- Primary Colonic Follicular Lymphoma Presenting as Four Diminutive Sessile Polyps Found Incidentally During Colonoscopy. [Journal Article]
- CEClin Endosc 2018 Apr 18
- Follicular lymphomas, which typically arise in the lymph nodes with spleen, liver, and bone marrow involvement, have generally low occurrence rates in Asian countries as compared with Western countri...
Follicular lymphomas, which typically arise in the lymph nodes with spleen, liver, and bone marrow involvement, have generally low occurrence rates in Asian countries as compared with Western countries. Follicular lymphomas of the gastrointestinal tract are rare, and primary colonic follicular lymphomas are particularly rare compared with others found in the small intestine and duodenum. Colonoscopic imaging of colonic lymphomas, including follicular lymphoma, may reveal mucosal ulcerations, erosions, indurations, polypoid mass-like lesions, and diffuse mucosal nodularity. Herein, we report a unique case of a follicular lymphoma of the transverse colon characterized by four sessile diminutive polyps located intermittently with multiple lymph node involvement in a 62-year-old man.
- Loss of ZG16 is associated with molecular and clinicopathological phenotypes of colorectal cancer. [Journal Article]
- BCBMC Cancer 2018 Apr 16; 18(1):433
- CONCLUSIONS: For the first time, our study demonstrated that ZG16 expression was sequentially reduced from normal, adenoma, to carcinoma. Association with multiple clinicopathological features indicates that ZG16 may play an important role in cancer initiation and progression. ZG16 may serve as a potential biomarker for diagnosis and prognosis of CRC.
- The application value of capsule endoscopy in diagnosing small intestinal carcinoma. [Journal Article]
- JCJ Cancer Res Ther 2018; 14(1):57-60
- CONCLUSIONS: Capsule endoscopy demonstrated a high diagnostic value for various small bowel diseases, including both tumor and inflammatory lesions. Given its simplicity, safety, and reliability, capsule endoscopy was an important examination tool for the diagnosis of small bowel diseases.
- A novel bioactive derivative of eicosapentaenoic acid (EPA) suppresses intestinal tumor development in ApcΔ14/+ mice. [Journal Article]
- CCarcinogenesis 2018 Mar 08; 39(3):429-438
- Familial adenomatous polyposis (FAP) is a genetic disorder characterized by the development of hundreds of polyps throughout the colon. Without prophylactic colectomy, most individuals with FAP devel...
Familial adenomatous polyposis (FAP) is a genetic disorder characterized by the development of hundreds of polyps throughout the colon. Without prophylactic colectomy, most individuals with FAP develop colorectal cancer at an early age. Treatment with EPA in the free fatty acid form (EPA-FFA) has been shown to reduce polyp burden in FAP patients. Since high-purity EPA-FFA is subject to rapid oxidation, a stable form of EPA compound has been developed in the form of magnesium l-lysinate bis-eicosapentaenoate (TP-252). We assessed the chemopreventive efficacy of TP-252 on intestinal tumor formation using ApcΔ14/+ mice and compared it with EPA-FFA. TP-252 was supplemented in a modified AIN-93G diet at 1, 2 or 4% and EPA-FFA at 2.5% by weight and administered to mice for 11 weeks. We found that administration of TP-252 significantly reduced tumor number and size in the small intestine and colon in a dose-related manner and as effectively as EPA-FFA. To gain further insight into the cancer protection afforded to the colon, we performed a comprehensive lipidomic analysis of total fatty acid composition and eicosanoid metabolites. Treatment with TP-252 significantly decreased the levels of arachidonic acid (AA) and increased EPA concentrations within the colonic mucosa. Furthermore, a classification and regression tree (CART) analysis revealed that a subset of fatty acids, including EPA and docosahexaenoic acid (DHA), and their downstream metabolites, including PGE3 and 14-hydroxy-docosahexaenoic acid (HDoHE), were strongly associated with antineoplastic activity. These results indicate that TP-252 warrants further clinical development as a potential strategy for delaying colectomy in adolescent FAP patients.
- Extensive colorectal lymphomatous polyposis complicated by acute intestinal obstruction: a case report. [Case Reports]
- JMJ Med Case Rep 2017 Jul 13; 11(1):190
- CONCLUSIONS: Mantle cell lymphoma develops as a progressive and aggressive disease with widespread polyposis of the gastrointestinal tract. The intensive chemotherapeutic regimens usually result in the regression of macroscopic and microscopic lesions; however, remissions are short in duration, and the median length of patient survival is 3-4 years. Mantle cell lymphoma is a rare disease that should be part of the differential diagnosis of polypoid diseases of the large intestine.
- Stat6 Promotes Intestinal Tumorigenesis in a Mouse Model of Adenomatous Polyposis by Expansion of MDSCs and Inhibition of Cytotoxic CD8 Response. [Journal Article]
- NNeoplasia 2017; 19(8):595-605
- Intestinal tumorigenesis in the ApcMin/+ model is initiated by aberrant activation of Wnt pathway. Increased IL-4 expression in human colorectal cancer tissue and growth of colon cancer cell lines im...
Intestinal tumorigenesis in the ApcMin/+ model is initiated by aberrant activation of Wnt pathway. Increased IL-4 expression in human colorectal cancer tissue and growth of colon cancer cell lines implied that IL-4-induced Stat6-mediated tumorigenic signaling likely contributes to intestinal tumor progression in ApcMin/+ mice. Stat6 also appears to promote expansion of myeloid-derived suppressor cells (MDSCs) cells. MDSCs promote polyp formation in the ApcMin/+ model. Hence, Stat6 could have a broad role in coordinating both polyp cell proliferation and MDSC expansion. We found that IL-4-induced Stat6-mediated proliferation of intestinal epithelial cells is augmented by platelet-derived growth factor-BB, a tumor-promoting growth factor. To determine whether polyp progression in ApcMin/+ mice is dependent on Stat6 signaling, we disrupted Stat6 in this model. Total polyps in the small intestine were fewer in ApcMin/+ mice lacking Stat6. Furthermore, proliferation of polyp epithelial cells was reduced, indicating that Stat6 in part controlled polyp formation. Stat6 also promoted expansion of MDSCs in the spleen and lamina propria of ApcMin/+ mice, implying regulation of antitumor T-cell response. More CD8 cells and reduced PD-1 expression on CD4 cells correlated with reduced polyps. In addition, a strong CD8-mediated cytotoxic response led to killing of tumor cells in Stat6-deficient ApcMin/+ mice. Therefore, these findings show that Stat6 has an oncogenic role in intestinal tumorigenesis by promoting polyp cell proliferation and immunosuppressive mediators, and preventing an active cytotoxic process.
- Protein-losing pseudomembranous colitis with cap polyposis-like features. [Case Reports]
- WJWorld J Gastroenterol 2017 Apr 28; 23(16):3003-3010
- Protein-losing enteropathy (PLE) is characterized by loss of serum proteins into the gastrointestinal tract. It may lead to hypoproteinemia and clinically present as protein deficiency edema, ascites...
Protein-losing enteropathy (PLE) is characterized by loss of serum proteins into the gastrointestinal tract. It may lead to hypoproteinemia and clinically present as protein deficiency edema, ascites, pleural or pericardial effusion and/or malnutrition. In most cases the site of protein loss is the small intestine. Here we present an unusual case of severe PLE in a 55-year old female with a one-year history of recurrent diarrhea, crampy abdominal pain, and peripheral edema. Endoscopy and MRI showed a diffuse inflammatory thickening of the sigmoid colon and the rectum. Surgical resection of the involved colon was performed and the symptoms were significantly resolved. The final histologic evaluation confirmed a diagnosis of a pseudomembranous colitis with cap polyposis-like features. Such a cause of PLE has never been described before.
- New insights into the earliest stages of colorectal tumorigenesis. [Review]
- ERExpert Rev Gastroenterol Hepatol 2017; 11(8):723-729
- Tumors in the large intestine have been postulated to arise via a stepwise accumulation of mutations, a process that takes up to 20 years. Recent advances in lineage tracing and DNA sequencing, howev...
Tumors in the large intestine have been postulated to arise via a stepwise accumulation of mutations, a process that takes up to 20 years. Recent advances in lineage tracing and DNA sequencing, however, are revealing new evolutionary models that better explain the vast amount of heterogeneity observed within and across colorectal tumors. Areas covered: A review of the literature supporting a novel model of colorectal tumor evolution was conducted. The following commentary examines the basic science and clinical evidence supporting a modified view of tumor initiation and progression in the colon. Expert commentary: The proposed 'cancer punctuated equilibrium' model of tumor evolution better explains the variability seen within and across polyps of the colon and rectum. Small colorectal polyps (6-9mm) followed longitudinally by interval imaging with CT colonography have been reported to have multiple fates: some growing, some remaining static in size, and others regressing in size over time. This new model allows for this variability in growth behavior and supports the hypothesis that some tumors can be 'born to be bad' as originally postulated by Sottoriva and colleagues, with very early molecular events impacting tumor fitness and growth behavior in the later stages of the disease process.
- Peutz-Jeghers syndrome with intermittent upper intestinal obstruction: A case report and review of the literature. [Case Reports]
- MMedicine (Baltimore) 2017; 96(17):e6538
- CONCLUSIONS: In this case, the patient was characteristic with pigmentations on his lips and intermittent upper intestinal obstruction (due to mass duodenal polyps), there are no definitive guidelines for the treatment to duodenal PJS hamartomatous polyp, each case requires tailor-made management.
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- GeneReviews® [BOOK]
- BOOKUniversity of Washington, Seattle: Seattle (WA)
- Juvenile polyposis syndrome (JPS) is characterized by predisposition to hamartomatous polyps in the gastrointestinal (GI) tract, specifically in the stomach, small intestine, colon, and rectum. The t...
Juvenile polyposis syndrome (JPS) is characterized by predisposition to hamartomatous polyps in the gastrointestinal (GI) tract, specifically in the stomach, small intestine, colon, and rectum. The term "juvenile" refers to the type of polyp rather than to the age of onset of polyps. Most individuals with JPS have some polyps by age 20 years; some may have only four or five polyps over their lifetime, whereas others in the same family may have more than 100. If the polyps are left untreated, they may cause bleeding and anemia. Most juvenile polyps are benign; however, malignant transformation can occur. Risk for GI cancers in families with JPS ranges from 9% to 50%. Most of this increased risk is attributed to colon cancer, but cancers of the stomach, upper GI tract, and pancreas have also been reported. A combined syndrome of JPS and hereditary hemorrhagic telangiectasia (JPS/HHT) is present in most individuals with an SMAD4 pathogenic variant.