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A teacher with intermittent rectal bleeding
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
As with any disease, risk factors are important in establishing a suitable index of clinical suspicion. For colorectal cancer these include: diet: a Westernised diet containing increased amounts of animal protein and low in fibrefamily history: particularly if family members have developed the disease at a young age (<45 years) – families may benefit from genetic screening and counsellingulcerative colitis: risk increases over time – there is a 10–20% chance of developing cancer in patients who have had ulcerative colitis with total colonic involvement for 10 years. Distal colitis does not confer a high riskadenomatous colonic polyps: many undergo malignant change if left untreatedfamilial adenomatous polyposis coli: multiple adenomas throughout the colon from a young age confer a very high risk, even 100% by the 4th decadeacromegaly.
Nucleic Acids as Therapeutic Targets and Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Familial adenomatous polyposis (FAP) is a hereditary condition that occurs in approximately 1:10,000 individuals worldwide, and is caused by mutations in the Adenomatous Polyposis Coli (APC) gene. As a result of these mutations, epithelial cells lining the intestinal tract have increased levels of the protein beta-catenin, which, in turn, results in uncontrolled cell growth. Proliferation of the epithelial cells results in the formation of numerous (hundreds to thousands) noncancerous growths (polyps) throughout the large intestine. CEQ508 is the first drug candidate in a novel class of therapeutic agents utilizing the “transkingdom” RNA interference (tkRNAi) platform developed by Marina Biotech Inc and which is an expressed RNA in a bacterial delivery system. The agent CEQ508 comprises attenuated bacteria that are engineered to enter dysplastic tissue and release a payload of short-hairpin RNA (shRNA) targeting the mRNA of beta-catenin, which is known to be dysregulated in classical FAP. CEQ508 was being developed by Marina as an orally administered treatment to reduce the levels of beta-catenin protein in the epithelial cells of the small and large intestine. In 2012 the company announced positive results for CEQ508 in safety Phase I trials, and the FDA granted fast track designation in 2015.
General Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Rebecca Fish, Aisling Hogan, Aoife Lowery, Frank McDermott, Chelliah R Selvasekar, Choon Sheong Seow, Vishal G Shelat, Paul Sutton, Yew-Wei Tan, Thomas Tsang
What is the genetic basis of colon cancer?APC (adenomatous polyposis coli) gene mutations Occur early in 60% of all adenomas and carcinomasK-ras mutations (induce cell growth) Occur later in large adenomas and carcinomasp53 mutation (involved in DNA repair and induction of apoptosis) Later, in invasive colonic cancersAccompanied by invasion
Expression Levels of WNT Signaling Pathway Genes During Early Tooth Development
Published in Organogenesis, 2023
Yuhan Song, Fujie Song, Xuan Xiao, Zhifeng Song, Shangfeng Liu
Adenomatous polyposis coli (APC) gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in cell migration and adhesion, transcriptional activation, and apoptosis.61 Mutations in Apc may cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy.62 Besides, other diseases such as Gardner syndrome, which is characterized by the presence of multiple intracolonic polyps and extracolonic tumors, can also be caused by Apc mutation. Our previous study found that patients with Gardner syndrome also had multiple impacted and supernumerary teeth.16 We found that Apc was expressed at E14.5-P7 and there are up to 2037 different mutation forms in Apc, suggesting that Apc played an important role in all stages of early tooth development.
Targeted deep sequencing reveals APC mutations as predictors of overall survival in Chinese colorectal patients receiving adjuvant chemotherapy
Published in Scandinavian Journal of Gastroenterology, 2022
Xin Chen, Mengjun Hu, Ying Chen, Ajian Li, Yutong Hua, Huihong Jiang, Huaguang Li, Moubin Lin
Adenomatous polyposis coli (APC) is a key tumor suppressor gene consisting of multiple functional domains enabling APC to interact with various proteins to regulate cell adhesion, chromosome segregation, survival, cell cycle progression and DNA repair [11–13]. APC can antagonize oncogenic transformation through repression of Wnt signaling [14–16]. APC is frequently mutated in CRC, occurring in over 70% of tumors. Somatic mutations of APC are scattered over its large coding sequence (CDS) of ∼8kb and 16 exons, and the mutational spectrum varies among different tumors and even within the same tumor, which makes it technically challenging to precisely identify all somatic mutations of APC in a large number of tumor samples, especially for rare mutations. Recently, deep NGS has overcome this challenge and identified a large number of nonsense mutations and a small number of frameshift and missense mutations in the APC gene [14,17,18]. APC mutations occur early in the premalignant lesion adenoma and persist through invasive carcinoma [14,17–19]. Despite its clear involvement in early carcinogenesis, the role of APC mutations in the clinical outcome of CRC is not clear and has not been assessed in The Cancer Genome Atlas (TCGA).
5-Hydroxymethylfurfural (HMF) formation, occurrence and potential health concerns: recent developments
Published in Toxin Reviews, 2021
Ankit Choudhary, Vikas Kumar, Satish Kumar, Ishrat Majid, Poonam Aggarwal, Sheenam Suri
At the preclinical level, HMF and its derivative, SMF, have been referred to as potent carcinogens (Shapla et al.2018). The end product of Maillard reaction i.e. HMF promotes the growth of human tumor cells and also found to have the opposite effect against human tumor cells (Markowicz et al.2012). Micro-adenomas and aberrant crypt foci (ACF) act as markers in the multistep stage which occurs during colon cancer. A study concluded that the incorporation of small doses of HMF and SMF in multiple intestinal neoplasia mice resulted in an increase in the formation of small adenomas and flat ACF (Svendsen et al.2009). When HMF was administered orally to F344 female rats, it resulted in an increment in both size and number of ACF (Zhang et al.1993). Adenomas formation in small and large intestines due to mutation in tumor suppressor gene i.e. adenomatous polyposis coli (ACP) which resulted in similar human familial adenomatous polyposis syndrome (Paulsen et al.2005).