腸癌
- 関
- bowel cancer、intestinal cancer
WordNet
- of or relating to or inside the intestines; "intestinal disease" (同)enteric, enteral
- any malignant tumor derived from epithelial tissue; one of the four major types of cancer
PrepTutorEJDIC
- 腸[内]の
- がん,がん腫
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English Journal
- Chronic ulcerative colitis and colorectal cancer.
- Rogler G.Author information Division of Gastroenterology and Hepatology, Department of Visceral Medicine, University Hospital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland. Electronic address: gerhard.rogler@usz.ch.AbstractOne of the most important consequences of chronically active ulcerative colitis (UC) or Crohn's disease (CD) - the two major forms of inflammatory bowel disease (IBD) - is the development of colorectal cancer (CRC). An increased risk for the occurrence of CRC in up to 30% of affected patients after 35years of UC has been reported. Recent evidence from population based studies indicates a lower risk. Nevertheless the incidence is still significantly increased as compared to individuals without chronic colitis. Colitis-associated CRC (CAC) does not display the adenoma-carcinoma sequence which is typical for sporadic CRC and the pathophysiology appears to be different. Chronic inflammation and the increased turnover of epithelial cells contribute to the development of low- and high-grade dysplasia which may further transform into CAC. Reactive oxygen species (ROS) generated by the inflammatory infiltrate are thought to contribute to the generation of dysplastic lesions. In sporadic CRC the sequence of mutations that finally lead to malignancy involves early activation of Wnt/β-catenin pathway (in 90% of cases) including mutations in adenomatous polyposis coli (APC) tumor suppressor gene, its regulating kinase GSK3β and β-catenin itself. β-catenin mutations are rarer in CAC and mutations in APC occur rather late during the disease progression, whereas there are earlier mutations in p53 and K-ras. Recent data indicate that the intestinal microbiome and its interaction with a functionally impaired mucosal barrier may also play a role in CAC development. CACs frequently show aggressive growth and early metastases. The treatment of CAC in patients with colitis always includes proctocolectomy with ileoanal anastomosis as meta- or synchronic lesions are frequent.
- Cancer letters.Cancer Lett.2014 Apr 10;345(2):235-41. doi: 10.1016/j.canlet.2013.07.032. Epub 2013 Aug 11.
- One of the most important consequences of chronically active ulcerative colitis (UC) or Crohn's disease (CD) - the two major forms of inflammatory bowel disease (IBD) - is the development of colorectal cancer (CRC). An increased risk for the occurrence of CRC in up to 30% of affected patients after
- PMID 23941831
- Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).
- Thakker RV.Author information Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford OX3 7LJ, United Kingdom. Electronic address: rajesh.thakker@ndm.ox.ac.uk.AbstractMultiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previously MEN2A) due to mutations of a tyrosine kinase receptor encoded by the rearranged during transfection (RET) protoncogene; MEN3 (previously MEN2B) due to RET mutations; and MEN4 due to cyclin-dependent kinase inhibitor (CDNK1B) mutations. Each MEN type is associated with the occurrence of specific tumors. Thus, MEN1 is characterized by the occurrence of parathyroid, pancreatic islet and anterior pituitary tumors; MEN2 is characterized by the occurrence of medullary thyroid carcinoma (MTC) in association with phaeochromocytoma and parathyroid tumors; MEN3 is characterized by the occurrence of MTC and phaeochromocytoma in association with a marfanoid habitus, mucosal neuromas, medullated corneal fibers and intestinal autonomic ganglion dysfunction, leading to megacolon; and MEN4, which is also referred to as MENX, is characterized by the occurrence of parathyroid and anterior pituitary tumors in possible association with tumors of the adrenals, kidneys, and reproductive organs. This review will focus on the clinical and molecular details of the MEN1 and MEN4 syndromes. The gene causing MEN1 is located on chromosome 11q13, and encodes a 610 amino-acid protein, menin, which has functions in cell division, genome stability, and transcription regulation. Menin, which acts as scaffold protein, may increase or decrease gene expression by epigenetic regulation of gene expression via histone methylation. Thus, menin by forming a subunit of the mixed lineage leukemia (MLL) complexes that trimethylate histone H3 at lysine 4 (H3K4), facilitates activation of transcriptional activity in target genes such as cyclin-dependent kinase (CDK) inhibitors; and by interacting with the suppressor of variegation 3-9 homolog family protein (SUV39H1) to mediate H3K methylation, thereby silencing transcriptional activity of target genes. MEN1-associated tumors harbor germline and somatic mutations, consistent with Knudson's two-hit hypothesis. Genetic diagnosis to identify individuals with germline MEN1 mutations has facilitated appropriate targeting of clinical, biochemical and radiological screening for this high risk group of patients for whom earlier implementation of treatments can then be considered. MEN4 is caused by heterozygous mutations of CDNK1B which encodes the 196 amino-acid CDK1 p27Kip1, which is activated by H3K4 methylation.
- Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Apr 5;386(1-2):2-15. doi: 10.1016/j.mce.2013.08.002. Epub 2013 Aug 8.
- Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previou
- PMID 23933118
- Adenocarcinoma of the minor duodenal papilla and its precursor lesions: a clinical and pathologic study.
- Shia J1, Agaram NP, Olgac S, Cobanov B, Adsay V, Klimstra DS.Author information 1*Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY †Department of Pathology, Emory University Hospital, Atlanta, GA.AbstractThe minor duodenal papilla drains the accessory pancreatic duct of Santorini and lies proximal to the ampulla of Vater. Adenocarcinoma and its precursor lesions arising in the minor papilla are rare. Literature data thus far are limited to a few individual case reports, and the condition is consequently poorly defined. Our study cases were composed of carcinomas fulfilling all of the following criteria: location at 1.5 to 2.5 cm proximal to the major papilla; presence of associated submucosal pancreatobiliary-type ducts with periductal glands or acinar tissue; a predominant submucosal location of the tumor; and lack of an intestinal-type adenoma in the adjacent duodenal mucosa. Tumors were studied morphologically, immunohistochemically, and clinically. Nine cases fulfilling the inclusion criteria were identified. There were 5 men and 4 women with an age range of 50 to 76 years (median, 72 y). The tumor size ranged from 1.2 to 4.4 cm (median, 3 cm). The carcinomas were of colloid type (3 tumors), pancreatobiliary type (4), or nonmucinous intestinal type (2). Five cases were associated with an intraductal papillary mucinous neoplasm (IPMN)-like precursor lesion within the residual structures of the minor papilla in the duodenal submucosa. Immunohistochemically, the intestinal-type and mucinous-type tumors tended to be positive for CK20, CDX2, MUC2, and B72.3, and pancreatobiliary-type tumors tended to be positive for CK7, MUC1, B72.3, and CA125. Loss of DPC4 (Smad4) expression was found in the pancreatobiliary-type carcinomas only. Two tumors showed loss of DNA mismatch-repair protein expression, one losing MLH1 and PMS2 and the other losing MSH6. Both patients were older than 60 years, and neither had germline mutation testing. Follow-up information was available for 6 patients (median follow-up time, 67.5 mo): 3 of the 6 patients died of disease at 60, 75, and 85 months after surgery, respectively, and all 3 patients had an intestinal-type carcinoma (1 colloid and 2 nonmucinous). The patient whose tumor was MSH6 deficient was alive without evidence of disease 51 months after surgery. In conclusion, adenocarcinomas of the minor papilla are rare tumors occurring predominantly in the sixth to seventh decade. Some of them arise from IPMN-like precursors in the residual submucosal minor papilla tissue. Morphologically, immunohistochemically, and clinically they are similar to ampullary or IPMN-associated pancreatic carcinomas and can exhibit either an intestinal, colloid, or pancreaticobiliary phenotype. DNA mismatch-repair deficiency may occur. A careful gross and histologic examination is essential to accurately recognize the site of origin of minor papilla carcinomas.
- The American journal of surgical pathology.Am J Surg Pathol.2014 Apr;38(4):526-33. doi: 10.1097/PAS.0000000000000123.
- The minor duodenal papilla drains the accessory pancreatic duct of Santorini and lies proximal to the ampulla of Vater. Adenocarcinoma and its precursor lesions arising in the minor papilla are rare. Literature data thus far are limited to a few individual case reports, and the condition is conseque
- PMID 24625417
Japanese Journal
- 膵Gastric Type Intraductal Papillary-Mucinous NeoplasmsのMIB-1 Labeling Index (Ki67)
- 渡邊 利広,高須 直樹,竹下 明子,手塚 康二,平井 一郎,木村 理
- 山形大学紀要. 医学 : 山形医学 32(2), 59-66, 2014-08-15
- … examined the relationship between the MIB-1 labeling index (Ki67) and the four morphological and immunohistological subtypes of intraductal papillary-mucinous neoplasms of the pancreas (IPMN).Methods :Between 2000 and 2007, we retrospectively evaluated 46 patients who had undergone surgery, were histopathologically diagnosed as IPMN, and in whom immunohistochemical staining was possible.Results :Histological grades of the 46 IPMNs were adenoma (n = 27), carcinoma in situ (n = 9), and invasive carcinoma derived from IPMN (n = …
- NAID 110009825046
- 症例 小腸転移により小腸穿孔をきたした肺多形癌の1例
- 寺田 百合子,檜山 紀子,古畑 善章
- 胸部外科 = The Japanese journal of thoracic surgery 67(9), 856-859, 2014-08
- NAID 40020162308
- Histological phenotype is correlated with the wall-invasion pattern of gallbladder adenocarcinoma
- TOBA Takahito,KIJIMA Hiroshi,HAKAMADA Kenichi,IGARASHI Yoshinori
- Biomedical Research 35(5), 295-302, 2014
- … Gallbladder carcinoma (GBC) is one of the most aggressive malignancies, and frequently shows vascular invasion and lymph node metastasis. … Histologically, the 61 cases were classified into the biliary (44 cases, 72.1%), gastric foveolar (13 cases, 21.3%), and intestinal (4 cases, 6.6%) types. …
- NAID 130004701679
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★リンクテーブル★
[★]
腸癌、腸がん
- 関
- bowel cancer、cancer of the intestine、intestinal carcinoma、intestinal neoplasm
[★]
- 英
- bowel cancer、intestinal cancer、intestinal carcinoma
- 関
- 小腸癌、腸がん、腸腫瘍
[★]
腸癌
- 関
- intestinal cancer、intestinal carcinoma
[★]
胃腸癌、消化器癌
- 関
- cancer of the gastrointestinal tract、gastrointestinal cancer
[★]
- 関
- alimentary system、bowel、digestive system、enteric、enteric canal、entero、gastrointestinal、gastrointestinal system、GI、gut、intestinal tract、intestine