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Journal articles on the topic 'Digestive cancers'
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1
Zhang, Tao, Bofang Wang, Baohong Gu, Fei Su, Lin Xiang, Le Liu, Xuemei Li, Xueyan Wang, Lei Gao, and Hao Chen. "Genetic and Molecular Characterization Revealed the Prognosis Efficiency of Histone Acetylation in Pan-Digestive Cancers." Journal of Oncology 2022 (April 5, 2022): 1–21. http://dx.doi.org/10.1155/2022/3938652.
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The imbalance between acetylation and deacetylation of histone proteins, important for epigenetic modifications, is closely associated with various diseases, including cancer. However, knowledge regarding the modification of histones across the different types of digestive cancers is still lacking. The purpose of this research was to analyze the role of histone acetylation and deacetylation in pan-digestive cancers. We systematically characterized the molecular alterations and clinical relevance of 13 histone acetyltransferase (HAT) and 18 histone deacetylase (HDAC) genes in five types of digestive cancers, including esophageal carcinoma, gastric cancer, hepatocellular carcinoma, pancreatic cancer, and colorectal cancer. Recurrent mutations and copy number variation (CNV) were extensively found in acetylation-associated genes across pan-digestive cancers. HDAC9 and KAT6A showed widespread copy number amplification across five pan-digestive cancers, while ESCO2, EP300, and HDAC10 had prevalent copy number deletions. Accordingly, we found that HAT and HDAC genes correlated with multiple cancer hallmark-related pathways, especially the histone modification-related pathway, PRC2 complex pathway. Furthermore, the expression pattern of HAT and HDAC genes stratified patients with clinical benefit in hepatocellular carcinoma and pancreatic cancer. These results indicated that acetylation acts as a key molecular regulation of pan-digestive tumor progression.
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Yang, Ting-Fang, Xin-Rui Li, and Mo-Wei Kong. "Molecular mechanisms underlying roles of long non-coding RNA small nucleolar RNA host gene 16 in digestive system cancers." World Journal of Gastrointestinal Oncology 16, no. 11 (November 15, 2024): 4300–4308. http://dx.doi.org/10.4251/wjgo.v16.i11.4300.
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This editorial reviews the molecular mechanisms underlying the roles of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16 ) in digestive system cancers based on two recent studies on lncRNAs in digestive system tumors. The first study, by Zhao et al , explored how hBD-1 affects colon cancer, via the lncRNA TCONS_00014506 , by inhibiting mTOR and promoting autophagy. The second one, by Li et al , identified the lncRNA prion protein testis specific (PRNT ) as a factor in oxaliplatin resistance by sponging ZNF184 to regulate HIPK2 and influence colorectal cancer progression and chemoresistance, suggesting PRNT as a potential therapeutic target for colorectal cancer. Both of these two articles discuss the mechanisms by which lncRNAs contribute to the development and progression of digestive system cancers. As a recent research hotspot, SNHG16 is a typical lncRNA that has been extensively studied for its association with digestive system cancers. The prevailing hypothesis is that SNHG16 participates in the development and progression of digestive system tumors by acting as a competing endogenous RNA, interacting with other proteins, regulating various genes, and affecting downstream target molecules. This review systematically examines the recently reported biological functions, related molecular mechanisms, and potential clinical significance of SNHG16 in various digestive system cancers, and explores the relationship between SNHG16 and digestive system cancers. The findings suggest that SNHG16 may serve as a potential biomarker and therapeutic target for human digestive system cancers.
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Stokłosa, Paulina, Anna Borgström, Sven Kappel, and Christine Peinelt. "TRP Channels in Digestive Tract Cancers." International Journal of Molecular Sciences 21, no. 5 (March 9, 2020): 1877. http://dx.doi.org/10.3390/ijms21051877.
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Cancers of the digestive tract are among the most prevalent types of cancer. These types of cancers are often diagnosed at a late stage, which results in a poor prognosis. Currently, many biomedical studies focus on the role of ion channels, in particular transient receptor potential (TRP) channels, in cancer pathophysiology. TRP channels show mostly non-selective permeability to monovalent and divalent cations. TRP channels are often dysregulated in digestive tract cancers, which can result in alterations of cancer hallmark functions, such as enhanced proliferation, migration, invasion and the inability to induce apoptosis. Therefore, TRP channels could serve as potential diagnostic biomarkers. Moreover, TRP channels are mostly expressed on the cell surface and ion channel targeting drugs do not need to enter the cell, making them attractive candidate drug targets. In this review, we summarize the current knowledge about TRP channels in connection to digestive tract cancers (oral cancer, esophageal cancer, liver cancer, pancreatic cancer, gastric cancer and colorectal cancer) and give an outlook on the potential of TRP channels as cancer biomarkers or therapeutic targets.
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Zhang, Nan, Yueying Wang, Gary Tse, Guangping Li, Shouling Wu, and Tong Liu. "Association of Visit-to-Visit Variability in Fasting Plasma Glucose with Digestive Cancer Risk." Oxidative Medicine and Cellular Longevity 2022 (July 13, 2022): 1–12. http://dx.doi.org/10.1155/2022/4530894.
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Background and Aims. The aim of this study is to investigate the association between visit-to-visit variability in fasting plasma glucose (FPG) and the risk of digestive cancers among individuals with and without diabetes. Methods. Using data from Kailuan cohort, a prospective population-based study, individuals who had at least two measurements of FPG between 2006 and 2012 without prior cancer were included in this study. Four indexes of variability were used, including standard deviation (SD), coefficient of variation (CV), variability independent of the mean (VIM), and average successive variability (ARV). Cox regression was used to evaluate the relationship between the quartiles of FPG variability and digestive cancers. Results. A total of 98,161 individuals were studied. Over a mean follow-up of 9.32 ± 0.81 years, 1103 individuals developed incident digestive cancer (1.21 per 1000 person-years). Compared to the individuals in the lowest quartile, those in the highest quartile of FPG variability by SD had 38.7% higher risk of developing overall digestive cancers after adjusting for the significant confounders (hazard ratio, 1.387; 95% confidence interval, 1.160-1.659; P = 0.0003 ). Higher FPG variability was associated with significantly higher risks of colorectal cancer (fully adjusted HR 1.432, 95% CI [1.073-1.912], P = 0.015 ) and pancreatic cancer (fully adjusted HR 2.105, 95% CI [1.024-4.329], P = 0.043 ), but not liver cancer (fully adjusted HR 1.427, 95% CI [0.973-2.092], P = 0.069 ) or esophageal and gastric cancer (fully adjusted HR 1.139, 95% CI [0.776-1.670], P = 0.506 ). Subgroup analyses showed that individuals who were younger (<65 years), male, and those without diabetes experienced a predominantly higher risk of developing digestive cancers. Similar results were observed when using CV, VIM, and ARV. Conclusions. FPG variability was significantly associated with increasing risk of digestive cancers, especially for pancreatic and colorectal cancer. Our study suggested a potential role of FPG variability in risk stratification of digestive cancers. Approaches that reduce FPG variability may lower the risks of incident digestive cancers among the general population. This trial is registered with ChiCTR-TNRC-11001489.
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Ishikawa, Marin, Kohei Nakamura, Ryutaro Kawano, Hideyuki Hayashi, Tatsuru Ikeda, Makoto Saito, Yo Niida, et al. "Clinical and Diagnostic Utility of Genomic Profiling for Digestive Cancers: Real-World Evidence from Japan." Cancers 16, no. 8 (April 15, 2024): 1504. http://dx.doi.org/10.3390/cancers16081504.
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The usefulness of comprehensive genomic profiling (CGP) in the Japanese healthcare insurance system remains underexplored. Therefore, this large-scale study aimed to determine the usefulness of CGP in diagnosing digestive cancers. Patients with various cancer types recruited between March 2020 and October 2022 underwent the FoundationOne® CDx assay at the Keio PleSSision Group (19 hospitals in Japan). A scoring system was developed to identify potentially actionable genomic alterations of biological significance and actionable genomic alterations. The detection rates for potentially actionable genomic alterations, actionable genomic alterations, and alterations equivalent to companion diagnosis (CDx), as well as the signaling pathways associated with these alterations in each digestive cancer, were analyzed. Among the 1587 patients, 547 had digestive cancer. The detection rates of potentially actionable genomic alterations, actionable genomic alterations, and alterations equivalent to CDx were 99.5%, 62.5%, and 11.5%, respectively. APC, KRAS, and CDKN2A alterations were frequently observed in colorectal, pancreatic, and biliary cancers, respectively. Most digestive cancers, except esophageal cancer, were adenocarcinomas. Thus, the classification flowchart for digestive adenocarcinomas proposed in this study may facilitate precise diagnosis. CGP has clinical and diagnostic utility in digestive cancers.
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Reitano, Elisa, Nicola de’Angelis, Paschalis Gavriilidis, Federica Gaiani, Riccardo Memeo, Riccardo Inchingolo, Giorgio Bianchi, Gian Luigi de’Angelis, and Maria Clotilde Carra. "Oral Bacterial Microbiota in Digestive Cancer Patients: A Systematic Review." Microorganisms 9, no. 12 (December 14, 2021): 2585. http://dx.doi.org/10.3390/microorganisms9122585.
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The relation between the gut microbiota and human health is increasingly recognized. Recently, some evidence suggested that dysbiosis of the oral microbiota may be involved in the development of digestive cancers. A systematic review was conducted according to the PRISMA guidelines to investigate the association between the oral microbiota and digestive cancers. Several databases including Medline, Scopus, and Embase were searched by three independent reviewers, without date restriction. Over a total of 1654 records initially identified, 28 studies (2 prospective cohort studies and 26 case-controls) were selected. They investigated oral microbiota composition in patients with esophageal squamous cell carcinoma (n = 5), gastric cancer (n = 5), colorectal cancer (n = 9), liver carcinoma (n = 2), and pancreatic cancer (n = 7). In most of the studies, oral microbiota composition was found to be different between digestive cancer patients and controls. Particularly, oral microbiota dysbiosis and specific bacteria, such as Fusobacterium nucleatum and Porphyromonas gingivalis, appeared to be associated with colorectal cancers. Current evidence suggests that differences exist in oral microbiota composition between patients with and without digestive cancers. Further studies are required to investigate and validate oral–gut microbial transmission patterns and their role in digestive cancer carcinogenesis.
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Turati, Federica, Marta Rossi, Claudio Pelucchi, Fabio Levi, and Carlo La Vecchia. "Fruit and vegetables and cancer risk: a review of southern European studies." British Journal of Nutrition 113, S2 (April 2015): S102—S110. http://dx.doi.org/10.1017/s0007114515000148.
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High intakes of fruit and vegetables may reduce the risk of cancer at several sites. Evidence has been derived mainly from case–control studies. We reviewed the relationship between consumption of vegetables and fruit and the risk of several common cancers in a network of Italian and Swiss case–control studies including over 10 000 cases of fourteen different cancers and about 17 000 controls. Data were suggestive of a protective role of vegetable intake on the risk of several common epithelial cancers. OR for the highest compared with the lowest levels of consumption ranged from 0·2 (larynx, oral cavity and pharynx) to 0·9 (prostate). Inverse associations were found for both raw and cooked vegetables, although for upper digestive tract cancers the former were somewhat stronger. Similar inverse associations were found for cruciferous vegetables. Frequent consumption of allium vegetables was also associated with reduced risk of several cancers. Fruit was a favourable correlate of the risk of several cancers, particularly of the upper digestive tract, with associations generally weaker than those reported for vegetables. A reduced risk of cancers of the digestive tract and larynx was found for high consumption of citrus fruit. Suggestive protections against several forms of cancer, mainly digestive tract cancers, were found for high consumption of apples and tomatoes. High intakes of fibres, flavonoids and proanthocyanidins were inversely related to various forms of cancer. In conclusion, data from our series of case–control studies suggested a favourable role of high intakes of fruit and vegetables in the risk of many common cancers, particularly of the digestive tract. This adds evidence to the indication that aspects of the Mediterranean diet may have a favourable impact not only on CVD, but also on several common (epithelial) cancers, particularly of the digestive tract.
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Capparelli, Rosanna, Paola Cuomo, Antonio Gentile, and Domenico Iannelli. "Microbiota–Liver Diseases Interactions." International Journal of Molecular Sciences 24, no. 4 (February 15, 2023): 3883. http://dx.doi.org/10.3390/ijms24043883.
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Gut microbiota regulates essential processes of host metabolism and physiology: synthesis of vitamins, digestion of foods non-digestible by the host (such as fibers), and—most important—protects the digestive tract from pathogens. In this study, we focus on the CRISPR/Cas9 technology, which is extensively used to correct multiple diseases, including liver diseases. Then, we discuss the non-alcoholic fatty liver disease (NAFLD), affecting more than 25% of the global population; colorectal cancer (CRC) is second in mortality. We give space to rarely discussed topics, such as pathobionts and multiple mutations. Pathobionts help to understand the origin and complexity of the microbiota. Since several types of cancers have as target the gut, it is vital extending the research of multiple mutations to the type of cancers affecting the gut–liver axis.
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Xiong, Zuming, Yongjun Yang, Wenxin Li, Yirong Lin, Wei Huang, and Sen Zhang. "Exploring Key Biomarkers and Common Pathogenesis of Seven Digestive System Cancers and Their Correlation with COVID-19." Current Issues in Molecular Biology 45, no. 7 (June 30, 2023): 5515–33. http://dx.doi.org/10.3390/cimb45070349.
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Digestive system cancer and COVID-19 significantly affect the digestive system, but the mechanism of interaction between COVID-19 and the digestive system cancers has not been fully elucidated. We downloaded the gene expression of COVID-19 and seven digestive system cancers (oral, esophageal, gastric, colorectal, hepatocellular, bile duct, pancreatic) from GEO and identified hub differentially expressed genes. Multiple verifications, diagnostic efficacy, prognostic analysis, functional enrichment and related transcription factors of hub genes were explored. We identified 23 common DEGs for subsequent analysis. CytoHubba identified nine hub genes (CCNA2, CCNB1, CDKN3, ECT2, KIF14, KIF20A, KIF4A, NEK2, TTK). TCGA and GEO data validated the expression and excellent diagnostic and prognostic ability of hub genes. Functional analysis revealed that the processes of cell division and the cell cycle were essential in COVID-19 and digestive system cancers. Furthermore, six related transcription factors (E2F1, E2F3, E2F4, MYC, TP53, YBX1) were involved in hub gene regulation. Via in vitro experiments, CCNA2, CCNB1, and MYC expression was verified in 25 colorectal cancer tissue pairs. Our study revealed the key biomarks and common pathogenesis of digestive system cancers and COVID-19. These may provide new ideas for further mechanistic research.
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Adianto Nugroho, Fransicus Arifin, Perwira Widianto, Agung Ari Wibowo, A. Yuda Handaya, Iwan Kristian, M Iqbal Rivai, et al. "Digestive Surgery Services in COVID-19 Pandemic Period: Indonesian Society of Digestive Surgeons Position Statement." Journal Of The Indonesian Medical Association 70, no. 6 (July 16, 2020): 132–41. http://dx.doi.org/10.47830/jinma-vol.70.6-2020-239.
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Digestive surgery service including surgical management of gastrointestinal disease and digestive cancers are experiencing the impact of COVID-19 pandemic. Therefore it is necessary to formulate recommendation for digestives surgery service, as guidelines to engage in case-by-case assessment of particular patients with digestive diseases. We are aware that the knowledge and science of COVID-19 are still evolving, with new progression every day. This recommendation reflect actual condition and are subject for future adjustment in the future.
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Auwercx, Julie, Pierre Rybarczyk, Philippe Kischel, Isabelle Dhennin-Duthille, Denis Chatelain, Henri Sevestre, Isabelle Van Seuningen, Halima Ouadid-Ahidouch, Nicolas Jonckheere, and Mathieu Gautier. "Mg2+ Transporters in Digestive Cancers." Nutrients 13, no. 1 (January 13, 2021): 210. http://dx.doi.org/10.3390/nu13010210.
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Despite magnesium (Mg2+) representing the second most abundant cation in the cell, its role in cellular physiology and pathology is far from being elucidated. Mg2+ homeostasis is regulated by Mg2+ transporters including Mitochondrial RNA Splicing Protein 2 (MRS2), Transient Receptor Potential Cation Channel Subfamily M, Member 6/7 (TRPM6/7), Magnesium Transporter 1 (MAGT1), Solute Carrier Family 41 Member 1 (SCL41A1), and Cyclin and CBS Domain Divalent Metal Cation Transport Mediator (CNNM) proteins. Recent data show that Mg2+ transporters may regulate several cancer cell hallmarks. In this review, we describe the expression of Mg2+ transporters in digestive cancers, the most common and deadliest malignancies worldwide. Moreover, Mg2+ transporters’ expression, correlation and impact on patient overall and disease-free survival is analyzed using Genotype Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) datasets. Finally, we discuss the role of these Mg2+ transporters in the regulation of cancer cell fates and oncogenic signaling pathways.
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Yuan, Xiao, Ya Yuan, Zhi He, Diyan Li, Bo Zeng, Qingyong Ni, Mingyao Yang, and Deying Yang. "The Regulatory Functions of Circular RNAs in Digestive System Cancers." Cancers 12, no. 3 (March 24, 2020): 770. http://dx.doi.org/10.3390/cancers12030770.
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Circular ribonucleic acids (circRNAs), which are a type of covalently closed circular RNA, are receiving increasing attention. An increasing amount of evidence suggests that circRNAs are involved in the biogenesis and development of multiple diseases such as digestive system cancers. Dysregulated circRNAs have been found to act as oncogenes or tumour suppressors in digestive system cancers. Moreover, circRNAs are related to ageing and a wide variety of processes in tumour cells, such as cell apoptosis, invasion, migration, and proliferation. Moreover, circRNAs can perform a remarkable multitude of biological functions, such as regulating splicing or transcription, binding RNA-binding proteins to enable function, acting as microRNA (miRNA) sponges, and undergoing translated into proteins. However, in digestive system cancers, circRNAs function mainly as miRNA sponges. Herein, we summarise the latest research progress on biological functions of circRNAs in digestive system cancers. This review serves as a synopsis of potential therapeutic targets and biological markers for digestive system cancer.
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Valean, Simona, Romeo Chira, and Dan Dumitrascu. "Epidemiological trends in digestive cancers compared to trends in alcohol consumption. Facts from Romania: correlation or coincidence?" Medicine and Pharmacy Reports 91, no. 4 (October 30, 2018): 376–86. http://dx.doi.org/10.15386/cjmed-1067.
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Cancer has emerged as the leading cause of death in human populations, according to recent estimations. Epidemiological studies emphasized the role of life style and of environmental factors in promoting the risk for digestive cancers. The contribution of alcohol was highly suspected. Even for digestive cancers with dominant infection etiology, like liver cancer and gastric cancer, the contribution of alcohol should be assessed. At population level there is therefore a need to compare trends in epidemiological data of gastrointestinal cancers and data on alcohol consumption, in order to extrapolate any causative relationship. The purpose of this review was to analyze the time trend of digestive cancers in Romania, in terms of mortality rates (between 1955-2012), and incidence rates (between 2008-2012), in males and females, and to analyze the alcohol consumption data, aiming to find out if there is any association.
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Valean, Simona, Monica Acalovschi, Mircea Diculescu, Mircea Manuc, Adrian Goldis, Catalin Sfarti, and Anca Trifan. "Mortality in Digestive Cancers, 2012: International Data and Data from Romania." Journal of Gastrointestinal and Liver Diseases 24, no. 4 (December 1, 2015): 507–14. http://dx.doi.org/10.15403/jgld.2014.1121.244.rom.
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We aimed to compare the difference in case fatality rate between more developed and very high Human Development Index (HDI) regions, less developed and low HDI regions, and Romania. The incidence and mortality rates for digestive cancers were obtained from the IARC/WHO 2012 database. World mean mortality-to-incidence ratios registered the highest values in pancreatic cancer (0.97/0.94), and liver cancer (0.93/0.96) in males/females, respectively. The lowest values were recorded in colorectal cancer (0.48 in both sexes). Mortality-to-incidence ratios were generally higher in less developed areas, low HDI populations, and in Romania. The difference in case fatality rate between different areas showed higher variations for colorectal, gastric and gallbladder cancers, and smaller variations for esophageal, liver, and pancreatic cancers. In summary, mortality-to-incidence ratios of digestive cancers were high in 2012; higher values were registered in less developed and low HDI regions, and in Romania. Mortality-to-incidence ratios were similar in both sexes, even though the incidence was generally higher in men. Digestive cancer mortality variation suggests the necessity of finding better strategies for prevention, early diagnosis and treatment of digestive cancers.
Abbreviations: ASRWs: age-standardized rate (World Standard Population) per 100,000 population; CRC: colorectal cancer; GC: gastric cancer; HDI: Human Development Index; HCC: hepatocellular carcinoma; IARC: International
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Chen, Siyuan, Hui Dong, Shiming Yang, and Hong Guo. "Cathepsins in digestive cancers." Oncotarget 8, no. 25 (March 29, 2017): 41690–700. http://dx.doi.org/10.18632/oncotarget.16677.
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Gonzalez, A. Llopis, M. Morales Suarez-Varela, and R. Rodriguez Martin. "Other digestive tract cancers." European Journal of Cancer Prevention 1 (October 1991): 28. http://dx.doi.org/10.1097/00008469-199110001-00049.
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Vaque, J., L. Armadans, J. Penella, P. Quesada, and J. Rossello. "Other digestive tract cancers." European Journal of Cancer Prevention 1 (October 1991): 29. http://dx.doi.org/10.1097/00008469-199110001-00050.
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Paz-Houza, J. I., M. M. Abad, E. Munoz, and A. Bullon. "Other digestive tract cancers." European Journal of Cancer Prevention 1 (October 1991): 29. http://dx.doi.org/10.1097/00008469-199110001-00051.
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McCarthy, Michael. "Aspirin and digestive cancers." Lancet 341, no. 8848 (March 1993): 821. http://dx.doi.org/10.1016/0140-6736(93)90589-9.
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Tron, Laure, Mathieu Fauvernier, Anne-Marie Bouvier, Michel Robaszkiewicz, Véronique Bouvier, Mélanie Cariou, Valérie Jooste, et al. "Socioeconomic Environment and Survival in Patients with Digestive Cancers: A French Population-Based Study." Cancers 13, no. 20 (October 14, 2021): 5156. http://dx.doi.org/10.3390/cancers13205156.
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Social inequalities are an important prognostic factor in cancer survival, but little is known regarding digestive cancers specifically. We aimed to provide in-depth analysis of the contextual social disparities in net survival of patients with digestive cancer in France, using population-based data and relevant modeling. Digestive cancers (n = 54,507) diagnosed between 2006–2009, collected through the French network of cancer registries, were included (end of follow-up 30 June 2013). Social environment was assessed by the European Deprivation Index. Multidimensional penalized splines were used to model excess mortality hazard. We found that net survival was significantly worse for individuals living in a more deprived environment as compared to those living in a less deprived one for esophageal, liver, pancreatic, colon and rectal cancers, and for stomach and bile duct cancers among females. Excess mortality hazard was up to 57% higher among females living in the most deprived areas (vs. least deprived) at 1 year of follow-up for bile duct cancer, and up to 21% higher among males living in the most deprived areas (vs. least deprived) regarding colon cancer. To conclude, we provide a better understanding of how the (contextual) social gradient in survival is constructed, offering new perspectives for tackling social inequalities in digestive cancer survival.
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Zhang, Hongli, Qingqing Feng, Wei-Dong Chen, and Yan-Dong Wang. "HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers." International Journal of Molecular Sciences 19, no. 11 (October 23, 2018): 3295. http://dx.doi.org/10.3390/ijms19113295.
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The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c-MET signaling may have therapeutic potential. Various HGF/c-MET signaling inhibitors, mainly c-MET inhibitors, have been tested in clinical trials. The observed efficacy and adverse events of some c-MET inhibitors were not very suitable for treating digestive system cancers. The development of new HGF/c-MET inhibitors in preclinical studies may bring promising treatments and synergistic combination (traditional anticancer drugs and c-MET inhibitors) strategies provided anacceptable safety and tolerability. Insights into miRNA biology and miRNA therapeutics have made miRNAs attractive tools to inhibit HGF/c-MET signaling. Recent reports show that several microRNAs participate in inhibiting HGF/c-MET signaling networks through antagonizing c-MET or HGF in digestive system cancers, and the miRNAs-HGF/c-MET axis plays crucial and novel roles for cancer treatment. In the current review, we will discuss recent findings about inhibitors of HGF/c-MET signaling in treating digestive system cancers, and how miRNAs regulate digestive system cancers via mediating HGF/c-MET pathway.
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Zhao, Zhou, Zhaolun Cai, Tianxiang Jiang, Junhong Han, and Bo Zhang. "Histone Chaperones and Digestive Cancer: A Review of the Literature." Cancers 14, no. 22 (November 14, 2022): 5584. http://dx.doi.org/10.3390/cancers14225584.
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Background: The global burden of digestive cancer is expected to increase. Therefore, crucial for the prognosis of patients with these tumors is to identify early diagnostic markers or novel therapeutic targets. There is accumulating evidence connecting histone chaperones to the pathogenesis of digestive cancer. Histone chaperones are now broadly defined as a class of proteins that bind histones and regulate nucleosome assembly. Recent studies have demonstrated that multiple histone chaperones are aberrantly expressed and have distinct roles in digestive cancers. Objective: The purpose of this review is to present the current evidence regarding the role of histone chaperones in digestive cancer, particularly their mechanism in the development and progression of esophageal, gastric, liver, pancreatic, and colorectal cancers. In addition, the prognostic significance of particular histone chaperones in patients with digestive cancer is discussed. Methods: According to PRISMA guidelines, we searched the PubMed, Embase, and MEDLINE databases to identify studies on histone chaperones and digestive cancer from inception until June 2022. Results: A total of 104 studies involving 21 histone chaperones were retrieved. Conclusions: This review confirms the roles and mechanisms of selected histone chaperones in digestive cancer and suggests their significance as potential prognostic biomarkers and therapeutic targets. However, due to their non-specificity, more research on histone chaperones should be conducted in the future to elucidate novel strategies of histone chaperones for prognosis and treatment of digestive cancer.
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Profir, Monica, Oana Alexandra Roşu, Sanda Maria Creţoiu, and Bogdan Severus Gaspar. "Friend or Foe: Exploring the Relationship between the Gut Microbiota and the Pathogenesis and Treatment of Digestive Cancers." Microorganisms 12, no. 5 (May 8, 2024): 955. http://dx.doi.org/10.3390/microorganisms12050955.
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Digestive cancers are among the leading causes of cancer death in the world. However, the mechanisms of cancer development and progression are not fully understood. Accumulating evidence in recent years pointing to the bidirectional interactions between gut dysbiosis and the development of a specific type of gastrointestinal cancer is shedding light on the importance of this “unseen organ”—the microbiota. This review focuses on the local role of the gut microbiota imbalance in different digestive tract organs and annexes related to the carcinogenic mechanisms. Microbiota modulation, either by probiotic administration or by dietary changes, plays an important role in the future therapies of various digestive cancers.
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Vithayathil, Mathew, Paul Carter, Siddhartha Kar, Amy M. Mason, Stephen Burgess, and Susanna C. Larsson. "Body size and composition and risk of site-specific cancers in the UK Biobank and large international consortia: A mendelian randomisation study." PLOS Medicine 18, no. 7 (July 29, 2021): e1003706. http://dx.doi.org/10.1371/journal.pmed.1003706.
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Background Evidence for the impact of body size and composition on cancer risk is limited. This mendelian randomisation (MR) study investigates evidence supporting causal relationships of body mass index (BMI), fat mass index (FMI), fat-free mass index (FFMI), and height with cancer risk. Methods and findings Single nucleotide polymorphisms (SNPs) were used as instrumental variables for BMI (312 SNPs), FMI (577 SNPs), FFMI (577 SNPs), and height (293 SNPs). Associations of the genetic variants with 22 site-specific cancers and overall cancer were estimated in 367,561 individuals from the UK Biobank (UKBB) and with lung, breast, ovarian, uterine, and prostate cancer in large international consortia. In the UKBB, genetically predicted BMI was positively associated with overall cancer (odds ratio [OR] per 1 kg/m2 increase 1.01, 95% confidence interval [CI] 1.00–1.02; p = 0.043); several digestive system cancers: stomach (OR 1.13, 95% CI 1.06–1.21; p < 0.001), esophagus (OR 1.10, 95% CI 1.03, 1.17; p = 0.003), liver (OR 1.13, 95% CI 1.03–1.25; p = 0.012), and pancreas (OR 1.06, 95% CI 1.01–1.12; p = 0.016); and lung cancer (OR 1.08, 95% CI 1.04–1.12; p < 0.001). For sex-specific cancers, genetically predicted elevated BMI was associated with an increased risk of uterine cancer (OR 1.10, 95% CI 1.05–1.15; p < 0.001) and with a lower risk of prostate cancer (OR 0.97, 95% CI 0.94–0.99; p = 0.009). When dividing cancers into digestive system versus non-digestive system, genetically predicted BMI was positively associated with digestive system cancers (OR 1.04, 95% CI 1.02–1.06; p < 0.001) but not with non-digestive system cancers (OR 1.01, 95% CI 0.99–1.02; p = 0.369). Genetically predicted FMI was positively associated with liver, pancreatic, and lung cancer and inversely associated with melanoma and prostate cancer. Genetically predicted FFMI was positively associated with non-Hodgkin lymphoma and melanoma. Genetically predicted height was associated with increased risk of overall cancer (OR per 1 standard deviation increase 1.09; 95% CI 1.05–1.12; p < 0.001) and multiple site-specific cancers. Similar results were observed in analyses using the weighted median and MR–Egger methods. Results based on consortium data confirmed the positive associations between BMI and lung and uterine cancer risk as well as the inverse association between BMI and prostate cancer, and, additionally, showed an inverse association between genetically predicted BMI and breast cancer. The main limitations are the assumption that genetic associations with cancer outcomes are mediated via the proposed risk factors and that estimates for some lower frequency cancer types are subject to low precision. Conclusions Our results show that the evidence for BMI as a causal risk factor for cancer is mixed. We find that BMI has a consistent causal role in increasing risk of digestive system cancers and a role for sex-specific cancers with inconsistent directions of effect. In contrast, increased height appears to have a consistent risk-increasing effect on overall and site-specific cancers.
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Vecchia, Carlo La, and Cristina Bosetti. "Diet and cancer risk in Mediterranean countries: open issues." Public Health Nutrition 9, no. 8A (December 2006): 1077–82. http://dx.doi.org/10.1017/s1368980007668475.
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AbstractObjectiveTo analyse various aspects of the Mediterranean diet in relation to the risk of several common cancers in Italy.DesignData from a series of case-control studies conducted in northern Italy between 1983 and 2004 on over 20 000 cases of several major cancers and 18 000 controls.ResultsFor most digestive tract cancers, the risk decreased with increasing vegetable and fruit consumption, with relative risks between 0.3 and 0.7 for the highest level of intake, and the population-attributable risks for low intake of vegetables and fruit ranged between 15 and 40%. Less strong inverse relations were observed for other (epithelial) cancers, too. A number of micronutrients contained in vegetables and fruit showed an inverse relation with cancer risk. In particular, flavones, flavonols and resveratrol were inversely related to breast cancer risk. Olive oil, which is a typical aspect of the Mediterranean diet, has also been inversely related to cancers of the colorectum and breast, and mainly of the upper digestive and respiratory tract. Consumption of pizza, one of the most typical Italian foods, was related to a reduced risk of digestive tract cancers, although pizza may simply be an aspecific indicator of the Italian diet.ConclusionsAdherence to the Mediterranean diet is a favourable indicator of the risk of several common epithelial cancers in Italy. A score summarising the major characteristics of the Mediterranean diet was related to a priori defined reduced risks of several digestive tract neoplasms by over 50%.
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Constantin, Adrian, Roxana Constantin, Florin Achim, Bogdan Socea, and Dragos Predescu. "Pregnancy and Gastric Cancer: A Narrative Review." Diagnostics 13, no. 11 (May 29, 2023): 1909. http://dx.doi.org/10.3390/diagnostics13111909.
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Cases of digestive cancers diagnosed during pregnancy are rare. The increasing prevalence of pregnancy in women aged 30–39 years (and not exceptionally 40–49 years) could explain the frequent co-occurrence of cancers and pregnancy. The diagnosis of digestive cancers in pregnancy is difficult due to the overlap between neoplasm symptomatology and the clinical picture of pregnancy. A paraclinical evaluation may also be difficult depending on the trimester of the pregnancy. Diagnosis is also delayed by practitioners’ hesitation to use invasive investigations (imaging, endoscopy, etc.) due to fetal safety concerns. Therefore, digestive cancers are often diagnosed during pregnancy in advanced stages, where complications such as occlusions, perforations, and cachexia have already arisen. In this review, we highlight the epidemiology, clinical aspects, paraclinical evaluation, and particularities of the diagnosis and treatment of gastric cancer during pregnancy.
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Thioubou, M. A., O. Sow, K. Diallo, M. L. Bassène, Diallo S, M. N. Gueye, M. P. Fall, Dia D, and Mbengue M. "Problematics in Medical Management of Digestive Cancers in Ziguinchor." Scholars Journal of Applied Medical Sciences 9, no. 10 (October 6, 2021): 1511–14. http://dx.doi.org/10.36347/sjams.2021.v09i10.005.
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Background: In Senegal, digestive cancers often cause an issue in their management, especially in semi-urban areas. The aim of our study was to evaluate the medical management of digestive cancers at Peace hospital in Ziguinchor. Patients and methodology: It was a retrospective study during 20 months, including all patients of medicine, general surgery and digestive endoscopy departments, with a diagnosis of primary digestive cancer. Data’s were collected and analyzed with Microsoft Excel. Results: Seventy and fourteen patients were included. There were 49 men and 25 women (sex-ratio 1,96). The average age was 45,2 years. Thirty and five patients (47,3%) presented a hepatocellular carcinoma. They all had a symptomatic treatment. Twelve patients died. An oesophageal cancer was diagnosed for 10 patients (13,5%). The tumor was located at upper third for 4 patients, middle third for 1 patient and lower third for 5 patients. The treatment was a feeding gastrostomy. A gastric cancer was diagnosed in 12 patients (16,2%). The tumor was in antrum for 8 patients (66,7%). A jejunostomy and a gastro-entero-anastomosis were realized for 2 patients. Ten patients (13,5%) had a colorectal cancer. The tumor was in lower rectum for 3 patients, middle rectum for 4 patients, upper rectum for 1 patient, rectosigmoid junction for 1 patient and right colon for 1 patient. A monobloc resection was realized for 1 patient. Four (4) patients had a colostomy. A pancreatic cancer was diagnosed for 7 patients (9,5%). Five patients (5) had a head cancer, one (1) had a tail cancer and another one (1) had a body-tail cancer. They all had a symptomatic treatment. Conclusion: In Senegal, primary digestive cancers are frequent in semi-urban areas especially hepatocellular carcinoma. The diagnosis is often delayed and the treatment is symptomatic. The primary prevention and a better local technical equipment would improve their management.
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Gamradt, Pia, Christelle De La Fouchardière, and Ana Hennino. "Stromal Protein-Mediated Immune Regulation in Digestive Cancers." Cancers 13, no. 1 (January 5, 2021): 146. http://dx.doi.org/10.3390/cancers13010146.
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The stromal tumor microenvironment (TME) consists of immune cells, vascular and neural structures, cancer-associated fibroblasts (CAFs), as well as extracellular matrix (ECM), and favors immune escape mechanisms promoting the initiation and progression of digestive cancers. Numerous ECM proteins released by stromal and tumor cells are crucial in providing physical rigidity to the TME, though they are also key regulators of the immune response against cancer cells by interacting directly with immune cells or engaging with immune regulatory molecules. Here, we discuss current knowledge of stromal proteins in digestive cancers including pancreatic cancer, colorectal cancer, and gastric cancer, focusing on their functions in inhibiting tumor immunity and enabling drug resistance. Moreover, we will discuss the implication of stromal proteins as therapeutic targets to unleash efficient immunotherapy-based treatments.
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Yeh, Kun-Huei. "Awardee Summary of 2023 Taiwan Oncology Society Clinical Research Award Recipient: Persistent Endeavors on Research of Digestive Cancers for Three Decades." Journal of Cancer Research and Practice 11, no. 1 (2024): 1–6. http://dx.doi.org/10.4103/ejcrp.ejcrp-d-23-00044.
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Abstract Objective: Digestive cancers account for five of the top ten cancer-related deaths in Taiwan. Our team has made persistent endeavors in translational research and clinical trials of digestive cancers for almost three decades. Data Sources and Study Selection: We enrolled relevant translational and clinical studies for digestive cancers published by our groups in the past three decades. Results: First, we developed a unique weekly 24-h infusion of high-dose 5-fluorouracil (5-FU) and leucovorin regimen (HDFL) in 1992. HDFL exhibits satisfactory single-agent activity, minimal myelosuppression, and mild toxicity. A variety of HDFL-based doublet combinations (such as cisplatin-HDFL, oxaliplatin-HDFL, and paclitaxel-HDFL) have become cornerstone regimens for three decades for the treatment of gastric cancers, with high efficacy and manageable toxicity at our hospital. Second, we have made persistent efforts in translational research and clinical trials on early-stage gastric mucosa-associated lymphoid tissue lymphomas (MALTomas), gastric diffuse large B-cell lymphomas, colorectal cancers (CRCs), pancreatic cancers, and immuno-oncology. Third, on behalf of the Taiwan Oncology Society, we participated in and published the Pan-Asian adapted European Society for Medical Oncology (ESMO) Clinical Practice Guidelines for locally advanced and metastatic CRC, gastric, and esophageal cancers, and the consensus meeting on tumor-agnostic indications of microsatellite instability-high (MSI-H) and NTRK. Conclusion: In the future, our team will make persistent endeavors in research on digestive cancers for immunotherapy and precision medicine to further improve treatment outcomes.
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Xie, Liling, Yun Song, Tengfei Lin, Huiyuan Guo, Binyan Wang, Genfu Tang, Chengzhang Liu, et al. "Association of plasma retinol levels with incident cancer risk in Chinese hypertensive adults: a nested case–control study." British Journal of Nutrition 122, no. 03 (July 29, 2019): 293–300. http://dx.doi.org/10.1017/s000711451900120x.
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AbstractWe aimed to investigate the association between plasma retinol and incident cancer among Chinese hypertensive adults. We conducted a nested case–control study, including 231 patients with incident cancer and 231 matched controls during a median 4·5-year follow-up of the China Stroke Primary Prevention Trial. There was a significant, inverse association between retinol levels and digestive system cancer (per 10 μg/dl increases: OR 0·79; 95 % CI 0·69, 0·91). When compared with participants in the first quartile of retinol (< 52·3 μg/dl), a significantly lower cancer risk was found in participants in quartile 2–4 ( ≥ 52·3 μg/dl: OR 0·31; 95 % CI 0·13, 0·71). However, there was a U-shaped association between retinol levels and non-digestive system cancers where the risk of cancers decreased (although not significantly) with each increment of plasma retinol (per 10 μg/dl increases: OR 0·89; 95 % CI 0·60, 1·31) in participants with retinol < 68·2 μg/dl, and then increased significantly with retinol (per 10 μg/dl increase: OR 1·65; 95 % CI 1·12, 2·44) in participants with retinol ≥ 68·2 μg/dl. In conclusion, there was a significant inverse dose–response association between plasma retinol and the risk of digestive system cancers. However, a U-shaped association was observed between plasma retinol and the risk of non-digestive cancers (with a turning point approximately 68·2 μg/dl).
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Bytnar, Julie A., Craig D. Shriver, and Kangmin Zhu. "Incidence rates of digestive cancers among U.S. military servicemen: Comparison with the rates in the general U.S. population." PLOS ONE 16, no. 9 (September 3, 2021): e0257087. http://dx.doi.org/10.1371/journal.pone.0257087.
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Background Digestive cancers greatly contribute to the cancer burden in the United States. These cancers are more common among men and some are increasing among adults under age 50. Military population, which is dominantly male and young, and general populations differ in exposure to risk factors for these cancers. However, no studies have systematically investigated whether the incidence rates of these cancers differ between the two populations. This study aimed to compare incidence rates and trends of select digestive cancers between active-duty military and general populations in men aged 20–59 years. Methods Data were from the Department of Defenses’ Automated Central Tumor Registry (ACTUR) and the National Cancer Institute’s Surveillance, Epidemiology, and End Results 9 (SEER-9) registries. Age-adjusted incidence rates of colorectal, stomach, liver, and pancreatic cancers among men aged 20–59 years during 1990–2013 were compared between the two populations. Stratified analyses by age were done for colorectal and stomach cancers. The joinpoint regression analysis was conducted to examine temporal trends for colorectal cancer. Results The age-adjusted incidence rates of colorectal, stomach, liver, and pancreatic cancers were overall lower among active-duty than SEER (IRR = 0.86, 95% CI = 0.81–0.92; IRR = 0.65, 95% CI = 0.55–0.76; IRR = 0.39, 95% CI = 0.30–0.49; IRR = 0.51, 95% CI = 0.41–0.62, respectively). This was observed in the groups of both ages 20–39 and 40–59 years for stomach cancer, and in the group of ages 40–59 years for colorectal cancer. The incidence rates of colorectal cancer tended to decrease since 2008 in ACTUR. Conclusion The incidence rates for selected digestive cancers overall were lower in the active-duty military population than the U.S. general population. This study highlights the need for more research enhancing our understanding of variations in these cancers between the two populations.
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Niemiec, Rafał, Justyna Branewska, Barbara Ostrowska, Mikołaj Matysek, Anna Olszanicka, Jan Imioło, Anna Maciąg, Izabela Hop, Kacper Kołodziejczyk, and Adam Galas. "role of flavonoids in digestive tract cancer prevention - a review article." Journal of Education, Health and Sport 37, no. 1 (June 6, 2023): 41–52. http://dx.doi.org/10.12775/jehs.2023.37.01.003.
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Introduction: Flavonoids are bioactive chemical compounds crucial for the functioning of plant organisms. Recently, they have been intensively studied in search of their potential application in medicine. One of the most popular fields in that regard is oncology. Digestive tract cancers are still a challenge for contemporary medicine. Our diet seems to have a direct impact on the etiology of colorectal, gastric, and esophageal cancers. The relationship between the consumption of flavonoids, their specific fractions, and digestive tract cancer morbidity is nowadays frequently investigated.Purpose: This review article aims to discuss the most recent scientific reports and summarize the current state of knowledge, considering the role of flavonoids in digestive tract cancer prevention.Materials and methods: Our work is based on articles accessed through medical information databases (Google Scholar, PubMed, CrossRef), various scientific books, and official NFZ and WHO-certified sites.Results: Total flavonoid intake lowers gastric and esophageal cancer morbidity. A high amount of dietary catechins prevents the growth of gastric and colorectal cancer. Increased consumption of anthocyanidins, flavones, and flavanones decreases esophageal cancer morbidity. Isoflavones, procyanidines, anthocyanidins, flaonols, and flavones severely decrease the chance of developing colorectal cancer.Conclusions: Flavonoids can play an important role in digestive tract cancer prevention. They suppress the growth of colorectal, gastric, and esophageal cancers. Nevertheless, new, high-quality studies are needed in order to compile adequate procedures and bring new, potential drugs to the market.
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PITU, FLAVIU, SERGIU PASCA, CALIN POPA, and AL HAJJAR NADIM. "The importance of MLH1, MSH2, MSH6 and PMS2 in determining DNA damage response in digestive cancers." Romanian Biotechnological Letters 26, no. 1 (January 1, 2021): 2289–94. http://dx.doi.org/10.25083/rbl/26.1/2289.2294.
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Introduction: Genomic instability is a common feature across human cancers, but presents variation across different types of cancer, patients and cells of from the same tumor.This can be caused either by changes in the DNA damage repair pathways, aberrant histone modifications or methylation. The aim of this study was to determine the common mutated genes between digestive cancers that present genomic instability and to determine the biological processes in which these are implicated. Material and Methods: Mutational profiles for patients presenting digestive cancers and mutations in MLH1, MSH2, MSH6 and PMS2 were downloaded from the MSK impact cohort via cBioPortal. PANTHER was used to determine the GO SLIM processes in which the mutated genes are involved. R 3.5.3 and the R package circlize were used to generate chord diagrams. Results and Discussions: Considering the number of mutated genes from different digestive cancers it could be observed that the deregulated processes are general cellular processes, while when taking into consideration the fold change in overrepresentation of certain processes, the main deregulated processes are represented by DNA damage repair pathways, showing their overrepresentation in the selected cohort based on a few mutated genes. Conclusion: MLH1,MSH2,MSH6 and PMS2 mutations dictate the alterations in DNA damage repair pathways in digestive cancers.
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Chai, Sanbao, Shuqing Yu, Zhirong Yang, Shanshan Wu, Le Gao, Haining Wang, Yuan Zhang, Siyan Zhan, Linong Ji, and Feng Sun. "Effect of incretin-based therapies on cancers of digestive system among 101 595 patients with type 2 diabetes mellitus: a systematic review and network meta-analysis combining 84 trials with a median duration of 30 weeks." BMJ Open Diabetes Research & Care 7, no. 1 (September 2019): e000728. http://dx.doi.org/10.1136/bmjdrc-2019-000728.
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ObjectivesTo evaluate the risk of cancers of digestive system with incretin-based therapies among patients with type 2 diabetes mellitus.Research design and methodsMedline, Embase, Cochrane Library and ClinicalTrials.gov databases were searched for randomized controlled clinical trials that compared incretin-based drugs with placebo or other antidiabetic drugs. Paired reviewers independently screened citations, extracted data and assessed risk of bias of included studies. Network meta-analysis was performed, followed by subgroup analysis. The Grading of Recommendations Assessment, Development and Evaluation system was used to assess the quality of evidence.ResultsA total of 84 studies (n=101 595) involving cancers of digestive system were identified (a median follow-up of 30 weeks). The risk of cancers of digestive system with incretin-based therapies was comparable with insulin (OR: 0.86, 95% CI 0.27 to 2.69), metformin (OR: 0.32, 95% CI 0.07 to 1.38), sodium-glucose co-transporter 2 (OR: 5.26, 95% CI 0.58 to 47.41), sulfonylureas (OR: 1.27, 95% CI 0.68 to 2.39), thiazolidinediones (OR: 0.42, 95% CI 0.13 to 1.42), alpha-glucosidase inhibitors (OR: 2.98, 95% CI 0.12 to 73.80), and placebo (OR: 0.87, 95% CI 0.71 to 1.05). The results of subgroup analysis based on the type of digestive system cancers indicated that incretin-based therapies did not increase the risk of gastrointestinal cancers, respectively. The results of subgroup analysis based on age, duration, mean HbA1c, trial duration, and sample size did not indicate the risk of digestive system cancers.ConclusionsModerate to high Grading of Recommendations Assessment, Development and Evaluation evidence suggests that incretin-based therapies were not associated with an increased risk of cancer of digestive system in patients with type 2 diabetes mellitus.
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Gilly, F. N., A. C. Sayag-Beaujard, P. Y. Carry, O. Glehen, B. Sadeghi-Looyeh, Y. Francois, J. B. Griot, et al. "INTRAPERITONEAL CHEMOHYPERTHERMIA IN DIGESTIVE CANCERS." Southern Medical Journal 89, Supplement (October 1996): S142. http://dx.doi.org/10.1097/00007611-199610001-00303.
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Zhou, Ying, and Guang-Hua Luo. "Porphyromonas gingivalisand digestive system cancers." World Journal of Clinical Cases 7, no. 7 (April 6, 2019): 819–29. http://dx.doi.org/10.12998/wjcc.v7.i7.819.
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Bedenne, L., E. Dorval, F. Tusseau, M. Ducreux, J. L. Legoux, C. Louvet, F. Mornex, Y. Panis, J. F. Bretagne, and M. Amouretti. "French Guidelines for Digestive Cancers." Gastroentérologie Clinique et Biologique 30 (September 2006): 3–4. http://dx.doi.org/10.1016/s0399-8320(06)73583-7.
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Wu, Ruo-Lin, Lei Huang, Hong-Chuan Zhao, and Xiao-Ping Geng. "Hyaluronic acid in digestive cancers." Journal of Cancer Research and Clinical Oncology 143, no. 1 (August 17, 2016): 1–16. http://dx.doi.org/10.1007/s00432-016-2213-5.
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Yaméogo, P. B., R. A. Djigemde, M. Ilboudo, A. S. Ouedraogo, and N. Zongo. "Descriptive epidemiology of colorectal cancer in Burkina Faso." African Journal of Oncology 2, no. 2 (July 1, 2022): 54–57. http://dx.doi.org/10.54266/ajo.2.2.54.
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OBJECTIVE: To describe the epidemiological profile of colorectal cancers in Burkina Faso. MATERIALS AND METHODS: This was a cross-sectional and descriptive study of colorectal cancers diagnosed in all anatomy and pathology laboratories in Burkina Faso from 1988 to 2018. Age, sex, nature of the specimens, histo-genetic and histological types were studied. Comparisons were possible using Student's t test and Fisher's Khi2 test. RESULTS: In 31 years, 802 colorectal cancers were diagnosed, representing a mean annual incidence of 25.9 cases ± 7.6. These cancers represented 30.9% of all digestive cancers and were therefore the 2nd most common digestive cancer. The mean age of the patients was 50 years ± 18.1. The sex-ratio was 1.2. In men, the mean age was 50 years ± 11.6 and in women 50 years ± 13. Endoscopic biopsy specimens were studied in 60.7% of cases. The cancers were located in the left colon in 44% of cases, in the right colon in 30.4% of cases and in the rectum in 25.6% of cases. Carcinomas constituted 93.5% of the histo-genetic types. Adenocarcinoma was the histological type in 77.9% of cases. CONCLUSION: The second most common digestive cancer in Burkina Faso, colorectal cancer occurs at a relatively young age. It is predominantly male. However, the average age of occurrence is identical in both sexes. Adenocarcinoma is the most frequent histological type. Access to mass screening would allow a better understanding of the frequencies. KEYWORDS: Epidemiology; Colorectal cancers; Burkina Faso.
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Zheng, Jiachen, Ming Zhao, Jiahui Li, Guoying Lou, Yanyan Yuan, Shizhong Bu, and Yang Xi. "Obesity-associated digestive cancers: A review of mechanisms and interventions." Tumor Biology 39, no. 3 (March 2017): 101042831769502. http://dx.doi.org/10.1177/1010428317695020.
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The prevalence of obesity has steadily increased over the past few decades. Previous studies suggest that obesity is an oncogenic factor and that over 20% of all cancers are obesity-related. Among such cancers, digestive system malignancies (including esophageal adenocarcinomas, colorectal cancers, and cancers of the gastric cardia, liver, and pancreas) are reported most frequently. While the 5-year survival rates of cancers of the breast and prostate are 90%, that rate is only 45% for digestive cancers. In this review, the mechanisms of obesity-associated digestive cancers are discussed, with an emphasis on obesity-related gene mutations, insulin and insulin-like growth factor signaling pathways, chronic inflammation, and altered adipokine levels. Evidence that these factors often function interdependently rather than independently in carcinogenesis is presented. Recommended interventions that may reduce the burden of obesity-associated digestive cancers, such as participation in physical activity, diet modulation, and calorie restriction, are also described.
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Yishak, Hasset, Kareem Halwah, and Jiyun Rhim. "Exploring the Therapeutic Potential of PTPN Families in Lung and Digestive Cancers." Berkeley Pharma Tech Journal of Medicine 3, no. 2 (December 30, 2023): 82–100. http://dx.doi.org/10.52243/bptjm.v3i2.49.
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Protein phosphorylation and dephosphorylation are pivotal in regulating protein activity. Two key players, protein tyrosine kinases and protein tyrosine phosphatases (PTPN), especially non-receptor PTPNs, exert opposing influences in this process. While all PTPNs dephosphorylate substrates, their impact on different cancers varies. Some act as tumor suppressors in specific cancers, while in others, they may function as tumor promoters. This review focuses on comprehending the roles of PTPNs in lung and digestive cancers. Notably, lung cancer ranks as the third most common cancer in the United States, with around 200,000 new cases reported annually. Despite declining rates in the US, stomach cancer remains a major cause of cancer-related deaths worldwide. The objective of this review article is to elucidate the functions of PTPN1, PTPN2, PTPN3, PTPN6, PTPN11, PTPN12, and PTPN13 in lung and/or digestive cancers. Emphasis is placed on exploring their potential as prognostic markers or therapeutic targets.
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Westcott, James, Christopher A. Luckhurst, Grahame McKenzie, Danish Memon, Li-Chiung Lin, Sinead Knight, Elizabeth J. Blaikley, et al. "Abstract 454: Validation of GPR35 as a novel cancer target in digestive tract cancers and discovery of potent, selective GPR35 inverse agonists." Cancer Research 83, no. 7_Supplement (April 4, 2023): 454. http://dx.doi.org/10.1158/1538-7445.am2023-454.
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Abstract Cancers of the digestive tract are a major area of unmet clinical need with incidence rates of some cancers increasing and early onset forms becoming more prevalent. Environmental factors, such as poor diet and microbiota, as well as inflammatory conditions, are strongly associated with occurrence of digestive system cancers. Obesogenic diet combined with microbiotic metabolism can lead to high levels of secondary bile acids in the human gut. Secondary bile acids deoxy- and litho-cholic acid have been shown to have oncogenic potential and their levels are increased in the intestines of cancer patients relative to healthy controls. GPR35 is an orphan class A G protein-coupled receptor primarily expressed in digestive system epithelial tissues and cells of myeloid lineage. GPR35 polymorphisms are strongly associated with inflammatory bowel diseases. In particular, rs37947171, a missense variant that codes for a threonine to methionine substitution at position 108 (T108M) and has been shown to have hypermorphic function, is strongly associated with Crohn’s disease and ulcerative colitis. GPR35 is also overexpressed in adenocarcinomas of the digestive tract, including those of esophageal, hepatic/bile ductal, pancreatic, gastric and colorectal origin, and high expression has been shown to confer poor prognosis in various digestive system cancers. Consistent with a proposed role in digestive tract cancers we now show that GPR35 is activated by lithocholic acid. Furthermore, we demonstrate through CRISPR-gene editing of cancer cells and RNAseq analysis that GPR35 can regulate transcriptional and cytoskeletal modules associated with hallmarks of cancer, including chemokine and growth factor expression and F-actin formation. GPR35 activates a transcriptional program that is enriched for genes containing pro-oncogenic serum response factor response element in their upstream promoters. High throughput screening and medicinal chemistry optimization has led to the discovery of potent antagonists of GPR35 signalling. Pharmacological characterisation of lead series has shown that they are able to prevent Gα and β-arrestin protein binding, while also inhibiting phospho-ERK, calcium flux, receptor internalisation and serum response factor-induced gene transcription. Furthermore, the series are competitive with predicted orthosteric agonist, can block activation of receptor signalling by lithocholic acid and act as inverse agonists of constitutive receptor tone. Profiling these inhibitors in cancer models is currently ongoing. This work provides the basis for the pre-clinical development of GPR35 inverse agonists as anti-cancer drugs. Citation Format: James Westcott, Christopher A. Luckhurst, Grahame McKenzie, Danish Memon, Li-Chiung Lin, Sinead Knight, Elizabeth J. Blaikley, Martin Pearce, Hannah R. Warren, Eleanor Parker, Graeme Milligan, Stuart W. Hughes, Tom McCarthy. Validation of GPR35 as a novel cancer target in digestive tract cancers and discovery of potent, selective GPR35 inverse agonists [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 454.
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Wang, Weijie, Donghua Xu, Bin Wang, Shushan Yan, Xiaochen Wang, Yin Yin, Xuehao Wang, Beicheng Sun, and Xiaoyang Sun. "Increased Risk of Cancer in relation to Gout: A Review of Three Prospective Cohort Studies with 50,358 Subjects." Mediators of Inflammation 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/680853.
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Gout is a common inflammatory disease characterized by acute arthritis and hyperuricemia. A number of epidemiological studies have suggested the critical role of gout in carcinogenesis. The aim of this study was to estimate the association between gout and cancer risk by meta-analysis of all relevant studies published to date. A comprehensive literature search in PubMed and Embase databases from their inception up to July 1, 2014, was performed to identify eligible studies. The strength for relationship between gout and the risk of different cancers was evaluated by calculating pooled relative risks (RRs) with 95% confidence intervals (95% CIs). All analyses were carried out by STATA 12.0 software. Gout patients were at an increased risk of cancer, particularly urological cancers, digestive system cancers, and lung cancer. No such significant association between gout and the risk of breast or brain cancers was observed. Sensitivity analysis did not materially alter the pooled results. Gout is a risk factor of cancer, particularly that of urological cancers, digestive system cancers, and lung cancer. The pooled data further support the hypothesis of a link between gout and carcinogenesis.
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Zhao, Feng, Chan Li, Yun Wu, Jianling Xia, Ming Zeng, Tao Li, and Ke Xie. "Connective Tissue Growth Factor in Digestive System Cancers: A Review and Meta-Analysis." BioMed Research International 2020 (December 27, 2020): 1–10. http://dx.doi.org/10.1155/2020/8489093.
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Aim. A meta-analysis was conducted to estimate the impact of connective tissue growth factor (CTGF) on outcomes in patients with digestive system cancers. Methods. A systemic literature survey was performed by searching the Cochrane Library and PubMed databases for articles that evaluated the impact of CTGF on outcomes in patients with digestive system cancers. Hazard ratios and 95% confidence intervals were calculated for prognostic factors, overall and recurrence-free survival using RevMan 5.3 software. Results. This meta-analysis was conducted to evaluate a total of 11 studies that included 1730 patients. The results showed that elevated CTGF expression was significantly correlated with advanced age, larger tumor size, multiple tumors, and vascular invasion. Subgroup analysis by cancer type revealed increased risk for lymph node metastasis and advanced tumor node metastasis (TNM) stage in gastric cancer, compared with colorectal cancer. An unfavorable effect of elevated CTGF levels on overall survival was found in patients with hepatocellular carcinoma and patients with gastric cancer, while survival was improved in colorectal cancer patients with high CTGF expression, compared to those with normal levels of CTGF. Conclusions. Elevated CTGF expression may be a novel biomarker for disease status and predicted survival outcomes in patients with specific digestive system cancers.
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Chen, Zhiqiang, Long Zhang, Guoyong Han, Xueliang Zuo, Yao Zhang, Qin Zhu, Jindao Wu, and Xuehao Wang. "A Meta-Analysis of the Diagnostic Accuracy of Circular RNAs in Digestive System Malignancy." Cellular Physiology and Biochemistry 45, no. 3 (2018): 962–72. http://dx.doi.org/10.1159/000487291.
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Background/Aims: Circular RNAs (circRNAs), a novel class of noncoding RNAs, have been found to be dysregulated in various cancers. However, the clinical application value of these circRNAs in digestive system cancers remains to be clarified. We aimed to comprehensively explore the potential role of circRNAs as diagnostic indicators in digestive system malignancies. Methods: Relevant studies were systematically retrieved from PubMed, Web of Science and the Cochrane Library. The data that were required to complete 2 × 2 contingency tables were obtained from the included studies. Stratified analyses by cancer type, sample size and publication year were performed. Results: Thirteen studies with 2,276 individuals were included in the meta-analysis. The pooled sensitivity and specificity of circRNAs in the diagnosis of digestive system malignancy were 0.72 [95% confidence interval (CI): 0.65-0.77] and 0.77 (95% CI: 0.72-0.81), respectively. The overall positive likelihood ratio was 3.09 (95% CI: 2.64-3.62), and the overall negative likelihood ratio was 0.37 (95% CI: 0.31-0.44). The pooled diagnostic odds ratio was 8.38 (95% CI: 6.86-10.25), and the overall area under the curve was 0.81 (95% CI: 0.77-0.84), indicating good discriminative ability of circRNAs as biomarkers for digestive system malignancy. Conclusion: circRNAs distinguish patients with digestive system cancer from controls with relatively high diagnostic accuracy. circRNAs may be used as potential biomarkers for the diagnosis of digestive system malignancy.
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Lai, Yue, Jun Mi, and Qiang Feng. "Fusobacterium nucleatum and Malignant Tumors of the Digestive Tract: A Mechanistic Overview." Bioengineering 9, no. 7 (June 28, 2022): 285. http://dx.doi.org/10.3390/bioengineering9070285.
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Fusobacterium nucleatum (F. nucleatum) is an oral anaerobe that plays a role in several oral diseases. However, F. nucleatum is also found in other tissues of the digestive tract, and several studies have recently reported that the level of F. nucleatum is significantly elevated in malignant tumors of the digestive tract. F. nucleatum is proposed as one of the risk factors in the initiation and progression of digestive tract malignant tumors. In this review, we summarize recent reports on F. nucleatum and its role in digestive tract cancers and evaluate the mechanisms underlying the action of F. nucleatum in digestive tract cancers.
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Song, Lele, Yan Chen, Yuan Gong, Jun Wan, Shaohua Guo, Hongyi Liu, Yuemin Li, Zhen Zeng, and Yinying Lu. "Opportunistic screening and survival prediction of digestive cancers by the combination of blood mSEPT9 with protein markers." Therapeutic Advances in Medical Oncology 12 (January 2020): 175883592096296. http://dx.doi.org/10.1177/1758835920962966.
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Background: The early detection of digestive cancers and precancerous diseases remains a significant challenge. This study aimed to investigate the performance of the blood methylated SEPT9 ( mSEPT9) assay, and the combination of this assay with serum protein markers, in hospital-based opportunistic screening strategies for digestive cancers. Methods: Opportunistic screening was performed in the participating hospitals on outpatients and inpatients who met specific inclusion criteria. We recruited a total of 2030 subjects, including 764 cancer patients [291 colorectal cancer (CRC), 239 gastric cancer (GC), 106 esophageal cancer (EC), and 128 hepatocellular carcinoma (HCC)], 423 subjects with precancerous diseases, and 843 normal subjects. All samples were transported to an authenticated clinical laboratory where the mSEPT9 tests were performed. Results: When used separately, the mSEPT9 detected CRC, GC, EC, and HCC, with a sensitivity of 76.6% [area under the receiver operating characteristic curve (AUC) = 0.86)], 47.7% (AUC = 0.76), 42.6% (AUC = 0.69), and 76.7% (AUC = 0.85) and a specificity of 94.6%, 92.3%, 92.5%, and 87.7%, respectively. The mSEPT9 assay also had potent ability to discriminate cancer from non-cancer subjects. The combination of mSEPT9 with CEA, CA724, SNCG, or AFP significantly enhanced the sensitivity for CRC, GC, EC, and HCC to 86.4% (AUC = 0.99, specificity = 92.8%), 63.6% (AUC = 0.86, specificity = 91.1%), 71.3% (AUC = 0.81, specificity = 82.1%), and 83.3% (AUC = 0.93, specificity = 85.1%), respectively. The performance of the mSEPT9 assay was influenced by cancer stage, patient age, pathological types, and the location of cancer. We also identified that mSEPT9 was an independent risk factor and was a valuable predictor for the long-term survival of digestive cancer patients, with a hazard ratio of 2.84, 2.07, 1.88, and 2.45, for CRC, GC, EC, and HCC, respectively. Conclusion: The blood mSEPT9 assay, whether used alone or in combination with serum protein markers, is effective for the opportunistic screening of digestive cancers. Furthermore, mSEPT9 is an independent risk factor and a predictive marker for the long-term survival of digestive cancer patients.
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Nakanishi, Risa, Takahiro Shimizu, Ken Kumagai, Atsushi Takai, and Hiroyuki Marusawa. "Genetic Pathogenesis of Inflammation-Associated Cancers in Digestive Organs." Pathogens 10, no. 4 (April 9, 2021): 453. http://dx.doi.org/10.3390/pathogens10040453.
Full textAbstract:
Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal reflux. Cancer is a genomic disease, and stepwise accumulation of genetic and epigenetic alterations of tumor-related genes leads to the development of tumor cells. Recent genome analyses show that genetic alterations, which are evoked by inflammation, are latently accumulated in inflamed epithelial cells of digestive organs. Production of reactive oxygen and aberrant expression of activation-induced cytidine deaminase, a nucleotide-editing enzyme, could be induced in inflamed gastrointestinal epithelial cells and play a role as a genomic modulator of inflammation-associated carcinogenesis. Understanding the molecular linkage between inflammation and genetic alterations will open up a new field of tumor biology and provide a novel strategy for the prevention of inflammation-associated tumorigenesis.
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Sumantran, Venil N., and Girish Tillu. "Cancer, Inflammation, and Insights from Ayurveda." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/306346.
Full textAbstract:
A recent, exciting discovery relates to the concept of “shared pathology” between cancer and metabolic syndrome. One major pathway common to cancer and metabolic syndrome is chronic inflammation, which is a major driving force in carcinogenesis. Indeed, chronic inflammation precedes most cancers and is considered a “hallmark” of the neoplastic process. We discuss molecular and biochemical evidence which links diet, obesity, abnormal lipid metabolism, and type 2 diabetes mellitus with chronic inflammation. We also explain how each of these factors is linked with biochemical aberrations of carcinogenesis and the prevalence and risk of cancer. While there are reliable biomarkers for chronic inflammation, there are few markers for a mechanistic link between early inflammation and digestive disorders. Discovery of such a marker could lead to identification of a new subtype of patients with digestive disorders that predispose them to cancer and/or metabolic syndrome. In this context, we discuss the ayurvedic concept of “Ama” which is thought to be a toxic, proinflammatory waste-product of improper digestion. We then develop hypotheses and outline preclinical and clinical experiments designed to prove whether “Ama” can serve as a novel and reliable biomarker that links abnormal digestive status, with the onset of chronic inflammation.
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Zarin, Bahare, Laleh Rafiee, Parnaz Daneshpajouhnejad, and Shaghayegh Haghjooy Javanmard. "A review on the role of CAFs and CAF-derived exosomes in progression and metastasis of digestive system cancers." Tumor Biology 43, no. 1 (August 18, 2021): 141–57. http://dx.doi.org/10.3233/tub-200075.
Full textAbstract:
Cancers evolve as a result of the accelerated proliferation of cancer cells in a complicated, enriched, and active microenvironment. Tumor microenvironment (TME) components are the master regulators of any step of cancer development. The tumor microenvironment is composed of many cellular and noncellular components that contribute to the evolution of cancer cells. Cancer-associated fibroblasts (CAFs) are activated fibroblasts in the TME that implicate in tumor progression and metastasis dissemination through secretion of oncogenic factors which are carried to the secondary metastatic sites through exosomes. In this review, we aimed to assess the role of CAF-derived exosomes in TME construction and pre-metastatic niche formation in different cancers of the digestive system in order to better understand some important mechanisms of metastasis and provide possible targets for clinical intervention. This review article is divided into two thematic parts explaining the general mechanisms of pre-metastatic niche formation and metastasis and the role of CAF-derived exosomes in different digestive system cancers including colorectal, gastric, esophageal, pancreatic, and liver cancers.