin C for CRCs with KRAS or BRAF mutations.
[Mh] MeSH terms primary: Ascorbic Acid/therapeutic use
Colorectal Neoplasms/drug therapy
Colorectal Neoplasms/genetics
Proto-Oncogene Proteins B-raf/genetics
Proto-Oncogene Proteins/genetics
ras Proteins/genetics
[Mh] MeSH terms secundary: Adenomatous Polyposis Coli Protein/genetics
Animals
Ascorbic Acid/administration & dosage
Ascorbic Acid/pharmacology
Cell Line, Tumor
Dehydroascorbic Acid/metabolism
Female
Glucose Transporter Type 1/metabolism
Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism
Glycolysis/drug effects
Humans
Mice
Mice, Mutant Strains
Mice, Nude
Proto-Oncogene Proteins p21(ras)/genetics
Reactive Oxygen Species/metabolism
Xenograft Model Antitumor Assays
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (APC protein, human); 0 (Adenomatous Polyposis Coli Protein); 0 (Glucose Transporter Type 1); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); 0 (Reactive Oxygen Species); 0 (SLC2A1 protein, human); EC 1.2.1.12 (Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins); PQ6CK8PD0R (Ascorbic Acid); Y2Z3ZTP9UM (Dehydroascorbic Acid)
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:151215
[St] Status:MEDLINE
[do] DOI:10.1126/science.aaa5004

  6 / 2037601 MEDLINE  
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[PMID]: 26365305
[Au] Autor:Schinasi LH; De Roos AJ; Ray RM; Edlefsen KL; Parks CG; Howard BV; Meliker JR; Bonner MR; Wallace RB; LaCroix AZ
[Ad] Address:Department of Environmental and Occupational Health, School of Public Health, Drexel University, Philadelphia, PA. Electronic address: lhs36@drexel.edu....
[Ti] Title:Insecticide exposure and farm history in relation to risk of lymphomas and leukemias in the Women's Health Initiative observational study cohort.
[So] Source:Ann Epidemiol;25(11):803-10, 2015 Nov.
[Is] ISSN:1873-2585
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Relationships of farm history and insecticide exposure at home or work with lymphohematopoietic (LH) neoplasm risk were investigated in a large prospective cohort of US women. METHODS: In questionnaires, women self-reported history living or working on a farm, personally mixing or applying insecticides, insecticide application in the home or workplace by a commercial service, and treating pets with insecticides. Relationships with non-Hodgkin lymphoma (NHL), chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, plasma cell neoplasms, and myeloid leukemia were investigated using Cox proportional hazard models. Age and farming history were explored as effect modifiers. RESULTS: The analysis included 76,493 women and 822 NHL cases. Women who ever lived or worked on a farm had 1.12 times the risk of NHL (95% confidence interval [CI] = 0.95-1.32) compared to those who did not. Women who reported that a commercial service ever applied insecticides in their immediate surroundings had 65% higher risk of CLL/SLL (95% CI = 1.15-2.38). Women aged less than 65 years who ever applied insecticides had 87% higher risk of DLBCL (95% CI = 1.13-3.09). CONCLUSIONS: Insecticide exposures may contribute to risk of CLL/SLL and DLBCL. Future studies should examine relationships of LH subtypes with specific types of household insecticides.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Em] Entry month:1510
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Process

  7 / 2037601 MEDLINE  
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[PMID]: 25616580
[Au] Autor:Bele A; Mirza S; Zhang Y; Ahmad Mir R; Lin S; Kim JH; Gurumurthy CB; West W; Qiu F; Band H; Band V
[Ad] Address:a Departments of Genetics ; Cell Biology and Anatomy ; Nebraska Medical Center , Omaha , NE USA.
[Ti] Title:The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells.
[So] Source:Cell Cycle;14(7):990-1000, 2015.
[Is] ISSN:1551-4005
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The mammalian ortholog of Drosophila ecdysoneless (Ecd) gene product regulates Rb-E2F interaction and is required for cell cycle progression. Ecd is overexpressed in breast cancer and its overexpression predicts shorter survival in patients with ErbB2-positive tumors. Here, we demonstrate Ecd knock down (KD) in human mammary epithelial cells (hMECs) induces growth arrest, similar to the impact of Ecd Knock out (KO) in mouse embryonic fibroblasts. Furthermore, whole-genome mRNA expression analysis of control vs. Ecd KD in hMECs demonstrated that several of the top 40 genes that were down-regulated were E2F target genes. To address the role of Ecd in mammary oncogenesis, we overexpressed Ecd and/or mutant H-Ras in hTERT-immortalized hMECs. Cell cycle analyses revealed hMECs overexpressing Ecd+Ras showed incomplete arrest in G1 phase upon growth factor deprivation, and more rapid cell cycle progression in growth factor-containing medium. Analyses of cell migration, invasion, acinar structures in 3-D Matrigel and anchorage-independent growth demonstrated that Ecd+Ras-overexpressing cells exhibit substantially more dramatic transformed phenotype as compared to cells expressing vector, Ras or Ecd. Under conditions of nutrient deprivation, Ecd+Ras-overexpressing hMECs exhibited better survival, with substantial upregulation of the autophagy marker LC3 both at the mRNA and protein levels. Significantly, while hMECs expressing Ecd or mutant Ras alone did not form tumors in NOD/SCID mice, Ecd+Ras-overexpressing hMECs formed tumors, clearly demonstrating oncogenic cooperation between Ecd and mutant Ras. Collectively, we demonstrate an important co-oncogenic role of Ecd in the progression of mammary oncogenesis through promoting cell survival.
[Mh] MeSH terms primary: Breast Neoplasms/metabolism
Carrier Proteins/physiology
Mammary Glands, Human/pathology
Proto-Oncogene Proteins p21(ras)/physiology
[Mh] MeSH terms secundary: Animals
Autophagy
Breast Neoplasms/pathology
Cell Movement
Cell Proliferation
Cell Transformation, Neoplastic
Cells, Cultured
Female
Humans
Mice, Inbred NOD
Mice, SCID
Microtubule-Associated Proteins/metabolism
Neoplasm Transplantation
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Carrier Proteins); 0 (ECD protein, human); 0 (Microtubule-Associated Proteins); 0 (light chain 3, human); EC 3.6.5.2 (HRAS protein, human); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:150402
[St] Status:MEDLINE
[do] DOI:10.1080/15384101.2015.1006982

  8 / 2037601 MEDLINE  
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[PMID]: 25802834
[Au] Autor:Reams RR; Jones-Triche J; Chan OT; Hernandez BY; Soliman KF; Yates C
[Ad] Address:College of Pharmacy & Pharmaceutical Sciences, Florida A&M University, Tallahassee, FL 32307, USA....
[Ti] Title:Immunohistological analysis of ABCD3 expression in Caucasian and African American prostate tumors.
[So] Source:Biomed Res Int;2015:132981, 2015.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In a previously published study, we showed that expression of the ABCD3 gene increased with increasing metastatic potential in a panel of prostate cancer cell lines derived from African American and Caucasian American men. Given importance of identifying biomarker(s) that can distinguish indolent versus aggressive prostate tumors, we conducted an immunohistochemical analysis of ABCD3 expression Caucasian and African American prostate tumors. ABCD3 expression in each patient population was compared with clinicopathologic characteristics, Gleason score, and age. ABCD3 expression increased with increasing Gleason score (P = 0.0094), age (P = 0.0014), and pathology grade (P = 0.0007) in Caucasian patients. Interestingly, in the AA patients, ABCD3 expression highly increased to the same degree in both low and high Gleason score tumors. Similarly, ABCD3 expression was elevated to the same degree in BPH derived from AA. Our findings demonstrate that increased ABCD3 expression correlates with Gleason Score in CA prostate tumors. However, in AA prostate tumors, ABCD3 expression was higher and was sustained in both low Gleason and high Gleason AA tumors. While the functional role of ABCD3 in prostate cancer is not completely elucidated, this gene warrants further study as a potential biomarker for aggressive prostate.
[Mh] MeSH terms primary: ATP-Binding Cassette Transporters/metabolism
Prostate/metabolism
Prostate/pathology
Prostatic Neoplasms/metabolism
Prostatic Neoplasms/pathology
[Mh] MeSH terms secundary: African Continental Ancestry Group
Aged
Case-Control Studies
European Continental Ancestry Group
Humans
Male
Neoplasm Grading
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (ABCD3 protein, human)
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:150324
[St] Status:MEDLINE
[do] DOI:10.1155/2015/132981

  9 / 2037601 MEDLINE  
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[PMID]: 25738355
[Au] Autor:Armaiz-Pena GN; Gonzalez-Villasana V; Nagaraja AS; Rodriguez-Aguayo C; Sadaoui NC; Stone RL; Matsuo K; Dalton HJ; Previs RA; Jennings NB; Dorniak P; Hansen JM; Arevalo JM; Cole SW; Lutgendorf SK; Sood AK; Lopez-Berestein G
[Ad] Address:Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA....
[Ti] Title:Adrenergic regulation of monocyte chemotactic protein 1 leads to enhanced macrophage recruitment and ovarian carcinoma growth.
[So] Source:Oncotarget;6(6):4266-73, 2015 Feb 28.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increased adrenergic signaling facilitates tumor progression, but the underlying mechanisms remain poorly understood. We examined factors responsible for stress-mediated effects on monocyte/macrophage recruitment into the tumor microenvironment, and the resultant effects on tumor growth. In vitro, MCP1 was significantly increased after catecholamine exposure, which was mediated by cAMP and PKA. Tumor samples from mice subjected to daily restraint stress had elevated MCP1 gene and protein levels, increased CD14+ cells, and increased infiltration of CD68+ cells. hMCP1 siRNA-DOPC nanoparticles significantly abrogated daily restraint stress-induced tumor growth and inhibited infiltration of CD68+ and F4/80+ cells. In ovarian cancer patients, elevated peripheral blood monocytes and tumoral macrophages were associated with worse overall survival. Collectively, we demonstrate that increased adrenergic signaling is associated with macrophage infiltration and mediated by tumor cell-derived MCP1 production.
[Mh] MeSH terms primary: Carcinoma/pathology
Chemokine CCL2/metabolism
Macrophages/metabolism
Ovarian Neoplasms/pathology
Stress, Psychological/metabolism
[Mh] MeSH terms secundary: Animals
Carcinoma/metabolism
Carcinoma/mortality
Chemotaxis, Leukocyte/physiology
Enzyme-Linked Immunosorbent Assay
Epinephrine/metabolism
Female
Humans
Kaplan-Meier Estimate
Mice
Mice, Nude
Norepinephrine/metabolism
Ovarian Neoplasms/metabolism
Ovarian Neoplasms/mortality
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (CCL2 protein, human); 0 (Chemokine CCL2); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:150318
[St] Status:MEDLINE

  10 / 2037601 MEDLINE  
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[PMID]: 25738607
[Au] Autor:Li J; Chanrion M; Sawey E; Wang T; Chow E; Tward A; Su Y; Xue W; Lucito R; Zender L; Lowe SW; Bishop JM; Powers S
[Ad] Address:Cancer Genome Center, Cold Spring Harbor Laboratory, Woodbury, NY 11740, United States of America....
[Ti] Title:Reciprocal interaction of Wnt and RXR-α pathways in hepatocyte development and hepatocellular carcinoma.
[So] Source:PLoS One;10(3):e0118480, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Genomic analysis of human hepatocellular carcinoma (HCC) is potentially confounded by the differentiation state of the hepatic cell-of-origin. Here we integrated genomic analysis of mouse HCC (with defined cell-of-origin) along with normal development. We found a major shift in expression of Wnt and RXR-α pathway genes (up and down, respectively) coincident with the transition from hepatoblasts to hepatocytes. A combined Wnt and RXR-α gene signature categorized HCCs into two subtypes (high Wnt, low RXR-α and low Wnt, high RXR-α), which matched cell-of-origin in mouse models and the differentiation state of human HCC. Suppression of RXR-α levels in hepatocytes increased Wnt signaling and enhanced tumorigenicity, whereas ligand activation of RXR-α achieved the opposite. These results corroborate that there are two main HCC subtypes that correspond to the degree of hepatocyte differentation and that RXR-α, in part via Wnt signaling, plays a key functional role in the hepatocyte-like subtype and potentially could serve as a selective therapeutic target.
[Mh] MeSH terms primary: Carcinogenesis
Carcinoma, Hepatocellular/pathology
Hepatocytes/pathology
Liver Neoplasms/pathology
Retinoid X Receptor alpha/metabolism
Wnt Proteins/metabolism
Wnt Signaling Pathway
[Mh] MeSH terms secundary: Animals
Carcinoma, Hepatocellular/genetics
Carcinoma, Hepatocellular/metabolism
Cell Differentiation
Cell Line, Tumor
Female
Genomics
Humans
Liver Neoplasms/genetics
Liver Neoplasms/metabolism
Mice
Protein Binding
Retinoid X Receptor alpha/genetics
Wnt Proteins/genetics
beta Catenin/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Retinoid X Receptor alpha); 0 (Wnt Proteins); 0 (beta Catenin)
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[Da] Date of entry for processing:150305
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0118480


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