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[PMID]: 29524808
[Au] Autor:Zhao C; Liu Q; Xu S; Xiao Y; Wang W; Yang J; Yang Y; Wang Y; Song Z; Li J
[Ad] Address:Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, China; University of Chinese Academy of Sciences, Beijing 100049, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technolog
[Ti] Title:Identification of type A spermatogonia in turbot (Scophthalmus maximus) using a new cell-surface marker of Lymphocyte antigen 75 (ly75/CD205).
[So] Source:Theriogenology;113:137-145, 2017 Dec 16.
[Is] ISSN:1879-3231
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Turbot (Schophthalmus maximus) is one of the most important economic marine flatfish species. However, due to rapid development of the industry, genetic resource recession has brought down the efficiency of aquaculture. Therefore, conservation of the genetic resource is increasingly demanded. Recent research proved that type A spermatogonia possesses the properties of spermatogonia stem cell, and it might provide an ideal solution. Therefore, it is necessary to develop an appropriate molecular marker on type A spermatogonia to further isolate and purify of type A spermatogonia in turbot. In this study, turbot lymphocyte antigen 75 (smly75) gene was identified and its localizations of expressions and the temporal transcription patterns were evaluated qualitatively and semiquantitatively. Investigation in testes of development of spermatogonia showed that smly75 mRNA, contrast with vasa and dnd mRNA, was exclusively localized in type A spermatogonia and not detected in type B spermatogonia, spermatocytes or gonadal somatic cells by in situ hybridization. Thus, the smly75 could be a new and convincing molecular marker on identification of type A spermatogonia. In addition, specifically to development pattern of type A spermatogonia, from 7- to 14- month testes, spermatogonia were dominated and the number of type A spermatogonia was increased, corresponding that smly75 expression was up-regulated gradually, while, in 16 month testes, accompanied by that several spermatogonia differentiated into primary spermatocytes, the smly75 expression down-regulated. Finally, broaden in the whole reproductive cycle, the smly75 transcription significantly variated with the differentiation of germ cells and in accordance with the number of type A spermatogonia. It is suggested that testes from 8 to 14 month old males could be used for further isolation and purification of type A-SG. These results will not only help to better understand type A spermatogonia, but also further facilitate type A spematogonia-mediated germ cell manipulation in turbot.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 129704 MEDLINE  
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[PMID]: 29524576
[Au] Autor:Kumari P; Singh SK; Raman R
[Ad] Address:Cytogenetics Laboratory, Department of Zoology, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India.
[Ti] Title:A novel non-coding RNA within an intron of CDH2 and association of its SNP with non-syndromic cleft lip and palate.
[So] Source:Gene;, 2018 Mar 07.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Genome-wide linkage analysis and whole genome sequencing in a Van der Woude syndrome (VWS) family revealed that the SNP, rs539075, within intron 2 of the cadherin 2 gene (CDH2) co-segregated with the disease phenotype. RESULTS: A study with nonsyndromic cleft lip with or without cleft palate (NSCL ±â€¯P) cases (N = 292) and controls (N = 287) established association of this SNP with NSCL ±â€¯P as a risk factor. RT-PCR based expression analysis of the SNP-harbouring region of intron 2 of CDH2 in the clefted lip and/or palate tissues of 16 patients revealed that the mutant allele expressed in all those individuals having it (hetero-/homozygous), whereas the wild type allele expressed in <50% of the samples in which it was present. The intronic transcript was also present in the prospective lip and palate region of 13.5 dpc mouse embryo, detected by RNA in situ hybridization and RT-PCR. CONCLUSIONS: These results including the in silico, characterization of the ~200 nt-intronic transcript showed that conformationally it fits best with noncoding small RNA, possibly a precursor of miRNA. Its function in the orofacial organogenesis remains to be elucidated which will enable us to define the role of this mutant ncRNA in the clefting of lip and palate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 129704 MEDLINE  
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[PMID]: 29510730
[Au] Autor:Zhao Y; Liu Y; Lin L; Huang Q; He W; Zhang S; Dong S; Wen Z; Rao J; Liao W; Shi M
[Ad] Address:Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
[Ti] Title:The lncRNA MACC1-AS1 promotes gastric cancer cell metabolic plasticity via AMPK/Lin28 mediated mRNA stability of MACC1.
[So] Source:Mol Cancer;17(1):69, 2018 Mar 06.
[Is] ISSN:1476-4598
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Metabolic plasticity has been increasingly thought to be a determinant of tumor growth and metastasis. MACC1, a transcriptional regulator of MET, was recognized as an oncogene in gastric cancer (GC); however, its transcriptional or post-translational regulation was not clear. We previously reported the metabolic role of MACC1 in glycolysis to promote GC progression. MACC1-AS1 is the antisense lncRNA of MACC1, yet its function was previously unknown. METHODS: We profiled and analyzed the expression of MACC1-AS1 utilizing the TCGA database as well as in situ hybridization using 123 pairs of GC tissues and matched adjacent normal gastric mucosa tissues (ANTs). The biological role of MACC1-AS1 in cell growth and metastasis was determined by performing in vitro and in vivo functional experiments. Glycolysis and antioxidant capabilities were assayed to examine its metabolic function. Further, the specific regulatory effect of MACC1-AS1 on MACC1 was explored transcriptionally and post-transcriptionally. RESULTS: MACC1-AS1 was shown to be expressed significantly higher in GC tissues than in ANTs, which predicted poor prognosis in GC patients. MACC1-AS1 promoted GC cell proliferation and inhibited cell apoptosis under metabolic stress. Mechanistically, MACC1-AS1 stabilized MACC1 mRNA and post-transcriptionally augmented MACC1 expression. Further, MACC1-AS1 was shown to mediate metabolic plasticity through MACC1 upregulation and subsequent enhanced glycolysis and anti-oxidative capabilities, and this was suggested to be coordinated by the AMPK/Lin28 pathway. CONCLUSIONS: Elevated expression of MACC1-AS1 in gastric cancer tissues is linked to poor prognosis and promotes malignant phenotype upon cancer cells. MACC1-AS1 is elevated under metabolic stress and facilitates metabolic plasticity by promoting MACC1 expression through mRNA stabilization. Our study implicates lncRNA MACC1-AS1 as a valuable biomarker for GC diagnosis and prognosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12943-018-0820-2

  4 / 129704 MEDLINE  
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[PMID]: 29443014
[Au] Autor:Weinreb I; Bishop JA; Chiosea SI; Seethala RR; Perez-Ordonez B; Zhang L; Sung YS; Chen CL; Assaad A; Oliai BR; Antonescu CR
[Ad] Address:Department of Pathology, University Health Network.
[Ti] Title:Recurrent RET Gene Rearrangements in Intraductal Carcinomas of Salivary Gland.
[So] Source:Am J Surg Pathol;42(4):442-452, 2018 Apr.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Intraductal carcinoma (IC) is the World Health Organization designation for lesions previously called low-grade cribriform cystadenocarcinoma. The relationship of IC to salivary duct carcinoma (SDC) is controversial, but currently these are considered distinct entities. It is hypothesized that IC and SDC should have different genomic signatures that may be identifiable by next-generation sequencing. A total of 23 ICs were identified: 14 pure IC and 9 invasive carcinomas with an intraductal component. Five invasive carcinomas were subjected to next-generation paired-end RNA sequencing. Data analysis was performed using FusionSeq and Mutation detection algorithms (MuTect and VarScan) for variant callers. Gene fusion candidates were validated by fluorescence in situ hybridization and reverse transcription polymerase chain reaction, and mutations by Sanger sequencing. Among the 9 invasive carcinomas, all except 1 were apocrine SDCs with an intraductal component. The remaining case showed typical intercalated duct type IC with invasive adenocarcinoma. The 14 pure ICs had typical intercalated duct features (2 showed hybrid intercalated/apocrine features). RNA sequencing predicted a NCOA4-RET fusion, confirmed by reverse transcription polymerase chain reaction, in the intercalated duct type IC invasive component. Six additional cases of pure IC showed RET rearrangement by fluorescence in situ hybridization (7/15=47%). No apocrine carcinomas showed RET rearrangement. RNA sequencing and Sanger sequencing identified PIK3CA (p.E545K/p.H1047R) and/or HRAS (p.Q61R) hotspot mutations in 6 of 8 (75%) apocrine carcinomas. In conclusion, 2 distinctive types of intraductal lesions are emerging based on molecular analysis. Classic intercalated type ICs commonly harbor fusions involving RET and rarely show widespread invasion. Apocrine intraductal lesions are typically associated with widespread invasion with no pure examples and show similar PIK3CA and HRAS mutations to SDC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000000952

  5 / 129704 MEDLINE  
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[PMID]: 29386359
[Au] Autor:Platt DJ; Smith AM; Arora N; Diamond MS; Coyne CB; Miner JJ
[Ad] Address:Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
[Ti] Title:Zika virus-related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice.
[So] Source:Sci Transl Med;10(426), 2018 Jan 31.
[Is] ISSN:1946-6242
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although Zika virus (ZIKV) infection in pregnant women can cause placental damage, intrauterine growth restriction, microcephaly, and fetal demise, these disease manifestations only became apparent in the context of a large epidemic in the Americas. We hypothesized that ZIKV is not unique among arboviruses in its ability to cause congenital infection. To evaluate this, we tested the capacity of four emerging arboviruses [West Nile virus (WNV), Powassan virus (POWV), chikungunya virus (CHIKV), and Mayaro virus (MAYV)] from related (flavivirus) and unrelated (alphavirus) genera to infect the placenta and fetus in immunocompetent, wild-type mice. Although all four viruses caused placental infection, only infection with the neurotropic flaviviruses (WNV and POWV) resulted in fetal demise. WNV and POWV also replicated efficiently in second-trimester human maternal (decidua) and fetal (chorionic villi and fetal membrane) explants, whereas CHIKV and MAYV replicated less efficiently. In mice, RNA in situ hybridization and histopathological analysis revealed that WNV infected the placenta and fetal central nervous system, causing injury to the developing brain. In comparison, CHIKV and MAYV did not cause substantive placental or fetal damage despite evidence of vertical transmission. On the basis of the susceptibility of human maternal and fetal tissue explants and pathogenesis experiments in immunocompetent mice, other emerging neurotropic flaviviruses may share with ZIKV the capacity for transplacental transmission, as well as subsequent infection and injury to the developing fetus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  6 / 129704 MEDLINE  
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[PMID]: 29309308
[Au] Autor:Kao YC; Flucke U; Eijkelenboom A; Zhang L; Sung YS; Suurmeijer AJH; Antonescu CR
[Ad] Address:Department of Pathology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
[Ti] Title:Novel EWSR1-SMAD3 Gene Fusions in a Group of Acral Fibroblastic Spindle Cell Neoplasms.
[So] Source:Am J Surg Pathol;42(4):522-528, 2018 Apr.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Benign/low-grade fibroblastic tumors encompass a broad spectrum of tumors with different morphologies and molecular genetic abnormalities. However, despite significant progress in recent genomic characterization, there are still tumors in this histologic spectrum that are difficult to classify, lacking known molecular characteristics. Triggered by a challenging congenital spindle cell neoplasm arising in the heel of a 1-year-old boy, we applied RNA sequencing for genetic discovery and identified a novel EWSR1-SMAD3 gene fusion. On the basis of the index case superficial acral location and fibroblastic appearance with a nonspecific immunophenotype, we searched our files for similar cases and screened them by fluorescence in situ hybridization for these abnormalities. Thus an identical EWSR1-SMAD3 fusion was identified in 2 additional spindle cell tumors with similar clinicopathologic features. Both cases occurred in the feet of adult women (58 and 61 y old) and were characterized by distinctive nodular growth with zonation pattern of peripheral hypercellular areas arranged in short fascicles, transitioning to hypocellular central areas of hyalinization and infarction. Focal stippled calcification in the collagenous area was present in 1 case. All 3 tumors had similar immunoprofiles, being negative for SMA, CD34, CD31, and S100, but showing consistent ERG positivity of uncertain significance. Follow-up information was available in 2 patients who developed local recurrences after incomplete initial excisions, at 5 and 14 months, respectively. None developed metastatic disease. In summary, we report a group of locally recurrent superficial acral tumors, characterized by bland spindle cell fascicular growth, occasional zonation pattern, ERG positivity, and recurrent EWSR1-SMAD3 gene fusions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000001002

  7 / 129704 MEDLINE  
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[PMID]: 29309307
[Au] Autor:Antonescu CR; Agaram NP; Sung YS; Zhang L; Swanson D; Dickson BC
[Ad] Address:Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY.
[Ti] Title:A Distinct Malignant Epithelioid Neoplasm With GLI1 Gene Rearrangements, Frequent S100 Protein Expression, and Metastatic Potential: Expanding the Spectrum of Pathologic Entities With ACTB/MALAT1/PTCH1-GLI1 Fusions.
[So] Source:Am J Surg Pathol;42(4):553-560, 2018 Apr.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:ACTB-GLI1 fusions have been reported as the pathognomonic genetic abnormality defining an unusual subset of actin-positive, perivascular myoid tumors, known as "pericytoma with the t(7;12) translocation." In addition, GLI1 oncogenic activation through a related MALAT1-GLI1 gene fusion has been recently reported in 2 unrelated gastric tumors, namely plexiform fibromyxoma and gastroblastoma. Triggered by unexpected targeted RNA-sequencing results detecting GLI1-related fusions in a group of malignant neoplasms with round to epithelioid morphology, and frequently strong S100 protein immunoreactivity, we investigated their clinicopathologic features in relation to other known pathologic entities sharing similar genetics. On the basis of a combined approach of targeted RNA sequencing and fluorescence in situ hybridization screening, we identified 6 cases with GLI1 gene fusions, including 4 fused to ACTB, 1 with MALAT1 and 1 with PTCH1 gene. Patients had a mean age of 36 years at diagnosis (range, 16 to 79 y) and slight female predilection all except 1 tumor originated in the soft tissue. Microscopically, the tumors had a monomorphic epithelioid phenotype arranged in a distinctive nested or cord-like architecture, separated by thin septae and delicate capillary network. All except 2 cases were strongly positive for S100 protein, whereas being negative for SOX10, SMA, and EMA. Only 1 tumor showed focal cytokeratin positivity in rare cells. Although the tumors showed some resemblance to pericytic/glomus tumors or myoepithelial tumors, the immunoprofile was not supportive of either lineage. Moreover, in contrast to the benign course of so-called pericytoma with t(7;12), 3 patients in this series developed metastatic disease to either lymph nodes or lung. In fact the only patient with lung metastases showed a novel PTCH1-GLI1 gene fusion. It remains to be determined whether these tumors represent a clinically and immunohistologically distinct subset of pericytoma, or an altogether novel soft tissue sarcoma. Our findings open new opportunities for targeted therapy, as tumors with GLI1 oncogenic activation, and subsequent PTCH1 overexpression, might be sensitive to sonic hedgehog pathway inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000001010

  8 / 129704 MEDLINE  
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[PMID]: 29524147
[Au] Autor:Beckman W; Vuist IM; Kempe H; Verschure PJ
[Ad] Address:Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands.
[Ti] Title:Cell-to-Cell Transcription Variability as Measured by Single-Molecule RNA FISH to Detect Epigenetic State Switching.
[So] Source:Methods Mol Biol;1767:385-393, 2018.
[Is] ISSN:1940-6029
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Single-molecule RNA fluorescent in situ hybridization (smRNA FISH) allows for the visualization, localization, and quantification of RNA transcripts within individual cells and tissues using custom-designed fluorescently labeled oligonucleotide probes. Here we describe a protocol for the preparation, imaging, and analysis of a smRNA FISH experiment that can be applied to any RNA of choice. We also provide insights as to how this powerful tool can be used to study epigenetic regulation, for example, following the epigenetic editing of genes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1007/978-1-4939-7774-1_21

  9 / 129704 MEDLINE  
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[PMID]: 29523241
[Au] Autor:Garribba L; Wu W; Özer Ö; Bhowmick R; Hickson ID; Liu Y
[Ad] Address:Center for Chromosome Stability, University of Copenhagen, Copenhagen, Denmark.
[Ti] Title:Inducing and Detecting Mitotic DNA Synthesis at Difficult-to-Replicate Loci.
[So] Source:Methods Enzymol;601:45-58, 2018.
[Is] ISSN:1557-7988
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Our conventional understanding of the process of DNA replication is that it occurs in the S-phase of the cell division cycle. However, during investigations into the mechanism by which common fragile sites (CFSs) drive genome instability, we observed that some DNA synthesis was still occurring in early mitosis at these loci. This curious phenomenon of mitotic DNA synthesis (which we now term "MiDAS") appears to be a form of break-induced DNA replication (BIR), a DNA repair process based on homologous recombination that has been characterized in detail only in lower eukaryotes. During MiDAS, it is proposed that parts of the human genome that are not fully replicated when cells enter mitotic prophase complete their replicative cycle at that point. To date, the loci that most depend upon this process are those whose replication can be affected by oncogene-induced DNA replication stress (RS), most notably, CFSs. From our studies, it is clear that the successful completion of MiDAS at CFSs can minimize chromosome missegregation and nondisjunction. Nevertheless, it is still not clear which loci that can undergo MiDAS, whether MiDAS is associated with mutations or genome rearrangements, or whether MiDAS really is a form of BIR. In this review, we describe methods for detecting MiDAS both in prometaphase cells and directly on isolated metaphase chromosomes. In addition, we have included methods for combining MiDAS detection either with immunofluorescence (IF) detection of proteins that are recruited to the MiDAS loci, or with fluorescence in situ hybridization using probes that target specific genomic loci.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  10 / 129704 MEDLINE  
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[PMID]: 29523116
[Au] Autor:Ryska A; Berzinec P; Brcic L; Cufer T; Dziadziuszko R; Gottfried M; Kovalszky I; Olszewski W; Oz B; Plank L; Timar J
[Ad] Address:The Fingerland Department of Pathology, Charles University Faculty of Medicine and University Hospital, Hradec Králové, Czech Republic. ryskaale@gmail.com.
[Ti] Title:NSCLC molecular testing in Central and Eastern European countries.
[So] Source:BMC Cancer;18(1):269, 2018 Mar 09.
[Is] ISSN:1471-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The introduction of targeted treatments for subsets of non-small cell lung cancer (NSCLC) has highlighted the importance of accurate molecular diagnosis to determine if an actionable genetic alteration is present. Few data are available for Central and Eastern Europe (CEE) on mutation rates, testing rates, and compliance with testing guidelines. METHODS: A questionnaire about molecular testing and NSCLC management was distributed to relevant specialists in nine CEE countries, and pathologists were asked to provide the results of EGFR and ALK testing over a 1-year period. RESULTS: A very high proportion of lung cancer cases are confirmed histologically/cytologically (75-100%), and molecular testing of NSCLC samples has been established in all evaluated CEE countries in 2014. Most countries follow national or international guidelines on which patients to test for EGFR mutations and ALK rearrangements. In most centers at that time, testing was undertaken on request of the clinician rather than on the preferred reflex basis. Immunohistochemistry, followed by fluorescent in situ hybridization confirmation of positive cases, has been widely adopted for ALK testing in the region. Limited reimbursement is a significant barrier to molecular testing in the region and a disincentive to reflex testing. Multidisciplinary tumor boards are established in most of the countries and centers, with 75-100% of cases being discussed at a multidisciplinary tumor board at specialized centers. CONCLUSIONS: Molecular testing is established throughout the CEE region, but improved and unbiased reimbursement remains a major challenge for the future. Increasing the number of patients reviewed by multidisciplinary boards outside of major centers and access to targeted therapy based on the result of molecular testing are other major challenges.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1186/s12885-018-4023-4


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