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Nutraceutical’s Role in Proliferation and Prevention of Colorectal Cancer
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Mayur M. Patel, Shruti U. Rawal, Jayvadan K. Patel
Colorectal carcinoma is the cancer that starts in distal alimentary canal (large intestine) involving colon and/or rectum. Most of the CRC initiate with the development of “polyps,” which are small growth on the inner lining (mucosa) of colon or rectum. Some of these polyps are precancerous and may progress to the development of cancer. Polyps that are flat or have raised growths are termed as sessile polyps, and those having a growth on short stalks are termed as pedunculated polyps. The presence of polyps, however, does not always indicate a cancerous or even precancerous condition. Noncancerous polyps include small hyperplastic polyps, inflammatory polyps, and hamartomatous polyps, which are not part of an inherited polyp syndrome. Cancerous polyps are hyperplastic polyps and adenomas. Polyps have to be extracted during colonoscopy in order to determine their nature and prevent CRC incidence [11].
Clinical Features of Colorectal Adenoma and Adenocarcinoma
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Jamie Murphy, Norman S. Williams
A full clinical examination is clearly essential in all cases of suspected colorectal carcinoma. Not only is the clinician looking for signs that may help to confirm the diagnosis, but also in cases where the diagnosis has already been made, it is important to assess the extent of spread and the fitness of the patient for surgical treatment.
Gastrointestinal system
Published in David A Lisle, Imaging for Students, 2012
Staging of colorectal carcinoma may be summarized as follows:Stage I: tumour confined to the bowel wallStage II: invasion through the full thickness of the bowel wall ± invasion of adjacent structuresStage III: metastasis to regional lymph node(s)Stage IV: metastasis to distant site(s) such as liver, non-regional lymph node(s), lung.
Utilizing network pharmacological analysis to investigate the key targets and mechanisms of kaempferol against oxaliplatin-induced neurotoxicity
Published in Toxicology Mechanisms and Methods, 2023
Hongxing Wang, Jing Quan, Youming Deng, Jie Chen, Ke Zhang, Zhan Qu
Chemotherapy-induced peripheral neuropathic pain is a serious adverse observed in up to 80% of patients during anti-cancer drug therapy (Sisignano et al. 2014). Colorectal carcinoma is common cancer in the world. Oxaliplatin is a third-generation platinum-based anti-cancer drug, which was widely applied to treat colorectal carcinoma. Although oxaliplatin is well known for its efficacy in the treatment of colorectal cancer, it can induce severe peripheral neurotoxicity (Graham et al. 2004). This neurotoxicity can be hazardous because it could disrupt treatment plans by decreasing doses or interrupting treatment (Han et al. 2016). Neuroinflammation, glial activation, oxidative stress, mitochondrial injury, and nuclear DNA injury were considered the major mechanisms of chronic peripheral neuropathy (Xu et al. 2018; Gui et al. 2020; Kang et al. 2021). Growing evidence indicated that the activation of astrocytes plays a pro-inflammatory effect in the pathological process of neurotoxicity (Ji et al. 2014). It has been reported that the pro-inflammatory cytokine and PI3K-mTOR signal pathways lead to oxaliplatin-induced neurotoxicity (Duan et al. 2018). Besides, curcumin could improve oxaliplatin-induced neurotoxicity by mitigating neuroinflammation (Zhang et al. 2020). Astragaloside IV alleviated oxaliplatin-induced neuropathic pain via the regulation of oxidative stress and neuroinflammation (Xu et al. 2021). Therefore, suppression of neuroinflammation may be a novel treatment strategy for oxaliplatin-induced neurotoxicity.
Colorectal carcinoma screening: Established methods and emerging technology
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
Erika Hissong, Meredith E. Pittman
Colorectal carcinoma remains a significant cause of global morbidity and mortality; it is the 2nd most common cancer and 4th most common cause of cancer-related death worldwide [1–3]. Risk factors for the development of colorectal carcinoma are well documented, and many are associated with a “Western” lifestyle, including cigarette smoking, obesity, high consumption of alcohol and red meat, and physical inactivity [4–8]. Colorectal carcinoma risk is also associated with family history, multiple hereditary cancer syndromes, and certain medical conditions such as inflammatory bowel disease [9–12]. Molecular and epidemiologic studies have shown that in patients without underlying cancer-predisposition syndromes or inflammatory bowel disease, colorectal neoplasia progresses from premalignant adenomas to invasive carcinoma over a period of approximately 10 years [13–15].
Lactate dehydrogenase: a marker of diminished antitumor immunity
Published in OncoImmunology, 2020
Sandra Van Wilpe, Rutger Koornstra, Martijn Den Brok, Jan Willem De Groot, Christian Blank, Jolanda De Vries, Winald Gerritsen, Niven Mehra
Patients with elevated LDH levels not only benefit less from immunotherapy, but also from many other anticancer therapies such as chemotherapy and targeted therapy.1,68 However, previous studies suggest that patients with high LDH levels benefit more from VEGF (receptor) inhibitors, such as vatalanib69 and bevacizumab,70,71 than patients with normal LDH levels. Two large, randomized controlled trials studied the efficacy of chemotherapy (FOLFOX) plus vatalanib versus FOLFOX alone in patients with colorectal carcinoma. Patients were randomized stratified according to baseline LDH levels (≤ or >1.5xULN). In the overall population, the addition of vatalanib exerted only moderate effects on PFS (HR 0.85, p = .005), whereas a major improvement was seen in patients with high LDH levels (HR 0.65, p < .001).69 It is not surprising that patients with elevated LDH levels benefit most from anti–VEGF therapy, since both glycolysis and hypoxia are associated with active angiogenesis.72,73 Moreover, previous studies found an association between high serum LDH levels and VEGF (receptor) overexpression in various tumors.74