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Relevant bibliographies by topics / Colorectal neoplasia

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Academic literature on the topic 'Colorectal neoplasia'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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Journal articles on the topic "Colorectal neoplasia"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Colorectal neoplasia"

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Pye, G. "Gastrointestinal pH and colorectal neoplasia." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381466.

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Kim, Sangmi Sandler Robert Samuel. "Obesity, inflammation and colorectal neoplasia." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,2164.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Feb. 26, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Epidemiology, School of Public Health." Discipline: Epidemiology; Department/School: Public Health.

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LaPointe, Lawrence C., and larry lapointe@flinders edu au. "Gene expression biomarkers for colorectal neoplasia." Flinders University. School of Medicine, 2009. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20091011.090028.

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The aim of this research was to assemble sufficient experimental evidence about candidate gene transcript expression changes between non-neoplastic and neo- plastic colorectal tissues to justify future assay development involving promis- ing leads. To achieve this aim, this thesis explores the hypothesis that gene expression-based biomarkers can be used to accurately discriminate colorectal neoplastic tissues from non-neoplastic controls. This hypothesis was tested by first analysing multiple, large, quality controlled data sets comprising gene expression measurements across colorectal phenotypes to discover potential biomarkers. Candidate biomarkers were then subjected to validation testing using a custom-design oligonucleotide microarray applied to independently derived clinical specimens. A number of novel conclusions are reached based on these data. The most important conclusion is that a defined subset of genes expressed in the colorectal mucosa are reliably differentially ex- pressed in neoplastic tissues. In particular, the apparently high prediction accu- racy achieved for single gene transcripts to discriminate hundreds of neoplastic and non-neoplastic tissues provides compelling evidence that the resulting can- didate genes are worthy of further biomarker research. In addition to addressing the central hypothesis, additional contributions are made to the field of colorectal neoplasia gene expression profiling. These contributions include: The first systematic analysis of gene expression in non-diseased tissues along the colorectum To better understand the range of gene expression in non-diseased tissues, RNA extracts taken from along the longitudinal axis of the large intestine were studied. The development of quality control methodologies for high dimen- sional gene expression data Complex data collection platforms such as oligonucleotide microarrays introduce the potential for unrecognized confound- ing variables. The exploration of quality control parameters across five hundred microarray experiments provided insights about quality control techniques. The design of a custom microrray comprised of oligonucleotide probe- sets hybridising to RNA transcripts differentially expressed in neo- plastic colorectal specimens A custom design oligonucleotide microarray was designed and tested combining the results of multiple biomarker discovery projects. Introduction of a method to filter differentially expressed genes dur- ing discovery that may improve validation efficiencies of biomarker discovery based on gene expression measurements Differential expression discovery research is typically focused only on quantitative changes in transcript concentration between phenotype contrasts. This work introduces a method for generating hypotheses related to transcripts which may be quali- tatively switched-on between phenotypes. Identification of mRNA transcripts which are differentially expressed between colorectal adenomas and colorectal cancer tissues Transcripts differentially expressed between adenomatous and cancerous RNA extracts were discovered and then tested in independent tissues. In conclusion, these results confirm the hypothesis that gene expression profiling can discriminate colorectal neoplasia (including adenomas) from non-neoplastic controls. These results also establish a foundation for an ongoing biomarker development program.

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Hubner, Richard Anthony. "Low penetrance polymorphisms and colorectal neoplasia susceptibility." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499095.

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Bhaskar, P. "Molecular mechanisms of colorectal neoplasia in acromegaly." Thesis, University of Newcastle upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405070.

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Liu, Lin, Karen Messer, John A. Baron, David A. Lieberman, Elizabeth T. Jacobs, Amanda J. Cross, Gwen Murphy, Maria Elena Martinez, and Samir Gupta. "A prognostic model for advanced colorectal neoplasia recurrence." SPRINGER, 2016. http://hdl.handle.net/10150/621531.

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Following colonoscopic polypectomy, US Multisociety Task Force (USMSTF) guidelines stratify patients based on risk of subsequent advanced neoplasia (AN) using number, size, and histology of resected polyps, but have only moderate sensitivity and specificity. We hypothesized that a state-of-the-art statistical prediction model might improve identification of patients at high risk of future AN and address these challenges. Data were pooled from seven prospective studies which had follow-up ascertainment of metachronous AN within 3-5 years of baseline polypectomy (combined n = 8,228). Pooled data were randomly split into training (n = 5,483) and validation (n = 2,745) sets. A prognostic model was developed using best practices. Two risk cut-points were identified in the training data which achieved a 10 percentage point improvement in sensitivity and specificity, respectively, over current USMSTF guidelines. Clinical benefit of USMSTF versus model-based risk stratification was then estimated using validation data. The final model included polyp location, prior polyp history, patient age, and number, size and histology of resected polyps. The first risk cut-point improved sensitivity but with loss of specificity. The second risk cut-point improved specificity without loss of sensitivity (specificity 46.2 % model vs. 42.1 % guidelines, p < 0.001; sensitivity 75.8 % model vs. 74.0 % guidelines, p = 0.64). Estimated AUC was 65 % (95 % CI: 62-69 %). This model-based approach allows flexibility in trading sensitivity and specificity, which can optimize colonoscopy over- versus underuse rates. Only modest improvements in prognostic power are possible using currently available clinical data. Research considering additional factors such as adenoma detection rate for risk prediction appears warranted.

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Parra, del Riego A., Sparks A. Olivares, B. F. Barreda, and Nilton Yhuri Carreazo. "Advanced colorectal neoplasia: The importance of adequate classification." Asociación Mexicana de Gastroenterología, 2016. http://hdl.handle.net/10757/605890.

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Sardo, Christine Louise. "The Biological Role of Fruit Phenolics, Sedentary Behavior, and Inflammation on Colorectal Neoplasia." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/297045.

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Background: Clinical and epidemiologic studies have investigated the effects of diet, physical activity, and inflammation on the risk of colorectal adenoma occurrence and recurrence. Inflammation has been proposed as a mechanism of action for the development of colorectal adenoma and cancer. Research indicates that fruit phenolic exposure may attenuate the inflammatory response and some data suggest that berries are effective in mitigating this process. Inflammatory cytokines such as interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) are of particular interest due to their role in adenoma development. Epidemiological investigations have studied the association between bioactive fruit phenolic compounds and colorectal neoplasia; however, epidemiological data for the association between consumption of berries, which contain high concentrations of these compounds, and colorectal adenoma recurrence are limited. In addition to a potential role of phenolics in reducing inflammation, physical activity has also been proposed as a mitigator of this process. Numerous studies have investigated the association between physical activity and colorectal neoplasia, yet data on sedentary behavior and colorectal adenoma recurrence are limited. This dissertation was designed to further elucidate the role of fruit phenolics and sedentary behavior on colorectal adenoma recurrence and to specifically highlight the potential role of black raspberries in mitigating the postprandial inflammatory response among overweight and obese individuals. Methods: Ten overweight or obese males (BMI>25 kg/m²), ages 55-72, participated in an open-label, randomized, 14-day, pilot crossover study. Subjects consumed a high- fat, high- calorie (HFHC) meal, with (Group 1) or without (Group 2) a 5 day regimen of 45 g of black raspberry powder in the form of a slurry. The study included a two-day washout period before Group 1 and Group 2 were crossed over. The two-day washout period was based on a pharmacokinetic study conducted with black raspberry powder (1); peak plasma concentrations of ellagic acid and anthocyanin metabolites peaked at 1 to 2 hours following consumption of 45 grams of black raspberry powder and by 12 hours, plasma concentrations of these metabolites were almost fully washed out, with plasma concentrations returning to near baseline levels. Blood samples were obtained prior to consumption of the HFHC breakfast and at 1, 2, 4, 8, and 12 hours afterwards, during two 14-hour clinic visits. The primary study outcomes were changes in areas under the curves (AUCs) of serum biomarkers of TNF-α, CRP, and IL-6. A secondary pooled analysis was conducted among participants from two randomized, double blind, placebo-controlled Phase III clinical trials to investigate the association between berry consumption and colorectal adenoma recurrence, and the association between sedentary behavior and colorectal adenoma recurrence. Analyses included 2,502 subjects who had completed the baseline Arizona Food Frequency Questionnaire to ascertain berry consumption history in the past year and 1,730 men and women who had completed the baseline Arizona Activity Frequency Questionnaire to ascertain sedentary behavior. All subjects had a follow-up colonoscopy during the trial. Logistic regression modeling was employed to estimate the effect of sedentary behavior or berry consumption on colorectal adenoma recurrence. Results: The mean AUC of serum IL-6 was significantly lower (p=0.03) with black raspberry (BRB) feeding (45.5±36.3 pg/mL; mean±SD), compared to high fat, high calorie meal alone (56.7±50.0 pg/mL). No statistically significant differences were observed in the mean AUC of serum TNF-α or CRP. In the pooled analysis, no significant associations were observed between berry consumption and adenoma recurrence in the pooled population or when stratified by sex. In the evaluation of association between sedentary behavior and adenoma recurrence, subjects in the second, third, and fourth quartiles of sedentary behavior experienced higher odds of adenoma recurrence; however, the difference was only statistically significant for the third quartile. Sex-stratified analyses revealed that in men, sedentary activity was statistically significantly associated with 45% higher odds of adenoma recurrence. Compared to the lowest quartile of sedentary activity, the ORs (95% CIs) for the second, third, and fourth quartiles among men were 1.31 (0.93, 1.84), 1.47 (1.04, 2.09), and 1.45 (1.02, 2.06) respectively (P trend=0.03). In contrast, no association with sedentary activity was observed in women. Conclusion: Polyphenol exposure in the form of a black raspberry slurry significantly decreased post-prandial IL-6 in a clinical trial among ten older overweight and obese men. These findings suggest short-term attenuation of an inflammatory maker may not translate to decreased adenoma recurrence, however, long term randomized clinical trials with black raspberries are needed to evaluate this further. However, in an epidemiological analysis, consumption of up to 1 cup per week of whole berries was not associated with lower odds for adenoma recurrence among a pooled population of participants in the Wheat Bran Fiber and Ursodeoxycholic Acid Phase III clinical trials. While the epidemiological results indicated that berry consumption are not associated with the development of early colorectal neoplasia, the effects on later stages of carcinogenesis are unknown. Higher levels of berry consumption may be required in order to reach a cancer inhibitory effect. Finally, results of the physical activity study suggest that sedentary behavior is associated with a higher risk of adenoma recurrence among men, providing evidence of detrimental effects of a sedentary lifestyle early in the carcinogenesis pathway. Efforts to further evaluate these findings in other cohorts or in an intervention trial should be considered.

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Wong, Justin Jong Leong Medical Sciences Faculty of Medicine UNSW. "The role of DNA methylation in the development of colorectal neoplasia." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43359.

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DNA methylation is increasingly recognised as a significant epigenetic event that may initiate and drive the process of neoplasia in humans. In the colon, DNA methylation of key genes is common in a subset of colorectal cancers. The extent to which DNA methylation at various genes contributes to initiation of colorectal neoplasms is less clear. This study sought to clarify the biological and clinicopathological significance of methylation of various genes in the development of sporadic and familial colorectal neoplasia. Quantitative methylation-specific PCR (qMSP) assays (capable of detecting down to a measureable proportion of 0.1% of the total input DNA) were developed to determine the presence of CpG methylation at a given gene. Methylation of MLH1-C was found in the apparently normal mucosa samples from seven of 104 (7%) of individuals with sporadic colorectal cancer (CRC) showing microsatellite instability (MSI). No methylation of MLH1-C was found in the biological samples of individuals with microsatellite stable (MSS) counterparts (n=131). MLH1-C methylation may be a field defect that predisposes to the development of sporadic colorectal neoplasia, particularly those demonstrating MSI. Methylation of three of five genes within the 3p22 region including AB002340, MLH1, ITGA9, PLCD1 and DLEC1 (regional 3p22 methylation) was found in 83% of sporadic MSI (n=86) and 12% of MSS cancers demonstrating BRAF V600E mutation (n=42). Regional 3p22 correlated strongly with CpG island methylator phenotype (CIMP), and other clinicopathological characteristics typical of CIMP. Thus, regional 3p22 methylation and CIMP may be overlapping phenomena. Regional 3p22 methylation and the BRAF V600E mutation were found in normal colonic mucosa of four individuals with sporadic MSI CRC, and these cases also had multiple synchronous serrated polyps. These molecular aberrancies may predispose some individuals to the development of metachronous serrated neoplasia. Germline epimutations of APC do not contribute towards the development of FAP, AFAP, or hyperplastic polyposis syndromes. However, APC methylation in normal colonic mucosa of these individuals may represent a field defect in the development of futher neoplasms. In conclusion, different patterns of DNA methylation in normal colonic mucosa may represent a field defect important in the development of different subtypes of colorectal neoplasia.

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Khoo, Kong Kheong. "The influence of metabolic phenotypes upon the development of colorectal neoplasia /." Title page, table of contents and conclusions only, 1995. http://web4.library.adelaide.edu.au/theses/09MD/09mdk45.pdf.

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Books on the topic "Colorectal neoplasia"

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Church, James, and Graham Casey. Molecular Genetics of Colorectal Neoplasia. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6.

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Chan, Andrew T., and Elmar Detering, eds. Prospects for Chemoprevention of Colorectal Neoplasia. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-30331-9.

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G, Williams Bryan R., and Casey Graham, eds. Molecular genetics and colorectal neoplasia: A primer for the clinician. New York: Igaku-Shoin, 1996.

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Beauchemin, Nicole, and Jacques Huot. Metastasis of colorectal cancer. Dordrecht: Springer, 2010.

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M, Goldberg Stanley, and Garcia-Aguilar Julio, eds. Colorectal cancer. Oxford: Health Press, 1999.

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Colorectal cancer. Philadelphia: Saunders/Elsevier, 2010.

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Cancer Quality Council of Ontario Signature Event on Colorectal Cancer. Improving the management of colorectal cancer: Summary of the Cancer Quality Council of Ontario Signature Event on Colorectal Cancer. Toronto, Ont: Cancer Quality Council of Ontario, 2003.

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Kudō, Shin'ei. Early colorectal cancer: Detection of depressed types colorectal carcinomas. Tokyo: Igaku-Shoin, 1996.

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Young, Annie M. ABC of colorectal cancer. 2nd ed. Chichester, West Sussex, UK: Wiley-Blackwell, 2011.

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Kerr, David J. ABC of colorectal cancer. London: BMJ Books, 2001.

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Book chapters on the topic "Colorectal neoplasia"

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Park, Seong Ho. "Nonpolypoid Colorectal Neoplasia." In Atlas of Virtual Colonoscopy, 133–43. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-5852-5_9.

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Church, James, and Graham Casey. "Pathology of Colorectal Neoplasia." In Molecular Genetics of Colorectal Neoplasia, 57–67. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_5.

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Kune, Gabriel A. "Morphology of Colorectal Neoplasia." In Causes and Control of Colorectal Cancer, 29–46. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1273-4_4.

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al-Najami, Issam, and Ravish Narotam Jootun. "Management of Rectal Neoplasia." In Multidisciplinary Treatment of Colorectal Cancer, 47–54. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58846-5_7.

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Church, James, and Graham Casey. "Molecular Genetics of Colorectal Neoplasia." In Molecular Genetics of Colorectal Neoplasia, 69–89. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_6.

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Schwartzberg, David M., and Michael J. Grieco. "Invasive Anal Canal Neoplasia." In Clinical Decision Making in Colorectal Surgery, 213–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-65942-8_28.

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Church, James, and Graham Casey. "An Introduction to Genetics." In Molecular Genetics of Colorectal Neoplasia, 1–12. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_1.

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Church, James, and Graham Casey. "A Registry for Inherited Colorectal Cancer." In Molecular Genetics of Colorectal Neoplasia, 139–48. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_10.

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Church, James, and Graham Casey. "Practical Applications of the Molecular Genetics of Colorectal Cancer." In Molecular Genetics of Colorectal Neoplasia, 149–57. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_11.

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Church, James, and Graham Casey. "Changes in Gene Function: Mutations, Methylation, and Variation in Expression." In Molecular Genetics of Colorectal Neoplasia, 13–26. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9310-6_2.

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Conference papers on the topic "Colorectal neoplasia"

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Ahlquist, David A. "Abstract IA13: Stool DNA detection of colorectal neoplasia." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-ia13.

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Adams, Scott V., Polly A. Newcomb, Andrea N. Burnett-Hartman, Melissa P. Upton, Lee-Ching Zhu, Margaret Mandelson, John D. Potter, and Karen W. Makar. "Abstract 299: Circulating microRNAs in association with colorectal neoplasia." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-299.

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Adams, Gregory, Sharifeh Mehrabi, Tesfamariam Mehreteab, Edward E. Grizzle, and Felix O. Aikhionbare. "Abstract 3806: Mitochondrial DNA (MtDNA) analysis in colorectal neoplasia." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3806.

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Fábián, A., R. Bor, Ö. Szabó, M. Rutka, B. Vasas, L. Andrási, A. Bálint, et al. "OUTCOMES OF ENDOSCOPIC AND SURGICAL REMOVAL OF EARLY COLORECTAL NEOPLASIA." In ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637556.

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Poole, Elizabeth M., Liren Xiao, Rachel L. Galbraith, Martha L. Slattery, David Duggan, Anna E. Coghill, Lisel Koepl, et al. "Abstract 927: Interleukin-23 receptor tagSNPs and colorectal neoplasia risk." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-927.

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Abbenhardt, Clare, Elisabeth M. Poole, Liren Xiao, Marty L. Slattery, Rachel L. Galbraith, David Duggan, Li Hsu, et al. "Abstract 934: Phospholipase A2A polymorphisms and risk of colorectal neoplasia." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-934.

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Montrose, David C., Levy Kopelovich, Xi Kathy Zhou, Rhonda Yantiss, Kotha Subbaramaiah, and Andrew Dannenberg. "Abstract 1634: Metabolomic profiling for early detection of colorectal neoplasia." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1634.

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Keku, Temitope O., Romin Bonakdar, Felix Araujo Perez, Amber N. McCoy, Patrick Edmundson, and Kevin Smith. "Abstract 1259: Gut microbiota and mucosal inflammation and colorectal neoplasia." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1259.

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Zhan, T., S. Belle, E. Valentini, S. Herrmann, T. Miersch, M. Li, T. Gaiser, M. Boutros, MP Ebert, and J. Betge. "Cancer-associated mutations in normal colorectal mucosa adjacent to sporadic neoplasia." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716208.

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Whitehall, Vicki, Jennifer Borowsky, Catherine Bond, Mark Bettington, Sally-Ann Pearson, Murugan Kalimutho, John Liu, et al. "Abstract PR04: Wnt and MAPK pathway activation in conventional and serrated colorectal neoplasia." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-pr04.

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