Journal articles: 'Colon'

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Olegovich, Ten Dmitry. "Results Of Colon Anastomosis Formation After Sigmoid Colon Resection." American Journal of Medical Sciences and Pharmaceutical Research 02, no. 07 (July 30, 2020): 31–37. http://dx.doi.org/10.37547/tajmspr/volume02issue07-05.

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Spencer, Nick J., Melinda Kyloh, David A. Wattchow, Anthony Thomas, Tiong Cheng Sia, Simon J. Brookes, and Sarah J. Nicholas. "Characterization of motor patterns in isolated human colon: are there differences in patients with slow-transit constipation?" American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 1 (January 2012): G34—G43. http://dx.doi.org/10.1152/ajpgi.00319.2011.

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The patterns of motor activity that exist in isolated full-length human colon have not been described. Our aim was to characterize the spontaneous motor patterns in isolated human colon and determine whether these patterns are different in whole colons obtained from patients with slow-transit constipation (STC). The entire colon (excluding the anus), was removed from patients with confirmed STC and mounted longitudinally in an organ bath ∼120 cm in length, containing oxygenated Krebs' solution at 36°C. Changes in circular muscle tension were recorded from multiple sites simultaneously along the length of colon, by use of isometric force transducers. Recordings from isolated colons from non-STC patients revealed cyclical colonic motor complexes (CMCs) in 11 of 17 colons, with a mean interval and half-duration of contractions of 4.0 ± 0.6 min and 51.5 ± 15 s, respectively. In the remaining six colons, spontaneous irregular phasic contractions occurred without CMCs. Interestingly, in STC patients robust CMCs were still recorded, although their CMC pacemaker frequencies were slower. Intraluminal balloon distension of the ascending or descending colon evoked an ascending excitatory reflex contraction, or evoked CMC, in 8 of 30 trials from non-STC (control) colons, but not from colons obtained from STC patients. In many control segments of descending colon, spontaneous CMCs consisted of simultaneous ascending excitatory and descending inhibitory phases. In summary, CMCs can be recorded from isolated human colon, in vitro, but their intrinsic pacemaker frequency is considerably faster in vitro compared with previous human recordings of CMCs in vivo. The observation that CMCs occur in whole colons removed from STC patients suggests that the intrinsic pacemaker mechanisms underlying their generation and propagation are preserved in vitro, despite impaired transit along these same regions in vivo.

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Schusser, Gerald F., and Nathaniel A. White. "Morphologic and quantitative evaluation of the myenteric plexuses and neurons in the large colon of horses." Journal of the American Veterinary Medical Association 210, no. 7 (April 1, 1997): 928–34. http://dx.doi.org/10.2460/javma.1997.210.07.928.

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Objective— To determine the number of myenteric plexuses and neurons in the large colon of clinically normal horses and whether the number was decreased in the large colon of horses with colon disease. Design— Prospective study. Sample Population— Colon samples from 15 clinically normal horses and 31 horses with colon disease. Procedure— Samples were obtained, fixed, and stained with H&E. The number of myenteric plexuses and neurons and longitudinal muscle thickness were determined in each segment of colon for clinically normal horses. Counts for segments were compared with each other and with counts in the same segment from horses with colon disease. Results— Myenteric plexus and neuron densities and longitudinal muscle thickness in clinically normal horses were significantly greater in the pelvic flexure and left dorsal and transverse colons. Horses with chronic obstruction (> 24 hours' duration) or with previous obstruction had significantly lower neuron density in the pelvic flexure. Myenteric plexus density in horses with strangulating large colon torsion/volvulus was significantly less in the right ventral, right dorsal, and transverse colons, and neuron density in these horses was significantly less in all segments of colon, except the left ventral colon. Horses with colon strangulation that survived had significantly greater neuron density than horses with colon strangulation that died. Enteroglial cell numbers were increased in myenteric plexuses of horses with acute and chronic obstruction. Clinical Implications— Myenteric plexus and neuron densities can be estimated by evaluating linear counts of H&E-stained colon samples. Enteroglial cells may increase in number in response to myenteric plexus inflammation, which may affect bowel function. (J Am Vet Med Assoc 1997;210:928–934)

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Holmqvist, O. H. "Colon heat and colon cancer." Medical Hypotheses 54, no. 3 (March 2000): 469–71. http://dx.doi.org/10.1054/mehy.1999.0878.

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Serrano-Morales, José M., María D. Vázquez-Carretero, Pablo García-Miranda, Ana E. Carvajal, María L. Calonge, Anunciación A. Ilundain, and María J. Peral. "Reelin Protects Against Colon Pathology via p53 and May Be a Biomarker for Colon Cancer Progression." Biology 11, no. 10 (September 26, 2022): 1406. http://dx.doi.org/10.3390/biology11101406.

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Previous observations made in human and mouse colons suggest that reelin protects the colon from pathology. In this study, we evaluated reelin expression during the transition from either colitis or precancerous lesions to colon cancer and tried to elucidate reelin regulation under these transition processes. Samples of healthy and pathological colons from humans and mice treated with either azoxymethane/dextran sulfate sodium (DSS) or azoxymethane alone were used. The relative abundances of reelin, DNMT-1 and ApoER2 mRNAs were determined by PCR in the colon samples cited above and in the tissue adjacent to mouse colon polyps and adenocarcinomas. In both, humans and mice, reelin mRNA abundance increased significantly in ulcerative colitis and slightly in polyps and decreased in adenomas and adenocarcinomas. Reelin expression was higher in the tissue adjacent to the colon adenocarcinoma and lower in the lesion itself. The reelin expression changes may result, at least in part, from those in DNMT-1 and appear to be independent of ApoER2. Lack of reelin downregulated p-Akt and p53 in healthy colon and prevented their increases in the inflamed colon, whereas it increased GSK-3β in DSS-untreated mice. In conclusion, reelin mRNA abundance depends on the severity of the colon pathology, and its upregulation in response to initial injuries might prevent the beginning of colon cancer, whereas reelin repression favors it. Increased p53 expression and activation may be involved in this protection. We also propose that changes in colon reelin abundance could be used to predict colon pathology progression.

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Gao, Chang, Rui Sun, Ya-Rong Xie, An-Li Jiang, Mei Lin, Min Li, Zheng-Wang Chen, Ping Zhang, Honglin Jin, and Jue-Ping Feng. "The soy-derived peptide Vglycin inhibits the growth of colon cancer cells in vitro and in vivo." Experimental Biology and Medicine 242, no. 10 (March 1, 2017): 1034–43. http://dx.doi.org/10.1177/1535370217697383.

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Vglycin, a novel natural polypeptide isolated from pea seeds, possesses antidiabetic properties. Our previous studies have shown that Vglycin can induce the differentiation of human colon adenocarcinoma cells. We aimed to determine the anticancer activity of Vglycin against colon cancer cells and to elucidate related apoptosis-inducing mechanisms. Treatment with purified Vglycin significantly reduced growth, viability, and colony formation of CT-26, SW480, and NCL-H716 colon cancer cells in a dose-dependent manner while down-regulating the expression of proliferating cell nuclear antigen. Mouse xenograft studies showed a 38% inhibition of colon cancer growth in mice treated with Vglycin (20 mg/kg/day) at day 21. Furthermore, the potential mechanisms involved in Vglycin-induced cell apoptosis were examined using cell cycle studies, ultrastructural examination, as well as apoptosis-associated pathway analysis. The results showed that Vglycin significantly promoted apoptosis and G1/S phase cell cycle arrest. As revealed by Western blot, the expression of CDK2 and Cyclin D1 was down-regulated in all three Vglycin-treated colon cancer cells, indicating that the CDK2/Cyclin D1 cell cycle pathway involved in the initiation and progression of colon cancer. Moreover, the inhibition of Vglycin-induced cell proliferation in colon cancer cells was accompanied by alteration of the expression levels of the apoptosis-related proteins Bax, Bcl-2 and Mcl-1, and an increase of caspase-3 activity. Together, our results suggest that Vglycin may be another plant-derived peptide that suppresses colon cancer, supporting the continued investigation of Vglycin as therapeutic agent for colon cancer. Impact statement The antidiabetic properties and the capability of inducing differentiation of human colon adenocarcinoma cells of Vglycin have been reported in our previous studies. However, the anticancer potential of Vglycin on colon cancer cells and its possible related mechanisms were still unknown. In this study, we found that Vglycin could reduce growth, viability, and colony formation or colony size of CT-26, SW480, and NCL-H716 colon cancer cells. Moreover, Vglycin decreased tumor volume by 38% in xenograft mice transplanted with CT-26 cells. The mechanisms of these phenomena may be due to the down-regulated CDK2 and Cyclin D1, G1/S phase cell cycle arrest, and the dysregulated expression of Bax, Bcl-2, and Mcl-1. The findings highlight the anticancer potential of Vglycin against colon cancer cells, and suggest Vglycin may be another colon cancer potential suppressive component of plant-derived peptides.

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Liu, Y., H. Huang, B. Yuan, L. Zhuang, T. Luo, and Q. Zhang. "Lentivirus-Mediated Knockdown of NOB1 Suppresses the Proliferation of Colon Cancer Cells." Zeitschrift für Gastroenterologie 52, no. 05 (May 2014): 429–35. http://dx.doi.org/10.1055/s-0033-1356338.

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AbstractNOB1 is important for ribosome biogenesis and protein degradation. Previous studies showed that it could regulate the growth and colony-formation ability of ovarian, breast and hepatocellular carcinoma cells. However, its function in colon cancer cells is largely unknown. In this study, we found that NOB1 could express in 6 different colon cancer cell lines. Lentivirus-mediated shRNA targeted NOB1 could suppress the endogenous gene expression. NOB1 depletion significantly inhibited cell proliferation and colony formation ability, as determined by MTT and colony formation assays. Flow cytometry analysis showed NOB1 silencing arrested cell cycle in G0 / G1 phase. Moreover, the percentage of cells at sub-G1 phase dramatically increased after NOB1 knockdown. These results indicate that NOB1 may play an important role in the growth and tumorigensis of colon cancer and knockdown of NOB1 may be a potential therapeutic method for colon cancer in the future.

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Phillips, M., A. Patel, P. Meredith, O. Will, and C. Brassett. "Segmental colonic length and mobility." Annals of The Royal College of Surgeons of England 97, no. 6 (September 1, 2015): 439–44. http://dx.doi.org/10.1308/003588415x14181254790527.

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Introduction Locoregional variation in the human colon is important in surgical practice; the length and mobility of different colonic regions impacts on laparoscopic and endoscopic colorectal procedures. The aim of this study was to refine anatomical understanding of the colon in terms of segmental length and mobility. Methods The colons of 35 cadavers were examined to determine lengths of caecum as well as ascending, transverse, descending and rectosigmoid colon, and to characterise colonic mobility at each location in terms of the mesenteric attachments. The presence of Jackson’s membrane (a congenital peritoneal band of the right colon) was also documented. Results The mean total colonic length was 131.2cm (standard deviation [SD]: 13.4cm). There was no correlation with height, age or sex; the best predictor of total colonic length was the length of the rectosigmoid segment. The mean height of the transverse mesocolon was 7.4cm (SD: 3.6cm) and that of the sigmoid mesocolon was 6.3cm (SD: 2.6cm). Two-thirds of the subjects had a mobile portion of the ascending colon and nearly one-third had a mobile descending colon. A mobile ascending colon was significantly more common in females. Jackson’s membrane was present in 66% of the subjects. Conclusions This cadaveric study suggests that rectosigmoid length accounts for most of the variability in total colonic length. The significant proportion of colons with mobility of the ascending and descending segments prompts revision of the traditional anatomical teaching of these segments as fixed and retroperitoneal. Mobility of the ascending colon may account for the anecdotal finding that colonoscopy is more challenging in female patients. Jackson’s membrane was identified in most colons.

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Wiese, Maria, Yan Hui, Dennis S. Nielsen, Andrew R. Williams, Julie C. Lynegaard, Nicolai R. Weber, and Charlotte Amdi. "Color of Colon Content of Normal and Intrauterine Growth-Restricted Weaned Piglets Is Associated with Specific Microbial Taxa and Physiological Parameters." Animals 10, no. 6 (June 22, 2020): 1073. http://dx.doi.org/10.3390/ani10061073.

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A well-balanced gut microbiome is associated with improved health outcomes, but to date, the GM of IUGR piglets have only been sparsely investigated. Here, we investigated GM composition, color of colon content, and blood parameters of 20 IUGR and 20 normal 24-day-old piglets. No significant differences were detected in colon microbiota composition between IUGR and the normal piglets with respect to alpha and beta diversity measures. The colon content of these piglets displayed three colors: brown, black, and yellow. Interestingly, the color of the colon content varied with microbial community composition, with significant differences in the relative abundance of taxa belonging to Fusobacteria and Treponema. Fusobacteria were most abundant in yellow fecal samples, with a mean relative abundance around 5.6%, whereas this was 0.51% within brown and 0.02% for the black fecal samples. Fusobacteria positively correlated with total blood protein, albumin, and triglycerides. Contrarily, Treponema was at 0.9% the most abundant in black fecal samples, while present at 0.1% of relative abundance in brown fecal samples and 0.01% in yellow samples, correlating positively with blood iron content. This study indicates that colon/fecal content color can be used as indicator for specific GM and metabolite signatures.

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Eluru, Jagadeesh Reddy, and Kailasam Koumaravelou. "Evaluation of aqueous and hydro alcoholic extracts of Clerodendrum viscosum V. leaves & Macrotyloma uniflorum L. seeds against DMH-induced colon cancer." International Journal of Research in Pharmaceutical Sciences 9, no. 1 (March 12, 2018): 174. http://dx.doi.org/10.26452/ijrps.v9i1.1227.

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Evaluation of anti-neoplastic activity of aqueous and hydro alcoholic extracts of Clerodendron viscosum V. leaves & Macrotyloma uniflorum L. seeds against DMH-induced colon cancer is the objective of this study. Extracts were obtained using cold maceration process. Six groups of animals, each containing ten male albino wistar rats (80 – 100 g) were administered with respective treatment to evaluate the anti-neoplastic activity. On the last day of experimental period, fecal matter was collected and colons were removed. Fecal matter was homogenized, and subjected to the measurement of fecal pH and bacterial enzymes. Colons of five animals were subjected for the presence of MPLs, ACFs in each colon, and histopathology by using standard methodology. Colons of remaining five animals were subjected to homogenization to measure the bacterial enzymes such as β-Glucosidase, β-Glucuronidase, and mucinase. The extracts showed significant protective effect by showing significant decrease in the levels of fecal and colon β-glucosidase, β-glucuronidase, mucinase; reduction in total number of ACFs in each colon and crypt multiplicity. Although, all the plant extracts has shown protective effect against colon carcinogenesis, treatment with hydro alcoholic extracts has produced more pronounced effect as compared with aqueous extracts.

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Bavil, Abolhassan Shakeri, Mohommad Hossein Somi, Masoud Nemati, Batool Seyfi Nadergoli, Kamyar Ghabili, Reshad Mirnour, and Hamideh Ashrafi. "Ultrasonographic Evaluation of Bowel Wall Thickness and Intramural Blood Flow in Ulcerative Colitis." ISRN Gastroenterology 2012 (May 9, 2012): 1–4. http://dx.doi.org/10.5402/2012/370495.

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Aim. This study aimed at assessing Doppler ultrasonographic findings of gut wall vessels and thickness in active and quiescent ulcerative colitis. Methods. Fifty patients with ulcerative colitis were studied using transabdominal grayscale and Doppler sonography of sigmoid, distal and middle parts of descending colon in different stages of the disease. Thickness of colon wall in the most involved site, number of color signals in each box, resistive index (RI), and pulsatility index (PI) were evaluated. Results. The median thickness of the colon wall in the most involved sites was 4.3 mm in acute phase and 4.4 mm in the inactive phase (P=0.47). The median number of the color signals in the active phase at the most involved site, distal part of descending colon and sigmoid was higher than that of the color signals in the inactive phase (P=0.0001). In the most involved site, the PI and RI were undetectable in the inactive phase. The median PI was 1.4 in the mild phase, 1.3 in the moderate phase, and 1.1 in the severe phase (P=0.002). Conclusion. In contrast to the colon wall thickness, increased intramural blood flow reflected the clinical severity in ulcerative colitis patients.

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Merting, Alyssa D., Dakota B. Poschel, Chunwan Lu, John D. Klement, Dafeng Yang, Honglin Li, Huidong Shi, et al. "Restoring FAS Expression via Lipid-Encapsulated FAS DNA Nanoparticle Delivery Is Sufficient to Suppress Colon Tumor Growth In Vivo." Cancers 14, no. 2 (January 12, 2022): 361. http://dx.doi.org/10.3390/cancers14020361.

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A hallmark of human colorectal cancer is lost expression of FAS, the death receptor for FASL of cytotoxic T lymphocytes (CTLs). However, it is unknown whether restoring FAS expression alone is sufficient to suppress csolorectal-cancer development. The FAS promoter is hypermethylated and inversely correlated with FAS mRNA level in human colorectal carcinomas. Analysis of single-cell RNA-Seq datasets revealed that FAS is highly expressed in epithelial cells and immune cells but down-regulated in colon-tumor cells in human colorectal-cancer patients. Codon usage-optimized mouse and human FAS cDNA was designed, synthesized, and encapsulated into cationic lipid to formulate nanoparticle DOTAP-Chol-mFAS and DOTAP-Chol-hFAS, respectively. Overexpression of codon usage-optimized FAS in metastatic mouse colon-tumor cells enabled FASL-induced elimination of FAS+ tumor cells in vitro, suppressed colon tumor growth, and increased the survival of tumor-bearing mice in vivo. Overexpression of codon-optimized FAS-induced FAS receptor auto-oligomerization and tumor cell auto-apoptosis in metastatic human colon-tumor cells. DOTAP-Chol-hFAS therapy is also sufficient to suppress metastatic human colon tumor xenograft growth in athymic mice. DOTAP-Chol-mFAS therapy exhibited no significant liver toxicity. Our data determined that tumor-selective delivery of FAS DNA nanoparticles is sufficient for suppression of human colon tumor growth in vivo.

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Urmonov, U. B., S. G. Afanasyev, A. Yu Dobrodeev, A. V. Avgustinovich, M. Yu Volkov, N. V. Vasiliev, and E. N. Samtsov. "COLON LIPOMA COMPLICATED BY COLON INVAGINATION." Grekov's Bulletin of Surgery 178, no. 6 (March 18, 2020): 63–65. http://dx.doi.org/10.24884/0042-4625-2019-178-6-63-65.

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Due to the lack of specific symptoms of colon lipoma, the disease is often complicated by invagination, bleeding, or colonic obstruction. The article presents a clinical case of successful treatment of complicated lipoma of the hepatic flexure of the colon.

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Fisher, Andrea, Alexander Podboy, and Vijay Pottathil. "Once a Colon, Always a Colon." Gastroenterology 157, no. 1 (July 2019): 29–30. http://dx.doi.org/10.1053/j.gastro.2019.03.058.

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Schroy, Paul C., and Robert C. Kurtz. "Colon cancer, colon polyps, and cholesterol." Gastroenterology 91, no. 1 (July 1986): 254–55. http://dx.doi.org/10.1016/0016-5085(86)90471-3.

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Kieran, Jennefer A., and Myriam J. Curet. "Laparoscopic colon resection for colon cancer." Journal of Surgical Research 117, no. 1 (March 2004): 79–91. http://dx.doi.org/10.1016/j.jss.2003.11.025.

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Chang, Xiaotian, Zhengbin Chai, Jiaorui Zou, Hongxing Wang, Yao Wang, Yabing Zheng, Hui Wu, and Chunyan Liu. "PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer." Cancer Biology & Medicine 16, no. 4 (November 1, 2019): 729–42. http://dx.doi.org/10.20892/j.issn.2095-3941.2019.0065.

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Objective As a member of the peptidyl arginine deiminase (PAD) family, PADI3 is weakly expressed in colon cancer tissues and highly expressed in adjacent colon cancer tissues. However, the role of PADI3 in colon cancer is unclear. In this study, we investigated the function and molecular mechanism of PADI3 in colon cancer tumorigenesis. Methods Western blot and real-time PCR were used to detect the expression levels of several genes. CCK-8, flow cytometry (FCM) and colony formation assays were used to examine cell proliferation, the cell cycle and colony formation ability. RNA-sequencing analysis was used to study the molecular mechanism of PADI3 in tumorigenesis. A truncation mutation experiment was performed to determine the key functional domain of PADI3. Results PADI3 overexpression inhibited cell proliferation and colony formation and led to G1 phase arrest in both HCT116 (originating from primary colon cancer) and LoVo (originating from metastatic tumor nodules of colon cancer) cells. PADI3-expressing HCT116 cells had a lower tumor formation rate and produced smaller tumors than control cells. PADI3 significantly decreased Sirtuin2 (Sirt2) and Snail expression and AKT phosphorylation and increased p21 expression, and Sirt2 overexpression partly reversed the effects induced by PADI3 overexpression. Immunocytochemistry showed that PADI3 is mainly localized in the cytoplasm. Truncation mutation experiments showed that the C-domain is the key domain involved in the antitumor activity of PADI3. Conclusions PADI3 suppresses Snail expression and AKT phosphorylation and promotes p21 expression by downregulating Sirt2 expression in the cytoplasm, and the C-domain is the key domain for its antitumor activity.

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Wang, Jia-Hua, Lee-Kiat Ban, Henry Hsin-Chung Lee, Yen-Hung Chen, Hui-Yu Lin, Zhe-Wei Zhu, Her-Young Su, et al. "Purification of Colon Carcinoma Cells from Primary Colon Tumor Using a Filtration Method via Porous Polymeric Filters." Polymers 13, no. 19 (October 5, 2021): 3411. http://dx.doi.org/10.3390/polym13193411.

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Cancer stem cells (CSCs) or cancer-initiating cells (CICs) are key factors for tumor generation and metastasis. We investigated a filtration method to enhance CSCs (CICs) from colon carcinoma HT-29 cells and primary colon carcinoma cells derived from patient colon tumors using poly(lactide-co-glycolic acid)/silk screen (PLGA/SK) filters. The colon carcinoma cell solutions were permeated via porous filters to obtain a permeation solution. Then, the cell cultivation media were permeated via the filters to obtain the recovered solution, where the colon carcinoma cells that adhered to the filters were washed off into the recovered solution. Subsequently, the filters were incubated in the culture media to obtain the migrated cells via the filters. Colon carcinoma HT-29 cells with high tumorigenicity, which might be CSCs (CICs), were enhanced in the cells in the recovered solution and in the migrated cells based on the CSC (CIC) marker expression, colony-forming unit assay, and carcinoembryonic antigen (CEA) production. Although primary colon carcinoma cells isolated from colon tumor tissues contained fibroblast-like cells, the primary colon carcinoma cells were purified from fibroblast-like cells by filtration through PLGA/SK filters, indicating that the filtration method is effective in purifying primary colon carcinoma cells.

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Voronov, Elena, and Ron N. Apte. "IL-1 in Colon Inflammation, Colon Carcinogenesis and Invasiveness of Colon Cancer." Cancer Microenvironment 8, no. 3 (December 2015): 187–200. http://dx.doi.org/10.1007/s12307-015-0177-7.

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Paggi, Silvia, Giuseppe Mogavero, Arnaldo Amato, Emanuele Rondonotti, Alida Andrealli, Gianni Imperiali, Nicoletta Lenoci, et al. "Linked color imaging reduces the miss rate of neoplastic lesions in the right colon: a randomized tandem colonoscopy study." Endoscopy 50, no. 04 (March 14, 2018): 396–402. http://dx.doi.org/10.1055/a-0580-7405.

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Abstract Background Linked color imaging (LCI) is a newly developed image-enhancing endoscopy technology that provides bright endoscopic images and increases color contrast. We investigated whether LCI improves the detection of neoplastic lesions in the right colon when compared with high definition white-light imaging (WLI). Methods Consecutive patients undergoing colonoscopy were randomized (1:1) after cecal intubation into right colon inspection at first pass by LCI or by WLI. At the hepatic flexure, the scope was reintroduced to the cecum under LCI and a second right colon inspection was performed under WLI in previously LCI-scoped patients (LCI–WLI group) and vice versa (WLI–LCI group). Lesions detected on first- and second-pass examinations were used to calculate detection and miss rates, respectively. The primary outcome was the right colon adenoma miss rate. Results Of the 600 patients enrolled, 142 had at least one adenoma in the right colon, with similar right colon adenoma detection rates (r-ADR) in the two groups (22.7 % in LCI–WLI and 24.7 % in WLI–LCI). At per-polyp analysis, double inspection of the right colon in the LCI–WLI and WLI–LCI groups resulted in an 11.8 % and 30.6 % adenoma miss rate, respectively (P < 0.001). No significant difference in miss rate was found for advanced adenomas or sessile serrated lesions. At per-patient analysis, at least one adenoma was identified in the second pass only (incremental ADR) in 2 of 300 patients (0.7 %) in the LCI – WLI group and in 13 of 300 patients (4.3 %) in the WLI – LCI group (P = 0.01). Conclusions LCI could reduce the miss rate of neoplastic lesions in the right colon.

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Wu, Szu-Yuan, Yan-Jiun Huang, Yew-Min Tzeng, Chi-Ying Huang, Michael Hsiao, Alexander Wu, and Tse-Hung Huang. "Destruxin B Suppresses Drug-Resistant Colon Tumorigenesis and Stemness Is Associated with the Upregulation of miR-214 and Downregulation of mTOR/β-Catenin Pathway." Cancers 10, no. 10 (September 25, 2018): 353. http://dx.doi.org/10.3390/cancers10100353.

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Background: Drug resistance represents a major challenge for treating patients with colon cancer. Accumulating evidence suggests that Insulin-like growth factor (IGF)-associated signaling promotes colon tumorigenesis and cancer stemness. Therefore, the identification of agents, which can disrupt cancer stemness signaling, may provide improved therapeutic efficacy. Methods: Mimicking the tumor microenvironment, we treated colon cancer cells with exogenous IGF1. The increased stemness of IGF1-cultured cells was determined by ALDH1 activity, side-population, tumor sphere formation assays. Destruxin B (DB) was evaluated for its anti-tumorigenic and stemness properties using cellular viability, colony-formation tests. The mimic and inhibitor of miR-214 were used to treat colon cancer cells to show its functional association to DB treatment. In vivo mouse models were used to evaluate DB’s ability to suppress colon tumor-initiating ability and growth inhibitory function. Results: IGF1-cultured colon cancer cells showed a significant increase in 5-FU resistance and enhanced stemness properties, including an increased percentage of ALDH1+, side-population cells, tumor sphere generation in vitro, and increased tumor initiation in vivo. In support, using public databases showed that increased IGF1 expression was significantly associated with a poorer prognosis in patients with colon cancer. DB, a hexadepsipeptide mycotoxin, was able to suppress colon tumorigenic phenotypes, including colony and sphere formation. The sequential treatment of DB, followed by 5-FU, synergistically inhibited the viability of colon cancer cells. In vivo studies showed that DB suppressed the tumorigenesis by 5-FU resistant colon cells, and in a greater degree when combined with 5-FU. Mechanistically, DB treatment was associated with decreased the mammalian target of rapamycin (mTOR) and β-catenin expression and an increased miR-214 level. Conclusion: We provided evidence of DB as a potential therapeutic agent for overcoming 5-FU resistance induced by IGF1, and suppressing cancer stem-like properties in association with miR-214 regulation. Further investigation is warranted for its translation to clinical application.

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Shen, Sha, Qingqing Guo, and Shuiping Zhan. "MicroRNA-612 regulates the proliferation and epithelial-to-mesenchymal transition of human colon cancer cells via G protein-coupled receptor 132 (GPR132)." Tropical Journal of Pharmaceutical Research 20, no. 7 (February 9, 2022): 1345–50. http://dx.doi.org/10.4314/tjpr.v20i7.4.

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Purpose: To investigate the effect of microRNA-612 (miR-612) on human colon cancer cells, and the mechanism involved. Methods: Expressions of miR-612 and GPR132 were determined by quantitative real-time polymerase chain reaction (qRT-PCR)el , while cell viability was evaluated using cell counting kit-8 (CCK8) and colony formation assays. Dual luciferase assay was used to determine the interaction between miR-612 and GPR132, while cell migration and invasion were measured by Transwell assay. Results: The expression levels of miR-612 in colon cancer tissues and cell lines were significantly down-regulated (p < 0.05). Overexpression of miR-612 in colon cancer cells led to significant inhibition of their proliferation and colony formation. Transwell assays revealed that miR-612 overexpression markedly stopped the migration, invasion and epithelial-to-mesenchymal transition. Conclusion: These results indicate that miR-612 exerts anti-cancer effect by suppressing the expression of GPR132 at the translational level. The in vitro tumor suppressive activity of miR-612 against colon cancer reveals its potential for the management of colon cancer.

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Yarze, Joseph C. "Evanescent Colon “Masses” due to Colon Ischemia." American Journal of Gastroenterology 113, no. 12 (December 2018): 1745. http://dx.doi.org/10.1038/s41395-018-0245-y.

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Dasari, Vijaya, Ali Ahmed, and Garrett Lawlor. "Ganglioneuromatosis of the Colon Mimicking Colon Cancer." American Journal of Gastroenterology 107 (October 2012): S486—S487. http://dx.doi.org/10.14309/00000434-201210001-01222.

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Ojha, Mini, NV Satheesh Madhav, and Anita Singh. "Synthesis and evaluation of sodium carboxymethyl cellulose azo polymer for colon specificity." International Current Pharmaceutical Journal 1, no. 8 (July 5, 2012): 209–12. http://dx.doi.org/10.3329/icpj.v1i8.11252.

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Sodium carboxymethyl cellulose is an excellent pharmaceutical excipient. It possesses good filmability, mucoadhesivity, viscolising capacity and bindability. The current aim of our research work is to synthesize a novel colon targeting polymer by using sodium carboxymethyl cellulose and glycine for colon targeting and to screen its colon specificity by in-vitro release model. Sodium carboxymethyl cellulose was subjected for synthesizing its derivative with glycine using azo linkage. The azo polymeric conjugate was evaluated for its color, solubility, Rf value, melting point, IR and 1HNMR spectral analysis. It was further subjected for evaluating its colon targeting property by in-vitro method using rat fecal matter. The research study revealed that the sodium carboxymethyl cellulose azo derivative showed promising colon specificity for a period of 120 minutes in a controlled manner along with modified solubility. So it can serve as a potential colon targeting polymer.DOI: http://dx.doi.org/10.3329/icpj.v1i8.11252 International Current Pharmaceutical Journal 2012, 1(8): 209-212

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Wibowo, Agung Ary, Andrian Sitompul, Alfi Yasmina, Ika Kustiyah Oktaviyanti, Ardik Lahdimawan, and Essy Dwi Damayanthi. "An increase in inflammatory cells related to the increase incidence of colitis and colorectal cancer." Bali Medical Journal 11, no. 1 (April 30, 2022): 499–502. http://dx.doi.org/10.15562/bmj.v11i1.2842.

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Background: Inflammation plays an important role in colorectal cancer formation, where colitis inflammatory cells can trigger the production of free radicals that interact with genes in carcinogenesis. Meanwhile, the colonic mucosal epithelium contains goblet cells that function to prevent inflammation. This study aims to examine the correlation between the number of goblet and inflammatory cells in the colon of patients with colorectal cancer, colitis, and healthy colon and their relationship with the incidence of colorectal cancer and colitis. Methods: Histopathological samples consisting of 30 healthy colons, 30 colons with colitis, and 31 colons with colorectal cancer were examined to obtain the average cell number in 10 or the entire field of view using a light microscope with 400 magnification. Using the Pearson correlation test and Multivariate Multinomial Logistic Regression, these samples were analyzed with SPSS version 26 for Windows. Results: Consequently, the results showed a weak but insignificant negative correlation between the number of goblet and inflammatory cells in the colon with colorectal cancer (r2=0.055; p=0.200), colitis (r2 = 0.002, p = 0.833), and healthy colon (r2 = 0.110, p = 0.073). The number of inflammatory cells is significantly associated with the incidence of colorectal cancer (OR=1.326; 95%CI=1.155-1.521; p=0.000) and colitis (OR=1.374; 95%CI=1.192-1.583; p=0.000) compared to normal colon. Conclusion: An increase in inflammatory cells is significantly associated with the incidence of colorectal cancer and colitis.

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Utano, Kenichi, Koichi Nagata, Tetsuro Honda, Takashi Kato, Alan Kawarai Lefor, and Kazutomo Togashi. "Bowel habits and gender correlate with colon length measured by CT colonography." Japanese Journal of Radiology 40, no. 3 (October 11, 2021): 298–307. http://dx.doi.org/10.1007/s11604-021-01204-7.

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Abstract Purpose CT colonography enables three-dimensional measurement of colon length. However, previous studies using CT colonography have not examined the association with gender, age, physique, a history of laparotomy and bowel habits, all possible contributory factors to colon length. The aim of this study is to investigate factors associated with colon length. Materials and methods We conducted a post hoc analysis based on data obtained from a previous multi-center trial including 321 patients with positive fecal immunochemical tests who underwent CT colonography. Colon length was measured using a computer-generated center line and was divided at the iliac crest level into the distal and proximal colons. Bowel habits were classified into three groups: A—daily; B—once every 2 or 3 days; and C—less than once in 3 days. Statistical comparison was made using one-way ANOVA with Bonferroni’s correction. Results A total of 295 patients were analyzed. The entire colon length (cm, mean ± standard deviation) of individual patients was 150.3 ± 18.5 cm and ranged from 109.7 to 195.9 cm. The female colon was significantly longer than the male colon (154.3 ± 18.1 cm vs. 147.1 ± 18.3 cm; p = 0.022). Colon length showed trends associated with age (p = 0.18) and a history of laparotomy (p = 0.14). According to bowel habits, the entire colon measured 147.4 ± 17.9 in group A, 154.7 ± 18.5 in group B and 158.6 ± 18.3 in group C, and significant differences were observed for “A vs. C” (p = 0.002) and “A vs. B” (p = 0.014). In subgroup analysis by colon segment, the proximal colon trended similarly to the entire colon while there were no trends for the distal colon. Conclusions This study has clearly demonstrated that bowel habits and gender both correlate with the length of the entire colon measured by CT colonography, and in particular, the proximal colon. Secondary abstract Using CT colonography, we measured the colon length in 295 patients. The entire colon length was 150.3 ± 18.5 cm on average. Females and constipated (less frequent defecation) patients have a significantly longer colon, and in particular, the proximal colon. Colon length showed trends associated with age and a history of laparotomy.

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Wang, Yiling, Jiantao He, Shenghui Zhang, Qingbo Yang, Bo Wang, Zhiyu Liu, and Xintian Wu. "Knockdown of Immature Colon Carcinoma Transcript 1 Inhibits Proliferation and Promotes Apoptosis of Non–Small Cell Lung Cancer Cells." Technology in Cancer Research & Treatment 16, no. 5 (July 13, 2016): 559–69. http://dx.doi.org/10.1177/1533034616657977.

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Non–small cell lung cancer, as the most frequent type lung cancer, has lower survival rate of 5 years, despite improvements in surgery and chemotherapy. Previous studies showed immature colon carcinoma transcript 1 is closely related to tumorigenesis of human cancer cells. In the present study, we found immature colon carcinoma transcript 1 was overexpressed in lung cancer tissues using Oncomine database mining, and the biological effect of immature colon carcinoma transcript 1 was investigated in non–small cell lung cancer cell lines 95D and A549. Lentivirus-mediated RNA interference was used to knock down immature colon carcinoma transcript 1 expression in 95D and A549 cells in vitro, and the knockdown efficiency was determined using quantitative real-time polymerase chain reaction and Western blot assay. Knockdown of immature colon carcinoma transcript 1 significantly suppressed non–small cell lung cancer cell proliferation and colony formation ability confirmed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Flow cytometry was applied to measure cell cycle arrest, and the result showed the cell cycle arrested in G2/M phase in 95D cells and arrested in G0/G1 phase in A549 cells. Furthermore, we measured the levels of cell cycle–associated proteins by Western blot analysis and found immature colon carcinoma transcript 1 –mediated cell proliferation inhibition appeared due to downregulation of cell cycle activator cyclin D1 and upregulation of cell cycle inhibitor p21. In addition, immature colon carcinoma transcript 1 silencing significantly induced non–small cell lung cancer cell apoptosis by annexin V/7-amino-actinomycin D double-staining assay. All our data suggest that immature colon carcinoma transcript 1 may play an important role for non–small cell lung cancer cell proliferation and could be a potential molecular target for diagnosing and treating human non–small cell lung cancer.

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Cuevas, Rolando. "CHARACTERIZATION OF COLON CANCER." CIRUGIA PARAGUAYA 41, no. 1 (April 30, 2017): 8–13. http://dx.doi.org/10.18004/sopaci.abril.8-13.

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Chaikham, Pittaya, Arunee Apichartsrangkoon, Srivilai Worametrachanon, and Tom Van de Wiele. "Impact of Encapsulated Lactobacillus casei 01 Along with Pasteurized Purple-Rice Drinks on Modulating Colon Microbiome using a Digestive Model." International Journal of Food Engineering 12, no. 7 (September 1, 2016): 637–46. http://dx.doi.org/10.1515/ijfe-2016-0008.

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Abstract The prospect of Lactobacillus casei 01 and pasteurized purple-rice drinks on modulating colon microbiome by using a simulator of the human intestinal microbial ecosystem was investigated. Accordingly, L. casei 01 alone and with pasteurized purple-rice drink were administered into the proximal and distal colons. In consequence, some colon bacteria and their metabolic activities were examined. The results showed that upon modulating the colon microbiota by L. casei 01 alone with pasteurized germinated-purple-rice drink in the distal colon, acetate and propionate (short-chain fatty acids) were equivalently elevated but other treatments performed differently. Based on the profile of colon microbiota, most treatments stimulated the highest number of lactobacilli followed by bifidobacteria, while other undesirable bacteria were moderately diminished. In overall, larger gelatinized starch in the rice drinks enabled by pasteurization triggered off better modulating impact than by pressurization.

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Liu, Weizhi, and Ke Meng. "COL11A1 is Downregulated by miR-339-5p and Promotes Colon Carcinoma Progression." Canadian Journal of Gastroenterology and Hepatology 2022 (May 28, 2022): 1–10. http://dx.doi.org/10.1155/2022/8116990.

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The roles of COL11A1 in cancer have been increasingly considered, but the understandings of the effects of COL11A1 on colon carcinoma progress are much limited yet. qRT-PCR and Western blot were utilized to evaluate COL11A1 expression at mRNA and protein levels, respectively, in colon carcinoma cell lines. Afterward, the tumorigenesis biological effects of COL11A1 were examined by CCK-8, colony formation, Transwell, and wound healing methods. Moreover, upstream miRNAs containing the binding sites with COL11A1 were predicted by the bioinformatics methods. The interplay between COL11A1 and miR-339-5p was identified by a dual-luciferase assay. COL11A1 expression was prominently upregulated in colon carcinoma cell lines relative to that in normal human colon mucosal epithelial cell lines, and it was related to tumor stages. The outcomes of in-vitro experiments suggested that interfering with COL11A1 remarkably repressed the malignant behaviors of SW480 and SW620 cells. MiR-339-5p was markedly lowly expressed in colon carcinoma cell lines. Furthermore, miR-339-5p directly targeted and negatively regulated COL11A1 expression. COL11A1 upregulation promoted colon carcinoma cell functions, while overexpressing miR-339-5p evidently attenuated the promotion. These results proved the modulation of the miR-339-5p/COL11A1 axis in colon carcinoma cells, and miR-339-5p repressed colon carcinoma progression via COL11A1 downregulation. These results offer new underlying targets for the accurate therapy of colon carcinoma patients.

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Tang, Chia-Pei, Chen-Hung Hsieh, and Tu-Liang Lin. "Computer-Aided Image Enhanced Endoscopy Automated System to Boost Polyp and Adenoma Detection Accuracy." Diagnostics 12, no. 4 (April 12, 2022): 968. http://dx.doi.org/10.3390/diagnostics12040968.

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Colonoscopy is the gold standard to detect colon polyps prematurely. Early detection, characterization and resection of polyps decrease colon cancer incidence. Colon polyp missing rate remains high despite novel methods development. Narrowed-band imaging (NBI) is one of the image enhance techniques used to boost polyp detection and characterization, which uses special filters to enhance the contrast of the mucosa surface and vascular pattern of the polyp. However, the single-button-activated system is not convenient for a full-time colonoscopy operation. We selected three methods to simulate the NBI system: Color Transfer with Mean Shift (CTMS), Multi-scale Retinex with Color Restoration (MSRCR), and Gamma and Sigmoid Conversions (GSC). The results show that the classification accuracy using the original images is the lowest. All color transfer methods outperform the original images approach. Our results verified that the color transfer has a positive impact on the polyp identification and classification task. Combined analysis results of the mAP and the accuracy show an excellent performance of the MSRCR method.

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Duvanskiy, V. A., and A. V. Belkov. "Modifi ed mode of fujinon intelligent color enhancement (FICE) in the diagnosis of colon lesions." Experimental and Clinical Gastroenterology 174, no. 5 (June 29, 2020): 67–71. http://dx.doi.org/10.31146/1682-8658-ecg-177-5-67-71.

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The study aims to evaluate the eff ectiveness of standard and modifi ed settings of the spectral color allocation technology in the diff erential diagnosis of the colon morphological type of epithelial formations. Materials and methods: video colonoscopy using standard and modifi ed mode of technology. A total of 746 patients were selected for spectral colour selection, of whom 80 were selected. There were 36 men, 44 women. The average age of the patients was 60 ± 9 years. There were 171 epithelial fomations, of which 106 (61.9%) were located in the left side of the large intestine: in the rectum — 33 (31.2%), in sigmoid — 52 (49%), in descending part — 21 (19.8%). In the right parts of the colon there were significant lower number of formations — 65 (38.1%): ascending intestine — 26 (40%), transversely — colon — 32 (49.2%), cecum — 7 (10.8%). Endoscopic studies were performed according to standard method using video colonoscopes from Fujinon, EC-590ZW / L, EC-530WL. Results: statistically revealed that the probability of determining the correct morphological type of epithelium is formation is 6 times higher when using the modifi ed spectral color technology highlight compared to standard technology settings. Conclusion: the modifi ed settings of the technology of spectral color highlighting allow much more accurative performance an optical biopsy of epithelial colon formations.

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Fruehwald, Christina, and Gary Ellison. "Successful Surgical Correction of Congenital Colonic Duplication and Anogenital Cleft in a Cat." Journal of the American Animal Hospital Association 56, no. 3 (May 1, 2020): 170–74. http://dx.doi.org/10.5326/jaaha-ms-6885.

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ABSTRACT A 17 wk old sexually intact female domestic shorthair kitten presented for an anogenital cleft and enlarged colon. The cat had experienced bacterial cystitis and constipation since weaning. Contrast referral images revealed an enlarged colon with a patent anus. Clinical examination revealed an anogenital cleft with a common anovulvar orifice. The rectum was patent upon digital rectal palpation, and fecal contamination of the vulva was present. Abdominal radiographs revealed two distinct colons, both filled with a moderate amount of formed fecal material. Contrast-enhanced computed tomography revealed segmental duplication of the descending colon with a dominant right colon and a smaller accessary left colon. The two structures conjoined at the transverse colon proximally and at the pubic brim distally. A common anogenital orifice with anovulvar communication was also noted. The anogenital cleft malformation was successfully repaired surgically. A celiotomy was performed to remove the smaller accessory colon. An ovariectomy and partial hysterectomy were also performed. The patient recovered uneventfully and showed no gross evidence of recurrent cystitis or urinary or fecal incontinence postoperatively. This is believed to be the first report of a congenital anogenital cleft and complete communicating colonic duplication in a cat.

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Trebollé, J. F., J. D. Escolar, F. M. Sánchez, V. E. García, M. J. Luesma, I. Cantarero, J. A. Fatás, J. Maestre, C. López, and J. Usón. "3d morphometric analysis of colon applied to a laparoscopic surgical approach. Cadaver study." ACTUALIDAD MEDICA 106, no. 106(814) (January 2022): 260–70. http://dx.doi.org/10.15568/am.2021.814.or03.

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Objective: The aim of this study is to define the changes that occurred in certain segments of the colons of cadavers after subjecting them to the conditions that are used in laparoscopic surgery of the colon. Methodology: Three cadavers were submitted to abdominal computerized tomography, first with no external, and then after the application of 15 mm of Hg of pneumoperitoneum and 15 degrees Trendelenburg, right or left lateral decubitus. Three-dimensional reconstruction of the images was performed for a morphological descriptive study of the pubic points, superior mesenteric artery, inferior mesenteric artery, hepatic flexure and splenic flexure. Results: A total of 390 measurements were performed, 159 showed changes. The inferior mesenteric artery point modifications were the most strongly related to the other points. The transverse colon – pubic symphysis – descending colon angle depended on the pubic symphysis – descending colon distance, and the transverse colon – inferior mesenteric artery – descending colon angle depended on the inferior mesenteric artery – transverse colon distance. Conclusions: The positional changes of the points studied were related to their attachment to the peritoneum, to the proximity of the neighboring viscera and to their location in the abdomen.

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Chen, J., C.-M. Chai, W. Dalu, L. Shen, F. Fromowitz, C. Compton, and MV Viola. "Oncogene Mutations in Cancer and Dysplasia Associated with Inflammatory Bowel Disease." Canadian Journal of Gastroenterology 4, no. 7 (1990): 384–89. http://dx.doi.org/10.1155/1990/329374.

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Chronic inflammatory bowel disease (IBO) predisposes affected individuals to the development of invasive colon cancer. Increased cancer risk has been seen in ulcerative colitis and Crohn's disease in Western societies as well as in schistosomal colitis in China. In this study it was found that the frequency of the 12th codon of c-Ki-ras, as well as the specific amino acid substitutions, were similar in sporadic colon cancers, cancers associated with ulcerative colitis in the United States, and colon cancers found in patients with schistosomal colitis in Jiangsu province in China. Further, activating mutations of codon 12 of e-Ki-ras were found in high grade dysplastic lesions in chronic ulcerative colitis. The latter finding indicates that some dysplasias are clonal proliferative lesions with genetic characteristics associated with invasive cancer.

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Cenariu, Diana, Alina-Andreea Zimta, Raluca Munteanu, Anca Onaciu, Cristian Silviu Moldovan, Ancuta Jurj, Lajos Raduly, et al. "Hsa-miR-125b Therapeutic Role in Colon Cancer Is Dependent on the Mutation Status of the TP53 Gene." Pharmaceutics 13, no. 5 (May 6, 2021): 664. http://dx.doi.org/10.3390/pharmaceutics13050664.

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Colon cancer is the third most common cancer type worldwide and is highly dependent on DNA mutations that progressively appear and accumulate in the normal colon epithelium. Mutations in the TP53 gene appear in approximately half of these patients and have significant implications in disease progression and response to therapy. miR-125b-5p is a controversial microRNA with a dual role in cancer that has been reported to target specifically TP53 in colon adenocarcinomas. Our study investigated the differential therapeutic effect of miR-125b-5p replacement in colon cancer based on the TP53 mutation status of colon cancer cell lines. In TP53 mutated models, miR-125b-5p overexpression slows cancer cells’ malignant behavior by inhibiting the invasion/migration and colony formation capacity via direct downregulation of mutated TP53. In TP53 wild type cells, the exogenous modulation of miR-125b-5p did not significantly affect the molecular and phenotypic profile. In conclusion, our data show that miR-125b-5p has an anti-cancer effect only in TP53 mutated colon cancer cells, explaining partially the dual behavior of this microRNA in malignant pathologies.

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Zhao, Jinlai, Yigang Wang, Yang Wang, Jianchao Gao, Haichao Yang, Xiaotang Wu, and Hua Li. "Transcription Factor FXR Activates DHRS9 to Inhibit the Cell Oxidative Phosphorylation and Suppress Colon Cancer Progression." Analytical Cellular Pathology 2022 (October 26, 2022): 1–13. http://dx.doi.org/10.1155/2022/8275574.

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Background. Colon cancer is a common gastrointestinal malignancy. It has been discovered that Farnesoid X receptor (FXR) plays an imperative regulatory role in multitype cancers in recent years. However, its regulatory mechanism in colon cancer has not been clearly explored. This study intended to explore the molecular regulatory mechanism of FXR and its downstream genes on the malignant progression of colon cancer. Methods. The mRNA and protein expression of FXR in colon cancer cells were measured by quantitative real-time polymerase chain reaction and Western blot. The effects of FXR on the biological function of colon cancer cells were measured by Cell Counting Kit-8, colony formation, and transwell assays. The downstream target gene of FXR was predicted by bioinformatics analysis and found to be associated with cellular oxidative phosphorylation. The binding relationship between FXR and its downstream gene dehydrogenase/reductase member 9 (DHRS9) was verified through luciferase reporter assay and chromatin immunoprecipitation assay. The changes of oxidative phosphorylation were detected by Western blot and oxygen consumption rate determination. The effect of FXR/DHRS9 axis on the malignant progression of colon cancer cells was further confirmed by rescue experiments. Results. FXR was underexpressed in colon cancer tissues and cells, and overexpressing FXR could repress the malignant behaviors of colon cancer cells. Besides, DHRS9 was a downstream gene of FXR, and FXR/DHRS9 inhibited the deterioration of colon cancer through inhibiting oxidative phosphorylation. Moreover, promoting FXR expression in colon cancer cells could partially reverse the biological function changes caused by silencing DHRS9 expression. Conclusion. FXR inhibited the oxidative phosphorylation and inhibited the malignant progression of colon cancer cells via targeting DHRS9.

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Wang, Rui, In-Kiu Kwon, Muthusamy Thangaraju, Nagendra Singh, Kebin Liu, Philippe Jay, Franz Hofmann, Vadivel Ganapathy, and Darren D. Browning. "Type 2 cGMP-dependent protein kinase regulates proliferation and differentiation in the colonic mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 2 (July 15, 2012): G209—G219. http://dx.doi.org/10.1152/ajpgi.00500.2011.

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Signaling through cGMP has emerged as an important regulator of tissue homeostasis in the gastrointestinal tract, but the mechanism is not known. Type 2 cGMP-dependent protein kinase (PKG2) is a major cGMP effector in the gut epithelium, and the present studies have tested its importance in the regulation of proliferation and differentiation in the mouse colon and in colon cancer cell lines. Tissue homeostasis was examined in the proximal colon of Prkg2 −/− mice using histological markers of proliferation and differentiation. The effect of ectopic PKG2 on proliferation and differentiation was tested in vitro using inducible colon cancer cell lines. PCR and luciferase reporter assays were used to determine the importance of Sox9 downstream of PKG2. The colons of Prkg2 −/− mice exhibited crypt hyperplasia, increased epithelial apoptosis, and reduced numbers of differentiated goblet and enteroendocrine cells. Ectopic PKG2 was able to inhibit proliferation and induce Muc2 and CDX2 expression in colon cancer cells, but did not significantly affect cell death. PKG2 reduced Sox9 levels and signaling, suggesting possible involvement of this pathway downstream of cGMP in the colon. The work presented here demonstrates a novel antiproliferative and prodifferentiation role for PKG2 in the colon. These homeostatic functions of PKG2 were reproducible in colon cancer cells lines where downregulation of Sox9 is a possible mechanism. The similarities in phenotype between PKG2 and GCC knockout mice positions PKG2 as a likely mediator of the homeostatic effects of cGMP signaling in the colon.

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Boutilier, Robert G., Shawn K. Murray, and Virginia M. Walley. "Green Colon." Archives of Pathology & Laboratory Medicine 124, no. 9 (September 1, 2000): 1397–98. http://dx.doi.org/10.5858/2000-124-1397-gc.

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Stefanik, Dawn Christine, and Esther Muscari Lin. "Colon Cancer." American Journal of Nursing 100, no. 4 (April 2000): 36. http://dx.doi.org/10.2307/3521934.

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Ahmed, Moiz, Nirali Sheth, and Raghav Bansal. "Black colon." Clinical Case Reports 9, no. 4 (March 13, 2021): 2502–3. http://dx.doi.org/10.1002/ccr3.4023.

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Kassir, Radwan. "Intrapericardial Colon." New England Journal of Medicine 384, no. 13 (April 1, 2021): e49. http://dx.doi.org/10.1056/nejmicm2028463.

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_, _. "Colon Cancer." Journal of the National Comprehensive Cancer Network 5, no. 9 (October 2007): 884. http://dx.doi.org/10.6004/jnccn.2007.0079.

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Colorectal cancer is the third most frequently diagnosed cancer in men and women in the United States. An estimated 112,340 new cases of colon cancer will occur in 2007 and an estimated 52,180 people will die from colon and rectal cancer in the same year. Despite these statistics, mortality from colon cancer has decreased over the past 30 years, possibly because of earlier diagnosis through screening and better treatment modalities. These guidelines begin with the clinical presentation of the patient to the primary care physician or gastroenterologist and address diagnosis, pathologic staging, surgical management, adjuvant treatment, management of recurrent and metastatic disease, and patient surveillance. For the most recent version of the guidelines, please visit NCCN.org

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Engstrom, Paul F., Juan Pablo Arnoletti, Al B. Benson, Yi-Jen Chen, Michael A. Choti, Harry S. Cooper, Anne Covey, et al. "Colon Cancer." Journal of the National Comprehensive Cancer Network 7, no. 8 (September 2009): 778–831. http://dx.doi.org/10.6004/jnccn.2009.0056.

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Benson, Al B., J. Pablo Arnoletti, Tanios Bekaii-Saab, Emily Chan, Yi-Jen Chen, Michael A. Choti, Harry S. Cooper, et al. "Colon Cancer." Journal of the National Comprehensive Cancer Network 9, no. 11 (November 2011): 1238–90. http://dx.doi.org/10.6004/jnccn.2011.0104.

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Allego, Mel M. "Colon Cancer." American Journal of Roentgenology 176, no. 4 (April 2001): 942. http://dx.doi.org/10.2214/ajr.176.4.1760942.

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Reddy, Bandaru S., and Chinthalapally V. Rao. "Colon Cancer." Drugs & Aging 16, no. 5 (May 2000): 329–34. http://dx.doi.org/10.2165/00002512-200016050-00002.

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Fuerst, Mark L. "Colon Cancer." Oncology Times 35, no. 20 (October 2013): 27–29. http://dx.doi.org/10.1097/01.cot.0000437208.82611.59.

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Carlson, Robert H. "Colon Cancer." Oncology Times 29, no. 8 (April 2007): 18. http://dx.doi.org/10.1097/01.cot.0000269625.81286.2e.

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Journal articles on the topic 'Colon'

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