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[PMID]: 29488037
[Au] Autor:Li WJ; Xu C; Wang K; Li TY; Wang XN; Yang H; Xing T; Li WX; Chen YH; Gao H; Ding L
[Ad] Address:The Cancer Center of Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
[Ti] Title:Severe Intestinal Inflammation in the Small Intestine of Mice Induced by Controllable Deletion of Claudin-7.
[So] Source:Dig Dis Sci;, 2018 Feb 27.
[Is] ISSN:1573-2568
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: As a potential tumor suppressor gene, Claudin-7 (Cldn7), which is a component of tight junctions, may play an important role in colorectal cancer occurrence and development. AIMS: To generate a knockout mouse model of inducible conditional Cldn7 in the intestine and analyze the phenotype of the mice after induction with tamoxifen. METHODS: We constructed Cldn7-flox transgenic mice and crossed them with Villin-CreERT2 mice. The Cldn7 inducible conditional knockout mice appeared normal and were well developed at birth. We induced Cldn7 gene deletion by injecting different dosages of tamoxifen into the mice and then conducted a further phenotypic analysis. RESULTS: After induction for 5 days in succession at a dose of 200 µl tamoxifen in sunflower oil at 10 mg/ml per mouse every time, the mice appeared dehydrated, had a lower temperature, and displayed inactivity or death. The results of hematoxylin-eosin staining showed that the intestines of the Cldn7 inducible conditional knockout mice had severe intestinal defects that included epithelial cell sloughing, necrosis, inflammation and hyperplasia. Owing to the death of ICKO mice, we adjusted the dose of tamoxifen to a dose of 100 µl in sunflower oil at 10 mg/ml per mouse (aged more than 8 weeks old) every 4 days. And we could induce atypical hyperplasia and adenoma in the intestine. Immunofluorescent staining indicated that the intestinal epithelial structure was destroyed. Electron microscopy experimental analysis indicated that the intercellular gap along the basolateral membrane of Cldn7 inducible conditional knockout mice in the intestine was increased and that contact between the cells and matrix was loosened. CONCLUSIONS: We generated a model of intestinal Cldn7 inducible conditional knockout mice. Intestinal Cldn7 deletion induced by tamoxifen initiated inflammation and hyperplasia in mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1007/s10620-018-4973-z

  2 / 25372 MEDLINE  
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[PMID]: 29471062
[Au] Autor:Karaca A; Malladi VR; Zhu Y; Tafaj O; Paltrinieri E; Wu JY; He Q; Bastepe M
[Ad] Address:Endocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Title:Constitutive stimulatory G protein activity in limb mesenchyme impairs bone growth.
[So] Source:Bone;110:230-237, 2018 Feb 20.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:GNAS mutations leading to constitutively active stimulatory G protein alpha-subunit (Gsα) cause different tumors, fibrous dysplasia of bone, and McCune-Albright syndrome, which are typically not associated with short stature. Enhanced signaling of the parathyroid hormone/parathyroid hormone-related peptide receptor, which couples to multiple G proteins including Gsα, leads to short bones with delayed endochondral ossification. It has remained unknown whether constitutive Gsα activity also impairs bone growth. Here we generated mice expressing a constitutively active Gsα mutant (Gsα-R201H) conditionally upon Cre recombinase (cGsα mice). Gsα-R201H was expressed in cultured bone marrow stromal cells from cGsα mice upon adenoviral-Cre transduction. When crossed with mice in which Cre is expressed in a tamoxifen-regulatable fashion (CAGGCre-ER™), tamoxifen injection resulted in mosaic expression of the transgene in double mutant offspring. We then crossed the cGsα mice with Prx1-Cre mice, in which Cre is expressed in early limb-bud mesenchyme. The double mutant offspring displayed short limbs at birth, with narrow hypertrophic chondrocyte zones in growth plates and delayed formation of secondary ossification center. Consistent with enhanced Gsα signaling, bone marrow stromal cells from these mice demonstrated increased levels of c-fos mRNA. Our findings indicate that constitutive Gsα activity during limb development disrupts endochondral ossification and bone growth. Given that Gsα haploinsufficiency also leads to short bones, as in patients with Albright's hereditary osteodystrophy, these results suggest that a tight control of Gsα activity is essential for normal growth plate physiology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  3 / 25372 MEDLINE  
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[PMID]: 29248442
[Au] Autor:Radyk MD; Burclaff J; Willet SG; Mills JC
[Ad] Address:Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St Louis, Missouri.
[Ti] Title:Metaplastic Cells in the Stomach Arise, Independently of Stem Cells, via Dedifferentiation or Transdifferentiation of Chief Cells.
[So] Source:Gastroenterology;, 2017 Dec 14.
[Is] ISSN:1528-0012
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Spasmolytic polypeptide-expressing metaplasia (SPEM) develops in patients with chronic atrophic gastritis due to infection with Helicobacter pylori; it might be a precursor to intestinal metaplasia and gastric adenocarcinoma. Lineage tracing experiments of the gastric corpus in mice have not established whether SPEM derives from proliferating stem cells or differentiated, post-mitotic zymogenic chief cells in the gland base. We investigated whether differentiated cells can give rise to SPEM using a nongenetic approach in mice. Mice were given intraperitoneal injections of 5-fluorouracil, which blocked gastric cell proliferation, plus tamoxifen to induce SPEM. Based on analyses of molecular and histologic markers, we found SPEM developed even in the absence of cell proliferation. SPEM therefore did not arise from stem cells. In histologic analyses of gastric resection specimens from 10 patients with adenocarcinoma, we found normal zymogenic chief cells that were transitioning into SPEM cells only in gland bases, rather than the proliferative stem cell zone. Our findings indicate that SPEM can arise by direct reprogramming of existing cells-mainly of chief cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  4 / 25372 MEDLINE  
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[PMID]: 29248441
[Au] Autor:He P; Yang JW; Yang VW; Bialkowska AB
[Ad] Address:Department of Medicine, Stony Brook University School of Medicine, Stony Brook, New York.
[Ti] Title:Krüppel-like Factor 5, Increased in Pancreatic Ductal Adenocarcinoma, Promotes Proliferation, Acinar-to-Ductal Metaplasia, Pancreatic Intraepithelial Neoplasia, and Tumor Growth in Mice.
[So] Source:Gastroenterology;, 2017 Dec 15.
[Is] ISSN:1528-0012
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: Activating mutations in KRAS (Kirsten rat sarcoma viral oncogene homolog) are detected in most pancreatic ductal adenocarcinomas (PDACs). Expression of an activated form of KRAS (KrasG12D) in pancreata of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precursor of PDAC. Pancreatitis increases formation of PanINs in mice that express KrasG12D by promoting acinar-to-ductal metaplasia (ADM). We investigated the role of the transcription factor Krüppel-like factor 5 (KLF5) in ADM and KRAS-mediated formation of PanINs. METHODS: We performed studies in adult mice with conditional disruption of Klf5 (Klf5 ) and/or expression of Kras (LSL-Kras ) via Cre recombinase regulated by an acinar cell-specific promoter (Ptf1a). Activation of KrasG12D and loss of KLF5 was achieved by administration of tamoxifen. Pancreatitis was induced in mice by administration of cerulein; pancreatic tissues were collected, analyzed by histology and immunohistochemistry, and transcriptomes were compared between mice that did or did not express KLF5. We performed immunohistochemical analyses of human tissue microarrays, comparing levels of KLF5 among 96 human samples of PDAC. UN-KC-6141 cells (pancreatic cancer cells derived from Pdx1-Cre;LSL-Kras mice) were incubated with inhibitors of different kinases and analyzed in proliferation assays and by immunoblots. Expression of KLF5 was knocked down with small hairpin RNAs or CRISPR/Cas9 strategies; cells were analyzed in proliferation and gene expression assays, and compared with cells expressing control vectors. Cells were subcutaneously injected into flanks of syngeneic mice and tumor growth was assessed. RESULTS: Of the 96 PDAC samples analyzed, 73% were positive for KLF5 (defined as nuclear staining in more than 5% of tumor cells). Pancreata from Ptf1a-Cre ;LSL-Kras mice contained ADM and PanIN lesions, which contained high levels of nuclear KLF5 within these structures. In contrast, Ptf1a-Cre ;LSL-Kras ;Klf5 mice formed fewer PanINs. After cerulein administration, Ptf1a-Cre ;LSL-Kras mice formed more extensive ADM than Ptf1a-Cre ;LSL-Kras ;Klf5 mice. Pancreata from Ptf1a-Cre ;LSL-Kras ;Klf5 mice had increased expression of the tumor suppressor NDRG2 and reduced phosphorylation (activation) of STAT3, compared with Ptf1a-Cre ;LSL-Kras mice. In UN-KC-6141 cells, PI3K and MEK signaling increased expression of KLF5; a high level of KLF5 increased proliferation. Cells with knockdown of Klf5 had reduced proliferation, compared with control cells, had reduced expression of ductal markers, and formed smaller tumors (71.61 ± 30.79 mm vs 121.44 ± 34.90 mm from control cells) in flanks of mice. CONCLUSION: Levels of KLF5 are increased in human PDAC samples and in PanINs of Ptf1a-Cre ;LSL-Kras mice, compared with controls. KLF5 disruption increases expression of NDRG2 and reduces activation of STAT3 and reduces ADM and PanINs formation in mice. Strategies to reduce KLF5 activity might reduce progression of acinar cells from ADM to PanIN and pancreatic tumorigenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 25372 MEDLINE  
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[PMID]: 29230665
[Au] Autor:Blok EJ; Kroep JR; Meershoek-Klein Kranenbarg E; Duijm-de Carpentier M; Putter H; Liefers GJ; Nortier JWR; Rutgers EJT; Seynaeve CM; van de Velde CJH; IDEAL Study Group
[Ad] Address:Department of Surgery, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
[Ti] Title:Relevant factors for the optimal duration of extended endocrine therapy in early breast cancer.
[So] Source:Breast Cancer Res Treat;168(2):413-420, 2018 Apr.
[Is] ISSN:1573-7217
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:PURPOSE: For postmenopausal patients with hormone receptor-positive early breast cancer, the optimal subgroup and duration of extended endocrine therapy is not clear yet. The aim of this study using the IDEAL patient cohort was to identify a subgroup for which longer (5 years) extended therapy is beneficial over shorter (2.5 years) extended endocrine therapy. METHODS: In the IDEAL trial, 1824 patients who completed 5 years of adjuvant endocrine therapy (either 5 years of tamoxifen (12%), 5 years of an AI (29%), or a sequential strategy of both (59%)) were randomized between either 2.5 or 5 years of extended letrozole. For each prior therapy subgroup, the value of longer therapy was assessed for both node-negative and node-positive patients using Kaplan Meier and Cox regression survival analyses. RESULTS: In node-positive patients, there was a significant benefit of 5 years (over 2.5 years) of extended therapy (disease-free survival (DFS) HR 0.67, p = 0.03, 95% CI 0.47-0.96). This effect was only observed in patients who were treated initially with a sequential scheme (DFS HR 0.60, p = 0.03, 95% CI 0.38-0.95). In all other subgroups, there was no significant benefit of longer extended therapy. Similar results were found in patients who were randomized for their initial adjuvant therapy in the TEAM trial (DFS HR 0.37, p = 0.07, 95% CI 0.13-1.06), although this additional analysis was underpowered for definite conclusions. CONCLUSIONS: This study suggests that node-positive patients could benefit from longer extended endocrine therapy, although this effect appears isolated to patients treated with sequential endocrine therapy during the first 5 years and needs validation and long-term follow-up.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s10549-017-4601-1

  6 / 25372 MEDLINE  
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[PMID]: 29523694
[Au] Autor:Lu Y; Roy S; Nuovo G; Ramaswamy B; Miller T; Shapiro C; Jacob ST; Majumder S
[Ti] Title:Anti-microRNA-222 (anti-miR-222) and -181B suppresses growth of tamoxifen-resistant xenografts in mouse by targeting TIMP3 protein and modulating mitogenic signal.
[So] Source:J Biol Chem;293(10):3588, 2018 Mar 09.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE; RETRACTION OF PUBLICATION
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.W118.002430

  7 / 25372 MEDLINE  
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[PMID]: 29521016
[Au] Autor:Hayata T; Chiga M; Ezura Y; Asashima M; Katabuchi H; Nishinakamura R; Noda M
[Ad] Address:Department of Biological Signaling and Regulation, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
[Ti] Title:Dullard deficiency causes hemorrhage in the adult ovarian follicles.
[So] Source:Genes Cells;, 2018 Mar 09.
[Is] ISSN:1365-2443
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In mammals, the ovarian follicles are regulated at least in part by bone morphogenetic protein (BMP) family members. Dullard (also known as Ctdnep1) gene encodes a phosphatase that suppresses BMP signaling by inactivating or degrading BMP receptors. Here we report that the Col1a1-Cre-induced Dullard mutant mice displayed hemorrhagic ovarian cysts, with red blood cells accumulated in the follicles, resulting in infertility. Cells expressing Cre driven by Col1a1 2.3-kb promoter and their descendants were found in granulosa cells in the ovary and in Sertoli cells in the testis. DullardmRNA was localized to granulosa cells in the ovary. Genes involved in steroid hormone genesis including Cyp11a1, Hsd3b1 and Star were reduced, whereas expression of Smad6 and Smad7, BMP-inducible inhibitory Smads, was up-regulated in the Dullard mutant ovaries. Tamoxifen-inducible Dullard deletion in the whole body using Rosa26-CreER mice also resulted in hemorrhagic ovarian cysts in 2 weeks, which was rescued by administration of LDN-193189, a chemical inhibitor of BMP receptor kinase, suggesting that the hemorrhage in the Dullard-deficient ovarian follicles might be caused by increased BMP signaling. Thus, we conclude that Dullard is essential for ovarian homeostasis at least in part via suppression of BMP signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1111/gtc.12575

  8 / 25372 MEDLINE  
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[PMID]: 29520654
[Au] Autor:Turashvili G; Gonzalez-Loperena M; Brogi E; Dickler M; Norton L; Morrow M; Wen HY
[Ad] Address:Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
[Ti] Title:The 21-Gene Recurrence Score in Male Breast Cancer.
[So] Source:Ann Surg Oncol;, 2018 Mar 08.
[Is] ISSN:1534-4681
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Given the limited data, systemic treatment of male breast cancer has been extrapolated from female patients. The 21-gene recurrence score (RS) assay estimates the risk of distant recurrence and chemotherapy benefit in early-stage, ER+/HER2- female breast cancer. We assessed the association between RS and type of treatment in male breast cancer. METHODS: We identified male patients with ER+/HER2- breast cancer and available RS results treated at our institution in 2006-2016. We collected data on clinicopathologic features, treatment, and outcome. The Institutional Review Board approved the study. RESULTS: The study cohort consists of 38 male breast cancer patients with a median age of 70 years. Median tumor size was 1.6 cm, and 81.6% (31) were node-negative. RS was low (≤ 17) in 26 (68.4%) cases, intermediate (18-30) in 9 (23.7%) cases, and high (≥ 31) in 3 (7.9%) cases, comparable to that in female patients at our institution. All patients underwent total mastectomy, and one received radiotherapy. Thirty-four (89.5%) patients received adjuvant endocrine therapy, mostly tamoxifen (81.6%; 31). Five (13.2%) patients with intermediate or high RS were treated with adjuvant chemotherapy. No locoregional recurrence was observed, and one patient developed distant recurrence (median follow-up 34 months). CONCLUSIONS: The RS distribution in male breast cancers was similar to that in females treated at our institution. With limited follow-up, patients with low RS were spared chemotherapy and did not develop recurrence. Our results suggest that the RS may have a clinical utility in male breast cancer patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1245/s10434-018-6411-z

  9 / 25372 MEDLINE  
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[PMID]: 29496489
[Au] Autor:Franco ME; Sutherland GE; Lavado R
[Ad] Address:Department of Environmental Science, Baylor University, Waco, TX 76706, USA.
[Ti] Title:Xenobiotic metabolism in the fish hepatic cell lines Hepa-E1 and RTH-149, and the gill cell lines RTgill-W1 and G1B: Biomarkers of CYP450 activity and oxidative stress.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;206-207:32-40, 2018 Feb 27.
[Is] ISSN:1532-0456
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of fish cell cultures has proven to be an effective tool in the study of environmental and aquatic toxicology. Valuable information can be obtained from comparisons between cell lines from different species and organs. In the present study, specific chemicals were used and biomarkers (e.g. 7-Ethoxyresorufin-O-deethylase (EROD) activity and reactive oxygen species (ROS)) were measured to assess the metabolic capabilities and cytotoxicity of the fish hepatic cell lines Hepa-E1 and RTH-149, and the fish gill cell lines RTgill-W1 and G1B. These cell lines were exposed to ß-naphthoflavone (BNF) and benzo[a]pyrene (BaP), the pharmaceutical tamoxifen (TMX), and the organic peroxide tert-butylhydroperoxide (tBHP). Cytotoxicity in gill cell lines was significantly higher than in hepatic cells, with BNF and TMX being the most toxic compounds. CYP1-like associated activity, measured through EROD activity, was only detected in hepatic cells; Hepa-E1 cells showed the highest activity after exposure to both BNF and BaP. Significantly higher levels of CYP3A-like activity were also observed in Hepa-E1 cells exposed to TMX, while gill cell lines presented the lowest levels. Measurements of ROS and antioxidant enzymes indicated that peroxide levels were higher in gill cell lines in general. However, levels of superoxide were significantly higher in RTH-149 cells, where no distinctive increase of superoxide-related antioxidants was observed. The present study demonstrates the importance of selecting adequate cell lines in measuring specific metabolic parameters and provides strong evidence for the fish hepatocarcinoma Hepa-E1 cells to be an excellent alternative in assessing metabolism of xenobiotics, and in expanding the applicability of fish cell lines for in vitro studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  10 / 25372 MEDLINE  
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[PMID]: 29415989
[Au] Autor:Li Z; Kabir I; Tietelman G; Huan C; Fan J; Worgall T; Jiang XC
[Ad] Address:Department of Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, 11203, USA.
[Ti] Title:Sphingolipid de novo biosynthesis is essential for intestine cell survival and barrier function.
[So] Source:Cell Death Dis;9(2):173, 2018 Feb 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Serine palmitoyltransferase (SPT) is the rate-limiting enzyme for sphingolipid biosynthesis. SPT has two major subunits, SPTLC1 and SPTLC2. We previously found that liver Sptlc2 deficiency in early life impairs the development of adherens junctions. Here, we investigated the role of Sptlc2 deficiency in intestine. We treated Sptlc2-Flox/villin-Cre-ER mice with tamoxifen (days 1, 2, and 3) to ablate Sptlc2 specifically in the intestine. At day 6 after tamoxifen treatment, Sptlc2-deficient mice had significantly decreased body weight with concurrent diarrhea and rectal bleeding. The number of goblet cells was reduced in both large and small intestine of Sptlc2-deficient mice compared with controls. Sptlc2 deficiency suppressed the level of mucin2 in the colon and increased circulating lipopolysaccharides, suggesting that SPT activity has a housekeeping function in the intestine. All Sptlc2-deficient mice died 7-10 days after tamoxifen treatment. Notably, supplementation with antibiotics and dexamethasone reduced lethality by 70%. We also found that colon specimens from patients with inflammatory bowel diseases had significantly reduced Sptlc2 expression, SPTLC2 staining, and goblet cell numbers. SPT activity is crucial for intestinal cell survival and barrier function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-017-0214-1


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