Relevant bibliographies by topics / Gastrointestinal system – Cancer

Academic literature on the topic 'Gastrointestinal system – Cancer'

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Published: 4 June 2021
Last updated: 31 January 2023

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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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Dissertations / Theses on the topic "Gastrointestinal system – Cancer"

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Royal, E. L. "Interplay between hypoxia and gastrin in gastrointestinal cancer." Thesis, University of Nottingham, 2009. http://eprints.nottingham.ac.uk/10805/.

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Tumour hypoxia has been linked to increased resistance to both radiotherapy and chemotherapy, especially in solid metastatic GI tumours. Under hypoxic conditions, genes that promote tumour growth and survival are up-regulated, via the transcription factor hypoxia-inducible factor-1 (HIF-1). The digestive hormone gastrin, which is often over-expressed in GI cancers, has also been shown to act as a pro-survival factor, up-regulating processes such as tumour proliferation, angiogenesis and migration, and down-regulating apoptosis. Due to the high level of similarity between the downstream events mediated by the two proteins, the relationship between gastrin and HIF-1 was investigated. HIF-1α nuclear protein expression was inducible under hypoxic conditions, which led to an expected increase in VEGF gene expression, followed by a 12-50 fold increase in hypoxic gastrin mRNA expression. HIF-1α expression and transcriptional activity were not consistently affected by exogenous gastrin. RNA-interference-mediated knockdown of HIF-1α resulted in a 40-60% down-regulation of gastrin gene expression under hypoxic conditions suggesting that HIF-1α is partially responsible for gastrin up-regulation in hypoxia. Potential hypoxia-response elements (HREs) were identified within the gastrin promoter, but were only partially responsive to hypoxic incubation in GI carcinoma cells in luciferase-reporter assays. Other possible mechanisms that may account for the increased gastrin gene expression induced under hypoxic conditions include interactions of gastrin with other transcriptional regulators, either in synergy with or independent from HIF-1, or the sequestration of gastrin within the cell by ‘P’-bodies or RNA-binding proteins. These findings may indicate that the addition of anti-gastrin agents such as CCK-2 receptor antagonists or gastrin immunogens to the treatment regime of patients with solid GI tumours may be clinically beneficial, especially if combined with agents used to reduce radiotherapy and chemotherapy resistance.
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Tse, Tak-fong. "Role of RON activation on chemoresistance in gastric cancer." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38592253.

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Almulhim, Zayed. "Imaging hypoxia in colorectal cancer and gastroesophageal cancer with positron emission tomography." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=232243.

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Purpose: Hypoxia in colorectal cancer (CRC) and gastroesophageal cancer (GEC) decreases tumour responsiveness to radio and chemotherapy leading to cancer progression and poor prognosis. This is the first study to utilise [18F]FAZA hypoxia radiotracer in patients with CRC and GEC. Methods: Six patients (mean age 68±8 years, 2 males and 4 females) with CRC and 4 patients diagnosed with GEC (mean age 65 years, 3 males and 1 female) were included in the study. [18F]FAZA was synthesised at the John Mallard Scottish PET Centre. After injection with 370 MBq of [18F]FAZA, PET/CT images with 60 min dynamic scan were acquired. In addition, 15 min static scans 2 hr post injection were performed. 3D PET images were reconstructed iteratively using an ordered subset expectation maximization (OSEM) method and fused to the corresponding low-dose CT images. [18F]FAZA uptake parameters including maximum standard uptake value (SUVmax), tumour-to-muscle ratio (T/M), tumour-to-bowel ratio (T/B) and volume of interest (VOI) were measured. Results: 4 out 6 patients with CRC (66%) showed clear uptake of [18F]FAZA in the primary tumour. The mean tumour SUVmax was 2.2±0.91 (range 1.12 - 3.71). The tumour SUVmax was significantly higher compared with muscle and bowel (t(5) =3.11, P=0.03), (t(5) =3.08, P=0.03), respectively. However, tumour SUVmean didn't differ significantly compared with muscle and bowel (t(5) =2.41 , P=0.06), (t(5) =2.46 , P=0.06) respectively. The mean tumour to muscle ratio (T/M) ratio was 1.89±0.64 (range 1.10 - 2.87), while the mean tumour to normal bowel (T/B) was 1.92±0.64 (range 1.08 - 2.74). However, [18F]FAZA did not accumulate in any of the tumours found in patients with GEC. Conclusions: [18F]FAZA PET/CT imaging is suitable and feasible for detecting CRC hypoxic tumour regions with image quality that can be used in clinical practice.
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Segara, Davendra St Vincents Hospital Clinical School UNSW. "Studies of retinoic acid signalling in pancreatic cancer." Awarded by:University of New South Wales. St Vincents Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/26269.

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Pancreatic cancer (PC) is the fourth leading cause of cancer death in Western societies. Despite significant progress in understanding the molecular pathology of PC and its precursor lesion: pancreatic intraepithelial neoplasia (PanIN), there remain no molecules with proven clinical utility. Affymetrix Genechipfi oligonucleotide microarrays were used to interrogate mRNA expression of PC and normal pancreas to identify molecular pathways dysregulated in PC. Analysis of these data identified altered expression of numerous components of the S100 Calcium Binding Protein Family, Retinoic Acid signalling pathway and the HOX transcriptional network in PC compared to normal pancreas. These pathways were assessed using immunohistochemistry (IHC) and in-situ hybridisation (ISH) in a cohort of patients with PC. Increased protein expression, of S100A2, S100A6 and S100P was observed in 43%, 60% and 48% of PC respectively. Expression of S100A2 was associated with a poor outcome (p = 0.009), whilst increased expression of S100A6 (p = 0.0008) and S100P (p = 0.0005) were associated with an improved outcome. Additionally, S100A2 expression was identified as an independent marker of outcome in resected tumours. Aberrant expression of retinoic acid signalling components was demonstrated in PC cell lines using semi-quantitative RT-PCR. ISH demonstrated expression of Retinoic Acid Induced 3 (RAI3), an orphan G protein coupled receptor normally expressed in the fetal lung, in 68% of PC, and this co-segregated with an improved overall survival (p = 0.026).Ectopic protein expression of HOXB2, a transcription factor normally expressed in the developing hindbrain and modulated by retinoic acid, was observed in 15% of early PanIN lesions and 38% of PC specimens. Expression of HOXB2 was associated with non-resectable tumours and was an independent predictor of poor survival in resected tumours. Suppression of HOXB2 protein expression using small interfering RNA, resulted in epithelioid trans-differentiation in the Panc-1 PC cell line, however no alteration in proliferation rates were observed compared to controls. This thesis has shown that transcript profiling and tissue validation has identified potential markers of early diagnosis and outcome in PC. Furthermore, pathways and molecules previously thought to be associated with normal human development have been implicated to play a role in the development and progression of PC. Further analyses of these markers will determine any potential role in future diagnostic and therapeutic strategies.
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McKernan, Margaret. "The relationship between quality of life (EORTC QLQ C-30) and survival and treatment in patients with gastro-oesophageal cancer." Connect to e-thesis, 2008. http://theses.gla.ac.uk/312/.

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Thesis (MSc(R)) - University of Glasgow, 2008.
Submitted to the University of Glasgow for the degree of Master of Science (Medical Science) in the Faculty of Medicine, 2008. Includes bibliographical references. Print version also available.
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Yip, Bon-ham, and 葉邦瀚. "Immunoglobulin gene translocations in gastric lymphoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37345321.

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Gutierrez, Orozco Fabiola. "Influence of tea catechins on the viability, IL-8 synthesis and secretion, and NF-[kappa]B activation of gastric epithelial AGS cancer cells." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1230670032.

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Tse, Tak-fong, and 謝德芳. "Role of RON activation on chemoresistance in gastric cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38592253.

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Ulander, Kerstin. "Assessments of well-being in caring of patients undergoing surgery for gastrointestinal cancer studies of nutrition, activities of daily living and health related quality of life /." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945119.html.

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Barnard, Desire. "Nucleotide sequence variation and expression levels of TP53 in cancers of the upper gastro-intestinal tract." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50046.

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Thesis (MSc)--Stellenbosch University, 2004.
ENGLISH ABSTRACT: The work presented in this thesis deals with the association between cancers of the upper gastro-intestinal tract and the tumor suppressor gene, TP53, and can be divided into three parts: (i) the analysis of the mutational spectrum of TP53 with respect to laryngeal cancer, (ii) the analysis of the mutational spectrum of TP53 with respect to esophageal cancer and (iii) the analysis of TP53 transcriptional levels in esophageal cancer. Laryngeal cancer (LC) is the 6th most common cancer in the world and the 2nd most common respiratory cancer, with approximately 500 000 new cases per annum detected worldwide. Over the last few years, LC has become increasingly prevalent within the Coloured Community of the Western Cape. The mechanisms of tumorigenesis in LC remain unknown, although smoking and alcohol consumption are considered to be major risk factors. Mutations within the gene TP53 have been strongly implicated as playing a role in cancer development, as they are frequently found in several cancer types. We therefore screened exons 5 - 8 of TP53 for mutations in DNA from tumor biopsies (n=44) and blood samples (n=42) from Coloured LC patients, using polymerase chain reaction - single strand conformation polymorphism (PCR-SSCP) analysis and direct sequencing. Blood samples from a healthy, matched control group (n=40) were included in the study as controls. Significant correlations were found between the occurrence of LC and age and smoking, whereas daily meat consumption was a possible protective factor. In tumor-derived samples, mutations were found in 3 of the exons under investigation, representing 25% of the samples. The mutations were unique to the tumor biopsies, indicating a somatic origin for mutations. The data confirms that the region between codons 175 and 273 of TP53 is a mutational hotspot for cancers in general. This study reports 6 novel mutations within this same region. Esophageal cancer (EC) has a very high incidence in South Africa, relative to the rest of the world, and is particularly common amongst the Black Transkei population. The goal of this study was to determine whether there are differences in the TP53 mutational pattern observed in the Coloured Western Cape community as compared to that observed in the Black Transkei community. This required the analysis of the molecular structure of TP53, specifically exons 5 - 8, in a group of Coloured EC patients (n=44) treated at Tygerberg Hospital, Cape Town, South Africa. DNA obtained from tumor biopsies and blood (from patients) as well as from apparently healthy surrounding tissue was screened via PCR-SSCP and direct sequencing analysis. Only 4 nucleotide changes were observed from a total of 124 sequences obtained, of which two were novel to esophageal squamous cell carcinoma. These 4 nucleotide alterations were found only within the tumor biopsy sample set, representing 9% of the tumors investigated. This study revealed that the mutational spectrum of TP53 within the Coloured population of the Western Cape greatly differs from that of the Black community of the Transkei. This suggests that a different set of etiological factors are involved in the tumorigenic process for each of these distinct geographical communities, which is the subject of an epidemiological study undertaken by the MRC. The final part of this thesis deals with the quantification and comparison of TP53 transcription levels in esophageal cancer tumor tissue to the TP53 levels in healthy esophageal tissue obtained from patients from a unique geographical and ethnic background. The cohort used in this study consisted of Coloured patients (n=2) treated at Tygerberg Hospital. The LightCycler system was implemented in order to try to accurately quantify TP53 mRNA levels. Unfortunately, the desired results were unattainable due to unforeseen difficulties encountered during the study. These difficulties included the insufficient preservation of samples for RNA based studies. Several recommendations were made concerning future similar studies, including an improved planning strategy as well as the employment of an RNA stabilizing agent. Additionally, a few important contributions were made through this study, including the design and optimization of TP53 primers specifically intended for future RNA studies. These primers would enable the identification of the presence of TP53 RNA species as well as the absence of DNA contamination in a single PCR amplification step. Other contributions include the development of a well-optimized RNA extraction method for the extraction of RNA from tough tissues (such as the human esophageal tissue used in this study). This method makes the extraction of large quantities of RNA from small amounts of tough tissue types possible. In conclusion, this study has made a significant contribution to the field of cancer research, by shedding light on the TP53 mutational spectrum with regards to laryngeal as well as esophageal cancer in a population unique to the Western Cape. The first part of this thesis has been published in Cancer Genetics and Cytogenetics (Barnard, D., K. Lehmann, E.G. Haal, P.O. van Heiden, and l.C. Victor. 2003. The spectrum of mutations in TP53 in laryngeal cancer patients from a high-incidence population shows similarities to many of the known mutational hotspots. Cancer Genetics and Cytogenetics 145:126-132), of which a copy can be found in Appendix I. This work has also been presented (by D. Barnard) at an international conference entitled "Cancer of the Esophagus and Gastric Cardia: From Gene to Cure", held in Amsterdam, the Netherlands during the period 13 - 15 December 2002.
AFRIKAANSE OPSOMMING: Die werk wat in hierdie tesis voorgelê word handel oor die assosiasie tussen kankers van die boonste gastrointestinale weg en die tumor suppressor geen, TP53, en kan in 3 dele gedeel word, (i) die analise van die mutasiespektrum van TP53 in laringiale kanker (LK), (ii) die analise van die mutasiespektrum van TP53 in slukderm kanker (SK) en (iii) die analise van die transkripsievlakke van TP53 in SK. Laringeal kanker (LK) is die 6de algemeenste kanker in die wêreld en die 2de algemeenste respiratoriese kanker, met "n benaderde 500 000 nuwe gevalle jaarliks wêreldwyd. Oor die afgelope paar jare het LK "n toenemende probleem geraak, veral in die Kleurling gemeenskap van die Wes Kaap. Die meganismes van die tumorvorming in LK is onbekend, alhoewel rook-en alkoholgebruik vername risiko faktore is. Die voorkoms van mutasies in TP53 is verskeie kere aangetoon in verskillende kanker tipes en daar word vermoed dat dit "n rol speel in tumorvorming. In hierdie studie is dus na mutasies in eksons 5 - 8 van TP53 gesoek in tumor biopsie weefsel (n=44) en bloed isolate (n=42) van Kleurling LK pasiënte d.m.v. polimerase ketting reaksie - enkelstring konformasie polimorfisme (PKR-ESKP) analisering en direkte volgorde bepaling. Bloed monsters van "n vergelykbare groep (n=40) is ook in die studie ingesluit as "n kontrole. Betekenisvolle positiewe korrelasies is gevind tussen die voorkoms van LK en ouderdom sowel as rook. Daarmee saam is daaglikse vleisinname as potensiële beskermende faktor gevind. In tumor biopsies is mutasies in 3 van die ondersoekte eksons gevind, wat 25% van die biopsie monsters verteenwoordig. Hierdie mutasies is uniek aan die tumor biopsie weefsels en dui op "n somatiese oorsprong van mutasies. Hierdie bevindinge bevestig dat die gedeelte tussen kodons 173 - 273 van TP53 "n hipermuteerbare gebied geassosieer met kankers is. Hierdie studie bevestig 6 nuwe mutasies. Daar is 'n hoë insidensie van slukderm kanker (SK) in Suid Afrika relatief tot die res van die wêreld. Hierdie soort kanker word veral gevind by die Swart populasie van die Transkei. Die doel van hierdie studie was om verskille tussen die TP53 mutasie patroon van die Kleurling gemeenskap van die Wes Kaap en die Swart gemeenskap van die Transkei te vergelyk. Hiervoor is die molekulêre struktuur van TP53, veral eksons 5 - 8, in 'n groep Kleurling SK pasiënte (n=42) wat behandel is by Tygerberg Hospitaal, Kaapstad, Suid Afrika, geanaliseer. Analisering is gedoen deur DNS van tumor, bloed en ook oënskynlike gesonde aangrensende weefsel van dieselfde pasiënte te onderwerp aan PKR-ESKP analise en direkte volgorde bepaling. Slegs 4 nukleotied veranderings is gevind in 124 volgorde bepalings, waarvan 2 nuwe veranderings is in SK. Hierdie 4 nukleotied veranderinge verteenwoordig 9% van al die tumors wat ondersoek is in die studie. Hierdie studie bewys dat die mutasiespektrum van TP53 in die Kleurling gemeenskap van die Wes Kaap grootliks verskil van die Swart gemeenskap van die Transkei. Dit impliseer dat verskillende etiologiese faktore moontlik 'n rol mag speel op die tumorvormingsproses in die 2 afsonderlike geografiese gemeenskappe. Hierdie is die onderwerp van 'n epidemiologiese studie wat deur die MNR onderneem word. Die laaste deel van hierdie tesis handel oor die kwantifisering en vergelyking van TP53 transkripsievlakke in SK tumor weefsel teenoor TP53 vlakke in gesonde slukderm weefsel van pasiënte in 'n unieke geografiese en etniese agtergrond. Die studie populasie in hierdie projek het bestaan uit Kleurling pasiënte (n=2) wat by Tygerberg hospitaal behandel is. Die "LightCycler" sisteem is gebruik vir die akkurate kwantifisering van TP53 boodskapper RNS vlakke. Ongelukkig is die verlangde resultate nie gekry nie as gevolg van onvoorsiene probleme wat ondervind is tydens die studie. Hierdie probleme sluit in die onvoldoende preserv RNS studies. Hierdie inleiers maak dit nou moontlik om die teenwoordigheid van TP53 RNS spesies sowel as die afwesigheid van DNS kontaminasie in een PKR amplifikasie stap te kan identifiseer. 'n Ander belangrike bydrae is die ontwikkeling van 'n goed geoptimaliseerde RNS ekstraksie metode vir moeilike starre weelfsel tipes (soos menslike slukderm weefsel in hierdie studie) en maak die ekstraksie van groot hoeveelhede RNS uit klein hoeveelhede van moeilik hanteerbare weefsel tipes moontlik. Om saam te vat, hierdie studie het betekenisvolle bydraes gemaak tot die veld van kankernavorsing deur die ontrafeling van die TP53 mutasiespektrum in beide laringeale sowel as slukderm kanker, in 'n populasie uniek aan die Wes Kaap. Die eerste deel van hierdie tesis is gepubliseer in Cancer Geneties and Cytogenetics (Barnard, D., K. Lehmann, E. G. Hoal, P. D. van Heiden, and T. C. Victor. 2003. The spectrum of mutations in TP53 in laryngeal cancer patients from a high-incidence population shows similarites to many of the known mutational hotspots. Cancer Genetics and Cytogenetics 145: 126-132) en 'n afskrif van die artikel is ingesluit in Appendix I. Hierdie werk is ook voorgedra (deur D. Barnard) by 'n internasionale kongres getiteld "Cancer of the Esophagus and Gastric Cardia: From Gene to Cure", wat in Amsterdam, Nederland gehou is gedurende 13 - 15 Desember 2002
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Books on the topic "Gastrointestinal system – Cancer"

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Al, Benson, ed. Gastrointestinal oncology. Boston: Kluwer Academic, 1998.

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Handbook of gastrointestinal cancer. Chichester, West Sussex: John Wiley & Sons, 2013.

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Hayat, M. A. Gastrointestinal Carcinoma. Dordrecht: Springer Netherlands, 2009.

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Abbruzzese, James L. Gastrointestinal oncology. New York: Oxford University Press, 2004.

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Evers, B. Mark. Molecular mechanisms in gastrointestinal cancer. Austin, Tex: R.G. Landes, 1999.

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Evers, B. Mark. Molecular mechanisms in gastrointestinal cancer. Austin, Tex: R.G. Landes, 1999.

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Markowitz, Sanford D. Energy Balance and Gastrointestinal Cancer. Boston, MA: Springer US, 2012.

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Gastrointestinal TNM cancer staging by endosonography. New York: Igaku-Shoin, 1995.

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Oxford American mini-handbook of gastrointestinal cancers. New York: Oxford University Press, 2011.

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Gastrointestinal endoscopy in the cancer patient. Chichester, West Sussex: Wiley-Blackwell, 2013.

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Book chapters on the topic "Gastrointestinal system – Cancer"

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Hodgson, Shirley V., William D. Foulkes, Charis Eng, and Eamonn R. Maher. "Gastrointestinal System." In A Practical Guide to Human Cancer Genetics, 47–87. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-2375-0_5.

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Valentini, M., R. Cannizzaro, F. Bortoluzzi, M. Sozzi, M. Fornasarig, and E. Bertolissi. "Gastrointestinal Damage by Cancer Chemotherapy." In Drug-Induced Injury to the Digestive System, 187–99. Milano: Springer Milan, 1993. http://dx.doi.org/10.1007/978-88-470-2220-1_12.

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Mayanagi, Shuhei, and Yuko Kitagawa. "Sentinel Node Navigation Surgery for Upper Gastrointestinal Cancer." In Cancer Metastasis Through the Lymphovascular System, 361–67. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-93084-4_33.

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Buchanan, K. D. "Effects of Sandostatin on Neuroendocrine Tumours of the Gastrointestinal System." In Recent Results in Cancer Research, 45–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84956-5_3.

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Yao, Kenshi, and Akinori Iwashita. "Diagnosis of Early Gastric Cancer: Endoscopic Diagnosis and Classification: VS Classification System for the Diagnosis of Early Gastric Cancer by Magnifying Endoscopy." In Endoscopy in Early Gastrointestinal Cancers, Volume 1, 43–55. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-10-6769-3_6.

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Mittal, B. R., Rahul Parghane, and J. Mohan Roop. "Application of PET and PET-CT in Cancer of the Gastrointestinal System." In Positron Emission Tomography, 113–22. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2098-5_13.

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Aikou, Takashi, Yuko Kitagawa, Yoshikazu Uenosono, Shoji Natsugoe, Anton J. Bilchik, and Naoto T. Ueno. "Gastrointestinal Cancer and the Lymphatic System: Patterns of Micrometastasis and Lymphatic Mapping with Clinical Outcome." In From Local Invasion to Metastatic Cancer, 29–43. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8_4.

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Kopp, Reinhard, Elisabeth Rothbauer, Maximilian Ruge, Hans Arnholdt, Joachim Spranger, M. Muders, Doris G. Pfeiffer, Friedrich Wilhelm Schildberg, and Andreas Pfeiffer. "Clinical Implications of the EGF Receptor/Ligand System for Tumor Progression and Survival in Gastrointestinal Carcinomas: Evidence for New Therapeutic Options." In Molecular Staging of Cancer, 115–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59349-9_10.

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Beyzadeoglu, Murat, Gokhan Ozyigit, Ugur Selek, and Ugur Selek. "Gastrointestinal System Cancers." In Radiation Oncology, 357–406. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27988-1_10.

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Hurmuz, Pervin, Gozde Yazici, Melis Gultekin, Sezin Yuce Sari, Mustafa Cengiz, and Gokhan Ozyigit. "Gastrointestinal System Cancers." In Radiation Oncology, 197–268. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97145-2_5.

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Conference papers on the topic "Gastrointestinal system – Cancer"

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Premasiri, Amaranath, Gemunu Happawana, Gary Evans, and Arye Rosen. "Design of a High Yielding Photonic Light Delivery System to be Used in Photodynamic Therapy for Esophageal Cancer, With Microwave Antenna Imprinted Balloon Catheter for Oxygen Enhancement." In ASME 2006 Frontiers in Biomedical Devices Conference. ASMEDC, 2006. http://dx.doi.org/10.1115/nanobio2006-18029.

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Photodynamic therapy (PDT) is a minimally invasive treatment with high effectiveness in the management of cancer of the upper gastrointestinal tract. A higher mortality rate associated with surgery and the higher morbidity in the older age group both make PDT a better treatment method for the treatment of esophageal cancer [1–3]. However, limitations in the best docimetry protocols performance of PDT are due to ineffectiveness of the light delivery and in the unavailability of sufficient oxygen required for singlet oxygen generation to bring cellular death [4–7]. The Introduction of an inexpensive high power semiconductor diode lasers for the light delivery system makes PDT efficient, low cost and portable [8–10]. However, the metallic water cooling systems used in the existing semiconductor cooling designs make those systems non-flexible and cumbersome in size [9].
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Mourant, Judith R., James D. Boyer, Tamara M. Johnson, JoAnne Lacey, Irving J. Bigio, Anthony G. Bohorfoush, and Mark H. Mellow. "Detection of gastrointestinal cancer by elastic scattering and absorption spectroscopies with the Los Alamos Optical Biopsy System." In Photonics West '95, edited by Robert R. Alfano. SPIE, 1995. http://dx.doi.org/10.1117/12.206824.

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Zeng, Haishan, Alan Weiss, Calum E. MacAulay, Nick MacKinnon, Richard W. Cline, and Remy Dawson. "Development of a fluorescence video endoscopy imaging system for the early detection of cancer in the gastrointestinal tract." In BiOS '97, Part of Photonics West, edited by Tuan Vo-Dinh, Robert A. Lieberman, Gerald G. Vurek, and Abraham Katzir. SPIE, 1997. http://dx.doi.org/10.1117/12.275550.

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Gupta, Sahil, Rasmi Palassery, Santhosh K. Devadas, Vinayak Maka, and Nalini Kilara. "Epidemiology of Adolescent and Young Adult Cancers in a Tertiary Hospital in South India." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735371.

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Abstract Introduction There has been an increase in the incidence of malignancies in young Indians, and there is no data reflecting the trend and profile of adolescent and young adult (AYA) cancers. Objectives This study was aimed to ascertain the epidemiology of AYA cancers in a tertiary care center in south India and the trend of AYA cancers during the past 9 years. Materials and Methods All patients aged 15 to 39 years with the diagnosis of cancer who were registered and received treatment with M.S. Ramaiah Hospital during a 9-year period from January 2011 to December 2019 were included. Basic demographic information on age, gender was available along with address and contact information. Using cancer site and morphology codes, the cancers were grouped by the ICD-O coding system of AYA cancers and their clinical information on disease and treatment status were collected retrospectively and analyzed. Results Of the total 946 registered AYA cancer patients, majority of AYA cancer were in age group of 35 to 39 years (39%) and females (58%). When analyzing the data and dividing the AYA population into early (15–24 years) and late (25–39 years), we found that whereas the majority of the patients had hematolymphoid malignancies (48%) in the early group (15–24 years), the late group (25–39 years) had more carcinomas (68%). The percentage distribution of AYA cancers among the study population, lymphoma and leukemia contribute 11% and 15%, respectively, to the patient load and still the carcinomas formed the bulk (58%) of the population. It is interesting to know that breast, genitourinary, and gastrointestinal (GI) malignancies constituted 17.75%, 14.16%, and 14.69% individually. Conclusion AYA oncology consists of a heterogeneous population and the profile differs by geography, sex, and other factors. There has been limited improvement in the past decade but there is a lot more to be done. To assess the problem, we have to identify and characterize the problem and look at the epidemiology of this population. This will require multicenter and international studies with focus on improving outcomes as in pediatric inspired ALL protocols. The trials should be started at local levels to ensure maximum participation. We need to generate data on epidemiology and channel our resources properly to save this precious but so called lost tribe of oncology.
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Schrock, Alexa B., Tzu-Hsiu Chen, Victor M. Rivera, and Joseph M. Gozgit. "Abstract B266: Ponatinib, a potent KIT inhibitor, suppresses the emergence of secondary resistance mutations in a gastrointestinal stromal tumor (GIST) model system." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b266.

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Nadeau, Valerie, Miles J. Padgett, Jacqueline Hewett, Wilson Sibbett, Khaled Hamdan, Sami Mohammed, Iain Tait, and Alfred Cushieri. "Compact endoscopic fluorescence detection system for gastrointestinal cancers." In BiOS 2001 The International Symposium on Biomedical Optics, edited by Thomas J. Dougherty. SPIE, 2001. http://dx.doi.org/10.1117/12.424440.

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Kandolf Sekulović, Lidija. "TOXICITIES OF TARGETED THERAPY AND IMMUNE-RELATED ADVERSE DRUG REACTIONS OF IMMUNOTHERAPY IN THE TREATMENT OF METASTATIC MELANOMA." In Okrugli sto s međunarodnim učešćem "Melanom". Akademija nauka i umjetnosti Bosne i Hercegovine, 2018. http://dx.doi.org/10.5644/pi2019.180.04.

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Targeted therapy and immunotherapy changed the treatment landscape for metastatic melanoma, which is chemotherapy resistant cancer. In pre-innovation era, the overall survival of patients with metastatic melanoma was 6 months, while today 5-year overall survival rate of 34% (and 50% in good prognostic groups) is evident. However, both treatments have their side effects, and cutaneous are the most frequent. Treating physicians in oncology centres, but also primary care specialists, need to be aware of their spectrum which differs for each class of drug: BRAF inhibitors, MEK inhibitors and immunotherapy with anti-PD1 and anti-CTLA4. While BRAF inhibitors have the most prominent adverse effects which are class specific, there are also drug-specific adverse effects. For example, vemurafenib causes photosensitivity, which is not specific for dabrafenib, while dabrafenib induces pyrexia, that occurs much less frequently with other BRAF inhibitors. Cutaneous rash and cutaneous neoplasms which develop due to paradoxical activation of RAS signalling are described with BRAF inhibitor monotherapy. These side-effects are much less common in combination therapy with BRAF and MEK inhibitor, but MEK inhibitor itself causes characteristic acneiform eruption, and serous retinopathy. Immune related adverse drug reactions are a hallmark of the immune checkpoint inhibitor immunotherapy, which can affect every organ system, and most commonly skin, lungs and gastrointestinal system, with differential frequencies recorded with anti-CTLA4 therapy and anti PD-1 therapy. Skin reactions most frequently include pruritus and eczematous reactions, as well as vitiligo-like hypopigmentation, which is linked Melanom 45 to the better response to treatment. In this review, frequent and rare side effects are presented, as well as the current algorithms for their treatment.
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Slawinski, Piotr R., Collin T. Garcia, Addisu Z. Taddese, Keith L. Obstein, and Pietro Valdastri. "Towards Recovering a Lost Degree of Freedom in Magnet-Driven Robotic Capsule Endoscopy." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3391.

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Flexible endoscopy, a procedure during which an operator pushes a semi-rigid endoscope through a patient’s gastrointestinal tract, has been the gold-standard screening method for colon cancer screening (colonoscopy) for over 50 years. Owing to the large amounts of tissue stress that result from the need for transmitting a force to the tip of the endoscope while the device wraps through the bowel, implementing a front-actuated endoscopy system has been a popular area of research [1]. The pursuit of such a concept was accelerated by the advent of ingestible capsule endoscopes, which, since then, have been augmented by researchers to include therapeutic capabilities, modalities for maneuverability, amongst other diagnostic functions [2]. One of the more common approaches investigated has been the use of magnetic fields to apply forces and torques to steer the tip of an endoscope [3]. Recent efforts in magnetic actuation have resulted in the use of robot manipulators with permanent magnets at their end effectors that are used to manipulate endoscopes with embedded permanent magnets. Recently, we implemented closed loop control of a tethered magnetic capsule by using real-time magnetic localization and the linearization of a magnetic wrench applied to the capsule by the actuating magnet [4]. This control was implemented in 2 degrees-of-freedom (DoF) in position (in the horizontal plane) and 2 DoF in orientation (panning and tilting). One DoF in position is lost owing to the tethered capsule being actuated in air and thus lacking a restoring force to counter the high field gradient. The 3rd orientation DoF is lost owing to the axial symmetry of the permanent magnet in the capsule; this prevents the application of torque in the axial direction and thus controlled roll and introduces a singularity in the capsule’s actuation. Although another dipole could be used to eliminate this singularity, this would complicate both the actuation and localization methods. In this manuscript, we consider the consequences of the embedded magnet (EM) being radially offset from the center of the capsule while being manipulated by an external actuating magnet (AM). We have developed a tethered capsule endoscope that contains a cylindrical EM (11.11 mm in length and diameter) with a residual flux density of 1.48 T that is offset by 1.85 mm from the center of the capsule; a distance that is less than 10% of the capsule diameter. Our investigation into the topic results from repeated observation of the capsule’s preference to align such that the internal magnet is closest to the actuating magnet (AM). The AM is a cylindrical magnet (101.6 mm in length and diameter) with a residual flux density of 1.48 T that is mounted at the end effector of a 6 DoF manipulator, as seen in Figure 1. In this manuscript, we evaluate the torqueing effects of the presence of this magnet offset with the goal of determining whether the torque effect is negligible, or impacts capsule motion and thus can potentially be used for the benefit of endoscope manipulation. A concept schematic of this effect is shown in Figure 2. A discussion of how to use this torque is beyond the scope of this manuscript. To the authors’ knowledge, the use of such concept in permanent-magnet based control has not been investigated.
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Nishikawa, Jun, Tsunemasa Taguchi, Yuji Uchida, Satoshi Kurai, Hideo Yanai, Shu Kiyotoki, Takeshi Okamoto, Shingo Higaki, and Isao Sakaida. "A novel imaging system of optical detection on cancers and tissues in gastrointestinal endoscope using high-color-rendering white and color tunable LEDs." In BiOS, edited by Guillermo J. Tearney and Thomas D. Wang. SPIE, 2010. http://dx.doi.org/10.1117/12.843386.

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Arora, Rahul D. "Definition, etiopathogenesis, management and role of flouroquinolone prophylaxis in prevention of spontaneous bacterial peritonitis complicating malignant ascites." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685345.

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Background: Malignancy related ascites encompasses multiple etiologies which include peritoneal carcinomatosis, hepatic synthetic dysfunction due to parenchymal involvement by the tumour, transcoeloemic metastasis and chylous ascites due to lymphatic obstruction. Primary Cancer type, liver metastasis and serum albumin have been listed as independent prognostic markers in malignant ascites. Spontaneous Bacterial Peritonitis is usually seen as a complication of decompensated chronic liver disease due to translocation of bacteria or haematogenous dissemination from a distant focus of infection. The combination of a positive peritoneal fluid culture and an ascitic fluid neutrophil count >250 cells/mm3 and no evidence of intra-abdominal source of infection; or 2) culture negative neutrocytic ascites: the combination of negative peritoneal fluid bacterial culture and neutrophil count >500 cells/mm3, without antibiotics within 7 days with no obvious source of infection are used to define spontaneous bacterialperitonitis. Ciprofloxacin prophylaxis has been proposed as a prophylaxis to reduce the incidence and prevent the recurrence of spontaneous bacterial peritonitis. Materials and Methods: A web search of indexed literature was carried out articles containing information on spontaneous bacterial peritonitis in the setting of malignancy or malignancy related ascites or malignant ascites. Articles that carried relevant information about etiopathogenesis, management and translational research in the context of malignant ascites were also included. Results: A total of 32 articles were analysed and about half of them included in the discussion to answer the research question. Discussion: Inflammatory cytokines released by tumor and immune cells compromise the mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach leading to formation of spheroids which imparts resistance to anoikis, apoptosis and chemotherapeutics leading to efficient feed forward progressive cycle of seeding and growth of peritoneal metastasis. Intraperitoneal metastasis can cause peritoneal dysfunction, adhesions and malignant ascites. Epithelial mesenchymal transistion and myofibroblastic transformation occur in the mesothelial cells in response to pathological stimuli. Vascular endothelial growth factor is an important mitogen for endothelial cells and plays an important role in increasing capillary vascular permeability. In preclinical studies systemic administration of VEGF Trap which acts as a decoy receptor for VEGF has shown to decrease the formation of ascites fluid and prevent tumour dissemination. Epithelial ovarian cancer cells have developed various mechanisms to evade immune surveillance like development of surface microvesicles which contain CD 95 ligand leading to apoptosis of immune cells. Higher levels of osteoproteogerin, IL 10 and leptin in the ascitic fluid have been associated with a poor prognosis in malignant ascites. Tethered bowel sign and presence of fluid in the omental bursa on CT have been shown to distinguish between malignant ascites and Cirrhotic ascites with accuracy. Immunological approaches to management of malignant ascites include use of intraperitoneal triamcinolone, interferon, long acting synthetic corticosteroids and the trifoliate antibody catumaxomab. VEGF Inhihibitors like octreotide and long acting depot preparations of lanreotide have also been shown to be feasible therapeutic options. Anti androgenic agents and PARP inhibitors have also been proposed as management options. Spontaneous bacterial peritonitis in the setting of malignancy in the absence of hepatic dysfunction has been reported to have a poorer prognosis than SBP in the setting of decompensated liver disease. Monomicrobial and polymicrobial bacterascites have been proposed in the absence of an elevated neutrophil ascitic fluid count that does not meet the diagnostic criteria. Extensive liver metastasis where the diseased liver can be expected to behave like a cirrhotic liver and gastrointestinal bleeding (on the basis of an isolated case report) have been considered as risk factors for the development of SBP in malignant ascites. In a case series of 8 patients with malignancy related ascites Patients with total ascitic fluid concentration of less than 1 gm per litre were found to be at risk for Spontaneous bacterial peritonitis and warrant flouroquinolone prophylaxis. Conclusion: Spontaneous Bacterial Peritonitis complicating malignant ascites is questionable entity. Good quality Audits and Randomised control trials are warranted to in this domain to enable the definition of incidence, antecedent complications, management and prophylaxis to ensure applicability of translational research to the clinical domain.
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Reports on the topic "Gastrointestinal system – Cancer"

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Newman-Toker, David E., Susan M. Peterson, Shervin Badihian, Ahmed Hassoon, Najlla Nassery, Donna Parizadeh, Lisa M. Wilson, et al. Diagnostic Errors in the Emergency Department: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2022. http://dx.doi.org/10.23970/ahrqepccer258.

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Objectives. Diagnostic errors are a known patient safety concern across all clinical settings, including the emergency department (ED). We conducted a systematic review to determine the most frequent diseases and clinical presentations associated with diagnostic errors (and resulting harms) in the ED, measure error and harm frequency, as well as assess causal factors. Methods. We searched PubMed®, Cumulative Index to Nursing and Allied Health Literature (CINAHL®), and Embase® from January 2000 through September 2021. We included research studies and targeted grey literature reporting diagnostic errors or misdiagnosis-related harms in EDs in the United States or other developed countries with ED care deemed comparable by a technical expert panel. We applied standard definitions for diagnostic errors, misdiagnosis-related harms (adverse events), and serious harms (permanent disability or death). Preventability was determined by original study authors or differences in harms across groups. Two reviewers independently screened search results for eligibility; serially extracted data regarding common diseases, error/harm rates, and causes/risk factors; and independently assessed risk of bias of included studies. We synthesized results for each question and extrapolated U.S. estimates. We present 95 percent confidence intervals (CIs) or plausible range (PR) bounds, as appropriate. Results. We identified 19,127 citations and included 279 studies. The top 15 clinical conditions associated with serious misdiagnosis-related harms (accounting for 68% [95% CI 66 to 71] of serious harms) were (1) stroke, (2) myocardial infarction, (3) aortic aneurysm and dissection, (4) spinal cord compression and injury, (5) venous thromboembolism, (6/7 – tie) meningitis and encephalitis, (6/7 – tie) sepsis, (8) lung cancer, (9) traumatic brain injury and traumatic intracranial hemorrhage, (10) arterial thromboembolism, (11) spinal and intracranial abscess, (12) cardiac arrhythmia, (13) pneumonia, (14) gastrointestinal perforation and rupture, and (15) intestinal obstruction. Average disease-specific error rates ranged from 1.5 percent (myocardial infarction) to 56 percent (spinal abscess), with additional variation by clinical presentation (e.g., missed stroke average 17%, but 4% for weakness and 40% for dizziness/vertigo). There was also wide, superimposed variation by hospital (e.g., missed myocardial infarction 0% to 29% across hospitals within a single study). An estimated 5.7 percent (95% CI 4.4 to 7.1) of all ED visits had at least one diagnostic error. Estimated preventable adverse event rates were as follows: any harm severity (2.0%, 95% CI 1.0 to 3.6), any serious harms (0.3%, PR 0.1 to 0.7), and deaths (0.2%, PR 0.1 to 0.4). While most disease-specific error rates derived from mainly U.S.-based studies, overall error and harm rates were derived from three prospective studies conducted outside the United States (in Canada, Spain, and Switzerland, with combined n=1,758). If overall rates are generalizable to all U.S. ED visits (130 million, 95% CI 116 to 144), this would translate to 7.4 million (PR 5.1 to 10.2) ED diagnostic errors annually; 2.6 million (PR 1.1 to 5.2) diagnostic adverse events with preventable harms; and 371,000 (PR 142,000 to 909,000) serious misdiagnosis-related harms, including more than 100,000 permanent, high-severity disabilities and 250,000 deaths. Although errors were often multifactorial, 89 percent (95% CI 88 to 90) of diagnostic error malpractice claims involved failures of clinical decision-making or judgment, regardless of the underlying disease present. Key process failures were errors in diagnostic assessment, test ordering, and test interpretation. Most often these were attributed to inadequate knowledge, skills, or reasoning, particularly in “atypical” or otherwise subtle case presentations. Limitations included use of malpractice claims and incident reports for distribution of diseases leading to serious harms, reliance on a small number of non-U.S. studies for overall (disease-agnostic) diagnostic error and harm rates, and methodologic variability across studies in measuring disease-specific rates, determining preventability, and assessing causal factors. Conclusions. Although estimated ED error rates are low (and comparable to those found in other clinical settings), the number of patients potentially impacted is large. Not all diagnostic errors or harms are preventable, but wide variability in diagnostic error rates across diseases, symptoms, and hospitals suggests improvement is possible. With 130 million U.S. ED visits, estimated rates for diagnostic error (5.7%), misdiagnosis-related harms (2.0%), and serious misdiagnosis-related harms (0.3%) could translate to more than 7 million errors, 2.5 million harms, and 350,000 patients suffering potentially preventable permanent disability or death. Over two-thirds of serious harms are attributable to just 15 diseases and linked to cognitive errors, particularly in cases with “atypical” manifestations. Scalable solutions to enhance bedside diagnostic processes are needed, and these should target the most commonly misdiagnosed clinical presentations of key diseases causing serious harms. New studies should confirm overall rates are representative of current U.S.-based ED practice and focus on identified evidence gaps (errors among common diseases with lower-severity harms, pediatric ED errors and harms, dynamic systems factors such as overcrowding, and false positives). Policy changes to consider based on this review include: (1) standardizing measurement and research results reporting to maximize comparability of measures of diagnostic error and misdiagnosis-related harms; (2) creating a National Diagnostic Performance Dashboard to track performance; and (3) using multiple policy levers (e.g., research funding, public accountability, payment reforms) to facilitate the rapid development and deployment of solutions to address this critically important patient safety concern.
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