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1. Sakai E, Fukuyo M, Ohata K, Matsusaka K, Doi N, Mano Y, Takane K, Abe H, Yagi K, Matsuhashi N, Fukushima J, Fukayama M, Akagi K, Aburatani H, Nakajima A, Kaneda A: Genetic and epigenetic aberrations occurring in colorectal tumors associated with serrated pathway. Int J Cancer; 2016 Apr 1;138(7):1634-44
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  • To clarify molecular alterations in serrated pathway of colorectal cancer (CRC), we performed epigenetic and genetic analyses in sessile serrated adenoma/polyps (SSA/P), traditional serrated adenomas (TSAs) and high-methylation CRC.
  • Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology

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  • [Copyright] © 2015 The Authors International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.
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  • (PMID = 26510091.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC4737347
  • [Keywords] NOTNLM ; DNA methylation / colorectal cancer (CRC) / gene mutation / sessile serrated adenoma/polyp (SSA/P) / traditional serrated adenoma (TSA)
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2. Baretton GB: [Serrated pathway of colorectal carcinogenesis]. Pathologe; 2010 Feb;31(1):9-15
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  • The low-risk-subtype of serrated adenocarcinomas is less frequent (<20% of all serrated adenocarcinomas) and characterized by proximal location, BRAF-mutation, high CpG-island methylation with loss of MLH1-expression and MSI-H phenotype.
  • The assumed precursor lesion of this subtype is the sessile serrated adenoma and the 5-year overall survival is >70%.
  • The high-risk-subtype is more frequent (>80% of all serrated adenocarcinomas) and characterized by distal location, KRAS mutation, MSI-L/MSS phenotype, lower CpG-island methylation, and possible p53 accumulation.
  • The assumed precursor lesion is the traditional serrated adenoma and the prognosis is unfavorable (<30% 5-year overall survival).
  • [MeSH-major] Adenocarcinoma / pathology. Cell Transformation, Neoplastic / pathology. Colorectal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Biomarkers, Tumor / genetics. Colonic Polyps / genetics. DNA Mutational Analysis. Gene Expression Regulation, Neoplastic / genetics. Humans. Intestinal Mucosa / pathology. Phenotype. Survival Rate

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  • (PMID = 19921196.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 32
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3. Stokowy T, Eszlinger M, Świerniak M, Fujarewicz K, Jarząb B, Paschke R, Krohn K: Analysis options for high-throughput sequencing in miRNA expression profiling. BMC Res Notes; 2014;7:144
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  • We use Illumina platforms for microarray analysis and miRNA sequencing of 20 samples from benign follicular thyroid adenoma and malignant follicular thyroid carcinoma.
  • [MeSH-major] Adenocarcinoma, Follicular / genetics. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. High-Throughput Nucleotide Sequencing / statistics & numerical data. MicroRNAs / genetics. Thyroid Neoplasms / genetics

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  • (PMID = 24625073.001).
  • [ISSN] 1756-0500
  • [Journal-full-title] BMC research notes
  • [ISO-abbreviation] BMC Res Notes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MIRN144 microRNA, human; 0 / MIRN197 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC4007773
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4. Ma L, Tao Y, Duran A, Llado V, Galvez A, Barger JF, Castilla EA, Chen J, Yajima T, Porollo A, Medvedovic M, Brill LM, Plas DR, Riedl SJ, Leitges M, Diaz-Meco MT, Richardson AD, Moscat J: Control of nutrient stress-induced metabolic reprogramming by PKCζ in tumorigenesis. Cell; 2013 Jan 31;152(3):599-611
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  • [Title] Control of nutrient stress-induced metabolic reprogramming by PKCζ in tumorigenesis.
  • Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress.
  • We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose.
  • PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity.
  • Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis.
  • Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors.
  • Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.

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  • [Copyright] Copyright © 2013 Elsevier Inc. All rights reserved.
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  • (PMID = 23374352.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK088107; United States / NIAID NIH HHS / AI / R01AI072581; United States / NIDDK NIH HHS / DK / R01DK088107; United States / NCI NIH HHS / CA / R21 CA147978; United States / NCI NIH HHS / CA / R01CA134530; United States / NIAID NIH HHS / AI / R01 AI072581; United States / NCI NIH HHS / CA / R01CA132847; United States / NCI NIH HHS / CA / R21CA147978; United States / NCI NIH HHS / CA / R01 CA132847; United States / NCATS NIH HHS / TR / UL1 TR000077; United States / NCI NIH HHS / CA / R01 CA134530
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 452VLY9402 / Serine; EC 2.7.1.- / protein kinase C eta; EC 2.7.11.13 / Protein Kinase C; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS431766; NLM/ PMC3963830
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5. Hornick JR, Johnston FM, Simon PO, Younkin M, Chamberlin M, Mitchem JB, Azar RR, Linehan DC, Strasberg SM, Edmundowicz SA, Hawkins WG: A single-institution review of 157 patients presenting with benign and malignant tumors of the ampulla of Vater: management and outcomes. Surgery; 2011 Aug;150(2):169-76
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  • BACKGROUND: Although benign ampullary tumors are removed endoscopically, due to their potential to progress to malignant disease, the favored treatment for adenocarcinoma is pancreaticoduodenectomy.
  • METHODS: We retrospectively reviewed 157 patients who presented with an ampullary mass, from 2001 to 2010, and identified 51 with benign adenoma and 106 with adenocarcinoma.
  • Based on our finding that nearly half the patients with T1 tumors had positive lymph nodes, we recommend pancreaticoduodenectomy for any patient with biopsy proven adenocarcinoma who is a suitable candidate for surgery.
  • [MeSH-major] Adenocarcinoma / surgery. Adenoma / surgery. Ampulla of Vater. Common Bile Duct Neoplasms / surgery

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  • (PMID = 21801957.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30 CA091842-01; United States / NCI NIH HHS / CA / T32 CA009621; United States / NCI NIH HHS / CA / T32 CA009621-22; United States / NCATS NIH HHS / TR / UL1 TR000448
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS309658; NLM/ PMC3155697
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6. Traverso LW, Moriya T, Hashimoto Y: Intraductal papillary mucinous neoplasms of the pancreas: making a disposition using the natural history. Curr Gastroenterol Rep; 2012 Apr;14(2):106-11
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  • The process of Intraductal papillary mucinous neoplasms (IPMN) follows the adenoma-to-carcinoma sequence.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Pancreatic Neoplasms / diagnosis

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7. Martínez-Aguilar J, Clifton-Bligh R, Molloy MP: Proteomics of thyroid tumours provides new insights into their molecular composition and changes associated with malignancy. Sci Rep; 2016 Mar 30;6:23660
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  • We applied data-independent acquisition mass spectrometry which enabled quantitative expression analysis of over 1,600 proteins from 32 specimens to compare normal thyroid tissue with the three most common tumours of the thyroid gland: follicular adenoma, follicular carcinoma and papillary carcinoma.
  • We made the novel observation that TGFβ-induced protein ig-h3 (TGFBI) was found frequently overexpressed in follicular carcinoma compared with follicular adenoma.
  • [MeSH-major] Adenocarcinoma, Follicular / metabolism. Adenoma / metabolism. Carcinoma, Papillary / metabolism. Proteome / metabolism. Thyroid Neoplasms / metabolism

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  • (PMID = 27025787.001).
  • [ISSN] 2045-2322
  • [Journal-full-title] Scientific reports
  • [ISO-abbreviation] Sci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteome
  • [Other-IDs] NLM/ PMC4812243
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8. Kim JG, Kim TO, Bae JH, Shim JW, Kang MJ, Yang K, Ting AH, Yi JM: Epigenetically regulated MIR941 and MIR1247 target gastric cancer cell growth and migration. Epigenetics; 2014 Jul;9(7):1018-30
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  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Cell Movement. Cell Proliferation. Epigenesis, Genetic. MicroRNAs / genetics. RNA, Messenger / metabolism. Stomach Neoplasms / pathology

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  • (PMID = 24785261.001).
  • [ISSN] 1559-2308
  • [Journal-full-title] Epigenetics
  • [ISO-abbreviation] Epigenetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC4143404
  • [Keywords] NOTNLM ; 5-aza-2'-deoxycytidine / DNA methylation / MIR1247 / MIR941 / epigenetics / gastric cancer / microRNA
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9. Takeyama H, Mizushima T, Nakajima K, Uemura M, Haraguchi N, Nishimura J, Hata T, Takemasa I, Yamamoto H, Doki Y, Mori M: Metachronous, colitis-associated rectal cancer that developed after sporadic adenocarcinoma in an adenoma in a patient with longstanding Crohn's disease: a case report. World J Surg Oncol; 2013;11:295
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  • [Title] Metachronous, colitis-associated rectal cancer that developed after sporadic adenocarcinoma in an adenoma in a patient with longstanding Crohn's disease: a case report.
  • Here, we describe a case of metachronous, colitis-associated rectal cancer that developed after the complete resection of an adenoma that became a sporadic adenocarcinoma in a patient with longstanding CD.
  • A histopathological examination showed an adenoma with sporadic adenocarcinoma.
  • A histopathological examination revealed a mucinous adenocarcinoma with signet ring cell carcinoma and lymph node metastasis.
  • [MeSH-major] Adenocarcinoma, Mucinous / secondary. Carcinoma, Signet Ring Cell / secondary. Crohn Disease / complications. Neoplasms, Second Primary. Rectal Neoplasms / pathology

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  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; Q573I9DVLP / Leucovorin
  • [Other-IDs] NLM/ PMC4225674
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10. Letellier E, Schmitz M, Baig K, Beaume N, Schwartz C, Frasquilho S, Antunes L, Marcon N, Nazarov PV, Vallar L, Even J, Haan S: Identification of SOCS2 and SOCS6 as biomarkers in human colorectal cancer. Br J Cancer; 2014 Aug 12;111(4):726-35
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  • Finally, we investigated the prognostic value of SOCS2 and SOCS6.
  • [MeSH-major] Adenocarcinoma / metabolism. Colorectal Neoplasms / metabolism. Suppressor of Cytokine Signaling Proteins / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Base Sequence. Biomarkers, Tumor. DNA Methylation. Disease-Free Survival. Down-Regulation. Female. Gene Expression. Humans. Male. Middle Aged. Molecular Sequence Data. Neoplasm Staging. Prognosis. Promoter Regions, Genetic. ROC Curve

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  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SOCS2 protein, human; 0 / SOCS6 protein, human; 0 / Suppressor of Cytokine Signaling Proteins
  • [Other-IDs] NLM/ PMC4134506
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