Relevant bibliographies by topics / Esophageal cancer

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Academic literature on the topic 'Esophageal cancer'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 June 2024

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Journal articles on the topic "Esophageal cancer"

_, _. "Esophageal Cancer." Journal of the National Comprehensive Cancer Network 6, no. 9 (October 2008): 818. http://dx.doi.org/10.6004/jnccn.2008.0062.

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Upper gastrointestinal (GI) tract cancers originating in the esophagus, gastroesophageal (GE) junctions, and stomach constitute a major health problem worldwide; esophageal cancer is the eighth most common cancer worldwide. An estimated 16,470 new cases of and 14,280 deaths from esophageal cancer will occur in the United States in 2008. Risk factors associated with development of esophageal cancer include age, male gender, Caucasian race, high body mass index, Barrett's esophagus, and history of gastroesophageal reflux disease. Important updates for the 2009 guidelines include a new page on “Principles of Best Supportive Care” that gives specific recommendations for esophageal cancer best supportive care throughout the guidelines. To view the NCCN Clinical Practice Guidelines in Oncology on Gastric Cancers, please visit the NCCN Web site at www.nccn.org. For the most recent version of the guidelines, please visit NCCN.org

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Daigo, Yataro, Atsushi Takano, and Yusuke Nakamura. "Cancer genomics-based screening of new therapeutic targets and biomarkers for esophageal cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16514-e16514. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16514.

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e16514 Background: Since the number of esophageal cancer patients who show objective response to standard therapies is still small, development of new anti-cancer agents with minimum risk of adverse events and highly precise molecular biomarkers is eagerly awaited. Methods: We have been screening novel therapeutic targets and their companion diagnostics for esophageal cancers as follows; i) To identify up-regulated genes in esophageal cancers by the gene expression profile analysis, ii) To verify the candidate genes for their low expression in normal tissues, iii) To validate the clinicopathological significance of their protein expression by tissue microarray covering 265 esophageal cancers, and iv) To verify their function for the growth of the esophageal cancer cells by siRNAs and gene transfection assays. Results: We identified dozens of candidate oncoproteins and selected a metyltransferase ESOC1 (esophageal cancer-associated oncoprotein 1). Immunohistochemical analysis revealed that ESOC1 positivity was observed in 68.5% of esophageal cancers and associated with tumor size. Moreover ESOC1 expression was an independent prognostic factor for esophageal cancer patients. Suppression of ESOC1 expression by its siRNAs inhibited growth of esophageal cancer cell lines. Introduction of ESOC1 increased the growth activity of mammalian cells, suggesting that ESOC1 is likely to be a prognostic biomarker and therapeutic target for esophageal cancers. Conclusions: Cancer genomics-based approach could be useful for the development of new cancer biomarkers as well as therapeutic targets for small molecules, antibodies, nucleic acid drugs, and immunotherapies.

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Boku, N. "Esophageal Cancer: Esophageal Cancer Drug Therapy." Annals of Oncology 23 (October 2012): xi67. http://dx.doi.org/10.1016/s0923-7534(20)32119-0.

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Pih, Gyu Young, and Do Hoon Kim. "Metachronous Cancer Occurring after Endoscopic Resection of Superficial Esophageal Cancer." Korean Journal of Helicobacter and Upper Gastrointestinal Research 20, no. 4 (December 10, 2020): 288–94. http://dx.doi.org/10.7704/kjhugr.2020.0046.

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Esophageal cancer has a relatively high prevalence of local recurrence, which is associated with a poor prognosis. Superficial esophageal cancer has shown a metachronous recurrence rate of 2.6~35.8% with the cumulative overall 3-year and 5-year metachronous cancer incidence being 9.9~15.5% and 20.6~24.5%, respectively. In addition to recurrences in the remnant esophagus, second metachronous primary tumors have been reported to arise in 4.0~37.4% of esophageal cancer survivors. The second primary cancers arising after a diagnosis of esophageal cancer are most commonly detected in the head and neck area, followed by the lungs and stomach. The field cancerization theory explains the high prevalence of head and neck cancer among esophageal cancer patients. The reported risk factors for metachronous esophageal recurrences include scattered-type Lugol staining, circumferential endoscopic resection of the primary lesion, heavy alcohol use, smoking, inactive aldehyde dehydrogenase-2 genes, alcohol dehydrogenase-1B genes, and young age at diagnosis of the primary cancer. The risk factors for metachronous second primary tumors include heavy alcohol use, smoking, and a previous history of radiation therapy. Consequently, periodic follow-up endoscopy using narrow-band imaging is essential for the screening of metachronous esophageal cancers and second primary tumors after endoscopic resection for superficial esophageal cancer.

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Tétreault, Marie-Pier. "Esophageal Cancer: Insights from Mouse Models." Cancer Growth and Metastasis 8s1 (January 2015): CGM.S21218. http://dx.doi.org/10.4137/cgm.s21218.

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Esophageal cancer is the eighth leading cause of cancer and the sixth most common cause of cancer-related death worldwide. Despite recent advances in the development of surgical techniques in combination with the use of radiotherapy and chemotherapy, the prognosis for esophageal cancer remains poor. The cellular and molecular mechanisms that drive the pathogenesis of esophageal cancer are still poorly understood. Hence, understanding these mechanisms is crucial to improving outcomes for patients with esophageal cancer. Mouse models constitute valuable tools for modeling human cancers and for the preclinical testing of therapeutic strategies in a manner not possible in human subjects. Mice are excellent models for studying human cancers because they are similar to humans at the physiological and molecular levels and because they have a shorter gestation time and life cycle. Moreover, a wide range of well-developed technologies for introducing genetic modifications into mice are currently available. In this review, we describe how different mouse models are used to study esophageal cancer.

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Flashner, Samuel, Kelley S. Yan, and Hiroshi Nakagawa. "3D Organoids: An Untapped Platform for Studying Host–Microbiome Interactions in Esophageal Cancers." Microorganisms 9, no. 11 (October 20, 2021): 2182. http://dx.doi.org/10.3390/microorganisms9112182.

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The microbiome is an emerging key co-factor in the development of esophageal cancer, the sixth leading cause of cancer death worldwide. However, there is a paucity of data delineating how the microbiome contributes to the pathobiology of the two histological subtypes of esophageal cancer: esophageal squamous cell carcinoma and esophageal adenocarcinoma. This critical knowledge gap is partially due to inadequate modeling of host–microbiome interactions in the etiology of esophageal cancers. Recent advances have enabled progress in this field. Three dimensional (3D) organoids faithfully recapitulate the structure and function of the normal, preneoplastic, and neoplastic epithelia of the esophagus ex vivo and serve as a platform translatable for applications in precision medicine. Elsewhere in the gastrointestinal (GI) tract, the co-culture of 3D organoids with the bacterial microbiome has fostered insight into the pathogenic role of the microbiome in other GI cancers. Herein, we will summarize our current understanding of the relationship between the microbiome and esophageal cancer, discuss 3D organoid models of esophageal homeostasis, review analogous models of host–microbiome interactions in other GI cancers, and advocate for the application of these models to esophageal cancers. Together, we present a promising, novel approach with the potential to ameliorate the burden of esophageal cancer-related morbidity and mortality via improved prevention and therapeutic interventions.

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Betancourt-Cuellar, Sonia L., Marcelo F. K. Benveniste, Diana P. Palacio, and Wayne L. Hofstetter. "Esophageal Cancer." Radiologic Clinics of North America 59, no. 2 (March 2021): 219–29. http://dx.doi.org/10.1016/j.rcl.2020.11.008.

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Harris, Christopher, Beth Croce, and Stine Munkholm-Larsen. "Esophageal cancer." Annals of Cardiothoracic Surgery 6, no. 2 (March 2017): 190. http://dx.doi.org/10.21037/acs.2017.03.01.

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Levine, Marc S. "ESOPHAGEAL CANCER." Radiologic Clinics of North America 35, no. 2 (March 1997): 265–79. http://dx.doi.org/10.1016/s0033-8389(22)00707-2.

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Saunders, H. Stuart, Neil T. Wolfman, and David J. Ott. "ESOPHAGEAL CANCER." Radiologic Clinics of North America 35, no. 2 (March 1997): 281–94. http://dx.doi.org/10.1016/s0033-8389(22)00708-4.

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Dissertations / Theses on the topic "Esophageal cancer"

Takala, H. (Heikki). "Biomarkers in esophageal cancer." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789514298400.

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Abstract Mediators of epithelial permeability, angiogenesis and invasion may serve as prognostic indicators and targets for therapies in esophageal cancer (EC). The expressions of claudins, hypoxia inducible factor-1α (HIF-1α), vascular endothelial growth factor-A (VEGF), nitric oxide synthases (iNOS, eNOS, nNOS) and toll-like receptor 9 (TLR9) were evaluated by immunohistochemistry in EC. The results were compared with clinicopathological variables, tumor proliferation and apoptosis. All of the claudins were expressed in most of the cancers. Esophageal adenocarcinomas (EAC) displayed more often increased claudin 3 and 5 expression than esophageal squamous cell carcinomas (ESCC). Loss of claudin 3 expression associated with distant metastases in EC and a tendency in this direction was also observed for claudin 4. Cancers with stronger claudin 4 expression showed increased apoptosis in both EAC and ESCC. HIF-1α was present in most of the ECs and like iNOS more often in ESCC than in EAC. Strong HIF-1α expression tended to associate with positive VEGF immunostaining. In ESCC, both strong HIF-1α expression and VEGF positivity tended to associate with increased microvessel density (MVD). In EAC, tumors showing VEGF positivity associated with increased MVD outside the tumor. Patients with strong HIF-1α expression had more often distant metastases than other patients in EC. There was no VEGF expression in normal esophageal mucosa and T3-4 tumors tended to be more often VEGF positive than T1-2 tumors. The expression of TLR9 was more intensive in dysplasia than in normal epithelium and ESCC and abundant TLR9 expression could serve as a marker of squamous cell high grade dysplasia. Intensive TLR9 expression was associated with higher grade tumors and the presence of nodal and distant metastases in ESCC. EC and its progression may be related to increased angiogenesis regulated by VEGF and HIF-1α. In EC, claudin expression varies along with the histology of the tumor. Claudin expression may be associated with apoptosis or proliferation and contribute to tumor behavior. An association was detected between moderate to strong expression of claudin 3 and a high TLR9 histoscore in ESCC. Altered expression of claudin 3 may result to upregulation of endosomal TLR9. TLR9 may serve as a marker for squamous cell dysplasia and ESCC progression
Tiivistelmä Solukerrosten läpäisevyyttä, verisuonten uudismuodostusta ja kasvainsolujen liikkuvuutta säätelevät tekijät voivat toimia ruokatorvisyövän ennustetekijöinä ja hoidon kohteina. Tässä tutkimuksessa selvitettiin klaudiinien, hypoksia-indusoituvan tekijän 1α (HIF-1α), verisuonen endoteelin kasvutekijän A (VEGF), kolmen typpioksidisyntaasin (iNOS, eNOS ja nNOS) sekä tollin kaltaisen reseptorin 9 (TLR9) ilmentymistä ja merkitystä ruokatorvisyövässä immunohistokemiallisin menetelmin. Tuloksia arvioitiin suhteessa proliferaatioon ja apoptoosiin. Useimmat syöpäkasvaimet ilmensivät jokaista tutkittua klaudiinia. Ruokatorven rauhassyövässä ilmeni levyepiteelisyöpää useammin klaudiineja 3 ja 5. Klaudiinin 3 vähäinen ilmentyminen oli yhteydessä etäpesäkkeiseen tautiin. Sama suuntaus näkyi klaudiinin 4 kohdalla. Apoptoosia todettiin enemmän kasvaimissa, jotka ilmensivät muita enemmän klaudiini 4:ä. Useimmat syöpäkasvaimet ilmensivät HIF-1α:a. Sekä iNOS että HIF-1α ilmentyivät runsaammin levyepiteeli- kuin rauhassyövässä. Tutkimus viittasi yhteyteen voimakkaan HIF-1α:n ilmentymisen ja VEGF:n ilmentymisen välillä. Voimakas HIF-1α:n ilmentyminen ja VEGF:n ilmentyminen vaikuttivat liittyvän ruokatorven levyepiteelisyövän uudissuonituksen lisääntymiseen. Rauhassyövän lisääntynyt uudissuonitus kasvaimen ulkopuolella saattaa liittyä VEGF:n ilmentymiseen. Potilailla, joiden kasvaimissa HIF-1α:n ilmentyminen oli voimakasta, todettiin etäpesäkkeitä muita useammin. VEGF:a ei todettu normaalissa limakalvossa, ja sen ilmentyminen vaikutti olevan yleisempää syvälle kasvavissa kuin pinnallisissa syövissä. TLR9 ilmentyi voimakkaammin levyepiteelin dysplasiassa kuin normaalissa tai kasvainepiteelissä. Huonosti erilaistuvissa ja levinneissä kasvaimissa TLR9 ilmentyi voimakkaammin kuin muissa kasvaimissa. Ruokatorvisyövän synty ja eteneminen voivat liittyä HIF:n ja VEGF:n säätelemään verisuonten uudismuodostukseen. Klaudiinit saattavat vaikuttaa syövän käyttäytymiseen myös apoptoosin ja proliferaation kautta. Tutkimuksessa todettiin yhteys lisääntyneen klaudiinin 3 ilmentymisen ja voimakkaasti ilmentyvän TLR9:n välillä. Muutos klaudiinin 3 ilmentymisessä saattaa lisätä levyepiteelin läpäisevyyttä johtaen TLR9:n aktivoitumiseen. TLR9 voi vaikuttaa ruokatorven levyepiteelin dysplasian ja syövän syntyyn sekä toimia vaikean dysplasian ja aggressiivisen levyepiteelisyövän merkkiaineena

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Chan, Pui-man Poemen. "Micrometastases of esophageal cancer /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36404652.

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Chan, Pui-man Poemen, and 陳培文. "Micrometastases of esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45012842.

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Rouvelas, Ioannis. "Esophageal cancer surgery - factors influencing survival /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-004-6/.

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Viklund, Pernilla. "Quality of life after esophageal cancer surgery /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-685-9/.

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Leung, Chi Chung. "Study of a candidate tumor suppressor gene on 9q32, deleted in esophageal cancer 1 (DEC1), in esophageal cancer /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20LEUNG.

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Stockeld, Dag. "Esophageal cancer : evaluation of some new strategies /." Stockholm : Karolinska institutet, 2002. http://diss.kib.ki.se/2002/91-7349-147-0.

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Fernandes, Elisabete Cristina Nunes. "Humoral responses against esophageal cancer-associated glycosylation." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/11301.

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Mestrado em Bioquímica Clínica
O cancro de esófago (CE) tem um mau prognóstico e uma baixa taxa de sobrevivência. É diagnosticado tardiamente, por endoscopia, um método invasivo que carece de especificidade e sensibilidade. Atualmente, não existem biomarcadores para melhorar a precisão do diagnóstico. A transformação maligna é acompanhada por alterações no padrão de glicosilação das células, que são utilizadas no diagnóstico não-invasivo, monitorização da doença, bem como terapêutica. Além disso, as proteínas exibindo glicosilação alterada são capazes de induzir respostas humorais. Os auto-anticorpos são uma nova geração de biomarcadores tumorais, com capacidade de amplificar alterações moleculares nos tumores. São ainda mais resistentes a proteólise o que os correspondentes epitopos. No entanto, pouco se sabe sobre a glicosilação em CE e a sua imunogenicidade. Assim, a primeira parte deste trabalho teve como objetivo identificar padrões de glicosilação no soro de doentes com CE por slot blotting. Foram considerados para este estudo os cinco antigénios tumorais Tn, sTn, T, sLea, e sLex. Verificou-se que os níveis de Tn, sTn, e do sLea estavam aumentados no soro de pacientes com EC, em comparação com um grupo de controlo, comparável em idade e género, sem doença maligna conhecida. A combinação dos antígenos Tn e sTn permitiu uma melhor discriminação entre CE e os controlos (sensibilidade de 93,8% e especificidade de 100%). A expressão destes antigénios nos tecidos de CE correspondentes, estimada por imuno-histoquímica, mostrou uma falta de correlação com as observações feitas no soro. Os dados sugerem que os padrões de glicosilação do soro são maioritariamente influenciados por proteínas não directamente secretadas ou libertadas por células tumorais, apesar de a sua contribuição não poder ser excluída. A segunda parte do trabalho visou identificar respostas humorais contra proteínas que transportam o sLea, um biomarcador associado à glicosilação com maior potencial de migração celular e metástase. A análise do perfil de IgG das amostras apresentou uma expressão aumentada de uma subclasse (IgG1) nos doentes com CE. As IgG1 produzidas de novo por indução tumoral demonstraram possuir sLea na sua estrutura, contribuindo assim para o aumento dos níveis deste antigénio no soro de doentes com EC. Ainda que os mecanismos biológicos por detrás deste evento não sejam ainda conhecidos, isso poderá permitir melhorar a sensibilidade e especificidade do teste sorológico de sLea (teste de CA19-9). Usando uma combinação de técnicas de immunoprecipiações e de Western blotting, foi ainda demonstrado, pela primeira vez, que as proteínas tumorais que transportam sLea podem induzir a produção de IgG1. A remoção do ácido siálico confirmou que a expressão de sLea era determinante para o reconhecimento de IgG1. Estas observações, bem como a identificação futura de proteínas imunogénicas transportadoras de sLea, prmitirão determinar o seu valor clínico e poderão ser um ponto de partida para o desenvolvimento de testes serológicos baseados em autoanticorpos. Em suma, eviências importantes foram encontradas com este estudo, que permitirão o desenvolvimento de testes serológicos não invasivos para a detecção de CE
Esophageal cancer (EC) has an extremely poor prognosis and decreased overall survival. It is generally diagnosed at a late stage, by endoscopy, which is invasive and lacks both specificity and sensitivity. At the moment, there are no biomarkers to improve the accuracy of diagnosis. The modification of cell glycosylation patterns is a recognized hallmark of cancer, explored in non-invasive diagnostic, therapeutic decision, disease monitoring as well as therapeutics. Moreover, abnormally glycosylated proteins have been proven capable of eliciting humoral responses. Autoantibodies are regarded as the new generation of tumor biomarkers, cable to amplifying events occurring in tumors and showing higher stability to proteolysis. Nevertheless, little is known about EC associated glycosylation nor and its immunogenicity. Based on these considerations, the first part of this work aimed to identify glycosylation patterns in serum associated with EC. Tn, sTn, T, sale, and sLex, the most studied tumors-associated carbohydrate antigens, were screened by slot blotting. The levels of Tn, sTn, and sLea antigens were found significantly increased in the serum of EC patients, when compared to a control group of matched age and gender, without known malignancy. Moreover, the combination of the Tn and sTn antigens allowed the best discrimination between EC and controls (93.8% sensitivity and 100% specificity). Still, the expression of these antigens in the corresponding EC tissues, estimated by immunohistochemistry, showed a lack of correlation with the observations made in serum. Data suggests that glycosylation patterns of serum are mostly influenced by proteins that are not directly secreted or released from tumor cells, even though their contribution cannot be excluded. The second part of the work aimed to identify humoral responses against proteins carrying the sLea, a glycosylated biomarker associated with increased potential of cellular migration and metastasis. The analysis of the IgG profile of the samples showed increased expression of IgG subclasse 1 (IgG1) in EC patients. De novo produced IgG1 were found to carry sLea, accounting for the increase in the levels of this glycan in the serum of EC patients. Even though the biological events underlying these observations remain to be clarified, this may allow improving the sensibility and specificity of the serological test for sLea (CA19-9 test). Using a combination of immunoprecipiations and western blotting techniques it was further demonstrated, for the first time, that tumor proteins carrying sLea could elicit IgG1 production. Furthermore, experiments using desialylated proteins confirmed that the expression of sLea expression was determinant for IgG1 recognition. These observations and the future identification of the immunogenic proteins carrying sLea will allow determining the clinical value of this explorative work and guiding the development of autoantibody-based serological tests. Altogether, important insights have been provided to guide the development of non-invasive serological tests for the detection of EC.

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Gallerani, Giulia <1986&gt. "Circulating Tumor Cells Investigation in Esophageal Cancer." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/7343/1/gallerani_giulia_tesi.pdf.

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Background: An increasing number of studies have established that circulating tumor cells (CTCs) are a heterogeneous population in which cells have different degrees of metastatic potential mainly due to epithelial-mesenchymal transition (EMT). This study aimed to assess the feasibility of circulating esophageal cancer cells identification, characterization and to evaluate their prognostic value in esophageal cancer Methods: In order to closely mimic CTC heterogeneity, MC10A and HMEL cell lines differently forced in EMT are used. Single cell analysis was conducted by DEPArray. We assigned a specific phenotypic tag to each potential CTC population: Epithelial-tag, Mesenchymal/stem-tag. We evaluated the basal cell phenotype and after EMT induction. Subsequently, the Grab all assay was performed on peripheral blood samples from patients with esophageal cancer. This feasibility study enrolled 11 patients (4 M1, 7 M0). Analyses were conducted on 3 peripheral blood samples (15/20 ml) per patients. Blood samples from non-metastatic patients were taken before and after primary neo-adjuvant therapy and after secondary treatment (surgery). Samples from metastatic patients were taken before and after first line therapy and after second line therapy. CTCs were identified and sorted singly by DEPArray system. Results: The assay was able to detect the phenotypic changes in cell lines mimicking CTC heterogeneity. Before therapy, CTCs were found in 3/4 metastatic patients. Of the 7 non-metastatic patients, 3 were positive for CTCs before therapy. Examining CTC status at different clinical time points, it was possible to suggest a correlation between the presence of CTCs and disease progression. Conclusions: Data showed that the assay is feasible, capable to analyze the phenotypic tags by DEPArray using a multiple staining without aspecific signals. Experiments carried out from both metastatic/non metastatic cancer patients showed the ability of the Grab-allassay to identify subpopulations of CTCs with different epithelial/stem/mesenchymal or hybrid phenotypes potentially related to disease progression.

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Gallerani, Giulia <1986&gt. "Circulating Tumor Cells Investigation in Esophageal Cancer." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/7343/.

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Books on the topic "Esophageal cancer"

Schlottmann, Francisco, Daniela Molena, and Marco G. Patti, eds. Esophageal Cancer. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91830-3.

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Saba, Nabil F., and Bassel F. El-Rayes, eds. Esophageal Cancer. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20068-2.

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Saba, Nabil F., and Bassel F. El-Rayes, eds. Esophageal Cancer. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-29832-6.

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C, Delarue Norman, Wilkins Earle W. 1919-, and Wong John M. D, eds. Esophageal cancer. St. Louis: Mosby, 1988.

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Eslick, Guy D. Esophageal cancer. Philadelphia, Pa., [etc.]: Saunders, 2009.

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Schlottmann, Francisco, Lorenzo Ferri, Daniela Molena, and Marco G. Patti, eds. Esophageal Cancer. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-39086-9.

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Sharma, Prateek, Richard Sampliner, and David Ilson, eds. Esophageal cancer and barrett's esophagus. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118655153.

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A, Jobe Blair, Thomas Charles R. 1957-, and Hunter John G, eds. Esophageal cancer: Principles and practice. New York: Demos Medical Pub., 2009.

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Casson, Alan G. Oncogene activation in esophageal cancer. Austin: R.G. Landes Co., 1992.

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Eslick, Guy D. Esophageal cancer: Epidemiology, diagnosis, and treatment. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Book chapters on the topic "Esophageal cancer"

Smith, Michael S., and Charles J. Lightdale. "Esophageal Cancer." In Practical Gastroenterology and Hepatology: Esophagus and Stomach, 315–24. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444327311.ch42.

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Yasuda, Shigeo. "Esophageal Cancer." In Carbon-Ion Radiotherapy, 197–201. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54457-9_23.

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Devaud, Nicolas, Vaibhav Gupta, Eran Shlomovitz, Jonathan C. Yeung, Michael Ko, and Gail Darling. "Esophageal Cancer." In Surgical Oncology Manual, 163–81. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48363-0_9.

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Yu, Yao, Hans T. Chung, and Mekhail Anwar. "Esophageal Cancer." In Handbook of Evidence-Based Radiation Oncology, 403–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_18.

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Zimmermann, Frank B. "Esophageal Cancer." In Target Volume Definition in Radiation Oncology, 149–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45934-8_8.

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Granov, Anatoliy, Leonid Tiutin, and Thomas Schwarz. "Esophageal Cancer." In Positron Emission Tomography, 89–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21120-1_6.

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Kornblum, Noah. "Esophageal Cancer." In Geriatric Gastroenterology, 571–79. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-1623-5_61.

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Natale, Di Martino, and Monaco Luigi. "Esophageal Cancer." In Surgical Management of Elderly Patients, 161–78. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-60861-7_10.

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Boshier, P. R., A. Wirsching, and Donald E. Low. "Esophageal Cancer." In A Mastery Approach to Complex Esophageal Diseases, 165–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75795-7_13.

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Chuy, Jennifer, and Noah Kornblum. "Esophageal Cancer." In Geriatric Gastroenterology, 1–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-90761-1_78-1.

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Conference papers on the topic "Esophageal cancer"

Nolte, David, Dawith Lim, Zhen Hua, and John Turek. "Coherence-Gated Digital Holography for Personalized Cancer Care." In Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/dh.2023.hm1c.2.

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Low-coherence digital holography of patient cancer biopsies shows promise as a method to select personalized chemotherapy. We review the status of current clinical trials of biodynamic imaging in human esophageal and triple-negative breast cancer.

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Hsu, Lun-Chen, Wen-Ding Huang, Shou-Jiang Tang, Stuart Spechler, H. F. Tibbals, and J. C. Chiao. "Nanofabricated Sensing Electrodes in a Batteryless Endoluminal Sensing Telemeter for Diagnosis of Gastroesophageal Reflux Disease (GERD)." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13313.

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Gastroesophageal reflux disease (GERD) is recognized the primary risk factor associated with esophageal cancers. Therefore, monitoring GERD symptoms accurately is important for early diagnosis of such cancers. In this work, interdigitated impedance sensing electrodes and nanofabricated IrOx-based pH sensing electrodes were made on the flexible substrates that can be easily embedded into an implantable device. The dual sensor electrodes were integrated into a batteryless wireless capsule packaged with biocompatible material for implant applications. The proposed sensing system has been tested with stimulated solutions of different pH values recording modulated sensor data in terms of frequency shifts to verify its performance. The experimental results showed that the impedance electrodes responded to ion content variations and the pH electrodes identified the pH values of various pH solutions. Our sensing system has demonstrated the ability to detect gastroesophageal reflux activities more accurately, which could help doctors to provide precise treatment methods, consequentially lowering the risks of esophageal cancer development.

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van der Bogt, RD, BJ van der Wilk, S. Nikkessen, KK Krishnadath, EJ Schoon, LE Oostenbrug, PD Siersema, FP Vleggaar, JJB van Lanschot, and MCW Spaander. "PREDICTIVE VALUE OF ENDOSCOPIC ESOPHAGEAL ABNORMALITIES FOR RESIDUAL ESOPHAGEAL CANCER AFTER NEOADJUVANT CHEMORADIOTHERAPY." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1704483.

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Janse, Markus H. A., Fons van der Sommen, Svitlana Zinger, Erik J. Schoon, and Peter H. N. de With. "Early esophageal cancer detection using RF classifiers." In SPIE Medical Imaging, edited by Georgia D. Tourassi and Samuel G. Armato. SPIE, 2016. http://dx.doi.org/10.1117/12.2208583.

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Panjehpour, Masoud, Bergein F. Overholt, Tuan Vo-Dinh, Christie Farris, James L. Schmidhammer, Rick E. Sneed, and Paul F. Buckley III. "Fluorescence spectroscopy for diagnosis of esophageal cancer." In OE/LASE '94, edited by Thomas J. Dougherty. SPIE, 1994. http://dx.doi.org/10.1117/12.179982.

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Al-Mayahi, Noor N., and Faisel G. Mohammed. "Esophageal cancer segmentation based on FCM algorithm." In 2ND INTERNATIONAL CONFERENCE FOR ENGINEERING SCIENCES AND INFORMATION TECHNOLOGY (ESIT 2022): ESIT2022 Conference Proceedings. AIP Publishing, 2024. http://dx.doi.org/10.1063/5.0185313.

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van der Sommen, Fons, Svitlana Zinger, Erik J. Schoon, and Peter H. N. de With. "Sweet-spot training for early esophageal cancer detection." In SPIE Medical Imaging, edited by Georgia D. Tourassi and Samuel G. Armato. SPIE, 2016. http://dx.doi.org/10.1117/12.2208114.

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Stranadko, E., V. Shabarov, M. Riabov, and V. Duvansky. "PHOTODYNAMIC THERAPY IN THE TREATMENT OF ESOPHAGEAL CANCER." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1704357.

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Trowers, Eugene A. "Endoscopic ultrasonography in the management of esophageal cancer." In BiOS 2000 The International Symposium on Biomedical Optics, edited by R. Rox Anderson, Kenneth E. Bartels, Lawrence S. Bass, C. Gaelyn Garrett, Kenton W. Gregory, Nikiforos Kollias, Harvey Lui, et al. SPIE, 2000. http://dx.doi.org/10.1117/12.386277.

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Fernandes, V., J. P. Pereira, T. M. Alfaro, A. J. Ferreira, and C. R. Cordeiro. "Flexible bronchoscopy and the prognosis of esophageal cancer." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1582.

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Reports on the topic "Esophageal cancer"

Li, Rongyang, Zheng Ma, and Jianhao Qiu. Prognostic and clinicopathological significance of pretreatment systemic immune-inflammation index in esophageal cancer: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0024.

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Review question / Objective: We performed this systematic review and meta-analysis to investigate the prognostic value of pretreatment systemic immune-inflammation index (SII) in esophageal cancer patients and the association between SII and the clinicopathological features of esophageal cancer. Eligibility criteria: (I) involved patients diagnosed with EC histopathologically; (II) hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) for pretreatment SII and survival outcomes were reported, or the correlation between SII and clinicopathological characteristics of EC was stated; (III) SII was calculated by the following formula: platelet count × neutrophil count/lymphocyte count; and (IV) a definite cut-off value of pretreatment SII was available to divide the patients into high or low SII group.

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Yu, Guocan, Wenfeng Yu, Xudong Xu, Bo Ye, and Kan Xu. Neoadjuvant immunotherapy for resectable esophageal cancer: A protocol of meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2021. http://dx.doi.org/10.37766/inplasy2021.2.0026.

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Liu, Ben, Zeyuan Liu, Xiaojie Xia, Shu Liu, Yuting Zeng, Yu Cheng, Xiaolin Ge, and Xinchen Sun. Prognostic value of nutritional risk index in patients with esophageal cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0038.

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Wang, Qing, Zi-Xu Wang, Nasu M. Otomi, and Shinji Mine. Association between cutoffs for classifying high- and low-volume hospitals and long-term survival after eophagectomy: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0023.

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Review question / Objective: It is still unclear about the association between cutoffs for classifying high- and low-volume hospitals and long-term survival after esophagectomy for patients with esophageal cancer. Condition being studied: It remains controversial whether size of hospital volume influences long-term survival outcomes for patients with esophageal cancer after esophagectomy. In addition, there is still no consensus for defining a reasonable cutoff of esophagectomies per year for classifying high- and low-volume hospitals. Information sources: After the retrieval of the relevant articles, they were screened to remove the duplicates. Search results were screened by two authors (Q.W. and Z.X.W.) independently according to the titles and abstracts. Next, the retained studies were searched for their full text and further were screened according to the following criteria: surgery for esophageal carcinoma as the theme; primary outcomes included hospital volume and long-term OS; comparison of OS between high- and low-volume hospitals; original articles with informative data; articles reporting adjusted hazard ratios (HRs) in multi-variate analysis; and articles in which procedural volume was an exact cutoff. Any disagreements were resolved through consultation with the third author.

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Qain, Jiekun, Zhangwei Tong, Yannan Zhang, and Chun Chen. Platinum vs immunotherapy for unresectable esophageal cancer: a systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2020. http://dx.doi.org/10.37766/inplasy2020.11.0012.

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Zhao, Chun-Lei, Bing Gu, Xiao-Bing Huo, and Feng-Fei Xia. I-125 seeds-loaded versus normal stent insertion for obstructive esophageal cancer: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0138.

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Li, Binfeng, Fei Xiong, Shengzhong Yi, and Sheng Wang. Prognostic and Clinicopathologic Significance of Neutrophil-to-lymphocyte Ratio in Esophageal Cancer: An Update Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0111.

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Lu, Jiaying, Na Li, Ji Ma, Nan Yao, and Yuanhu Yao. High-dose versus standard-dose radiotherapy in concurrent chemoradiotherapy for inoperable esophageal cancer: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0045.

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Wang, He, Jun Chen, Xiaoling Wang, and Jun Dang. Neoadjuvant immune checkpoint inhibitor in combination with chemotherapy or chemoradiotherapy in resectable esophageal cancer: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0052.

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Review question / Objective: It remains unclear whether addition of immune checkpoint inhibitor (ICI) to neoadjuvant chemoradiotherapy (nCRT) or neoadjuvant chemotherapy (nCT) can increase antitumor efficacy in resectable esophageal cancer (EC). we performed the systematic review and meta-analysis to assess antitumor efficacy and safety of nICRT and nICT, and made a comparison with nCRT and nICT. We used pathological complete response (pCR) as the primary outcomes of interest. Condition being studied: Initial findings from a number of phase 1 or 2 trials have supported the tolerability and/or antitumor efficacy of ICI plus nICRT (nICRT) and nICT (nICT). However, the superiority of this combination strategy remains uncertain due to lack of randomized control trials (RCTs) with long-term outcomes. Moreover, there are still outstanding questions such as the selection of nICRT or nICT, the ideal predictive biomarkers, and timing of surgical resection.

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wang, hesong, chunyang song, wenzhao deng, xiaohan zhao, and wenbin shen. Evaluation of Neoadjuvant Immune Combined Therapy and Traditional Neoadjuvant Therapy for Resectable Esophageal Cancer: A Systematic Review and Single-arm and Network Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0060.

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Review question / Objective: Population: Patients with histologically-confirmed resectable esophageal carcinoma; Intervention: Neoadjuvant immunotherapy combined with chemotherapy or neoadjuvant immunotherapy combined with chemoradiotherapy followed by surgery; Control: Neoadjuvant chemotherapy or neoadjuvant chemoradiotherapy followed by surgery; Outcomes: Treatment related adverse events, r0 resection rate, pathological complete response, major pathological response, objective response rate, disease control rate, postoperative complications, postoperative mortality, 1/2/3/5year overall survival, 1/2/3/5year disease free survival; Study Design: All prospective and restrospective studies.

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