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Journal articles on the topic 'Colorectal neoplasia'

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Published: 4 June 2021
Last updated: 19 February 2022

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1

Taylor, Irving. "Colorectal neoplasia." Current Opinion in Gastroenterology 7, no. 1 (February 1991): 25–29. http://dx.doi.org/10.1097/00001574-199102000-00006.

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2

Grega, Tomáš, Gabriela Vojtěchová, Michal Voška, Ondřej Májek, Miroslav Zavoral, Štěpán Suchánek, Monika Ambrožová, and Jarmila Jirkovská. "Predictors of advanced colorectal neoplasia in colorectal cancer screening – interim results of multicentric prospective study." Gastroenterologie a hepatologie 74, no. 5 (October 30, 2020): 386–92. http://dx.doi.org/10.14735/amgh2020386.

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ntroduction: The incidence of advanced colorectal neoplasia in the screening population shows great diversity with a prevalence of 3–12 %. Due to the uneven distribution in the population, potential risk factors that would allow the stratification of individuals according to the degree of risk of colorectal neoplasia are searched. Aim: To determine the risk factors associated with the occurrence of advanced colorectal neoplasia in the screening population. Methods: Asymptomatic individuals aged 45–75 years who underwent preventive colonoscopy in 2012–2016 in a multicenter prospective study monitoring metabolic risk factors for CRC (MRF CRC study) were included in the analysis. Data were analyzed using descriptive statistics. The Fisher’s exact test was used to compare the risk factors with the occurrence of advanced colorectal neoplasia. Results: There were 1,108 men (56.3%) and 859 women (43.7%) in the group; the average age of the individuals was 60 years. The majority of subjects were referred for primary screening colonoscopy (1,174 subjects; 59.7%) and 793 subjects (40.3%) underwent FOBT positive colonoscopy. The total number of advanced colorectal neoplasms in the cohort was 11,8% (233 individuals). The independent risk factors significantly associated with advanced colorectal neoplasia included age (p < 0.001), male gender (p = 0.001), smoking (p < 0.001), serum concentrations of triglycerides (p = 0.029; especially concentrations > 2 mmol/l) and low vitamin D (p = 0.033). These are preliminary results which will be specified in the following more detailed data analysis using logistic regression. Conclusion: The strongest risk factors associated with advanced colorectal neoplasia were age, gender and smoking. In addition to these factors, serum triglyceride levels and low vitamin D were significantly associated with advanced colorectal neoplasia. In the individuals with a higher incidence of advanced colorectal neoplasia according to the given factors, primary screening colonoscopy should be considered.
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3

Snover, Dale C., and Kenneth P. Batts. "Serrated Colorectal Neoplasia." Surgical Pathology Clinics 3, no. 2 (June 2010): 207–40. http://dx.doi.org/10.1016/j.path.2010.05.001.

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4

Ho Kim, W., J. Hoon Suh, T. Il Kim, S. Kwan Shin, Y. Han Paik, H. Won Chung, D. Young Kim, et al. "Colorectal flat neoplasia." Digestive and Liver Disease 35, no. 3 (March 2003): 165–71. http://dx.doi.org/10.1016/s1590-8658(03)00024-0.

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5

Cohen, A. M. "Colorectal neoplasia: surgery." Current Opinion in Gastroenterology 6, no. 1 (February 1990): 38–40. http://dx.doi.org/10.1097/00001574-199002000-00008.

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6

IJspeert, Joep Evert Godfried, Jan Paul Medema, and Evelien Dekker. "Colorectal Neoplasia Pathways." Gastrointestinal Endoscopy Clinics of North America 25, no. 2 (April 2015): 169–82. http://dx.doi.org/10.1016/j.giec.2014.11.004.

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7

CAMPOS, Fábio Guilherme, Magaly Gemio TEIXEIRA, Arceu SCANAVINI, Maristela Gomes de ALMEIDA, Sergio Carlos NAHAS, and Ivan CECCONELLO. "INTESTINAL AND EXTRAINTESTINAL NEOPLASIA IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE IN A TERTIARY CARE HOSPITAL." Arquivos de Gastroenterologia 50, no. 2 (April 2013): 123–29. http://dx.doi.org/10.1590/s0004-28032013000200021.

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Context The development of neoplasia is an important concern associated with inflammatory bowel disease (IBD), especially colorectal cancer (CRC). Objectives Our aim was to determine the incidence of intestinal and extraintestinal neoplasias among patients with inflammatory bowel disease. Methods There were retrieved information from 1607 patients regarding demographics, disease duration and extent, temporal relationship between IBD diagnosis and neoplasia, clinical outcomes and risk factors for neoplasia. Results Crohn's disease (CD) was more frequent among women (P = 0.0018). The incidence of neoplasia was higher in ulcerative colitis (UC) when compared to CD (P = 0.0003). Eight (0.99%) patients developed neoplasia among 804 with CD: 4 colorectal cancer, 2 lymphomas, 1 appendix carcinoid and 1 breast cancer. Thirty (3.7%) patients developed neoplasia among the 803 UC: 13 CRC, 2 lymphomas and 15 extraintestinal tumors. While CRC incidence was not different among UC and CD (1.7% vs 0.5%; P = 0.2953), the incidence of extraintestinal neoplasias was higher among UC (2.1% vs 0.5%, P = 0.0009). Ten (26.3%) patients out of 38 with neoplasia died. Conclusions CRC incidence was low and similar in both diseases. There was a higher incidence of extraintestinal neoplasia in UC when compared to CD. Neoplasias in IBD developed at a younger age than expected for the general population. Mortality associated with malignancy is significant, affecting 1/4 of the patients with neoplasia.
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8

Hunt, L. M., P. S. Rooney, J. D. Hardcastle, and N. C. Armitage. "Endoscopic screening of relatives of patients with colorectal cancer." Gut 42, no. 1 (January 1, 1998): 71–75. http://dx.doi.org/10.1136/gut.42.1.71.

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Background—The risk of colorectal cancer is higher among relatives of those affected. The neoplastic yield reported from screening such individuals varies enormously between studies and depends on the age and strength of the family history of those screened.Aims—To ascertain the neoplastic yield of endoscopic screening of first degree relatives of patients with colorectal cancer by age and familial risk.Subjects—A total of 330 individuals with a family history of colorectal cancer.Method—Endoscopic screening conducted according to a protocol.Results—Adenomas were found in 12%, and adenomas larger than 1 cm in 8%, of “high risk” individuals screened primarily by colonoscopy. Of those with neoplasia, 26% had lesions at or proximal to the splenic flexure. Neoplasia was found in 9.5% of individuals at lower familial risk, screened primarily by 60 cm flexible sigmoidoscopy, 4% of whom had neoplasia larger than 1 cm in size or cancer. Neoplastic yield was greatest in the fourth and fifth decades in those at highest risk, but increased with age in those at lower risk.Conclusions—For individuals with two or more first degree relatives, or relatives who have developed colorectal cancer at a young age, colonoscopy appears to be the only satisfactory method of screening, but 60 cm flexible sigmoidoscopy may be useful in those at lower levels of risk.
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9

Langenfeld, Sean J. "Advances in Colorectal Neoplasia." Surgical Clinics of North America 97, no. 3 (June 2017): i. http://dx.doi.org/10.1016/s0039-6109(17)30054-3.

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10

Carey, Frank. "Pathology of colorectal neoplasia." Surgery (Oxford) 35, no. 3 (March 2017): 126–31. http://dx.doi.org/10.1016/j.mpsur.2016.12.006.

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11

Inadomi, John M. "Screening for Colorectal Neoplasia." New England Journal of Medicine 376, no. 2 (January 12, 2017): 149–56. http://dx.doi.org/10.1056/nejmcp1512286.

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12

Jenkins, Paul J., and Peter D. Fairclough. "Colorectal neoplasia in acromegaly*." Clinical Endocrinology 55, no. 6 (December 2001): 727–29. http://dx.doi.org/10.1046/j.1365-2265.2001.01418.x.

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13

Fajardo, Alyssa, and Bruce Robb. "Chemoprevention for Colorectal Neoplasia." Clinics in Colon and Rectal Surgery 21, no. 04 (October 14, 2008): 304–12. http://dx.doi.org/10.1055/s-0028-1089947.

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14

Dolejs, Scott, Benjamin Gayed, and Alyssa Fajardo. "Prevention of Colorectal Neoplasia." Clinics in Colon and Rectal Surgery 29, no. 04 (November 21, 2016): 353–62. http://dx.doi.org/10.1055/s-0036-1584086.

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AbstractColorectal cancer (CRC) is one of the leading causes of cancer-related morbidity and mortality worldwide. There are well-established screening protocols involving fecal testing, radiographic, and endoscopic evaluations that have led to decreased incidence and mortality of CRC in the United States. In addition to screening for CRC, there is interest in preventing colorectal neoplasia by targeting the signaling pathways that have been identified in the pathway of dysplasia progressing to carcinoma. This review will detail the efficacy of multiple potential preventative strategies including lifestyle changes (physical activity, alcohol use, smoking cessation, and obesity); dietary factors (dietary patterns, calcium, vitamin D, fiber, folate, and antioxidants and micronutrients); and chemopreventive agents (nonsteroidal anti-inflammatory drugs, statins, metformin, bisphosphonates, and postmenopausal hormonal therapy).
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15

JENKINS, P. J., G. M. BESSER, and P. D. FAIRCLOUGH. "Colorectal neoplasia in acromegaly." Gut 44, no. 5 (May 1, 1999): 585–87. http://dx.doi.org/10.1136/gut.44.5.585.

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16

Anderson, Joseph, and Zvi Alpern. "Smoking and Colorectal Neoplasia." American Journal of Gastroenterology 103 (September 2008): S200—S201. http://dx.doi.org/10.14309/00000434-200809001-00519.

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17

Anderson, Joseph C., Zvi A. Alpern, Brendan J. Wiggins, Patricia M. Hubbard-Ells, and Carol M. Martin. "Smoking and Colorectal Neoplasia." American Journal of Gastroenterology 101 (September 2006): S211—S212. http://dx.doi.org/10.14309/00000434-200609001-00498.

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18

Holick, Michael F., and Peter R. Holt. "Chemoprevention of Colorectal Neoplasia." Gastroenterology 135, no. 4 (October 2008): 1427–28. http://dx.doi.org/10.1053/j.gastro.2008.06.092.

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19

Wakeman, Chris, Jacqueline Keenan, Jimmy Eteuati, Paul Hollington, Tim Eglinton, and Frank Frizelle. "Chemoprevention of colorectal neoplasia." ANZ Journal of Surgery 87, no. 12 (December 21, 2015): E228—E232. http://dx.doi.org/10.1111/ans.13392.

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20

Negrete Carballo, Eduardo, and Fidel David Huitzil Melendez. "Prevalence of advanced colorectal neoplasia according to risk categories at screening colonoscopy in a tertiary referral center." Journal of Clinical Oncology 36, no. 4_suppl (February 1, 2018): 578. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.578.

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578 Background: Colorectal cancer (CRC) is the third most common cancer in the world. There is strong evidence that screening for colorectal cancer improves survival in conutries with high incidence. Although Mexico is considered a country with a low incidence of CRC, 4694 potentially preventable deaths occur every year. There is no established CRC screening program in our country, risk stratification of the target populations to be screened may bring potential advantages, making the strategy more cost-effective. The Asia-Pacific Colorectal Screening (APCS) score, is a validated risk-stratification tool that helps identify individuals at risk for advanced colorectal neoplasm amongst the asymptomatic population. Methods: We performed a retrospective, cross-sectional analysis of database records from 1172 patients who underwent screening colonoscopy betwen january 2013 and november 2014. Results: The prevalence of advanced colorectal neoplasia was 2.9%. Applying the APCS stratification, 91 subjects (7.8%) were in the average risk tier, 849 subjects (72.4%) in the moderate risk tier and 232 (19.8%) subjects in the high risk tier. The prevalence of advanced neoplasia in the average risk, moderate risk and high risk groups was 0%, 2.6% and 5.1%, respectively. The subjects in the high risk tier had 2.21-fold (p = 0.021) increased prevalence of advanced neoplasia than those in the average-moderate tier. Conclusions: The APCS score is a simple risk stratification index for colorectal advanced neoplasm that uses elementary clinical information on age, gender, family history and smoking to stratify the risk of colorectal advanced neoplasm in asymptomatic subjects for priority of colorectal screening.
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21

Toiyama, Yuji, Keun Hur, Koji Tanaka, Yasuhiro Inoue, Tsutomu Tabata, Masato Kusunoki, C. Richard Boland, and Ajay Goel. "Methylated miR-124, -137, and -34b/c as predictive biomarkers for ulcerative colitis-associated colorectal neoplasia." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e14631-e14631. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e14631.

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e14631 Background: Accumulating evidence suggests that microRNAs (miRNAs) can be targets of methylation-induced silencing in colorectal cancer, which can occur in an age-dependent manner, and constitutes an epigenetic “field defect”. We hypothesized whether methylation of miR-124, -137 and -34b/c can predict colorectal neoplasia in patients with ulcerative colitis (UC). Methods: We examined 185 samples from 70 UC patients (45 patients without neoplasia, 12 with dysplasia and 13 with cancers) for the methylation status of miR-124, -137 and -34b/c by quantitative bisulfite pyrosequencing analysis. In addition, expression levels of these 3 miRNAs in dysplastic (n=12), cancerous (n=13) and non-neoplastic UC mucosa (n=20) were quantified by TaqMan qRT-PCR. Results: MiR-124 and -137 methylation levels were significantly higher in rectal tissues than in proximal mucosa from non-neoplastic UC tissues, and were significantly associated with age and disease duration in rectal tissues. Methylation levels of all 3 miRNAs were significantly higher in dysplasia and cancer compared to mucosa without neoplasia, and showed a “field defect” in the non-neoplastic rectal tissues from patients with cancer . Receiver operating characteristic (ROC) analysis revealed that methylation levels of all 3 miRNAs in non-neoplastic rectal tissues could discriminate patients with cancer from those without (miR-124 AUC value = 0.74; miR-137 AUC = 0.79; miR-34b/c AUC=0.72). Furthermore, methylated miR-137 in non-neoplastic rectal tissues allowed discrimination of UC patients with neoplasia from those without (AUC = 0.76), and independently predicted neoplasia (OR= 5.55; 95% CI: 1.40–22.05; P = 0.0148). Expression levels of all 3 miRNAs were significantly downregulated in dysplasia or cancer compared to non-neoplastic UC mucosa, and the expression and methylation were negatively correlated. Conclusions: Methylation of miR-124, -137 and -34b/c in rectal biopsies, particularly miR-137, may serve as novel predictive biomarkers for neoplasia in UC patients. Restoration of expression by reversing their methylation status could be an attractive strategy to slow or reverse age-related UC-associated neoplasia.
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22

Peng, S. M. "Rank-Based Fecal Hemoglobin Concentration for Assessing Colorectal Neoplasms of National-Wide Colorectal Cancer Screening in Taiwan." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 204s. http://dx.doi.org/10.1200/jgo.18.82500.

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Background: Fecal hemoglobin concentration has shown potential of predicting colorectal cancer and colorectal adenoma. Accordingly, it is of great interest to use fecal hemoglobin concentration to stratify population into risk groups of colorectal disease. Aim: This study aims to predict the risk of colorectal neoplasia by using quantitative fecal hemoglobin concentration with a rank-based method. Methods: Using data from Taiwanese nationwide colorectal cancer screening program between 2004 to 2009 following up until 2012, fecal hemoglobin concentration regarded as the ordinal outcome was used to predict the risk of colorectal adenoma. Accelerated failure time model on fecal hemoglobin was used to evaluate the differences across 4 categories of outcome, including colorectal cancer, advanced adenoma, nonadvanced adenoma, and normal colon. We converted the adjusted percentile values of each group of colorectal neoplasia into the corresponding risk with Bayesian underpinning. Results: The adjusted median fecal hemoglobin concentration of nonadvanced adenoma was 57.0, advanced adenoma was 82.4, and colorectal cancer was 163.1 µg/g feces compared with normal colon. The corresponding risks of 2 groups when the fecal hemoglobin concentration reached the median were 4.0%, 4.8%, and 29.5%. Risk of reaching other percentile of 2 groups of colorectal neoplasm can be acquired on the basis of adjusted percentile value of fecal hemoglobin. Conclusion: Based on quantitative fecal hemoglobin concentration and survival model analysis, we estimated the risk of developing colorectal neoplasia by percentile of fecal hemoglobin concentration.
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23

Falt, Přemysl. "Current status of endoscopic full-thickness resection for treatment of colorectal neoplastic lesions." Gastroenterologie a hepatologie 75, no. 3 (June 30, 2021): 194–99. http://dx.doi.org/10.48095/ccgh202194.

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Endoscopic full-thickness resection (FTR) is a novel technique for endoscopic treatment of colorectal neoplastic lesions that are not suitable for standard endoscopic resection. Published evidence on FTR suggests high technical success rate, high proportion of R0 resections and low risk of serious complications. According to limited data, FTR appears to be a recommendable alternative to the technically challenging and time consuming endoscopic submucosal dissection (ESD) in the treatment of carcinomas with superficial submucosal invasion and local residual neoplasia, specifically outside the rectum. The main limitations of FTR are the limited extent of resection and occasional residual neoplasia after resection. Further research including prospective and randomized comparison to other resection techniques is needed for a correct inclusion of FTR in the treatment algorithm of colorectal neoplasia.
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24

Brenner, D. E., Y. Su, D. P. Normolle, S. Syngal, R. Bresalier, N. Marcon, J. Baron, and T. Block. "Detection of colorectal neoplasia associated K-Ras mutations in human urine." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 1005. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.1005.

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1005 Background: Since colorectal neoplasia-associated genes have been detected in human blood, we hypothesized that small DNA fragments containing genetic mutations associated with colorectal neoplasias are filtered and excreted in the urine. If so, genes associated with colorectal cancer will be detected in the urine. K-ras mutations are commonly associated with colorectal neoplasia and do not occur in the urinary tract. Methods: K-ras mutation detection: 200 microl of urine was extracted with guanidine thiocyanate and purifed using a Wizard DNA isolation kit. Codon 12 K-ras mutation detection methods–1: restriction enriched PCR, 20 cycles, with primers that amplify both wild type and mutated DNA but with an artificial BstNI site at the 5’ end of the amplified product (>2 K-ras copies per assay); 2: Peptide nucleic acid clamping real time PCR (>15 K-ras copies per assay). Human subjects: Training set = 20 patients with known K-ras mutations in colorectal cancer tissue. Test set = blinded urine samples from colorectal adenocarcinoma (N=48), adenoma (N=31), hyperplastic polyp (N=12) and endoscopically normal colon and rectum (N=60). Results: 1. Human urine contains 150–250 base pair DNA fragments derived from the circulation. These fragments can be readily distinguished from high molecular weight DNA from sloughed urinary tract cells. 2. Training set for K-ras detection (tissue confirmed K-ras mutations): Serum 6/20 (30%), Plasma (11/20 (55%), Urine: 18/20 (90%), (p<0.15 for plasma, p<0.001 for serum). 3. Test set (blinded): a. >2 copies of mutated K-ras genes were detected in: 16/48 (33%) adenocarcinomas; 23/31 (74%) adenomas; 5/12 (42%) hyperplastic polyps, and 19/60 (31%) non-neoplasia controls. b. >15 copies of mutated K-ras genes were detected in: 12/48 (25%) adenocarinomas; 15/31 (48%) adenomas; 3/12 (25%) hyperplastic polyps, and 11/60 (18%) non-neoplasia controls. Conclusions: Small DNA fragments in human urine contain K-Ras mutations identical to those found in colorectal cancer DNA. The sensitivity for detection of K-ras mutations in urine appears equivalent or superior to K-ras mutation detection in feces or serum. DNA mutations from systemic epithelial neoplasias may be detected in filtered urinary DNA fragments and may be useful for early detection of neoplasia. No significant financial relationships to disclose.
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25

Acevedo, Alejandro, Yaritza Diaz, Cynthia M. Perez, Maria Garau, John Baron, and Marcia Cruz-Correa. "Diabetes Mellitus and Colorectal Neoplasia." Journal of Cancer Therapy 03, no. 06 (2012): 859–65. http://dx.doi.org/10.4236/jct.2012.326110.

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26

Jass, Jeremy R., Vicki L. J. Whitehall, Joanne Young, and Barbara A. Leggett. "Emerging concepts in colorectal neoplasia." Gastroenterology 123, no. 3 (September 2002): 862–76. http://dx.doi.org/10.1053/gast.2002.35392.

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27

Pai, Ajit, Slawomir Marecik, John Park, and Leela Prasad. "Robotic Colorectal Surgery for Neoplasia." Surgical Clinics of North America 97, no. 3 (June 2017): 561–72. http://dx.doi.org/10.1016/j.suc.2017.01.006.

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28

HARDCASTLE, J. D. "Screening for colorectal neoplasia: Introduction." Journal of Gastroenterology and Hepatology 6, no. 6 (December 1991): 537. http://dx.doi.org/10.1111/j.1440-1746.1991.tb00903.x.

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29

JOHN, D. J. B. ST. "Screening tests for colorectal neoplasia." Journal of Gastroenterology and Hepatology 6, no. 6 (December 1991): 538–44. http://dx.doi.org/10.1111/j.1440-1746.1991.tb00904.x.

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30

FETTMAN, MARTIN J., ROSS N. BUTLER, ANTHONY J. McMICHAEL, and IAN C. ROBERTS-THOMSON. "Metabolic phenotypes and colorectal neoplasia." Journal of Gastroenterology and Hepatology 6, no. 1 (February 1991): 81–89. http://dx.doi.org/10.1111/j.1440-1746.1991.tb01151.x.

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31

Jacobs, Elizabeth T., Patricia A. Thompson, and Mar??a Elena Mart??nez. "Diet, Gender, and Colorectal Neoplasia." Journal of Clinical Gastroenterology 41, no. 8 (September 2007): 731–46. http://dx.doi.org/10.1097/mcg.0b013e3180338e56.

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32

Gibson, Joanna A., and Robert D. Odze. "Pathology of premalignant colorectal neoplasia." Digestive Endoscopy 28, no. 3 (March 15, 2016): 312–23. http://dx.doi.org/10.1111/den.12633.

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33

Young, Graeme P., and Richard K. Le Leu. "Resistant Starch and Colorectal Neoplasia." Journal of AOAC INTERNATIONAL 87, no. 3 (May 1, 2004): 775–86. http://dx.doi.org/10.1093/jaoac/87.3.775.

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Abstract There are several approaches to examining the relationship between resistant starch (RS) and development of colorectal cancer (CRC). These include examination of epidemiological relationships, objective testing of effects of RS given to humans on biological events of relevance to CRC, and studies in animal models where protection and mechanisms of protection can be directly tested. Nine epidemiological studies have examined the relationship between starch and CRC and/or adenomas. Most show a significant protective effect. However, epidemiological tools for measuring consumption of RS are poorly developed and so a benefit for RS can only be inferred. On balance, the magnitude of protection by starch appears to be in the order of 25–50%. Human intervention studies have examined the effect of various types and amounts of RS consumption on colonic biology. To generalize from these studies, RS softens stools and increases stool bulk, decreases pH, increases short-chain fatty acids (SCFAs) including butyrate, reduces products of protein fermentation, and decreases bile salts in fecal water. Such changes seem to be achieved within about 4 weeks of commencing consumption. The greatest effects are seen with the highest doses where increased fecal starch recovery is observed. A modest number of animal studies have been undertaken. Those examining effects of RS on colonic biology and biomarkers for CRC confirm and extend the results in humans. RS modifies the lumenal environment, largely through altered fermentation of polysaccharides and proteins. RS also affects epithelial biology in that it increases apoptotic deletion of genetically damaged cells. More work is needed to define what types and combinations of RS, perhaps with probiotics, exert the greatest effects on colonic environment and epithelial biology, and then to test these in the cancer models for their protective effect. A few studies have examined effect of RS on cancer as an end point in several rodent models, but the results are not clear cut. In conclusion, consumption of RS dramatically affects the colonic lumenal environment and facilitates apoptotic deletion of genetically damaged cells in the colon, several of which are considered to be biomarkers associated with risk for CRC. These effects can be interpreted as reflecting improved colonic health, which might be of benefit in protection against CRC. Direct evidence for protection is still not available.
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34

Lang, Leslie H. "“Virtual colonoscopy” for colorectal neoplasia." Gastroenterology 126, no. 2 (February 2004): 390. http://dx.doi.org/10.1053/j.gastro.2003.12.043.

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35

Spigelman, A. D. "Endoscopic surveillance for colorectal neoplasia." British Journal of Surgery 81, no. 11 (November 1994): 1664–65. http://dx.doi.org/10.1002/bjs.1800811135.

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36

Schraibman, I. G. "Endoscopic surveillance for colorectal neoplasia." British Journal of Surgery 82, no. 4 (April 1995): 568. http://dx.doi.org/10.1002/bjs.1800820447.

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37

Morris, D. L. "Colorectal neoplasia: epidemiology and aetiology." Current Opinion in Gastroenterology 6, no. 1 (February 1990): 24–32. http://dx.doi.org/10.1097/00001574-199002000-00006.

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38

Ahlquist, D. A. "Colorectal neoplasia: diagnosis and screening." Current Opinion in Gastroenterology 6, no. 1 (February 1990): 33–37. http://dx.doi.org/10.1097/00001574-199002000-00007.

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39

Scott, N., and P. Quirke. "Molecular biology of colorectal neoplasia." Gut 34, no. 3 (March 1, 1993): 289–92. http://dx.doi.org/10.1136/gut.34.3.289.

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40

Ahlquist, David A. "Molecular Detection of Colorectal Neoplasia." Gastroenterology 138, no. 6 (May 2010): 2127–39. http://dx.doi.org/10.1053/j.gastro.2010.01.055.

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41

Sengupta, Shomik, Joe J. Tjandra, and Peter R. Gibson. "Dietary fiber and colorectal neoplasia." Diseases of the Colon & Rectum 44, no. 7 (July 2001): 1016–33. http://dx.doi.org/10.1007/bf02235491.

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42

Chang, George J. "Laparoscopic treatment of colorectal neoplasia." Current Treatment Options in Gastroenterology 9, no. 3 (June 2006): 256–64. http://dx.doi.org/10.1007/s11938-006-0044-1.

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43

Mueller, Rudolph, and Andrew Davis. "Flexible sigmoidoscopy for colorectal neoplasia." American Journal of Medicine 90, no. 4 (April 1991): 536–37. http://dx.doi.org/10.1016/0002-9343(91)80104-t.

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44

Mueller, Rudolph, and Andrew Davis. "Flexible sigmoidoscopy for colorectal neoplasia." American Journal of Medicine 90, no. 1 (January 1991): 536–37. http://dx.doi.org/10.1016/0002-9343(91)90624-7.

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45

Thomas, Melissa L., Susanne K. Pedersen, Aidan McEvoy, Emma Vizgoft, Snigdha Gaur, Iain Beeston, and Lawrence C. LaPointe. "Plasma Testing of Gene Expression Biomarkers for Colorectal Neoplasia Discovered in Neoplastic Colorectal Tissue." Gastroenterology 140, no. 5 (May 2011): S—416. http://dx.doi.org/10.1016/s0016-5085(11)61709-5.

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46

Saade, Rayan, Zhiyan Fu, and Hwajeong Lee. "Endoscopically Unresectable Paneth Cell (PC)–Containing Adenomas and the Risk of Developing Colorectal Neoplasia." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S73. http://dx.doi.org/10.1093/ajcp/aqz113.089.

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Abstract Objectives Whether the presence of Paneth cells (PCs) in colorectal adenomas indicates an increased risk of colorectal neoplasia or not is controversial. We examined the clinicopathologic features of PC-containing adenomas (PCAs) that were surgically removed, focusing on the risk of developing subsequent colorectal neoplasia on follow-up. Methods A retrospective cohort of 154 patients with endoscopically unresectable colorectal adenomas who underwent surgical removal was retrieved. Archived pathology slides were evaluated for the presence of PC, villous features, and high-grade dysplasia. Demographic and clinical data were obtained by reviewing electronic medical records. A minimum 12 months of follow-up was considered valid follow-up data. Fisher’s exact test and Student t test were performed when indicated (P < .05 was considered statistically significant). Results PCAs were identified in 84 out of 154 cases (54.5%), commonly in the proximal as compared to distal colorectum (60.7% vs 38.1%, P = .018). There was no significant difference in patient age (mean, 66.0 vs 63.8), gender (M:F, 42:42 vs 35:35), adenoma size (mean, 3.18 cm vs 2.78 cm), villous features (69.0% vs 68.6%), and high-grade dysplasia (44.0% vs 35.7%) between PCA and non-PCA groups. After the mean follow-up duration of 65.8 months (range 12-169), 11 out of 30 patients (36.7%) had recurrent colorectal neoplasia, including 2 adenocarcinomas in the PCA group, as compared to 8 out of 27 (29.6%) in non-PCA group with no adenocarcinoma (P > .05). No statistical difference in the risk of developing colorectal neoplasia was noted between proximal PCA (24%), distal PCA (33.3%), and non-PCA (29.6%) groups. Conclusion PCAs are more common in the proximal colon, consistent with normal anatomic distribution of PC in the colon. No association was observed between PCA and high-grade dysplasia or colorectal neoplasia risk in endoscopically unresectable adenomas. PCA location was not a significant marker for future adverse outcomes.
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Wong, Martin C. S., Thomas Y. T. Lam, Kelvin K. F. Tsoi, Victor C. W. Chan, Hoyee W. Hirai, Jessica Y. L. Ching, and Joseph J. Y. Sung. "Predictors of Advanced Colorectal Neoplasia for Colorectal Cancer Screening." American Journal of Preventive Medicine 46, no. 5 (May 2014): 433–39. http://dx.doi.org/10.1016/j.amepre.2013.12.008.

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48

Mori, Yuriko, Alexandru V. Olaru, Yulan Cheng, Rachana Agarwal, Jian Yang, Delgermaa Luvsanjav, Wayne Yu, et al. "Novel candidate colorectal cancer biomarkers identified by methylation microarray-based scanning." Endocrine-Related Cancer 18, no. 4 (June 2, 2011): 465–78. http://dx.doi.org/10.1530/erc-11-0083.

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DNA hypermethylation is a common epigenetic abnormality in colorectal cancers (CRCs) and a promising class of CRC screening biomarkers. We conducted a genome-wide search for novel neoplasia-specific hypermethylation events in the colon. We applied methylation microarray analysis to identify loci hypermethylated in 17 primary CRCs relative to eight non-neoplastic colonic mucosae (NCs) from neoplasia-free subjects. These CRC-associated hypermethylation events were then individually evaluated for their ability to discriminate neoplastic from non-neoplastic cases, based on real-time quantitative methylation-specific PCR (qMSP) assays in 113 colonic tissues: 51 CRCs, nine adenomas, 19 NCs from CRC patients (CRC–NCs), and 34 NCs from neoplasia-free subjects (control NCs). A strict microarray data filtering identified 169 candidate CRC-associated hypermethylation events. Fourteen of these 169 loci were evaluated using qMSP assays. Ten of these 14 methylation events significantly distinguished CRCs from age-matched control NCs (P<0.05 by receiver operator characteristic curve analysis); methylation of visual system homeobox 2 (VSX2) achieved the highest discriminative accuracy (83.3% sensitivity and 92.3% specificity, P<1×10−6), followed by BEN domain containing 4 (BEND4), neuronal pentraxin I (NPTX1), ALX homeobox 3 (ALX3), miR-34b, glucagon-like peptide 1 receptor (GLP1R), BTG4, homer homolog 2 (HOMER2), zinc finger protein 583 (ZNF583), and gap junction protein, gamma 1 (GJC1). Adenomas were significantly discriminated from control NCs by hypermethylation of VSX2, BEND4, NPTX1, miR-34b, GLP1R, and HOMER2 (P<0.05). CRC–NCs were significantly distinguished from control NCs by methylation of ALX3 (P<1×10−4). In conclusion, systematic methylome-wide analysis has identified ten novel methylation events in neoplastic and non-neoplastic colonic mucosae from CRC patients. These potential biomarkers significantly discriminate CRC patients from controls. Thus, they merit further evaluation in stool- and circulating DNA-based CRC detection studies.
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Manne, Upender, Chandrakumar Shanmugam, Venkat R. Katkoori, Harvey L. Bumpers, and William E. Grizzle. "Development and progression of colorectal neoplasia." Cancer Biomarkers 9, no. 1-6 (October 26, 2011): 235–65. http://dx.doi.org/10.3233/cbm-2011-0160.

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50

Tobi, M. ,. M. "Polyps as biomarkers for colorectal neoplasia." Frontiers in Bioscience 4, no. 1-3 (1999): d329. http://dx.doi.org/10.2741/tobi.

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