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The rectum
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The most common abnormality found in colorectal cancer is mutation in the Wnt signaling pathway, which increases cell signalling activity. The mutations can be inherited or acquired. The most commonly mutated gene is the APC gene, which results in accumulation of the P-catenin protein. P-catenin activates the transcription of various proto-oncogenes that are responsible for normal cell renewal and differentiation, but when overexpressed can cause cancer. Many other mutations, other than in the Wnt signaling pathway, are found in colorectal cancer, and include mutations in the TP53 gene that controls normal cell division and death, and mutations in genes responsible for programmed cell death, such as the gene encoding transforming growth factor (TGF)-P and DCC (deleted in colorectal cancer). Other genetic abnormalities include overexpression of oncogenes, including genes encoding the proteins KRAS (Kirsten rat sarcoma homologue), RAF (rapidly accelerated fibrosarcoma) and PI3K (phosphoinositide 3-kinase), which lead to increased cell proliferation, and inactivation of tumour suppressor genes, such as PTEN (phosphatase and tensin homologue), which normally inactivates the PI3K signalling pathway.
Gnetum montanum extract induces apoptosis by inhibiting the activation of AKT in SW480 human colon cancer cells
Published in Pharmaceutical Biology, 2022
Xianglong Pan, Xiaotao Hou, Fan Zhang, Peiling Tang, Wanruo Wan, Zixia Su, Yeguo Yang, Wei Wei, Zhengcai Du, Jiagang Deng, Erwei Hao
Colorectal cancer (CRC) is among the top three cancers with higher incident and mortality rate around the world. In 2020, the International Agency for Research on Cancer (IARC) documented that approximately 1.15 million of new CRC cases (which is about 10% of all types of cancers) and >570,000 of CRC-related deaths (which is about 9.4% of all cancer-related deaths) were reported worldwide (Jung et al. 2020; Sung et al. 2021). Colon cancer is a malignant tumour grows from the epithelium mucosal crypts of the large intestine (Iqbal and George 2017). Gene mutations (such as adenomatous polyposis (APC), deleted in colorectal cancer (DCC), K-Ras, p53, B-Raf proto-oncogene serine/threonine kinase (BRAF), mismatch repair gene) and microsatellite instability are the common factors that led to the development of colon cancer (Ahmed 2020; Benson et al. 2021). The common treatments of colon cancer include surgery, radiotherapy, chemotherapy, and molecular targeted therapy. Although the present diagnostic and therapeutic procedures have greatly been improved, the prognosis of colon cancer remains poor (Binefa et al. 2014; Li et al. 2021). The therapeutic drugs used to treat malignant tumours include chemo drugs, new technology drugs, and natural drugs. Research in exploring the novel natural compounds that can modulate apoptosis pathway of cancer cells for new drug development is intensively on-going. Various traditional plants with known medicinal properties are widely studied over the past decades (Hou et al. 2016; Aiello et al. 2019).
Relationship between circulating netrin-1 levels, obesity, prediabetes and newly diagnosed type 2 diabetes
Published in Archives of Physiology and Biochemistry, 2022
Iveta Nedeva, Antoaneta Gateva, Yavor Assyov, Vera Karamfilova, Tsvetelina Velikova, Zdravko Kamenov
Netrin-1 belongs to the laminin-related proteins of axon guidance, acts through its two classic receptor families, such as deleted in colorectal cancer (DCC) and uncoordinated 5 (UNC5) subfamilies and plays various key roles such as anti-inflammatory, anti-apoptotic and pro-angiogenic (Dun and Parkinson 2017). The purpose of this study was to evaluate the relationship between netrin-1, obesity and carbohydrate disturbances (from prediabetes to diabetes). As initially expected, in our patients with obesity and carbohydrate disturbances there were more significant abnormalities in regard to glucose level, HOMA, BMI, waist, WSR, WHR, VAI, TG, BP and HDL. The latter is frequently observed in such kind of patients and is in the context of the metabolic changes associated with these types of pathology. Mean netrin-1 levels were lower in patients with obesity, prediabetes and diabetes compared to the control group. Liu et al. (2016) similarly showed that in patients with newly diagnosed type 2 diabetes, netrin-1 levels were significantly lower than in normal controls which correspond to our results. Furthermore, in our study we described that the risk of carbohydrate disturbances was about three times higher in patients with netrin-1 levels ≤ 0.17 ng/ml versus those with higher values. In addition, we found a negative correlation between netrin-1 and anthropometric parameters (BMI, WSR, waist) and LDL.
The potential of Slit2 as a therapeutic target for central nervous system disorders
Published in Expert Opinion on Therapeutic Targets, 2020
Prativa Sherchan, Zachary D. Travis, Jiping Tang, John H. Zhang
Various regulatory genes control the expression of axonal guidance molecules and thereby regulate the path that axonal fibers travel. Among few studies that have explored the role of regulatory genes and transcription factors that controls expression of Slit and its receptor Robo, the transcription factor Pax6 seems to play a role in axonal pathfinding during brain development by regulating Slit proteins [46]. The expressions of Slit1 and Slit2 were downregulated whereas netrin-1 was upregulated in the dorsal thalamus of Pax6 deficient mice [46]. This was associated with aberrant pattern of axonal projections from mammillary bodies to thalamus and midbrain in Pax6 mutant mice [46]. The expression of Slit3 did not change, which was low in wild type and mutant mice. However, expression patterns of the receptor for netrin-1, deleted in colorectal cancer (DCC), and Robo1-3 was similar between Pax mutant and wild type embryonic mice [46]. Mutations in genes that encode Pax6 may lead to reduced Slit1 and Slit2 expression resulting in abnormal axonal pathfinding.