The Role of Metabolic Epidemiology and Laboratory Studies in the Etiology of Colon Cancer

Bridging the Gap of Drug Delivery in Colon Cancer: The Role of Chitosan and Pectin Based Nanocarriers System

Current Drug Delivery ◽

10.2174/1567201817666200717090623 ◽

2020 ◽

Vol 17 (10) ◽

pp. 911-924

Author(s):

Rohitas Deshmukh

Keyword(s):

Drug Delivery ◽

Colon Cancer ◽

Targeted Drug Delivery ◽

Targeted Delivery ◽

Therapeutic Agent ◽

Therapeutic Agents ◽

Delivery Systems ◽

Target Tissue ◽

Polymer Carriers

Colon cancer is one of the most prevalent diseases, and traditional chemotherapy has not been proven beneficial in its treatment. It ranks second in terms of mortality due to all cancers for all ages. Lack of selectivity and poor biodistribution are the biggest challenges in developing potential therapeutic agents for the treatment of colon cancer. Nanoparticles hold enormous prospects as an effective drug delivery system. The delivery systems employing the use of polymers, such as chitosan and pectin as carrier molecules, ensure the maximum absorption of the drug, reduce unwanted side effects and also offer protection to the therapeutic agent from quick clearance or degradation, thus allowing an increased amount of the drug to reach the target tissue or cells. In this systematic review of published literature, the author aimed to assess the role of chitosan and pectin as polymer-carriers in colon targeted delivery of drugs in colon cancer therapy. This review summarizes the various studies employing the use of chitosan and pectin in colon targeted drug delivery systems.

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Role of MicroRNAs in Colon Cancer Progression and Metastasis

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530320666200825184924 ◽

2020 ◽

Vol 20 ◽

Author(s):

Shruthi Sanjitha Sampath ◽

Sivaramakrishnan Venkatabalsubramanian ◽

Satish Ramalingam

Keyword(s):

Colon Cancer ◽

Cancer Progression ◽

Target Genes ◽

Tumour Progression ◽

Intestinal Barrier ◽

Colon Cancer Progression ◽

Bowel Diseases ◽

Inflammatory Bowel ◽

Novel Therapeutic Strategies

: MicroRNAs regulate gene expression at the posttranscriptional level by binding to the mRNA of their target genes. The dysfunction of miRNAs is strongly associated with the inflammation of the colon. Besides, some microRNAs are shown to suppress tumours while others promote tumour progression and metastasis. Inflammatory bowel diseases include Crohn’s disease and Ulcerative colitis which increase the risk factor for inflammation-associated colon cancer. MicroRNAs are shown to be involved in gastrointestinal pathologies, by targeting the transcripts encoding proteins of the intestinal barrier and their regulators that are associated with inflammation and colon cancer. Detection of these microRNAs in the blood, serum, tissues, faecal matter, etc will enable us to use these microRNAs as biomarkers for early detection of the associated malignancies and design novel therapeutic strategies to overcome the same. Information on MicroRNAs can be applied for the development of targeted therapies against inflammation-mediated colon cancer.

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Defecatory Dysfunction After Colon Cancer Resection: The Role of Inferior Mesenteric Artery Tie

Anticancer Research ◽

10.21873/anticanres.14276 ◽

2020 ◽

Vol 40 (5) ◽

pp. 2969-2974

Author(s):

ENRICO FIORI ◽

DANIELE CROCETTI ◽

ANTONIETTA LAMAZZA ◽

FRANCESCA DE FELICE ◽

GIORGIA BURRELLI SCOTTI ◽

...

Keyword(s):

Colon Cancer ◽

Mesenteric Artery ◽

Inferior Mesenteric Artery ◽

Cancer Resection ◽

Defecatory Dysfunction ◽

Colon Cancer Resection

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Activation of the GPR35 pathway drives angiogenesis in the tumour microenvironment

Gut ◽

10.1136/gutjnl-2020-323363 ◽

2021 ◽

pp. gutjnl-2020-323363

Author(s):

Ester Pagano ◽

Joshua E Elias ◽

Georg Schneditz ◽

Svetlana Saveljeva ◽

Lorraine M Holland ◽

...

Keyword(s):

Colon Cancer ◽

Tumour Growth ◽

Tumour Microenvironment ◽

Tube Formation ◽

Tissue Remodelling ◽

Colon Cancers ◽

Inflammatory Bowel ◽

Ion Pumping ◽

G Protein Coupled

ObjectivePrimary sclerosing cholangitis (PSC) is in 70% of cases associated with inflammatory bowel disease. The hypermorphic T108M variant of the orphan G protein-coupled receptor GPR35 increases risk for PSC and ulcerative colitis (UC), conditions strongly predisposing for inflammation-associated liver and colon cancer. Lack of GPR35 reduces tumour numbers in mouse models of spontaneous and colitis associated cancer. The tumour microenvironment substantially determines tumour growth, and tumour-associated macrophages are crucial for neovascularisation. We aim to understand the role of the GPR35 pathway in the tumour microenvironment of spontaneous and colitis-associated colon cancers.DesignMice lacking GPR35 on their macrophages underwent models of spontaneous colon cancer or colitis-associated cancer. The role of tumour-associated macrophages was then assessed in biochemical and functional assays.ResultsHere, we show that GPR35 on macrophages is a potent amplifier of tumour growth by stimulating neoangiogenesis and tumour tissue remodelling. Deletion of Gpr35 in macrophages profoundly reduces tumour growth in inflammation-associated and spontaneous tumour models caused by mutant tumour suppressor adenomatous polyposis coli. Neoangiogenesis and matrix metalloproteinase activity is promoted by GPR35 via Na/K-ATPase-dependent ion pumping and Src activation, and is selectively inhibited by a GPR35-specific pepducin. Supernatants from human inducible-pluripotent-stem-cell derived macrophages carrying the UC and PSC risk variant stimulate tube formation by enhancing the release of angiogenic factors.ConclusionsActivation of the GPR35 pathway promotes tumour growth via two separate routes, by directly augmenting proliferation in epithelial cells that express the receptor, and by coordinating macrophages’ ability to create a tumour-permissive environment.

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