Journal articles on the topic 'Gastrointestinal system – Cancer'
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GÜLŞEN, Muaz, and Sevban ARSLAN. "Home Care in Gastrointestinal System-Oriented Cancer Surgery." Turkiye Klinikleri Journal of Internal Medicine 6, no. 1 (2021): 44–48. http://dx.doi.org/10.5336/intermed.2020-76526.
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Ohuchida, Kenoki. "Robotic Surgery in Gastrointestinal Surgery." Cyborg and Bionic Systems 2020 (December 4, 2020): 1–7. http://dx.doi.org/10.34133/2020/9724807.
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Robotic surgery is expanding in the minimally invasive treatment of gastrointestinal cancer. In the field of gastrointestinal cancer, robotic surgery is performed using a robot-assisted surgery system. In this system, the robot does not operate automatically but is controlled by the surgeon. The surgery assistant robot currently used in clinical practice worldwide is the leader-follower type, including the da Vinci® Surgical System (Intuitive Surgical). This review describes the current state of robotic surgery in the treatment of gastrointestinal cancer and discusses the future development of robotic systems in gastrointestinal surgery.
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Zhong, Jia-Ling. "Ubiquitin proteasome system research in gastrointestinal cancer." World Journal of Gastrointestinal Oncology 8, no. 2 (2016): 198. http://dx.doi.org/10.4251/wjgo.v8.i2.198.
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Zawacki, Kristin L. "Hereditary Cancer Syndromes of the Gastrointestinal System." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 13, no. 4 (November 2002): 523–39. http://dx.doi.org/10.1097/00044067-200211000-00006.
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Brown, Kimberly. "Hereditary Cancer Syndromes of the Gastrointestinal System." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 13, no. 4 (November 2002): 590–92. http://dx.doi.org/10.1097/00044067-200211000-00015.
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Pazienza, Valerio, Manlio Vinciguerra, and Gianluigi Mazzoccoli. "PPARs Signaling and Cancer in the Gastrointestinal System." PPAR Research 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/560846.
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Nowadays, the study of the peroxisome proliferators activated receptors (PPARs) as potential targets for cancer prevention and therapy has gained a strong interest. From a biological point of view, the overall responsibility of PPARs in cancer development and progression is still controversial since several studies report both antiproliferative and tumor-promoting actions for these signaling molecules in human cancer cells and animal models. In this paper, we discuss PPARs functions in the context of different types of gastrointestinal cancer.
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Tajabadi, Z., M. E. Akbari, and A. A. Hafez. "Physical Activity and Gastrointestinal Cancer Risk: A Review." Acta Medica Bulgarica 46, no. 1 (February 1, 2019): 57–67. http://dx.doi.org/10.2478/amb-2019-0010.
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Abstract Introduction: Western lifestyle characterized by increased consumption of red meat, fat, processed food, smoking, alcohol drinking, lower consumption of vegetables and physical inactivity has been associated with a higher gastrointestinal cancer risk. Digestive system cancers are diagnosed at late stages when they show poor response to treatment and are associated with a high mortality rate. Colorectal, gastric, esophageal and pancreatic cancers are among the most common cancers worldwide. Studies show that more than 50% of gastrointestinal cancers develop as a result of inappropriate lifestyle. An inverse association between physical activity and many chronic diseases has been proved so far. However, the association between physical activity and some gastrointestinal cancers is still controversial. This study was aimed to determine the association between physical activity and gastrointestinal cancers risk. Methods: We conducted a comprehensive search of English and Persian databases from February 2007 till December 2017, for studies investigating the association of physical activity and risk of gastrointestinal cancers. Finally, after reading full text of articles, 123 studies were included. Results: Physical activity can be helpful in reducing the risk of gastrointestinal cancer, especially colon and pancreatic cancers. The risk reduction is not similar for different types of gastrointestinal cancers and also among males and females. Conclusion: Different types of physical activity are associated with a lower risk of gastrointestinal cancer. However, it is unknown which type and intensity of physical activity are associated with a protective effect against gastro-intestinal cancer.
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Yamashina, Takeshi, Masaaki Shimatani, Masahiro Takeo, Kotaro Sasaki, Masahiro Orino, Natsuko Saito, Hironao Matsumoto, et al. "Viral Infection in Esophageal, Gastric, and Colorectal Cancer." Healthcare 10, no. 9 (August 26, 2022): 1626. http://dx.doi.org/10.3390/healthcare10091626.
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The human gastrointestinal tract, which constitutes the digestive system, contains a large number of virus particles that maintain organizational homeostasis and health. Conversely, viral pathogens have also attracted attention for their involvement in the pathogenesis of certain cancers, including gastrointestinal cancers. To aid prevention and treatment of these cancers, the relevance of gastrointestinal viral factors as potential risk factors needs to be carefully investigated. This review summarizes and discusses the available literature on the relationship between the development of esophageal, gastric, and colorectal cancers and their corresponding viruses. This review reveals that research on the association between colorectal cancer and viruses, in particular, is still in its infancy compared to the association between HPV and esophageal cancer and between EBV and gastric cancer.
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Ghadyalpatil, Nikhil Suresh, Chopra Supriya, Patil Prachi, Dsouza Ashwin, and Saklani Avanish. "Gastrointestinal cancers in India: Treatment perspective." South Asian Journal of Cancer 05, no. 03 (July 2016): 126–36. http://dx.doi.org/10.4103/2278-330x.187585.
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AbstractGI cancer is not one cancer but is a term for the group of cancers that affect the digestive system including gastric cancer (GC), colorectal cancer (CRC), hepatocellular carcinoma (HCC), esophageal cancer (EC), and pancreatic cancer (PC). Overall, the GI cancers are responsible for more cancers and more deaths from cancer than any other organ. 5 year survival of these cancers remains low compared to western world. Unlike the rest of the world where organ based specialities hepatobiliary, pancreatic, colorectal and esophagogastric exist , these cancers are managed in India by either a gastrointestinal surgeons, surgical oncologist, or a general surgeon with varying outcomes.The aim of this review was to collate data on GI cancers in indian continent. In colorectal cancers, data from tertiary care centres identifies the unique problem of mucinous and signet colorectal cancer. Results of rectal cancer resection in terms of technique (intersphincteric resection, extralevator aper, minimal invasive approach ) to be comparable with world literature. However long term outcome and data regarding colon cancers and nationally is needed. Gastric cancer at presentation are advanced and in surgically resected patients, there is need for a trial to compare chemoradiation vs chemotherapy alone to prevent loco regional recurrence. Data on minimal invasive gastric cancer surgery may be sparse for the same reason. Theree is a lot of data on surgical techniques and perioperatve outcomes in pancreatic cancer. There is a high volume of locally advanced gallbladder cancers with efforts on to decide whether neoadjuvant chemotherapy or neoadjuvant chemoradiotherapy is better for down staging. Considering GI cancers, a heterogeneous disease with site specific treatment options and variable outcomes, the overall data and outcomes are extremely variable. Young patients with pathology unique to the Indian subcontinent (for example, signet ring rectal cancer, GBCs) need focussed attention. Solution for such pathology needs to come from the Indian continent itself. Joint efforts to improve outcomes for GI cancer can be integrated under the national cancer grid program.
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Giallongo, Sebastiano, Oriana Lo Re, and Manlio Vinciguerra. "Macro Histone Variants: Emerging Rheostats of Gastrointestinal Cancers." Cancers 11, no. 5 (May 15, 2019): 676. http://dx.doi.org/10.3390/cancers11050676.
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Gastrointestinal cancers (GC) are malignancies involving the gastrointestinal (GI) tract and accessory organs of the digestive system, including the pancreas, liver, and gall bladder. GC is one of the most common cancers and contributes to more cancer-related deaths than cancers of any other system in the human body. Causative factors of GC have been consistently attributed to infections, smoking, an unhealthy diet, obesity, diabetes, and genetic factors. More recently, aberrant epigenetic regulation of gene expression has emerged as a new, fundamental pathway in GC pathogenesis. In this review, we summarize the role of the macroH2A histone family in GI cell function and malignant transformation, and highlight how this histone family may open up novel biomarkers for cancer detection, prediction, and response to treatment.
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Javed, Aadil, Gianluca Malagraba, Mahdieh Yarmohammadi, Catalina M. Perelló-Reus, Carles Barceló, and Teresa Rubio-Tomás. "Therapeutic Potential of Mitotic Kinases’ Inhibitors in Cancers of the Gastrointestinal System." Future Pharmacology 2, no. 3 (June 30, 2022): 214–37. http://dx.doi.org/10.3390/futurepharmacol2030015.
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Mitosis entails mechanistic changes required for maintaining the genomic integrity in all dividing cells. The process is intricate and temporally and spatially regulated by the ordered series of activation and de-activation of protein kinases. The mitotic kinases ensure the stepwise progression of entry into mitosis after the G2 phase of the cell cycle, followed by prophase, pro-metaphase, metaphase, anaphase, telophase, and subsequently cytokinesis and birth of two daughter cells with equal segregation and distribution of the genome. The major mitotic kinases include cyclin-dependent kinase 1 (CDK1), Aurora A and B Kinases, and Polo-Like-Kinase 1 (PLK1), among others. Overexpression of some of these kinases has been reported in many cancers as the mitotic fidelity and genome integrity are interlinked and dependent on these regulators, the native irregularities in these factors can be targeted as therapeutic strategies for various cancers. Here, we report and summarize the recent updates on the literature describing the various mitotic inhibitors targeting kinases, which can be used as potential therapeutic interventions for gastrointestinal cancers including gastric cancer, liver cancer, pancreatic cancer and colorectal cancer.
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McGwin, Gerald. "The Association between Ranitidine Use and Gastrointestinal Cancers." Cancers 13, no. 1 (December 23, 2020): 24. http://dx.doi.org/10.3390/cancers13010024.
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N-nitrosodimethylamine (NDMA) is a carcinogen in experimental animals. It has been classified a probable human carcinogen and has been found in ranitidine. This study sought to evaluate the association between ranitidine use and cancer of the gastrointestinal system. Events reported to the FDA Adverse Events Reporting System that were associated with the use of proton pump inhibitors (PPIs) and H2 antagonists were selected. Proportionate reporting ratios (PRRs) and associated 95% confidence intervals (CIs) were calculated to compare the proportion of all reported adverse events that were for gastrointestinal system cancers among adverse event reports for ranitidine to adverse event reports for other H2 antagonists. The proportion of adverse events for any gastrointestinal system cancer relative to all other events was elevated for ranitidine compared to PPIs and other H2 antagonists (PRR 3.66, 95% CI 3.19–4.20). Elevated and significant PRRs were observed for pharyngeal (PRR 9.24), esophageal (PRR 3.56), stomach (PRR 1.48), colorectal (PRR 16.31), liver (PRR 2.64), and pancreatic (PRR 2.18) cancers. The PRRs for anal (PRR 4.62) and gallbladder (PRR 4.62) cancer were also elevated though not statistically significant. In conjunction with a large body of epidemiologic and human and animal basic science research, the study results support the hypothesis that NDMA-contaminated ranitidine increases the risk of cancer and supports the withdrawal of these medications from the market.
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Forde, Patrick F., Mira Sadadcharam, Michael G. Bourke, Thomas A. Conway, Shane R. Guerin, Marcel de Kruijf, Gerald C. O’Sullivan, Joseph Impellizeri, Anthony J. P. Clover, and Declan M. Soden. "Preclinical evaluation of an endoscopic electroporation system." Endoscopy 48, no. 05 (April 4, 2016): 477–83. http://dx.doi.org/10.1055/s-0042-101343.
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Background and study aims: Targeted delivery of specific chemotherapeutic drugs into tumors can be achieved by delivering electrical pulses directly to the tumor tissue. This causes a transient formation of pores in the cell membrane that enables passive diffusion of normally impermeant drugs. A novel device has been developed to enable the endoscopic delivery of this tumor permeabilizing treatment. The aim of the preclinical studies described here was to investigate the efficacy and safety of this nonthermal ablation system in the treatment of gastrointestinal cancer models. Methods: Murine, porcine, and canine gastrointestinal tumors and tissues were used to assess the efficacy and safety of electroporation delivered through the special device in combination with bleomycin. Tumor cell death, volume, and overall survival were recorded. Results: Murine tumors treated with electrochemotherapy showed excellent responses, with cell death being induced rapidly, mainly via an apoptotic-type mechanism. Use of the system in canine gastrointestinal cancers demonstrated successful local endoluminal tumor resolution, with no safety or adverse effects noted. Conclusions: Electroporation via the new device in combination with bleomycin offers a nonthermal tumor ablative approach, and presents clinicians with a new option for the management of gastrointestinal cancers.
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Tan, Yaohong, Monica T. Garcia-Buitrago, Jonathan C. Trent, and Andrew E. Rosenberg. "The immune system and gastrointestinal stromal tumor." Current Opinion in Oncology 27, no. 4 (July 2015): 338–42. http://dx.doi.org/10.1097/cco.0000000000000201.
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Yalcintepe, Sinem, Hakan Gurkan, Selma Demir, Hilmi Tozkir, Huseyin Ahmet Tezel, Emine Ikbal Atli, Engin Atli, Damla Eker, and Irfan Cicin. "Targeted next-generation sequencing as a diagnostic tool in gastrointestinal system cancer/polyposis patients." Tumori Journal 106, no. 6 (May 11, 2020): 510–17. http://dx.doi.org/10.1177/0300891620919171.
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Background: Recent advances in next-generation sequencing (NGS) technology have enabled multigene testing and changed the diagnostic approach to hereditary gastrointestinal cancer/polyposis syndromes. The aim of this study was to analyze different cancer predisposition genes in hereditary/sporadic gastrointestinal cancer/polyposis. Methods: Cancer predisposition genes were analyzed with an Illumina MiSeq NGS system in 80 patients with gastrointestinal cancer/polyposis who were examined between the years 2016 and 2019. Deletion/duplication analysis of MLH1, MSH2, and EPCAM genes was performed by using the multiplex ligation-dependent probe amplification method. Results: Germline testing of hereditary cancer-related genes was performed in 80 patients with gastrointestinal cancer/polyposis. A total of 30 variants in 30 cases (37.5%) were assessed as pathogenic/likely pathogenic. A total of 19 heterozygous variants were assessed as variants of uncertain clinical significance in 17 cases (21.25%) and 18 (22.5%) novel variations (9 pathogenic/likely pathogenic, 9 variants of uncertain significance) were determined. In 4 (5%) cases, multiplex ligation-dependent probe amplification detected deletions in MLH1, MSH2, and EPCAM genes. Conclusion: The accumulation of analyses with multigene testing will increase the available data for cancer predisposition genes in hereditary gastrointestinal cancer/polyposis. Educational campaigns for prevention, efficient screening programs, and more personalized care based on the profile of individual patients are necessary.
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Hubbard, Joleen M., and Axel Grothey. "Cancer Stem Cells and Cancer Stem Cell Inhibitors in Gastrointestinal Cancers." Oncology & Hematology Review (US) 12, no. 01 (2016): 41. http://dx.doi.org/10.17925/ohr.2016.12.01.41.
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Cancer stem cells (CSCs) are a subpopulation of phenotypically distinct cancer cells that may play an important role in tumor pathogenesis. The gastrointestinal (GI) system provides a good example for investigation of the role of CSCs in tumor proliferation; GI CSCs are suitable for study due to their abundance, proliferative potential, and consistent structural arrangement that is maintained under tightly controlled signaling pathways. GI stem cells have a long lifespan and this, combined with their rapid turnover, may predispose them to forming CSCs. Alternative possible sources of GI CSCs include differentiated intestinal cells, bone marrow, and cancer cells. Therapies that specifically target CSCs present an exciting opportunity to treat patients with cancer. Enhanced understanding of CSC markers, such as CD133, CD44, and epithelial cell adhesion molecule (EpCAM), may facilitate development of therapies that target them. Among the stemness pathways that have been targeted are Wnt/β-catenin, STAT, Notch, and Nanog.
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Bouzid, Rachid, Maikel Peppelenbosch, and Sonja I. Buschow. "Opportunities for Conventional and In Situ Cancer Vaccine Strategies and Combination with Immunotherapy for Gastrointestinal Cancers, A Review." Cancers 12, no. 5 (April 30, 2020): 1121. http://dx.doi.org/10.3390/cancers12051121.
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Survival of gastrointestinal cancer remains dismal, especially for metastasized disease. For various cancers, especially melanoma and lung cancer, immunotherapy has been proven to confer survival benefits, but results for gastrointestinal cancer have been disappointing. Hence, there is substantial interest in exploring the usefulness of adaptive immune system education with respect to anti-cancer responses though vaccination. Encouragingly, even fairly non-specific approaches to vaccination and immune system stimulation, involving for instance influenza vaccines, have shown promising results, eliciting hopes that selection of specific antigens for vaccination may prove useful for at least a subset of gastrointestinal cancers. It is widely recognized that immune recognition and initiation of responses are hampered by a lack of T cell help, or by suppressive cancer-associated factors. In this review we will discuss the hurdles that limit efficacy of conventional cancer therapeutic vaccination methods (e.g., peptide vaccines, dendritic cell vaccination). In addition, we will outline other forms of treatment (e.g., radiotherapy, chemotherapy, oncolytic viruses) that also cause the release of antigens through immunogenic tumor cell death and can thus be considered unconventional vaccination methods (i.e., in situ vaccination). Finally, we focus on the potential additive value that vaccination strategies may have for improving the effect immunotherapy. Overall, a picture will emerge that although the field has made substantial progress, successful immunotherapy through the combination with cancer antigen vaccination, including that for gastrointestinal cancers, is still in its infancy, prompting further intensification of the research effort in this respect.
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Khan, Zabiha, and R. Loganathan. "Transfer learning based classification of MSI and MSS gastrointestinal cancer." International journal of health sciences 6, S1 (March 22, 2022): 1857–72. http://dx.doi.org/10.53730/ijhs.v6ns1.4952.
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Gastrointestinal and Colorectal cancers are treated with chemotherapy and its other forms which are not able to provide higher survival rates [1]. Immunotherapy is increasingly becoming popular due to its promising response especially to mutated tumors such as MicroSatellite Instability (MSI) cancers with deficient DNA Mismatch-Repair system (dMMR). Generally, 85% of all the cases related to gastrointestinal and colorectal cancers have proficient DNA Mismatch-Repair system (pMMR) which are also called MicroSatellite Stability (MSS). Only about 15% of the gastrointestinal and colorectal cancer patients have deficient DNA Mismatch-Repair system (dMMR) causing MicroSatellite Instability (MSI) in their tumors. While Immunotherapy responds well to patients with MSI tumors, it is resistant to MSS tumors [2]. Hence, it’s important to classify MSI vs. MSS tumors so that appropriate treatment can be given to the patients. Clinically MSI cancers are difficult to be detected after stage III due to their sensitivity to pembrolizumab inhibitors [3] [4]. In this work, deep learning based transfer learning approach is detailed that can accurately classify MSI vs. MSS cancers using histological images which are derived from formalin-fixed paraffin-embedded (FFPE).
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Landry, Christine S., Kelly M. Mcmasters, Charles R. Scoggins, and Robert C. G. Martin. "Proposed Staging System for Gastrointestinal Carcinoid Tumors." American Surgeon 74, no. 5 (May 2008): 418–22. http://dx.doi.org/10.1177/000313480807400511.
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Gastrointestinal carcinoid tumors are rare neuroendocrine tumors with no staging system in existence. The goal of this study was to establish a staging system consistent with the American Joint Commission on Cancer Staging Systems using the TNM strategy. A retrospective review of our prospective database of 990 hepatopancreaticobiliary patients and our tumor registry identified 108 patients with gastrointestinal carcinoid tumors from June 1990 to September 2006. Tumors were classified into our staging system by depth of penetration, size of primary tumor, nodal status, and the presence/absence of distant metastasis. Patients were staged as Stage 1, 22 per cent; Stage II, 29 per cent; Stage 3, 12 per cent; and Stage 4, 35 per cent. There were 41 men and 57 women with a median age of 58.5 years (range, 19–86 years). Primary tumors included 52 small bowel, 12 colon, 19 rectum, nine stomach, and seven of unknown primary origin. The use of our initial staging system demonstrated a trend in differences in survival across all four stages. The use of our initial staging proposal delineates the biology of the disease with accurate overall survival estimates. The addition of a dedicated American Joint Commission on Cancer staging system is needed for gastrointestinal carcinoids. Widespread use of this staging system may contribute to the future management and treatment of gastrointestinal carcinoid tumors.
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Malagraba, Gianluca, Mahdieh Yarmohammadi, Aadil Javed, Carles Barceló, and Teresa Rubio-Tomás. "The Role of LSD1 and LSD2 in Cancers of the Gastrointestinal System: An Update." Biomolecules 12, no. 3 (March 17, 2022): 462. http://dx.doi.org/10.3390/biom12030462.
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Epigenetic mechanisms are known to play a key role in cancer progression. Specifically, histone methylation involves reversible post-translational modification of histones that govern chromatin structure remodelling, genomic imprinting, gene expression, DNA damage repair, and meiotic crossover recombination, among other chromatin-based activities. Demethylases are enzymes that catalyse the demethylation of their substrate using a flavin adenine dinucleotide-dependent amine oxidation process. Lysine-specific demethylase 1 (LSD1) and its homolog, lysine-specific demethylase 2 (LSD2), are overexpressed in a variety of human cancer types and, thus, regulate tumour progression. In this review, we focus on the literature from the last 5 years concerning the role of LSD1 and LSD2 in the main gastrointestinal cancers (i.e., gastric cancer, liver cancer, pancreatic cancer, and colorectal cancer).
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Nicolaides, Steven, and Alex Boussioutas. "Immune-Related Adverse Events of the Gastrointestinal System." Cancers 15, no. 3 (January 23, 2023): 691. http://dx.doi.org/10.3390/cancers15030691.
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Immune checkpoint inhibitors (ICI) are a form of immunotherapy that have revolutionized the treatment of a number of cancers. Specifically, they are antibodies targeted against established and emerging immune checkpoints, such as cytotoxic T-cell antigen 4 (CTLA4), programmed cell death ligand 1 (PD-L1) and programmed cell death 1 protein (PD-1) on CD8-positive T cells, which promote the destruction of tumor cells. While the immune checkpoint inhibitors are very effective in the treatment of a number of cancers, their use is limited by serious and in some cases life-threatening immune-related adverse events. While these involve many organs, one of the most prevalent serious adverse events is immune checkpoint inhibitor colitis, occurring in a significant proportion of patients treated with this therapy. In this review, we aim to broadly describe the immune-related adverse events known to occur within the gastrointestinal system and the potential role played by the intestinal microbiome.
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Arriaga, Yull Edwin, Karlis Draulis, Rezzan Hekmat, Suwei Wang, Winnie Felix, Irene Dankwa-Mullan, Kyu Rhee, and Gretchen Jackson. "Systematic review of gastrointestinal cancer studies of concordance with expert opinion for a clinical decision support system (CDSS)." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 250. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.250.
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250 Background: Watson for Oncology (WfO), a cognitive CDSS, provides therapeutic options to cancer-treating physicians. We reviewed the concordance of WfO therapeutic options in gastrointestinal cancers with experts’ treatment decisions. Methods: Systematic review to identify WfO concordance studies in gastrointestinal cancers, published from June 2015 to June 2019. Concordance was defined as agreement between WfO “Recommended” and “For Consideration” treatment options and decisions made by experts. Mean concordance rates were calculated as an average, weighted by the number of patients in each study. Results: 2,407 patients were identified (Table). Overall treatment decision concordance was 67.2% (SD 25.7%). Concordance for rectal, colon, hepatocellular, and gastric cancers were 90.5% (SD 9.4%), 80.9% (SD 24.3%), 58.5%, and 47.5% (SD 33.9%), respectively. Concordance with WfO were significantly higher for rectal versus colon cancer ( p = .001), rectal versus gastric cancer ( p < .0001) and for colon versus gastric cancer ( p <.0001). Conclusions: Concordance between WfO and treatment decisions by experts for rectal and colon cancers were high. Concordance for HCC and gastric cancer were the lowest. A higher discordance in gastric cancer is likely related to disease-specific and management differences compared to United States practice. Variable concordance between expert clinical decisions and CDSS suggestions and can be minimized by localization efforts. [Table: see text]
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Wan, Chunhua, Xiaoqin Yan, Baoying Hu, and Xinhua Zhang. "Emerging Roles of the Nervous System in Gastrointestinal Cancer Development." Cancers 14, no. 15 (July 30, 2022): 3722. http://dx.doi.org/10.3390/cancers14153722.
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Our understanding of the fascinating connection between nervous system and gastrointestinal (GI) tumorigenesis has expanded greatly in recent years. Recent studies revealed that neurogenesis plays an active part in GI tumor initiation and progression. Tumor-driven neurogenesis, as well as neurite outgrowth of the pre-existing peripheral nervous system (PNS), may fuel GI tumor progression via facilitating cancer cell proliferation, chemoresistance, invasion and immune escape. Neurotransmitters and neuropeptides drive the activation of various oncogenic pathways downstream of neural receptors within cancer cells, underscoring the importance of neural signaling pathways in GI tumor malignancy. In addition, neural infiltration also plays an integral role in tumor microenvironments, and contributes to an environment in favor of tumor angiogenesis, immune evasion and invasion. Blockade of tumor innervation via denervation or pharmacological agents may serve as a promising therapeutic strategy against GI tumors. In this review, we summarize recent findings linking the nervous system to GI tumor progression, set the spotlight on the molecular mechanisms by which neural signaling fuels cancer aggressiveness, and highlight the importance of targeting neural mechanisms in GI tumor therapy.
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Riddell, Robert H. "East Meets West: What Is Early Cancer?" Canadian Journal of Gastroenterology 13, no. 6 (1999): 495–97. http://dx.doi.org/10.1155/1999/384035.
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It has become increasingly apparent that the Japanese and Western systems of classifying dysplasia and carcinoma in the gastrointestinal tract are not the same. The implication of these differences is that in an article in a Western journal on gastrointestinal ‘cancer’ originating from Japan, it is often impossible to repeat the study to confirm or refute it because of these differences in definitions. ‘Carcinoma’ is diagnosed in Japan by virtue of its structural and cytological features but by invasion in the Western system. Adenoma does not mean a dysplastic lump in the Japanese system (although it can), but in most cases is similar to low grade dysplasia irrespective of the macroscopic and/or endoscopic appearances (hence flat and depressed adenomas in the Japanese system); however, most examples of high grade dysplasia in the Western system, as well as some low grade dysplasia, are ‘cancer’ in the Japanese system. Conversely, both have conceptual areas that are useful in the other’s system.
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Ogihara, Tatsuo, Haruo Watanabe, Akihiro Namihisa, Osamu Kobayashi, Hiroto Miwa, and Nobuhiro Sato. "Clinical Experience Using a Real Time Autofluorescence Endoscopy System in the Gastrointestinal Tract." Diagnostic and Therapeutic Endoscopy 5, no. 2 (January 1, 1999): 119–24. http://dx.doi.org/10.1155/dte.5.119.
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Autofluorescence spectra of neoplastic tissues have been reported to be significantly different from those of normal tissues when excited by blue or violet light. From this concept, a light-induced autofluorescence endoscopic imaging system for gastrointestinal mucosa (LIFE-GI; Xillix, Canada and Olympus, Japan) has been newly developed and the clinical evaluation of the prototype system has been conducted in hospitals in Canada, Netherlands and Japan.We examined the clinical usefulness of the prototype LIFE-GI system for the detection of gastrointestinal cancer and high and low grade dysplasia. The LIFE-GI system was also applied to the early detection of remnant lesions after endoscopic treatment of early gastric cancer and to the detection of laterally spreading superficial colonic tumors.This system has potential application for the diagnosis of dysplastic lesions and early cancers in the gastrointestinal tract as an adjunct to ordinary white light endoscopy. This system, which needs no administration of a photosensitive agent, may be suitable as a screening method for the early detection of neoplastic tissues.
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Cil, T., A. Y. Tuzun, A. Altintas, S. Batum, A. Isikdogan, and M. Yurt. "Reduced folat carrier gene status in colorectal, gastric, and pancreatic cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e13540-e13540. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e13540.
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e13540 Background: Folates play a key role in one-carbon metabolism essential for the biosynthesis of purines, thymidylate and hence DNA replication. Folates and antifolates which cannot traverse membranes must use specific transport systems for their cellular uptake. Antifolates such as raltitrexed and pemetrexed which will be used for gastrointestinal system cancer patients treatment are divalent anions which predominantly use the reduced folate carrier (RFC) for their cellular uptake. The aim of this prospective study; was documenting RFC gene status in gastric, colorectal and pancreatic cancers in southeast region of Turkey. Methods: We were evaluated homozygote, heterozygote mutations of RFC (SLC19A1) and wild type of RFC in new diagnosis gastric, colorectal and pancreas cancer patients who presented at the medical oncology and gastroenterology divisions of the Dicle University Hospital in Turkey between the dates August 2007 and October 2008 in southeast region of Turkey. Results: We were evaluated gene status of RFC in 62 (50%) colorectal, 45 (36.3%) gastric and 17 (13.7%) pancreatic cancer patients. In colorectal cancer patients group; 28 (45.9%), 19 (31.1%), 14 (23%), in gastric cancer 29 (64.4%), 7 (15.6%), 9 (20%), in pancreatic cancer 11 (64.7%), 2 (11.8%), 4 (23.5%) heterozygote, homozygote and wild type gene status, respectively. These results have no statistically significant (p=0.209) in three different gastrointestinal cancer types. Conclusions: New generation antifolat chemotherapeutic drugs such as pemetrexed which is multitargeted antifolat and enters the cells via the RFC system has demonstrated activity in gastrointestinal cancers. We think that antifolat drugs will be used in colorectal, gastric and pancreatic cancer patients in standard treatment protocols and RFC gene status will be an important of antifolat drugs activity in these tumors. No significant financial relationships to disclose.
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Zhang, Xiaoting, Hao Su, Hongyan Chen, Qing Li, Xiaodong Liu, Lin Zhang, William Ka Kei Wu, Matthew Tak Vai Chan, and Huarong Chen. "RNA Modifications in Gastrointestinal Cancer: Current Status and Future Perspectives." Biomedicines 10, no. 8 (August 8, 2022): 1918. http://dx.doi.org/10.3390/biomedicines10081918.
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Gastrointestinal (GI) cancer, referring to cancers of the digestive system such as colorectal cancer (CRC), gastric cancer (GC), and liver cancer, is a major cause of cancer-related deaths in the world. A series of genetic, epigenetic, and epitranscriptomic changes occur during the development of GI cancer. The identification of these molecular events provides potential diagnostic, prognostic, and therapeutic targets for cancer patients. RNA modification is required in the posttranscriptional regulation of RNA metabolism, including splicing, intracellular transport, degradation, and translation. RNA modifications such as N6-methyladenosine (m6A) and N1-methyladenosine (m1A) are dynamically regulated by three different types of regulators named methyltransferases (writers), RNA binding proteins (readers), and demethylases (erasers). Recent studies have pointed out that abnormal RNA modification contributes to GI tumorigenesis and progression. In this review, we summarize the latest findings on the functional significance of RNA modification in GI cancer and discuss the therapeutic potential of epitranscriptomic inhibitors for cancer treatment.
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Schonkeren, Simone L., Meike S. Thijssen, Nathalie Vaes, Werend Boesmans, and Veerle Melotte. "The Emerging Role of Nerves and Glia in Colorectal Cancer." Cancers 13, no. 1 (January 5, 2021): 152. http://dx.doi.org/10.3390/cancers13010152.
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The role of the nervous system as a contributor in the tumor microenvironment has been recognized in different cancer types, including colorectal cancer (CRC). The gastrointestinal tract is a highly innervated organ system, which is not only innervated by the autonomic nervous system, but also contains an extensive nervous system of its own; the enteric nervous system (ENS). The ENS is important for gut function and homeostasis by regulating processes such as fluid absorption, blood flow, and gut motility. Dysfunction of the ENS has been linked with multiple gastrointestinal diseases, such as Hirschsprung disease and inflammatory bowel disease, and even with neurodegenerative disorders. How the extrinsic and intrinsic innervation of the gut contributes to CRC is not fully understood, although a mutual relationship between cancer cells and nerves has been described. Nerves enhance cancer progression through the secretion of neurotransmitters and neuropeptides, and cancer cells are capable of stimulating nerve growth. This review summarizes and discusses the nervous system innervation of the gastrointestinal tract and how it can influence carcinogenesis, and vice versa. Lastly, the therapeutic potential of these novel insights is discussed.
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Popescu, George Denis Alexandru, Cristian Scheau, Ioana Anca Badarau, Mihai-Daniel Dumitrache, Ana Caruntu, Andreea-Elena Scheau, Daniel Octavian Costache, et al. "The Effects of Capsaicin on Gastrointestinal Cancers." Molecules 26, no. 1 (December 28, 2020): 94. http://dx.doi.org/10.3390/molecules26010094.
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Gastrointestinal (GI) cancers are a group of diseases with very high positions in the ranking of cancer incidence and mortality. While they show common features regarding the molecular mechanisms involved in cancer development, organ-specific pathophysiological processes may trigger distinct signaling pathways and intricate interactions with inflammatory cells from the tumoral milieu and mediators involved in tumorigenesis. The treatment of GI cancers is a topic of increasing interest due to the severity of these diseases, their impact on the patients’ survivability and quality of life, and the burden they set on the healthcare system. As the efficiency of existing drugs is hindered by chemoresistance and adverse reactions when administered in high doses, new therapies are sought, and emerging drugs, formulations, and substance synergies are the focus of a growing number of studies. A class of chemicals with great potential through anti-inflammatory, anti-oxidant, and anti-tumoral effects is phytochemicals, and capsaicin in particular is the subject of intensive research looking to validate its position in complementing cancer treatment. Our paper thoroughly reviews the available scientific evidence concerning the effects of capsaicin on major GI cancers and its interactions with the molecular pathways involved in the course of these diseases.
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Brown, Taurean, DeLawrence Sykes, and Antiño R. Allen. "Implications of Breast Cancer Chemotherapy-Induced Inflammation on the Gut, Liver, and Central Nervous System." Biomedicines 9, no. 2 (February 13, 2021): 189. http://dx.doi.org/10.3390/biomedicines9020189.
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Breast Cancer is still one of the most common cancers today; however, with advancements in diagnostic and treatment methods, the mortality and survivorship of patients continues to decrease and increase, respectively. Commonly used treatments today consist of drug combinations, such as doxorubicin and cyclophosphamide; docetaxel, doxorubicin, and cyclophosphamide; or doxorubicin, cyclophosphamide, and paclitaxel. Although these combinations are effective at destroying cancer cells, there is still much to be understood about the effects that chemotherapy can have on normal organ systems such as the nervous system, gastrointestinal tract, and the liver. Patients can experience symptoms of cognitive impairments or “chemobrain”, such as difficulty in concentrating, memory recollection, and processing speed. They may also experience gastrointestinal (GI) distress symptoms such as diarrhea and vomiting, as well as hepatotoxicity and long term liver damage. Chemotherapy treatment has also been shown to induce peripheral neuropathy resulting in numbing, pain, and tingling sensations in the extremities of patients. Interestingly, researchers have discovered that this array of symptoms that cancer patients experience are interconnected and mediated by the inflammatory response.
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Badipatla, Kanthi Rekha, Niharika Yadavalli, Trupti Vakde, Masooma Niazi, and Harish K. Patel. "Lung cancer metastasis to the gastrointestinal system: An enigmatic occurrence." World Journal of Gastrointestinal Oncology 9, no. 3 (2017): 129. http://dx.doi.org/10.4251/wjgo.v9.i3.129.
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Klubo-Gwiezdzinska, Joanna, David Morowitz, Douglas Van Nostrand, Kenneth D. Burman, Vasyl Vasko, Mark Soberman, and Leonard Wartofsky. "Metastases of Well-Differentiated Thyroid Cancer to the Gastrointestinal System." Thyroid 20, no. 4 (April 2010): 381–87. http://dx.doi.org/10.1089/thy.2009.0280.
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Dulal, Soniya, Bishnu D. Paudel, Aarati Shah, Bibek Acharya, Sandhya Chapagain Acharya, Rameej Revanta Thapa, and Lori Wood. "Delay in diagnosis and treatment of gastrointestinal cancer in Nepal." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e18269-e18269. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e18269.
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e18269 Background: Gastrointestinal (GI) cancers represent a major health challenge worldwide including Nepal where patients (pts) often present with advanced disease. The purpose of this study was to determine the time delay in diagnosis and treatment by evaluating time from first symptoms to diagnosis and treatment and to identify contributing factors from both pts and the health system in Nepal. Methods: An IRB approved cross sectional study was performed in pts with GI cancers. 50 newly diagnosed pts were enrolled and interviewed with a standardized questionnaire during the last 6 months of 2018. Diagnosis delay was defined as time from first symptoms to histopathological diagnosis. Treatment delay was defined as time from diagnosis to surgery and/or treatment by medical/ radiation oncologist. Results: The median age at diagnosis was 52.5 years. 52% had gastroesophageal cancer and 48% had colorectal cancer. 84% presented with Stage III/ IV disease. The median diagnosis delay was 217 days and the median treatment delay was 37 days. The median patient delay (time from first symptoms to first medical consultation) was 150 days. 64% were illiterate, 94% had a history of self medication prior to first medical consultation, 68% were from rural areas with limited healthcare facilities and 72% were unaware of causes of GI cancers. Reasons for diagnostic delay appear to be self diagnosis, self medication and lack of a prompt referral system. Reasons for treatment delay included financial constraint, prolonged wait times for procedures and treatment due to limited skilled manpower. Conclusions: Our data shows there is a significant delay in diagnosis and treatment especially in the time from first symptoms to first medical consultation. We found many preventable reasons for this that, if addressed appropriately, could have a significant impact on reducing the morbidity and mortality of GI cancers. There is an urgent need for intensive and comprehensive cancer education in Nepal and other developing countries.
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Caini, Saverio, Marco Del Riccio, Virginia Vettori, Sara Raimondi, Melania Assedi, Silvano Vignati, Guglielmo Bonaccorsi, et al. "The Prognostic Impact of Quitting Smoking at or around Diagnosis on the Survival of Patients with Gastrointestinal Cancers: A Systematic Literature Review." Cancers 14, no. 16 (August 9, 2022): 3857. http://dx.doi.org/10.3390/cancers14163857.
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Cigarette smoking is a strong risk factor for the occurrence of gastrointestinal cancers, and a substantial proportion of newly diagnosed patients is made up of active smokers, yet the impact of smoking cessation at or around diagnosis on the clinical course of these cancers (whose prognosis is often unfavourable) has never been summarized to date. We reviewed studies published until 30 April 2022 that investigated whether smoking cessation at or around diagnosis favourably affects the clinical course of gastrointestinal cancers patients. Six studies were included for colorectal cancer patients, which provided limited yet suggestive evidence that quitters may have longer disease-specific survival compared to continued smokers. Only one study each focused on patients with gastric or HBV-positive liver cancer (both reporting a survival advantage for quitters vs. continued smokers), while we found no eligible studies for patients with cancer at other sites within the digestive system. More research is urgently needed to expand the evidence on the topic, given the potentially major clinical implications for these patients. Moreover, health professionals should provide the necessary smoking cessation support to any smoker who is undergoing diagnostic work-up or treatment for gastrointestinal cancer.
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Stojanovska, Vanesa, Samy Sakkal, and Kulmira Nurgali. "Platinum-based chemotherapy: gastrointestinal immunomodulation and enteric nervous system toxicity." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 4 (February 15, 2015): G223—G232. http://dx.doi.org/10.1152/ajpgi.00212.2014.
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The efficacy of chemotherapeutic treatment of colorectal cancer is challenged by severe gastrointestinal side effects, which include nausea, vomiting, constipation, and diarrhea. These symptoms can persist long after the treatment has been ceased. An emerging concept is the ability of platinum-based drugs to stimulate immunity, which is in contrast to conventional chemotherapeutic agents that are immunosuppressive. Here, we review the immunomodulatory aspects of platinum-based anticancer chemotherapeutics and their impact on gastrointestinal innervation. Given the bidirectional communication between the enteric nervous system and gastrointestinal immune system; exploring the consequences of platinum-induced immunogenicity will facilitate better understanding of gut dysfunction caused by chemotherapeutic agents. We propose that the development of future successful chemotherapeutics should rely on targeting the mechanisms underlying long-term gastrointestinal side effects.
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Bawazir, A. A., G. Abdul Hamid, and E. Morales. "Available data on cancer in the south eastern governorate of Yemen." Eastern Mediterranean Health Journal 4, no. 1 (January 15, 1998): 107–13. http://dx.doi.org/10.26719/1998.4.1.107.
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We studied the distribution of cancer by sex, age, region of residence and system and organ affected of 685 patients obtained through the Treatment Abroad Register of the Aden Health Office [1989-1983]. The most common malignancies, excluding specific sites for each sex, were gastrointestinal tract [19.4%], lymphoma [16.4%], head and neck [13.2%], bone and soft tissue [12.2%] and thyroid [11.2%]. The most common malignancies among males were gastrointestinal, lymphoma, head and neck, bone and soft tissue and leukaemia;and among females were breast, female genital system, thyroid, gastrointestinal and lymphoma
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Marônek, Martin, René Link, Giovanni Monteleone, Roman Gardlík, and Carmine Stolfi. "Viruses in Cancers of the Digestive System: Active Contributors or Idle Bystanders?" International Journal of Molecular Sciences 21, no. 21 (October 30, 2020): 8133. http://dx.doi.org/10.3390/ijms21218133.
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The human virome, which is a collection of all the viruses that are present in the human body, is increasingly being recognized as an essential part of the human microbiota. The human gastrointestinal tract and related organs (e.g., liver, pancreas, and gallbladder)—composing the gastrointestinal (or digestive) system—contain a huge number of viral particles which contribute to maintaining tissue homeostasis and keeping our body healthy. However, perturbations of the virome steady-state may, both directly and indirectly, ignite/sustain oncogenic mechanisms contributing to the initiation of a dysplastic process and/or cancer progression. In this review, we summarize and discuss the available evidence on the association and role of viruses in the development of cancers of the digestive system.
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Hiraiwa, K., H. Takeuchi, Y. Kitagawa, H. Hasegawa, Y. Saikawa, T. Ando, T. Irino, T. Yoshikawa, S. Ishii, and M. Kitajima. "Circulating tumor cells detected in patients with gastrointestinal cancers associate with tumor stage and response to chemotherapy." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 4635. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.4635.
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4635 Background: Circulating tumor cells (CTCs) in metastatic breast cancer has been reported to correlate with shorter overall survival. The purpose of this study was to clarify the clinical significance of CTCs in gastrointestinal cancers. Methods: CTCs of 108 patients with stage III or IV gastrointestinal cancers and 38 healthy volunteers were measured by use of the CellSearch system. Correlation between CTC counts and clinicopathologic variables was examined. Results: The number of CTCs in stage IV patients (23.0 ± 109.1) was significantly larger than that in healthy donors (0.1 ± 0.2) and that in stage III patients (0.4 ± 1.8) (p < 0.001). =2 CTCs were more frequently found in stage IV patients (41.6%) than in healthy donors (0%) and in stage III patients (3.2%) (p < 0.001). =2 CTCs in gastric or colorectal cancer had significant correlation with peritoneal dissemination (p = 0.029). =2 CTCs in esophageal cancer had significant correlation with pleural dissemination (p = 0.030). In 10 of 32 CTC positive (=2) patients with stage IV gastrointestinal cancers, CTC was measured before initiation of a new line of chemotherapy and more than 3 weeks after initiation of therapy. The change in CTCs correlated with disease progression and reflected chemotherapeutic effect. Conclusions: This study suggested measurement of CTCs in gastrointestinal cancer patients shows promise as a tool for judging advanced tumor stage, predicting peritoneal or pleural dissemination and monitoring response to chemotherapy. No significant financial relationships to disclose.
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Mitra, Devarati, Helen Alice Shih, Kevin Oh, Priscilla Brastianos, Jennifer Y. Wo, William Curry, Jeffrey W. Clark, et al. "HER2 positivity in brain metastases from gastrointestinal primary malignancies." Journal of Clinical Oncology 36, no. 4_suppl (February 1, 2018): 61. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.61.
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61 Background: HER2 amplification in gastrointestinal (GI) cancers, beyond gastric cancer, is uncommon and as a result infrequently tested. In breast cancer, HER2 amplification has been associated with brain metastases (BM) with associated prognostic value and therapeutic opportunity. The purpose of this project was to determine if HER2 amplification is more frequent in GI cancer patients with brain metastases. Methods: Retrospective review of our institution’s medical record system identified all patients with GI primary malignancies who had resection of BM between 1999-2015 with tissue available. Fluorescence in-situ hybridization for HER2 amplification and immunohistochemistry for HER2 expression was performed on each sample and quantified by a board-certified pathologist. Results: Twenty-five GI cancer patients with BM were identified: 40% esophageal adenocarcinoma (AC), 12% esophageal squamous cell carcinoma (SCC), 44% colorectal AC and 4% pancreatic AC. At diagnosis 36% had metastatic disease. A BM was the isolated first site of metastasis in: 11/13 esophageal cancers, 1/11 colorectal cancers and 1/1 pancreatic cancer. Two esophageal cancer patients and one colon cancer patient had BM at diagnosis but otherwise median time to BM was 30 months (range 4-127 months). There was a median of 1 BM with a maximum of 4 lesions per patient. The most common intracranial site was the cerebellum (40%) with a median metastasis size of 27 mm (range 5-55 mm). Overall, HER2 was amplified in 24% (n=6) with 4 of these patients having paired primary tumor tissue available. None of the primary tumor tissue was HER2 amplified. No colorectal cancer patients had HER2 amplification but 67% of esophageal SCC, 30% of esophageal AC and the only pancreatic AC patient had Her2 amplified and overexpressed brain metastases. Conclusions: HER2 amplification was enriched in esophageal SCC and AC patients who developed resectable BM despite none of these patients having HER2 amplification in their primary tissue. HER2 amplification testing in esophageal cancer patients with BM (regardless of histology) may lead to additional therapeutic options, even if primary tissue was negative for HER2 amplification.
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Kit, Oleg I., Liubov Yu Vladimirova, Tatiana A. Zykova, Oksana V. Katelnitskaya, Andrey A. Maslov, Elena A. Shevyakova, Natalia A. Abramova, et al. "Polymorphism of genes of hemostasis system and methionin exchange in patients with gastrointestinal tumors." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e16011-e16011. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e16011.
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e16011 Background: The purpose of the study was to analyze the rates of polymorphic allelic variants of genes of the hemostasis system and methionin exchange in patients with gastrointestinal cancers (GICs). Methods: The study included 69 patients with histologically verified GICs (main group): gastric cancer (GC) – 17, colon cancer (CC) – 42, other tumors – 10 (pancreatic cancer – 6, liver cancer – 3, gallbladder cancer – 1) and 50 patients without cancer (control group). 12 polymorphic loci were determined in genomic DNA samples by Real-time PCR: F2 (G20210А, rs1799963), F5 (G1691A, rs6025), F7 (G10976A, rs6046), F13 (G226A, rs5985), FGB G(-455)A (rs1800790), ITGA2-α2 (C807T, rs1126643), ITGB3-b (Т1565С, rs5918), PAI-1 4G(-675)5G, rs1799889), MTHFR (С677Т, rs1801133 and A1298C, rs1801131), MTR (А2756G, rs1805087), MTRR (A66G, rs1801394). Results: The ratio of genotype frequencies maintained in the Hardy-Weinberg equilibrium in all gene loci except FGB G(-455)A in GC patients (p = 0.02). The rate of an alternative allele in the F2 gene among patients with GICs was 1.4%, in the control group – 1.0%; F5 – 1.0% and 4.0%; F7 – 13.0% and 11.0%; F13 – 31.9% and 32.0%; FGB – 29.7% and 22.0%; ITGA2 – 37.7% and 38.0%; ITGB3 – 17.4% and 21.0%; PAI-1 – 55.1% and 56.0%, MTHFR (Т) – 26.6% and 31.3%; MTHFR (С) – 33.0% and 27.5%; MTR – 29.8% and 26.3%; MTRR – 51.1% and 57.5%, respectively (p > 0.05). AA homozygotes at the FGB G(-455)A locus were more frequent in the main group, compared to controls: 4.3% vs 4.0%; p = 0.02. No differences in the frequency of alternative alleles of the studied genes were found between patients with GC and CC. GG genotype at the FGB G(-455)A locus was found in GC patients in 29.4%, in controls – in 60.0% (OR = 0.28, 95% CI 0.08-0.91); GA genotype – in 70.6% and 36.0% (OR = 4.27, 95% CI 1.29-14.06), AA genotype – in 0% and 4.0% (p = 0.04, χ2 = 6.34), respectively. Conclusions: The univariate analysis demonstrated that carriage of the GA genotype at the FGB G(-455)A (rs1800790) locus could be found more often in patients with GC.
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Lee, Yunna, Jeongbin Jo, Hae Young Chung, Charalabos Pothoulakis, and Eunok Im. "Endocannabinoids in the gastrointestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 4 (October 1, 2016): G655—G666. http://dx.doi.org/10.1152/ajpgi.00294.2015.
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The endocannabinoid system mainly consists of endogenously produced cannabinoids (endocannabinoids) and two G protein-coupled receptors (GPCRs), cannabinoid receptors 1 and 2 (CB1 and CB2). This system also includes enzymes responsible for the synthesis and degradation of endocannabinoids and molecules required for the uptake and transport of endocannabinoids. In addition, endocannabinoid-related lipid mediators and other putative endocannabinoid receptors, such as transient receptor potential channels and other GPCRs, have been identified. Accumulating evidence indicates that the endocannabinoid system is a key modulator of gastrointestinal physiology, influencing satiety, emesis, immune function, mucosal integrity, motility, secretion, and visceral sensation. In light of therapeutic benefits of herbal and synthetic cannabinoids, the vast potential of the endocannabinoid system for the treatment of gastrointestinal diseases has been demonstrated. This review focuses on the role of the endocannabinoid system in gut homeostasis and in the pathogenesis of intestinal disorders associated with intestinal motility, inflammation, and cancer. Finally, links between gut microorganisms and the endocannabinoid system are briefly discussed.
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Haakenstad, Ellana K., Lauren K. Brais, Arrien Bertram, Andrea Kruse, Alissa Gentile, Rachel A. Freedman, Neal Ian Lindeman, et al. "Defining equitable genomic testing uptake in gastrointestinal oncology: Ensuring capture of demographic data." Journal of Clinical Oncology 41, no. 4_suppl (February 1, 2023): 794. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.794.
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794 Background: Tumor genomic testing (GT) has increased diagnostic accuracy and treatment options for patients (pts) with cancer. Dana-Farber Cancer Institute (DFCI) has made GT accessible as an institute-supported research effort for >10 yrs. We estimate 50% standard therapies and 15-35% clinical trials in Gastrointestinal Cancer Clinic (GCC) require GT to determine eligibility. Pts in GCC with certain cancers are eligible for GT as a clinical test – these include metastatic/locally advanced colorectal, gastric, pancreatic, or biliary cancers. Clinical testing requires CLIA lab certification and insurance reimbursement; research does not. Herein we ID gaps in our GT database. Methods: We reviewed data on GT uptake in GCC between 4/2015 - 6/2022. 20,096 pts were captured by the GT tracking system. Data included: testing ordered and completed (proportion, type, time to receiving tissue for testing [TR], time to testing completion [TC]). Demographic data is not captured in the tracking system; matching unique patient identifiers with electronic health record is pending. Results: Most pts received GT (57.6%); 12% were not eligible; 30.4% declined consent. Most testing was completed (67.6%), but 21.3% of tests failed (45.5% of these from insufficient tissue). Research testing (71%) comprised most tests, but clinical tests were completed faster (median 34 days research vs 20 days clinical). Ampullary (91%), anal (90%), colon (90%) had highest completion rates; pancreatic (59%), hepatocellular carcinoma (56%) had lowest (from insufficient viable tumor in submitted specimens). Conclusions: GCC has a robust recruitment program that has yielded high GT uptake. Given the frequency that GT is used for treatment and trials, building a demographically representative dataset is crucial, especially for pts with largest burden of morbidity and mortality from cancer. We ID'd data gaps in the GT tracking system, which lacks demographics and reason for not testing. Demographic data is available in the electronic health record but does not speak with the GT tracking system so this analysis is not routinely done. Ability to visualize this data is important to ensure equitable GT uptake. Future efforts will focus on improving rates of consent in genomics databases and cancer clinical trials. Genomic testing at Dana-Farber Cancer Institute Gastrointestinal Cancer Center, 4/2015 – 6/2022.[Table: see text]
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Holland, Amy Marie, Ana Carina Bon-Frauches, Daniel Keszthelyi, Veerle Melotte, and Werend Boesmans. "The enteric nervous system in gastrointestinal disease etiology." Cellular and Molecular Life Sciences 78, no. 10 (March 26, 2021): 4713–33. http://dx.doi.org/10.1007/s00018-021-03812-y.
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AbstractA highly conserved but convoluted network of neurons and glial cells, the enteric nervous system (ENS), is positioned along the wall of the gut to coordinate digestive processes and gastrointestinal homeostasis. Because ENS components are in charge of the autonomous regulation of gut function, it is inevitable that their dysfunction is central to the pathophysiology and symptom generation of gastrointestinal disease. While for neurodevelopmental disorders such as Hirschsprung, ENS pathogenesis appears to be clear-cut, the role for impaired ENS activity in the etiology of other gastrointestinal disorders is less established and is often deemed secondary to other insults like intestinal inflammation. However, mounting experimental evidence in recent years indicates that gastrointestinal homeostasis hinges on multifaceted connections between the ENS, and other cellular networks such as the intestinal epithelium, the immune system, and the intestinal microbiome. Derangement of these interactions could underlie gastrointestinal disease onset and elicit variable degrees of abnormal gut function, pinpointing, perhaps unexpectedly, the ENS as a diligent participant in idiopathic but also in inflammatory and cancerous diseases of the gut. In this review, we discuss the latest evidence on the role of the ENS in the pathogenesis of enteric neuropathies, disorders of gut–brain interaction, inflammatory bowel diseases, and colorectal cancer.
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Sui, Guo-Yan, Feng Wang, Jin Lee, and Yoon Seok Roh. "Mitochondrial Control in Inflammatory Gastrointestinal Diseases." International Journal of Molecular Sciences 23, no. 23 (November 28, 2022): 14890. http://dx.doi.org/10.3390/ijms232314890.
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Mitochondria play a central role in the pathophysiology of inflammatory bowel disease (IBD) and colorectal cancer (CRC). The maintenance of mitochondrial function is necessary for a stable immune system. Mitochondrial dysfunction in the gastrointestinal system leads to the excessive activation of multiple inflammatory signaling pathways, leading to IBD and increased severity of CRC. In this review, we focus on the mitochondria and inflammatory signaling pathways and its related gastrointestinal diseases.
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Kladi-Skandali, Athina, Kleita Michaelidou, Andreas Scorilas, and Konstantinos Mavridis. "Long Noncoding RNAs in Digestive System Malignancies: A Novel Class of Cancer Biomarkers and Therapeutic Targets?" Gastroenterology Research and Practice 2015 (2015): 1–18. http://dx.doi.org/10.1155/2015/319861.
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High throughput methodologies have revealed the existence of an unexpectedly large number of long noncoding RNAs (lncRNAs). The unconventional role of lncRNAs in gene expression regulation and their broad implication in oncogenic and tumor suppressive pathways have introduced lncRNAs as novel biological tumor markers. The most prominent example of lncRNAs application in routine clinical practice is PCA3, a FDA-approved biomarker for prostate cancer. Regarding digestive system malignancies, the oncogenic HOTAIR is one of the most widely studied lncRNAs in the preclinical level and has already been identified as a potent prognostic marker for major malignancies of the gastrointestinal tract. Here, we provide an overview of recent findings regarding the emerging role of lncRNAs not only as key regulators of cancer initiation and progression in colon, stomach, pancreatic, liver, and esophageal cancers, but also as reliable tumor markers and therapeutic tools. lncRNAs can be easily, rapidly, and cost-effectively determined in tissues, serum, and gastric juice, making them highly versatile analytes. Taking also into consideration the largely unmet clinical need for early diagnosis and more accurate prognostic/predictive markers for gastrointestinal cancer patients, we comment upon the perspectives of lncRNAs as efficient molecular tools that could aid in the clinical management.
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Deniz, Zeynep, Suleyman Uraz, Ryan Holem, Resat Ozaras, and Veysel Tahan. "Human Papillomavirus Infection and Oropharyngeal and Gastrointestinal Cancers: A Causal Relationship?" Diseases 10, no. 4 (October 20, 2022): 94. http://dx.doi.org/10.3390/diseases10040094.
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The human papillomavirus (HPV) is one of the most common sexually transmitted infections worldwide. The risk of being infected at least once in a lifetime among both men and women is estimated to be 50%. Although the majority of HPV infections are asymptomatic and improve within 2 years, approximately 10% of individuals develop a persistent infection and have an increased risk of developing carcinomas. The association of HPV and genital cancer is well established. However, there is evidence that HPV may also be associated with other cancers, including those of the gastrointestinal system. The aim of this review is to organize the current evidence of associations between HPV infections and oropharyngeal and gastrointestinal cancers, including the following: oropharyngeal, esophageal, gastric, colorectal, and anal cancers. A comprehensive review of the most up-to-date medical literature concluded that an HPV infection might have a role in the oncogenesis of gastrointestinal tract cancers. HPV may have a causal relationship with oropharyngeal and esophageal squamous cell cancers. However, the association between HPV and gastric and colorectal cancers is weaker. The development of cancer in the oropharyngeal and gastrointestinal tract is usually multifactorial, with HPV having a role in at least a subset of these cancers. HPV infections pose a big challenge due to their burden of infection and their oncogenic potential.
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Bernard, Joseph, Rebecca Rose Henderson, Lenz Sacha Christyl Pierre, Lynn Gabrielle Alexis, Doukens Patrick Gilbert, and Vincent DeGennaro. "A five-year epidemiological profile of patients with cancer managed by a Haitian cancer program." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 10564. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.10564.
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10564 Background: Cancer epidemiology in Haiti is poorly understood. The national cancer registry is not functional, and data reported by GLOBOCAN are estimations that do not totally reflect the reality of cancers in Haiti. The aim of this study was to present the five-year epidemiology of malignancies managed by one of the main cancer programs in Haiti. Methods: A retrospective study was conducted on patients aged 15 years old and above with pathological and/or clinical diagnosis of cancer managed from January 2016 to December 2020 at Innovating Health International (IHI), a cancer center located in Port-au-Prince, Haiti. The chart review collected variables such as age, gender, date of admission and cancer type in order to present this epidemiological profile of cancers. Results: Overall, 3060 patients with cancer were managed during the study period. 84.4% of the patients were female and 15.6% male. The mean and median ages of the study population were respectively 52.5 [range: 15 –92] and 53.0 years. Adolescents and young adults (15-39 years old) represented 18.9 % of this cohort and geriatric cases (≥ 65 years old) were 21.0%. Breast cancer was the most common type (n = 1391, 45.5%%), followed by gynecological cancers (n = 746, 24.4%) with cervical cancer representing 77.5 % of these cases (n = 578); gastrointestinal cancers (n = 252, 8.2%) dominated by colorectal (n = 92, 36.5%) and gastric cancer (n = 58, 23.0%); head and neck cancers (n = 129, 4.2%); hematological malignancies (n = 128, 4.2%) with lymphomas representing 60.9% of the cases (n = 78); sarcomas (n = 114, 3.7%), urological cancers (n = 73, 2.4%) with prostate cancer representing 56.1% of the cases; skin cancers including melanoma (n = 60, 1.9%); lung cancer (n = 24, 0.8%); thyroid cancer (n = 13, 0.4%) and central nervous system (CNS) cancers (n = 6, 0.2%). 4.1% of the patients (n = 124) had a cancer of unknown primary (CUP). Breast (53.5%), cervical (28.9%) and gastrointestinal (5.0%) cancers were the most common types among women, while gastrointestinal (25.8%), hematological (16.1%), head and neck (14.7%) and urological (12.6%) cancers were the most diagnosed among men. Conclusions: Cancer mainly affects Haiti’s young, active and female population. Breast and cervical cancers were the most prevalent in this retrospective cohort regardless of the age group. The under-representation of prostate and other urological malignancies, lung cancer, acute leukemias and CNS cancers was likely due to underdiagnosis, misdiagnosis, under-referral or early mortality. An active cancer registry is needed to better evaluate the real cancer burden in Haiti.
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Prasad, Sahdeo, and Amit K. Tyagi. "Ginger and Its Constituents: Role in Prevention and Treatment of Gastrointestinal Cancer." Gastroenterology Research and Practice 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/142979.
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Gastrointestinal (GI) cancer, a cancer of different organs of the digestive system, is one of the most common cancers around the world. The incidence and death rate of some of these cancers are very high. Although a large variety of chemotherapeutic agents have been introduced since the last few decades to combat GI cancer, most of them are very expensive and have side effects. Therefore, the compounds derived from natural sources, which are considered to be safe and cost effective, are needed. Ginger (Zingiber officinale) is one of the most widely used natural products consumed as a spice and medicine for treating nausea, dysentery, heartburn, flatulence, diarrhea, loss of appetite, infections, cough, and bronchitis. Experimental studies showed that ginger and its active components including 6-gingerol and 6-shogaol exert anticancer activities against GI cancer. The anticancer activity of ginger is attributed to its ability to modulate several signaling molecules like NF-κB, STAT3, MAPK, PI3K, ERK1/2, Akt, TNF-α, COX-2, cyclin D1, cdk, MMP-9, survivin, cIAP-1, XIAP, Bcl-2, caspases, and other cell growth regulatory proteins. In this review, the evidences for the chemopreventive and chemotherapeutic potential of ginger extract and its active components usingin vitro, animal models, and patients have been described.
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AL-Ishaq, Raghad Khalid, Lenka Koklesova, Peter Kubatka, and Dietrich Büsselberg. "Immunomodulation by Gut Microbiome on Gastrointestinal Cancers: Focusing on Colorectal Cancer." Cancers 14, no. 9 (April 25, 2022): 2140. http://dx.doi.org/10.3390/cancers14092140.
Full textAbstract:
Gastrointestinal cancer (GI) is a global health disease with a huge burden on a patient’s physical and psychological aspects of life and on health care providers. It is associated with multiple disease related challenges which can alter the patient’s quality of life and well-being. GI cancer development is influenced by multiple factors such as diet, infection, environment, and genetics. Although activating immune pathways and components during cancer is critical for the host’s survival, cancerous cells can target those pathways to escape and survive. As the gut microbiome influences the development and function of the immune system, research is conducted to investigate the gut microbiome–immune interactions, the underlying mechanisms, and how they reduce the risk of GI cancer. This review addresses and summarizes the current knowledge on the major immune cells and gut microbiome interactions. Additionally, it highlights the underlying mechanisms of immune dysregulation caused by gut microbiota on four major cancerous pathways, inflammation, cellular proliferation, apoptosis, and metastasis. Overall, gut-immune interactions might be a key to understanding GI cancer development, but further research is needed for more detailed clarification.
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AL-Ishaq, Raghad Khalid, Lenka Koklesova, Peter Kubatka, and Dietrich Büsselberg. "Immunomodulation by Gut Microbiome on Gastrointestinal Cancers: Focusing on Colorectal Cancer." Cancers 14, no. 9 (April 25, 2022): 2140. http://dx.doi.org/10.3390/cancers14092140.
Full textAbstract:
Gastrointestinal cancer (GI) is a global health disease with a huge burden on a patient’s physical and psychological aspects of life and on health care providers. It is associated with multiple disease related challenges which can alter the patient’s quality of life and well-being. GI cancer development is influenced by multiple factors such as diet, infection, environment, and genetics. Although activating immune pathways and components during cancer is critical for the host’s survival, cancerous cells can target those pathways to escape and survive. As the gut microbiome influences the development and function of the immune system, research is conducted to investigate the gut microbiome–immune interactions, the underlying mechanisms, and how they reduce the risk of GI cancer. This review addresses and summarizes the current knowledge on the major immune cells and gut microbiome interactions. Additionally, it highlights the underlying mechanisms of immune dysregulation caused by gut microbiota on four major cancerous pathways, inflammation, cellular proliferation, apoptosis, and metastasis. Overall, gut-immune interactions might be a key to understanding GI cancer development, but further research is needed for more detailed clarification.