Database : MEDLINE
Search on : Colorectal and Neoplasms [Words]
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[PMID]: 29477967
[Au] Autor:Erben V; Carr PR; Holleczek B; Stegmaier C; Hoffmeister M; Brenner H
[Ad] Address:Division of Preventive Oncology, German Cancer Research Center (DKFZ), National Center for Tumor Diseases (NCT), Heidelberg, Germany; Medical Faculty Heidelberg, Heidelberg University, Heidelberg, Germany. Electronic address: vanessa.erben@nct-heidelberg.de.
[Ti] Title:Dietary patterns and risk of advanced colorectal neoplasms: A large population based screening study in Germany.
[So] Source:Prev Med;111:101-109, 2018 Feb 23.
[Is] ISSN:1096-0260
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Specific components of the diet such as red and processed meat have been associated with the risk of developing colorectal cancer. However, evidence on the association of dietary patterns with colorectal neoplasms is sparse. The aim of this study was to analyze the association of dietary patterns with prevalence of advanced colorectal neoplasms among older adults in Germany. A cross-sectional study was conducted among participants of screening colonoscopy in Saarland, Germany, who were enrolled in the KolosSal study (Effektivität der Früherkennungs-Koloskopie: eine Saarland-weite Studie) from 2005 to 2013. Information on diet and lifestyle factors was obtained through questionnaires and colonoscopy results were extracted from physicians' reports. Associations of a priori defined dietary patterns (vegetarian or adapted versions of the Healthy Eating Index [HEI] and the Dietary Approaches to Stop Hypertension [DASH] index) with the risk of advanced colorectal neoplasms were assessed by multiple logistic regression analyses with comprehensive adjustment for potential confounders. A total of 14,309 participants were included (1561 with advanced colorectal neoplasms). Healthier eating behavior was associated with lower prevalence of advanced colorectal neoplasms in a dose-response manner. Adjusted odds ratios (95% confidence intervals) comparing the highest with the lowest categories of adapted HEI and DASH were 0.61 (0.50, 0.76) and 0.70 (0.55, 0.89), respectively. No significant associations were observed for a vegetarian eating pattern (adjusted OR 0.80 (0.55, 1.17)). Healthy dietary patterns, as described by a high HEI or DASH score, but not a vegetarian diet alone, are associated with reduced risk of advanced colorectal neoplasms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 104068 MEDLINE  
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[PMID]: 29182684
[Au] Autor:Huo T; Canepa R; Sura A; Modave F; Gong Y
[Ad] Address:Department of Health Outcomes & Policy, College of Medicine, University of Florida, Gainesville, Florida, United States of America.
[Ti] Title:Colorectal cancer stages transcriptome analysis.
[So] Source:PLoS One;12(11):e0188697, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths in the United States. The purpose of this study was to evaluate the gene expression differences in different stages of CRC. Gene expression data on 433 CRC patient samples were obtained from The Cancer Genome Atlas (TCGA). Gene expression differences were evaluated across CRC stages using linear regression. Genes with p≤0.001 in expression differences were evaluated further in principal component analysis and genes with p≤0.0001 were evaluated further in gene set enrichment analysis. A total of 377 patients with gene expression data in 20,532 genes were included in the final analysis. The numbers of patients in stage I through IV were 59, 147, 116 and 55, respectively. NEK4 gene, which encodes for NIMA related kinase 4, was differentially expressed across the four stages of CRC. The stage I patients had the highest expression of NEK4 genes, while the stage IV patients had the lowest expressions (p = 9*10-6). Ten other genes (RNF34, HIST3H2BB, NUDT6, LRCh4, GLB1L, HIST2H4A, TMEM79, AMIGO2, C20orf135 and SPSB3) had p value of 0.0001 in the differential expression analysis. Principal component analysis indicated that the patients from the 4 clinical stages do not appear to have distinct gene expression pattern. Network-based and pathway-based gene set enrichment analyses showed that these 11 genes map to multiple pathways such as meiotic synapsis and packaging of telomere ends, etc. Ten of these 11 genes were linked to Gene Ontology terms such as nucleosome, DNA packaging complex and protein-DNA interactions. The protein complex-based gene set analysis showed that four genes were involved in H2AX complex II. This study identified a small number of genes that might be associated with clinical stages of CRC. Our analysis was not able to find a molecular basis for the current clinical staging for CRC based on the gene expression patterns.
[Mh] MeSH terms primary: Colorectal Neoplasms/genetics
Transcriptome
[Mh] MeSH terms secundary: Aged
Female
Gene Expression Regulation, Neoplastic
Humans
Linear Models
Male
Middle Aged
Principal Component Analysis
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Js] Journal subset:IM
[Da] Date of entry for processing:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188697

  3 / 104068 MEDLINE  
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[PMID]: 29520890
[Au] Autor:Deevi RK; Javadi A; McClements J; Vohhodina J; Savage K; Loughrey MB; Evergren E; Campbell FC
[Ad] Address:Centre for Cancer Research and Cell Biology, Queen's University of Belfast, Belfast, UK.
[Ti] Title:Protein kinase C zeta suppresses low- or high-grade colorectal cancer (CRC) phenotypes by interphase centrosome anchoring.
[So] Source:J Pathol;, 2018 Mar 09.
[Is] ISSN:1096-9896
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Histological grading provides prognostic stratification of colorectal cancer (CRC) by scoring heterogeneous phenotypes. Features of aggressiveness include aberrant mitotic spindle configurations, chromosomal breakage, and bizarre multicellular morphology, but pathobiology is poorly understood. Protein kinase C zeta (PKCz) controls mitotic spindle dynamics, chromosome segregation, and multicellular patterns, but its role in CRC phenotype evolution remains unclear. Here, we show that PKCz couples genome segregation to multicellular morphology through control of interphase centrosome anchoring. PKCz regulates interdependent processes that control centrosome positioning. Among these, interaction between the cytoskeletal linker protein ezrin and its binding partner NHERF1 promotes the formation of a localized cue for anchoring interphase centrosomes to the cell cortex. Perturbation of these phenomena induced different outcomes in cells with single or extra centrosomes. Defective anchoring of a single centrosome promoted bipolar spindle misorientation, multi-lumen formation, and aberrant epithelial stratification. Collectively, these disturbances induce cribriform multicellular morphology that is typical of some categories of low-grade CRC. By contrast, defective anchoring of extra centrosomes promoted multipolar spindle formation, chromosomal instability (CIN), disruption of glandular morphology, and cell outgrowth across the extracellular matrix interface characteristic of aggressive, high-grade CRC. Because PKCz enhances apical NHERF1 intensity in 3D epithelial cultures, we used an immunohistochemical (IHC) assay of apical NHERF1 intensity as an indirect readout of PKCz activity in translational studies. We show that apical NHERF1 IHC intensity is inversely associated with multipolar spindle frequency and high-grade morphology in formalin-fixed human CRC samples. To conclude, defective PKCz control of interphase centrosome anchoring may underlie distinct categories of mitotic slippage that shape the development of low- or high-grade CRC phenotypes. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1002/path.5035

  4 / 104068 MEDLINE  
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[PMID]: 29477926
[Au] Autor:McQuade C; Waters PS; O'Brien C; Crowther S; Torreggiani W; Kavanagh DO
[Ad] Address:Department of Colorectal Surgery, The Adelaide & Meath Hospital, Tallaght, Dublin 24, Ireland. Electronic address: colin.mc.quade@icloud.com.
[Ti] Title:Colorectal intussusception secondary to primary rectal melanoma: A novel case report.
[So] Source:Int J Surg Case Rep;44:78-81, 2018 Feb 14.
[Is] ISSN:2210-2612
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Intussusception in adults is a rare condition, accounting for just 5% of all cases. Approximately 50% of cases of large intestine intussusception occur due to a malignant neoplasm. We present here a novel case report of colo-rectal intussusception arising secondary to a primary rectal melanoma. PRESENTATION OF CASE: We present the case of an 85 year-old patient, who underwent a colonoscopy for investigation of weight loss and altered bowel habit. At colonoscopy, a pigmented polypoid mass was visualised in the upper third of the rectum. The lesion was causing colo-rectal intussusception. Initial biopsies of the specimen stained positive for S-100. The patient had an MRI (magnetic resonance imaging) pelvis, which demonstrated a mass at the rectosigmoid junction, which was diffusely high signal on the fat sat T1 weighted sequence. The patient proceeded to a laparoscopic anterior resection and had an uncomplicated post-operative course. The resected specimen was sent for pathological analysis. The morphological and immunohistochemical profile was consistent with malignant melanoma. There was no evidence of cutaneous melanoma following a full skin examination. DISCUSSION: Rectal melanoma is a rare condition. We present a novel case report of colo-rectal intussusception arising secondary to rectal melanoma. CONCLUSION: This is a rare entity. This patient's pre-operative MRI and biopsy samples suggested this lesion was a rectal melanoma, which was subsequently confirmed on analysis of the resected specimen. Surgical resection of such neoplasms should be attempted where possible.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  5 / 104068 MEDLINE  
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[PMID]: 29406563
[Au] Autor:Yanus GA; Akhapkina TA; Ivantsov AO; Preobrazhenskaya EV; Aleksakhina SN; Bizin IV; Sokolenko AP; Mitiushkina NV; Kuligina ES; Suspitsin EN; Venina AR; Holmatov MM; Zaitseva OA; Yatsuk OS; Pashkov DV; Belyaev AM; Togo AV; Imyanitov EN; Iyevleva AG
[Ad] Address:N.N. Petrov Institute of Oncology, Laboratory of Molecular Oncology, St.-Petersburg 197758, Russia.
[Ti] Title:Spectrum of APC and MUTYH germ-line mutations in Russian patients with colorectal malignancies.
[So] Source:Clin Genet;, 2018 Feb 06.
[Is] ISSN:1399-0004
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:Distribution of cancer-predisposing mutations demonstrates significant interethnic variations. This study aimed to evaluate patterns of APC and MUTYH germ-line mutations in Russian patients with colorectal malignancies. APC gene defects were identified in 26/38 (68%) subjects with colon polyposis; 8/26 (31%) APC mutations were associated with 2 known mutational hotspots (p.E1309Dfs*4 [n = 5] and p.Q1062fs* [n = 3]), while 6/26 (23%) mutations were novel (p.K73Nfs*6, p.S254Hfs*12, p.S1072Kfs*9, p.E1547Kfs*11, p.L1564X and p.C1263Wfs*22). Biallelic mutations in MUTYH gene were detected in 3/12 (25%) remaining subjects with polyposis and in 6/90 (6.7%) patients with colorectal cancer (CRC) carrying KRAS p.G12C substitution, but not in 231 early-onset CRC cases negative for KRAS p.G12C allele. In addition to known European founder alleles p.Y179C and p.G396D, this study revealed a recurrent character of MUTYH p.R245H germ-line mutation. Besides that, 3 novel pathogenic MUTYH alleles (p.L111P, p.R245S and p.Q293X) were found. Targeted next-generation sequencing of 7 APC/MUTYH mutation-negative DNA samples identified novel potentially pathogenic POLD1 variant (p.L460R) in 1 patient and known low-penetrant cancer-associated allele CHEK2 p.I157T in 3 patients. The analysis of 1120 healthy subjects revealed 15 heterozygous carriers of recurrent MUTYH mutations, thus the expected incidence of MUTYH-associated polyposis in Russia is likely to be 1:23 000.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1111/cge.13228

  6 / 104068 MEDLINE  
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[PMID]: 29270670
[Au] Autor:Lv C; Wang H; Tong Y; Yin H; Wang D; Yan Z; Liang Y; Wu D; Su Q
[Ad] Address:Department of General Surgery, Shengjing Hospital Affiliated to China Medical University, Shenyang City, Liaoning Province, 110004, People's Republic of China.
[Ti] Title:The function of BTG3 in colorectal cancer cells and its possible signaling pathway.
[So] Source:J Cancer Res Clin Oncol;144(2):295-308, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: B-cell translocation gene 3 (BTG3) has been identified as a candidate driver gene for various cancers, but its specific role in colorectal cancer (CRC) is poorly understood. We aimed to investigate the relationship between expression of BTG3 and clinicopathological features and prognosis, as well as to explore the effects and the role of a possible BTG3 molecular mechanism on aggressive colorectal cancer behavior. METHODS: BTG3 expression was assessed by immunohistochemistry (IHC) on specimens from 140 patients with CRC. The association of BTG3 expression with clinicopathological features was examined. To confirm the biological role of BTG3 in CRC, two CRC cell lines expressing BTG3 were used and BTG3 expression was knocked down by shRNA. CCK-8, cell cycle, apoptosis, migration, and invasion assays were performed. The influence of BTG3 knockdown was further investigated by genomic microarray to uncover the potential molecular mechanisms underlying BTG3-mediated CRC development and progression. RESULTS: BTG3 was downregulated in colorectal cancer tissues and positively correlated with pathological classification (p = 0.037), depth of invasion (p = 0.016), distant metastasis (p = 0.024), TNM stage (p = 0.007), and overall survival (OS) and disease-free survival (DFS). BTG3 knockdown promoted cell proliferation, migration, invasion, relieved G2 arrest, and inhibited apoptosis in HCT116 and LoVo cells. A genomic microarray analysis showed that numerous tumor-associated signaling pathways and oncogenes were altered by BTG3 knockdown. At the mRNA level, nine genes referred to the extracellular-regulated kinase/mitogen-activated protein kinase pathway were differentially expressed. Western blotting revealed that BTG3 knockdown upregulated PAK2, RPS6KA5, YWHAB, and signal transducer and activator of transcription (STAT)3 protein levels, but downregulated RAP1A, DUSP6, and STAT1 protein expression, which was consistent with the genomic microarray data. CONCLUSIONS: BTG3 expression might contribute to CRC carcinogenesis. BTG3 knockdown might strengthen the aggressive colorectal cancer behavior.
[Mh] MeSH terms primary: Colorectal Neoplasms/metabolism
Proteins/metabolism
[Mh] MeSH terms secundary: Cell Line, Tumor
Cell Movement/physiology
Cell Proliferation/physiology
Colorectal Neoplasms/genetics
Colorectal Neoplasms/pathology
Down-Regulation
Female
Gene Knockdown Techniques
HCT116 Cells
HT29 Cells
Humans
Immunohistochemistry
Male
Middle Aged
Paraffin Embedding
Proteins/genetics
Signal Transduction
Tumor Cells, Cultured
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (BTG3 protein, human); 0 (Proteins)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171223
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2561-9

  7 / 104068 MEDLINE  
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[PMID]: 29188362
[Au] Autor:Slattery ML; Mullany LE; Sakoda L; Samowitz WS; Wolff RK; Stevens JR; Herrick JS
[Ad] Address:Department of Medicine, University of Utah, 383 Colorow, Salt Lake City, UT, 84108, USA. marty.slattery@hsc.utah.edu.
[Ti] Title:The NF-κB signalling pathway in colorectal cancer: associations between dysregulated gene and miRNA expression.
[So] Source:J Cancer Res Clin Oncol;144(2):269-283, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: The nuclear factor-kappa B (NF-κB) signalling pathway is a regulator of immune response and inflammation that has been implicated in the carcinogenic process. We examined differentially expressed genes in this pathway and miRNAs to determine associations with colorectal cancer (CRC). METHODS: We used data from 217 CRC cases to evaluate differences in NF-κB signalling pathway gene expression between paired carcinoma and normal mucosa and identify miRNAs that are associated with these genes. Gene expression data from RNA-Seq and miRNA expression data from Agilent Human miRNA Microarray V19.0 were analysed. We evaluated genes most strongly associated and differentially expressed (fold change (FC) of > 1.5 or < 0.67) that were statistically significant after adjustment for multiple comparisons. RESULTS: Of the 92 genes evaluated, 22 were significantly downregulated and nine genes were significantly upregulated in all tumours. Two additional genes (CD14 and CSNK2A1) were dysregulated in MSS tumours and two genes (CARD11 and VCAM1) were downregulated and six genes were upregulated (LYN, TICAM2, ICAM1, IL1B, CCL4 and PTGS2) in MSI tumours. Sixteen of the 21 dysregulated genes were associated with 40 miRNAs. There were 76 miRNA:mRNA associations of which 38 had seed-region matches. Genes were associated with multiple miRNAs, with TNFSRF11A (RANK) being associated with 15 miRNAs. Likewise several miRNAs were associated with multiple genes (miR-150-5p with eight genes, miR-195-5p with four genes, miR-203a with five genes, miR-20b-5p with four genes, miR-650 with six genes and miR-92a-3p with five genes). CONCLUSIONS: Focusing on the genes and their associated miRNAs within the entire signalling pathway provides a comprehensive understanding of this complex pathway as it relates to CRC and offers insight into potential therapeutic agents.
[Mh] MeSH terms primary: Colorectal Neoplasms/genetics
Colorectal Neoplasms/metabolism
Gene Expression Regulation, Neoplastic
MicroRNAs/genetics
NF-kappa B/metabolism
[Mh] MeSH terms secundary: Adult
Aged
Case-Control Studies
Female
Humans
Male
MicroRNAs/biosynthesis
Middle Aged
NF-kappa B/genetics
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (MicroRNAs); 0 (NF-kappa B)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171201
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2548-6

  8 / 104068 MEDLINE  
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[PMID]: 28470797
[Au] Autor:O'Kane GM; Ryan É; McVeigh TP; Creavin B; Hyland JM; O'Donoghue DP; Keegan D; Geraghty R; Flannery D; Nolan C; Donovan E; Mehigan BJ; McCormick P; Muldoon C; Farrell M; Shields C; Mulligan N; Kennedy MJ; Green AJ; Winter DC; MacMathuna P; Sheahan K; Gallagher DJ
[Ad] Address:St. James's Hospital, Dublin 8, Ireland.
[Ti] Title:Screening for mismatch repair deficiency in colorectal cancer: data from three academic medical centers.
[So] Source:Cancer Med;6(6):1465-1472, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Reflex immunohistochemistry (rIHC) for mismatch repair (MMR) protein expression can be used as a screening tool to detect Lynch Syndrome (LS). Increasingly the mismatch repair-deficient (dMMR) phenotype has therapeutic implications. We investigated the pattern and consequence of testing for dMMR in three Irish Cancer Centres (CCs). CRC databases were analyzed from January 2005-December 2013. CC1 performs IHC upon physician request, CC2 implemented rIHC in November 2008, and CC3 has been performing rIHC since 2004. The number of eligible patients referred to clinical genetic services (CGS), and the number of LS patients per center was determined. 3906 patients were included over a 9-year period. dMMR CRCs were found in 32/153 (21%) of patients at CC1 and 55/536 (10%) at CC2, accounting for 3% and 5% of the CRC population, respectively. At CC3, 182/1737 patients (10%) had dMMR CRCs (P < 0.001). Additional testing for the BRAF V600E mutation, was performed in 49 patients at CC3 prior to CGS referral, of which 29 were positive and considered sporadic CRC. Referrals to CGS were made in 66%, 33%, and 30% of eligible patients at CC1, CC2, and CC3, respectively. LS accounted for CRC in eight patients (0.8%) at CC1, eight patients (0.7%) at CC2, and 20 patients (1.2%) at CC3. Cascade testing of patients with dMMR CRC was not completed in 56%. Universal screening increases the detection of dMMR tumors and LS kindreds. Successful implementation of this approach requires adequate resources for appropriate downstream management of these patients.
[Mh] MeSH terms primary: Colorectal Neoplasms/genetics
DNA Mismatch Repair
[Mh] MeSH terms secundary: Academic Medical Centers
Adolescent
Adult
Aged
Aged, 80 and over
Humans
Immunohistochemistry
Middle Aged
Mutation
Phenotype
Proto-Oncogene Proteins B-raf/genetics
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Name of substance:EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170505
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1025

  9 / 104068 MEDLINE  
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[PMID]: 28464467
[Au] Autor:Torigata M; Yamakawa D; Takakura N
[Ad] Address:Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
[Ti] Title:Elevated expression of Tie1 is accompanied by acquisition of cancer stemness properties in colorectal cancer.
[So] Source:Cancer Med;6(6):1378-1388, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Tie receptors 1 and 2 (Tie1/2) play crucial roles in embryonic angiogenesis. Recent studies suggest enhanced expression of Tie1 in several types of cancer and negative correlations between Tie1 levels and clinical outcome. These observations suggest important functions of Tie1 not only for vascular formation but also in tumorigenesis. Ligands for Tie2, that is angiopoietins 1-4, have been identified, but not for Tie1. To determine the molecular functions of Tie1, its detailed characterization in tumors would be helpful. Herein, we report that Tie1 is up-regulated in colorectal cancer. Detailed analysis using tumor-bearing models and immunohistochemistry combined with Flow cytometric analysis and cell sorting (FACS) revealed that Tie1 protein was expressed in a small population of malignant tumor cells. Intriguingly, Tie1 expression was observed and could be maintained only in vivo. Further analysis using sphere-formation culture revealed that Tie1-positive cells are enriched within the population of tumor cells with cancer stemness properties. Indeed, Tie1-positive tumor cells derived from a murine model overexpressed Lgr5, a typical stemness marker for colorectal cancer. Our results provide a novel insight into Tie1 function in tumorigenesis and suggest clinical applications to target cancer stem cells.
[Mh] MeSH terms primary: Colorectal Neoplasms/metabolism
Receptor, TIE-1/metabolism
[Mh] MeSH terms secundary: Animals
Cell Line, Tumor
Cell Proliferation
Colorectal Neoplasms/genetics
Humans
Mice
Mice, Nude
Neoplastic Stem Cells
RNA, Messenger/metabolism
Receptor, TIE-1/genetics
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (RNA, Messenger); EC 2.7.10.1 (Receptor, TIE-1)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1072

  10 / 104068 MEDLINE  
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[PMID]: 28453756
[Au] Autor:Hovde Ø; Høivik ML; Henriksen M; Solberg IC; Småstuen MC; Moum BA
[Ad] Address:Department of Gastroenterology, Innlandet Hospital Trust, Gjøvik, Norway.
[Ti] Title:Malignancies in Patients with Inflammatory Bowel Disease: Results from 20 Years of Follow-up in the IBSEN Study.
[So] Source:J Crohns Colitis;11(5):571-577, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background and Aims: Whether patients with inflammatory bowel diseases [IBDs] have increased risk of developing cancer has been debated. The aims of the study were to determine the prevalence of intestinal/extraintestinal cancers in an IBD cohort 20 years after diagnosis and to assess whether these patients had an increased cancer-specific risk compared with a matched control population. Methods: Patients with ulcerative colitis [UC] and Crohn's disease [CD] diagnosed 1990-1993 have been prospectively followed up for 20 years. Follow-up visits were carried out 1, 5, 10, and 20 years after inclusion. Data on all cancer cases, deaths, and causes of death were collected from the Cancer Registry of Norway and from the Norwegian Cause of Death Registry. Results: In all, 756 patients [519 UC and 237 CD] were diagnosed with IBD. Increased risk of cancer was seen in UC patients (hazard ratio [HR] = 1.40, 95% confidence interval [CI] 1.08-1.81, p < 0.01), but not in CD patients [HR = 1.23, 95% CI 0.80-2.03, p = 0.30]. Stratified by gender, our data revealed a statistically increased risk for all cancers only in male UC patients compared with the controls [HR = 1.51, 95% CI 1.08-2.11, p = 0.017]. In both groups breast cancer was seen more often than expected. Conclusions: Male UC patients display an increased risk of development of colorectal cancer and, also all cancers combined, compared with the controls. In both UC and CD, standardized incidence ratio for breast cancer was increased.
[Mh] MeSH terms primary: Inflammatory Bowel Diseases/complications
Intestinal Neoplasms/epidemiology
Neoplasms/epidemiology
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Aged, 80 and over
Cause of Death
Child
Child, Preschool
Colitis, Ulcerative/complications
Crohn Disease/complications
Female
Follow-Up Studies
Humans
Intestinal Neoplasms/etiology
Male
Middle Aged
Neoplasms/etiology
Neoplasms/mortality
Norway/epidemiology
Registries
Risk Factors
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw193


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