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Dissertations / Theses on the topic 'Esophageal cancer'

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Published: 4 June 2021
Last updated: 8 June 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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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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11

Sohma, Toshiya. "Chenodeoxycholic acid stimulates the progression of human esophageal cancer cells : a possible mechanism of angiogenesis in patients with esophageal cancer." Kyoto University, 2006. http://hdl.handle.net/2433/135635.

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12

Tam, Hok-nang Alex. "Epigenetic inactivation of protocadherin PCDH10 in esophageal cancer /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36586390.

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13

Bashash, Morteza. "Molecular epidemiology of gastric and esophageal cancer survival." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/30666.

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Introduction: Gastric and esophageal cancers are among the deadliest forms of cancer. Studies of human cancer susceptibility examine factors associated with the incidence of disease. Studies of human cancer prognosis and prediction examine factors associated with disease outcomes. This dissertation is about molecular and other factors that affect survival of gastric and esophageal cancer patients. Methods: Population-based registry data linked with patient outcome data was used to describe the epidemiology of gastric and esophageal cancers in BC; to compare survival of cancer patients in BC, and Ardabil, Iran and to describe differences in survival of BC patients of different ethnicity. The ethnicity of patients was determined based on lists of names corresponding to each ethnic group. A prospective cohort study was conducted to examine the effect of genetic polymorphisms in TIMP (1-4) and MMP (2, 7 and 9) genes. Results: Analysis of cancer registry data points to several factors associated with gastric and esophageal cancer survival. Patients with gastric cardia experience worse survival compared to other gastric cancers. Ethnicity of gastric and esophageal cancer patients is associated with their survival. Gastric and esophageal cancer patients diagnosed in British Columbia have better survival compared to those daignosed in Adabil, Iran. Genetic polymorphisms are also associated with survival. My prospective study identified 4 genetic polymorphisms at TIMP-3 associated with survival of esophageal adenocarcinoma and gastroesophageal junction (GEJ). Conclusion: Besides established prognostic indicators, other factors affect survival of gastric and esophageal cancers. Differences in survival by ethnicity support the importance of ethnicity as a prognostic factor. Survival differences between BC and Ardabil are likely due to disease characteristics and patient factors, in addition to differences in healthcare systems. TIMP3 genetic polymorphisms are promising prognostic factors for adenocarcinoma of esophagus and GEJ. Modeling prognosis based on host factors, including ethnicity and genetic polymorphisms, is an emerging field of translational cancer research. More research is needed to fully explore the functional effects of TIMP3 polymorphisms, and to identify both genetic and lifestyle factors underlying the effect ethnicity on survival.
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14

Tong, King-hung Daniel, and 唐琼雄. "Management strategies for advanced stage of esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42841549.

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15

Tam, Hok-nang Alex, and 譚學能. "Epigenetic inactivation of protocadherin PCDH10 in esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45011011.

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16

Tong, King-hung Daniel. "Management strategies for advanced stage of esophageal cancer." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42841549.

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17

Hui, King-cheung, and 許景祥. "Biomarkers for esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41634020.

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18

Essack, Magbubah. "Transcription Regulation and Candidate Diagnostic Markers of Esophageal Cancer." Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5306_1267148426.

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This thesis reports on the development of a novel comprehensive database (Dragon Database of Genes Implicated in Esophageal Cancer, DDEC) as an integrated knowledge database aimed at representing a gateway to esophageal cancer related data. More importantly, it illustrates how the biocurated genes in the database may represent a reliable starting point for divulging transcriptional regulation, diagnostic markers and the biology related to esophageal cancer.

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19

Bergquist, Henrik. "Aspects on the management of patients with esophageal cancer /." Göteborg : Dept. of Otorhinolaryngology, Head and Neck Surgery, the Sahlgrenska Academy, Göteborg University, 2007. http://hdl.handle.net/2077/4422.

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20

Lindblad, Mats. "Aspects on the etiology of esophageal and gastric cancer /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-110-5/.

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21

Yu, Zhuoyou, and 余卓由. "Role of DNAJB6 in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196454.

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Esophageal cancer (EC), which is geographically diverse, has only a 10.7% five-year survival rate. One of the histologic forms, esophageal squamous cell carcinoma (ESCC), in Hong Kong accounts for 81.5% of the total EC cases and its five-year survival rate is only ~14%, due to its high frequency of metastasis. In our previous studies, functional complementation study of chromosome 9 defects led to the discovery of a novel tumor suppressor gene, Deleted in Esophageal Cancer 1 (DEC1), mapping to 9q32. DEC1 was shown to reduce tumorigenicity in a mouse model and its expression was shown to be associated with lymph node metastasis, early onset of ESCC, and familial ESCC development in a tissue microarray (TMA) study. Moreover, DNAJ (Hsp40) homologue subfamily B member 6 (DNAJB6), a molecular co-chaperone protein and the focus of the current study, was identified as a DEC1-interacting protein through a yeast two-hybrid screening. The interaction was further confirmed by the GST pull-down assay and co-localization studies. Using a TMA constructed with ESCC tissues from Hong Kong, the clinical relevance of DNAJB6 expression was demonstrated. In the present study, the role of DNAJB6 in ESCC was investigated using cell line-based in vivo and in vitro studies. DNAJB6 was shown to be down-regulated in ESCC cell lines. The two isoforms of DNAJB6 have distinct subcellular localizations, with DNAJB6a mainly localized to the nucleus and DNAJB6b diffused throughout the cell. Existence of a functional nuclear localization signal peptide and a functional nuclear export signal peptide was verified in DNAJB6a and DNAJB6b, respectively. In vitro evidence of possible DNAJB6a truncation was found. In vivo subcutaneous nude mice tumorigenicity assays showed that over-expression of DNAJB6a, but not DNAJB6b, suppresses tumor growth at the primary site, while DNAJB6a silencing enhances tumor growth. The suppressive effect of DNAJB6a depends on nuclear localization of the protein and the HPD tripeptide motif in the N-terminal J domain. In vitro function studies show that DNAJB6a over-expression impairs cell proliferation by suppressing G1/S transition. AKT1 phosphorylation is down-regulated in DNAJB6a over-expressed cells, leading to up-regulation of p27KIP1 protein expression and down-regulation of cyclin E1 protein expression, the G1/S transition promoter, in an AKT1-dependent manner. DNAJB6a silencing results in the opposite effect. Over-expression of DNAJB6b, but not DNAJB6a, instead suppresses lung colonization in an experimental metastasis assay, and prolongs survival of the mice. Silencing of DNAJB6a in immortalized normal esophageal epithelial cells initially induces a senescence-like phenotype with greatly reduced proliferation possibly due to oncogenic stress from up-regulation of AKT1 phosphorylation and cyclin E1 protein expression, but promotes EMT-like molecular alterations by up-regulating STAT3 phosphorylation and TWIST1 protein expression and resumes proliferation after prolonged culture. In summary, these results suggest that DNAJB6 plays a critical role in ESCC initiation, development, and metastasis and provides valuable insight into the understanding of ESCC tumorigenesis and metastasis. This suggests its usefulness as a biomarker candidate for detecting early ESCC tumor initiation.
published_or_final_version
Clinical Oncology
Doctoral
Doctor of Philosophy
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22

Fu, Li. "Identification and characterization of cancer-related genes in esophageal squamous cell carcinoma." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557820.

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23

Yang, Zhiyi. "Mass spectrometry-based metabolomic and lipidomic characterization of esophageal cancer and lung cancer." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/819.

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Esophageal cancer and lung cancer are among the most common cancers worldwide with millions of new cases annually. Esophageal cancer patients at an advanced stage suffer from a poor five-year survival rate. However, only fewer than 30% of esophageal cancer cases were diagnosed at an early stage. For lung cancer, malignant pleural effusion (MPE) is an important hallmark for late-stage patients with metastasis. However, other causes of pleural effusions including tuberculosis bring difficulties in the diagnosis of MPE. It is necessary to develop novel diagnostic biomarkers and elucidate the pathological mechanism of esophageal cancer and lung cancer. Metabolic reprogramming is an emerging hallmark of cancer. It has been clear that metabolites play a critical role in cancer development and impose vulnerabilities that could be targeted for cancer therapy. The overall objective of this study is to comprehensively characterize the metabolic dysregulation in esophageal cancer and lung cancer for biomarker discovery and pathological elucidation, by using liquid chromatography--mass spectrometry (LC-MS)-based metabolomics and lipidomics. Paired tumors and normal adjacent tissues from esophageal squamous-cell carcinoma (ESCC) patients were first analyzed through global metabolomic and lipidomic profiling. Tumors were clearly separated from the normal tissues based on the partial least-square discriminant analysis (PLS-DA) model (R2Y >0.85 and Q2Y >0.79 in metabolomic profiling and R2Y >0.70 and Q2Y >0.67 in lipidomic profiling). A preliminary list of 41 polar metabolites and 65 lipids were identified to be significantly perturbed in tumor tissues. Kynurenine, spermidine, citicoline, as well as several glucosylceramides and phosphatidylcholines (PC) showed excellent predictive potential with area under curve (AUC) values better than 0.95 in receiver operating characteristic (ROC) models. Major elevated metabolic pathways were polyamine biosynthesis, glycerophospholipid metabolism, methionine mechanism, arginine and proline mechanism, and kynurenine metabolism, suggesting active amino acid biosynthesis and lipid biosynthesis in ESCC. The potential biomarkers and dysregulated pathways discovered above in ESCC tissue was further validated using targeted metabolomic, lipidomic and proteomic profiling. Polyamine biosynthesis was found to be activated in ESCC through the overexpression of tumor promoting ornithine decarboxylase and spermidine/spermine synthases. Upregulated levels of S-adenosylmethionine and DNA (cytosine-5)-methyltransferase 1 implied DNA hypermethylation in ESCC. Elevated purines in tumors were generated through the overexpression of methylenetetrahydrofolate dehydrogenases. Active phospholipid biosynthesis in tumors was promoted by overexpression of choline transporters and synthase of citicoline, which may accelerate the tumor growth. Dysregulation of coenzyme A species with different fatty acyl chains showed the same trend as of phospholipids, implying the specific activation of relevant acyltransferases in the phospholipid remodeling pathway. Moreover, essential amino acids exhibited a higher upregulation trends in patients with high-grade tumor or with cancer recurrence. Collectively, this study revealed the detailed metabolic dysregulations in ESCC tumor tissues, discovered potential metabolite biomarkers and identified therapeutic targets of ESCC. In order to explore the clinical application of the discovered biomarkers, metabolomic and lipidomic profiling was further performed on ESCC plasma samples. Eight metabolites were found to be simultaneously upregulated in ESCC tumors and plasma samples, indicating their potential as tumor-derived plasma biomarkers. Among them, a panel of five tumor-derived plasma biomarkers consisting of arginine, acetylspermidine, methylguanosine, dimethylguanosine and cystine showed good diagnostic potential in the cross validation. These biomarkers are related with polyamine biosynthesis and purine metabolism, which are critical to support tumor growth. For lung cancer, MPE from lung adenocarcinoma patients were investigated by LC-MS/MS-based metabolomic and lipidomic profiling. In PLS-DA models, the MPE samples were clearly separated from benign pleural effusion samples from pulmonary tuberculosis patients. A group of 17 polar metabolites and 45 lipids were identified to be significantly perturbed in MPE. For diagnostic purposes, ether lipid biomarkers, including PCs, lyso-PCs and phosphatidylethanolamines, showed an excellent predictive ability with the highest AUC value of 0.953 in ROC models. Furthermore, downregulated ether lipids and upregulated oxidized polyunsaturated fatty acids in MPE reflected the elevated oxidative stress and peroxisome disorder in lung cancer patients, which offers deeper understanding in lung cancer pathology.
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Fu, Li, and 付利. "Identification and characterization of cancer-related genes in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557820.

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25

Gopalan, Vinod. "Investigating the Role of the GAEC1 Oncogene in Human Cancers." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/365538.

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Cancer is now the most common cause of death in Australia, with an estimated 110,000 new cases in the country in 2009 and 42,000 deaths. Current Australian data indicates that 1 in 2 men and 1 in 3 women can expect to be diagnosed with cancer in the first 85 years of their life. Cancer is a disease where abnormal cells grow rapidly and spread throughout the body in an uncontrolled manner. Cancer occurs due to several damaging events that can occur in an individual cell or from a combination of many processes. DNA damage is a common feature to all cancers, though not all DNA damage will result in cancer. It has been proved that research on molecular pathways of cancers directly contributes in advanced care for cancer patients by more accurately refining prognosis and selecting the most appropriate adjuvant therapy for these patients. Gene amplified in esophageal cancer 1 (GAEC1) is a novel gene located at 7q22.1 identified using comparative DNA fingerprinting with inter-simple sequence repeat-polymerase chain reaction (ISSR-PCR). GAEC1 protein, based on its cDNA sequence showed no homology to any known protein. Preliminary work on GAEC1 suggested that it has tumorigenic potential and over expression of GAEC1 is a critical step for tumour transformation. GAEC1 was found to be expressed in several normal tissues, including oesophagus, small intestine, colon and non-gastrointestinal sites, such as lung, thymus and prostate. However, because the initial work on this gene was undertaken in oesophageal cancer, there is currently a lack of information of the molecular roles of this novel gene in other cancers.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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26

Chung, Man-fai Yvonne, and 鍾文暉. "Investigation of biomarkers in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43704025.

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27

Peralta, Robert C. "Allelotype analysis of chromosome 5 markers in human esophageal cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0008/MQ29311.pdf.

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28

Umeoka, Shigeaki. "Esophageal cancer : evaluation with triple-phase dynamic CT : initial experience." Kyoto University, 2006. http://hdl.handle.net/2433/143833.

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29

Hong, Tao. "The Epstein-Barr virus is rarely associated with esophageal cancer." Kyoto University, 2001. http://hdl.handle.net/2433/150567.

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30

Chen, Tong. "Chemoprevention of esophageal cancer investigation of inducible nitric oxide synthase as a chemopreventive target in n-nitrosomethylbenzylamine-induced esophageal tumorigenesis /." Columbus, Ohio : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1068585557.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xiv, 149 p.; also includes graphics (some col). Includes abstract and vita. Advisor: Gary D. Stoner, School of Public Health. Includes bibliographical references (leaves 125-149).
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31

Cheung, Pak-yan, and 張柏欣. "Esophageal carcinogenesis: immortalization, transformation and epithelial-mesenchymal transition." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290379.

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32

Law, Bic-fai Fian, and 羅璧輝. "Molecular genetics of esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3660446X.

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33

Fong, Sheri Fumiko Tsuda. "The LOX and LOXL2 amine oxidases in colon and esophageal cancer." Thesis, University of Hawaii at Manoa, 2003. http://hdl.handle.net/10125/1258.

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Several members of the lysyl oxidase family of copper-dependent amine oxidases have been implicated in tumor development. The Iysyl oxidase (LOX) and LOX-like 2 (LOXL2) genes have been mapped to chromosomal regions affected by loss of heterozygosity (LOH) in several cancers, including those of the colon and esophagus. Indeed, there have been numerous reports of reduced LOX and a few reports of reduced LOXL2 expression in various cancers. Identification of microsatellite markers within the LOX locus and the LOXL2 gene allowed for evaluation ofthe status of these gene alleles in colon and esophageal tumors. There was significant LOH of the LOX locus in colon tumors that was accompanied by reduced mRNA expression and a spectrum of alterations and mutations affecting the LOX gene. This study demonstrated, for the first time, that genetic events, namely LOH, deletions and mutations ofthe LOX gene, were responsible, at least partly, for the reduction of LOX gene expression. There was also significant LOH of the LOXL2 gene in both colon and esophageal tumors. However, instead of a reduction of LOXL2 expression, there was increased expression that correlated with less differentiated tumors and absent elastosis, both indicators of poor prognosis. Further studies indicated that both LOX and LOXL2 are absent in non-invasive tumor cell lines but re-expressed in invasive cell lines, likely as part of the thelial-mesenchymal transition that occurs in the last steps of tumorigenesis to facilitate metastasis. The results presented and research strategy outlined in this dissertation will define the importance of LOXL2 amine oxidase activity and protein interactions in the critical but poorly understood process oftumor cell migration and invasion.
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34

Verschuur, Elisabeth Maria Lutgardis. "Nurse-led Follow-up and Palliative Care of Esophageal Cancer Patients." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10551.

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35

Tatematsu, Noriatsu. "Impact of esophagectomy on physical fitness in patients with esophageal cancer." 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/174997.

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36

Sai, Heitetsu. "Long-term results of definitive radiotherapy for stage 1 esophageal cancer." Kyoto University, 2007. http://hdl.handle.net/2433/135890.

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37

Zhu, Cailei, and 祝彩磊. "Identification and characterization of CHL1 in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46329559.

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38

Zendehdel, Kazem. "Risk indicators for esophageal cancer : some medical conditions and tobacco-related factors /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-239-2/.

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39

Law, Ying-kit Simon, and 羅英傑. "Strategies to improve outcome of esophageal cancer: a study of morbidity, mortality, and prognosis afteresophagectomy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B25558353.

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40

祝彩磊 and Cailei Zhu. "Characterization of tumor suppressing function of PCAF in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557480.

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41

Fujii, Kota. "Association of Chemoradiotherapy With Thoracic Vertebral Fractures in Patients With Esophageal Cancer." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264656.

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42

Tewari, Abha. "A cranberry proanthocyanidin inhibits cancer-related processes in human esophageal adenocarcinoma cells." Connect to resource, 2006. http://hdl.handle.net/1811/24055.

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Thesis (Honors)--Ohio State University, 2006.
Title from first page of PDF file. Document formatted into pages: contains 20 p.; also includes graphics. Includes bibliographical references (p. 17-20). Available online via Ohio State University's Knowledge Bank.
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43

Ye, Weimin. "Aspects of gastroesophageal reflux and risk for esophageal cancer : an epidemiological approach /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-695-2/.

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44

Liston, Beth Wagner. "Investigation of HA-RAS mutation as a chemopreventive target in esophageal cancer /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486457871786712.

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45

Schein, Julia. "Retrospektive Analyse der operativ versorgten Patienten mit Ösophaguskarzinomen und Karzinomen des ösophagogastralen Übergangs der Jahre 2007 bis 2011 an der Universitätsklinik Leipzig." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-192291.

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Jährlich werden in Deutschland 5190 Neuerkrankungen an einem Ösophaguskarzinom registriert. Diese Tumorentität steht bei Männern an 13. Stelle der Häufigkeiten der Krebserkrankungen und bei den Frauen an 17. Stelle. Die Fünfjahresüberlebensrate wird in der Literatur für männliche Patienten mit 11-22% und für Frauen mit 15-20% angegeben. Somit hat das Ösophaguskarzinom nach wie vor eine schlechte Prognose. Ziel der durchgeführten Studie war es, retrospektiv einen Überblick über die Patienten zu erstellen, welche im Zeitraum von 2007 bis 2011 aufgrund eines Ösophaguskarzinoms in der Klinik für Viszeral-, Transplantations-, Thorax-, und Gefäßchirurgie der Universitätsklinik Leipzig operativ behandelt wurden und die gewonnenen deskriptiven Statistiken und Überlebenszeitanalysen mit denen der Fachliteratur zu vergleichen, sowie gegebenenfalls Rückschlüsse zur Therapieoptimierung zu ziehen. Insgesamt lag die mediane Überlebenszeit der Patienten bei 23,7 Monaten (95%KI 13,7-33,6). Die 5-Jahres-Überlebensrate lag bei 30,3%. Zusammenfassend konnten signifikante Überlebensvorteile für das männliche Geschlecht, eine niedrigere lokale Infiltrationstiefe des Tumors (pT), das Fehlen von regionalen Lymphknotenmetastasen im Gesamtkollektiv und in der Gruppe der Adenokarzinome (pN), ein niedrigeres pUICC-Stadium ebenfalls im Gesamtkollektiv und in der Gruppe der Adenokarzinome, eine R0-Resektion und in der Subgruppe der Plattenepithelkarzinom die alleinige Operation ohne neoadjuvante Therapie festgestellt werden.
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46

Hui, Cheuk-man, and 許卓文. "Role of Id-1 in proliferation and survival of esophageal carcinoma cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29947492.

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47

Leung, Cheuk-man, and 梁卓文. "A study of BARX2 expression in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47560460.

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Background Esophageal carcinoma mainly affects middle aged to elderly males. It ranks the ninth most common cancer world-wide. The main histological types are squamous cell carcinoma and adenocarcinoma. In Hong Kong, esophagus squamous cell carcinoma (ESCC) is by far the more common. BARX2 is a human homeobox gene located at 11q24-q25, encoding a protein of 254 amino acids. Recent researches show that its expression in breast cancer promotes cellular invasion. Objectives The study aimed to test the hypothesis that BARX2 is a prognostic marker in ESCC. BARX2 expression in ESCC was correlated with patient survival and other clinicopathologic parameters in a cohort of patients. Material and Methods Records of ESCC patients were obtained retrospectively from the computerized database of Queen Mary Hospital. ESCC patients, who underwent esophagectomy in the hospital from 1998 to 2005 but without receiving prior chemotherapy or radiotherapy directed to the tumor, were selected. Tumor staging was done according to the 6th edition of AJCC Cancer Staging Manual. Immunohistochemical staining for BARX2 expression was performed on paraffin sections of the primary ESCC tissues sampled in a tissue microarray constructed for research purposes. The pattern of BARX2 expression in nucleus and cell cytoplasm of tumor cells was recorded and the staining intensity scored on a 4-point scale. The scores were statistically analyzed together with the various clinicopathologic parameters. BARX2 expression and patient survival time were analyzed by the log-rank test. Results A total of 78 ESCC patients were recruited. At the time of data analysis, 52 (66.7%) patients were dead. The overall median survival of patients was 14.3 months. BARX2 was found to be mainly expressed in the cytoplasm of tumor cells while non-tumor epithelium showed strong nuclear expression. Patients with high level BARX2 expression had short survival time, though the difference did not reach statistical significance (p=0.075). Within the subgroup of lower T-stage ESCC (T1-3), high level BARX2 expression was significantly associated with shorter survival time (p=0.042). However, differential BARX2 expression did not affect survival time within the group of patients who had advanced stage (T4) disease (p=0.525). In patients who had no regional lymph node metastasis (N0), high level BARX2 expression was associated with shorter survival time (p=0.023). However, when patients had regional lymph node metastases (N1), BARX2 expression did not affect patient survival time (p=0.533). Patients whose ESCC showed moderate differentiation in a three-tier tumor grading system, when accompanied with low level BARX2 expression, had longer survival time (p=0.029). However, BARX2 expression did not affect survival time when ESCC showed either well differentiation (p=0.462) or poor differentiation (p=0.637). Multivariate analysis showed patient age and T-stage to be the only two independent parameters of prognostic significance (p=0.025 and p=0.036 respectively). Conclusions BARX2 expression in ESCC was aberrant and mainly cytoplasmic. It was inversely correlated with patient survival time in early ESCC disease (T1-T3 or N0). BARX2 expression evaluated by immunohistochemistry could be a useful and practical prognostic marker of ESCC in its early stages, when the proper decision on treatment would be critical for the patients.
published_or_final_version
Pathology
Master
Master of Medical Sciences
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48

Zhao, Yue. "Characterization and targeted therapy of stem cell-like side population cells in pancreatic cancer and esophageal cancer." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-168236.

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49

Hu, Qinghui, and 胡庆慧. "Characterization of oncogenic function of microRNA665 in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193480.

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Background: Esophageal squamous cell carcinoma (ESCC) has been increasing in incidence, but knowledge of the genetic basis of this disease remains limited. In general, esophageal carcinoma can be divided into two main types: Esophageal Squamous Cell Carcinoma (ESCC) and Esophageal Adenocarcinoma (EAC). The pathogenesis of esophageal carcinoma still remains unclear, although some risk factors like chronic irritation, or chronic inflammation which may be caused by diseases such as gastroesophageal reflux disease (GERD) or unhealthy lifestyles like smoking have been proved to be related to the carcinogenic process. Diagnosis and treatment for this kind of cancer have continue to develop and evolve, but the 5-year overall survival rate is still relatively low. Therefore, it is clinically important to identify any potential genetic changes which may help us to discover some useful biomarker targets for the further development of more direct and harmless targeted therapy for our esophageal cancer patients. Objectives: In this study, I aimed to identify some potential oncogenic microRNA (miRNA) and to study their clinical meaning in ESCC patients. Methods: Microarray was applied to identify differentially expressed miRNAs in ESCC tumour tissue, compared with corresponding adjacent non-tumour esophageal tissue. One candidate oncogenic miRNA, miR-665, was investigated in the present study. After testing the expression level of miR-665 in ESCC cell lines and patients’ samples with RT-PCR, miR-665 stably expressing cells was established using two ESCC cell lines (KYSE30 and KYSE510). Functional characterization was then conducted using in vitro and in vivo assays to examine the effect of miR-665 towards the development of ESCC. Bioinformatic software such as Target Scan was used to generate a list of predicted target genes that may be modulated by miR-665. Results: The high expression of miR-665 has been confirmed in ESCC tissues and cell lines, showing the potential carcinogenic function of miR-665. Ectopic expression of miR-665 also demonstrates its ability to enhance tumour growth and invasion in vitro and in vivo. Bioinformatic analysis of miR-665 predicted targets showed putative binding sites for miR-665 within the 3’UTR region of NLK. Conclusions: This study has identified a novel miRNA and a related gene which might play an important role in the pathogenesis of ESCC, affecting the cancer process and tumour growth. This may help to find potential new biomarker for the future improvement and development of new treatment of ESCC patients.
published_or_final_version
Clinical Oncology
Master
Master of Philosophy
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50

Hsu, Che-Wei, and 許哲瑋. "Epidemiological study on oral cancer and esophageal cancer." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/93430899365932208545.

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碩士
中國醫藥大學
環境醫學研究所
96
Aims: The objectives of this study are to, 1) evaluate the general trends and spatial-temporal patterns regarding incidence and mortality rates of oral and esophageal cancers in last twenty-five years in Taiwan; 2) to determine the age-, period- and cohort (APC)-specific effects for mortality rates and incidence rates of these two cancers; 3) to estimate whether the cancers are associated with smoking, drinking, and areca chewing. Methods: We calculated the standard incidence rates from 1979-2003 and standard mortality rates from 1982-2006, using WHO 1976 world population as standard. In order to present the spatial-temporal patterns, we drew three-level cancer map of cumulative incidence and mortality rates. And we respectively used age, period, and cohort as horizontal axe to plot the observed rates to analysis the effects of age, period and cohort. We also used age-period-cohort model to assess those effects. The 23 counties in Taiwan in regarding to the use of tobacco, alcohol, and areca were classified into high, medium and low prevalence areas. Poisson regression was used to analyze the association between risk factors and the disease. Results: Between 1979 and 2003, the oral cancer incidence rates had 6.19 times increase in males and 2.32 times in females, and the esophageal cancer had 1.99 times increase in males and 1.01 times in females. Compared with 1982, the oral cancer mortality rates in 2006 had 4.72 times increase in males and 0.98 times in females. The increasing trends were more precipitous in oral cancer than in esophageal cancer, and more precipitous among males than among females. The oral cancer was more severe in counties of eastern and mid-southern Taiwan; esophageal cancer was more severe in eastern and northern Taiwan. The incidence rates of oral and esophageal cancers were higher in younger male groups, but less in younger female groups. These diseases in male were in increasing trends in recent years, particularly in younger cohorts. However, the diseases in females were relatively stable and had a decreasing trend in younger cohorts. The areca chewing behavior had a significant effect (p<0.05) on diseases among males. Compared with people of less areca use, rate ratios (RR) of incidence were 1.58 for the oral cancer and 1.13 for the esophageal cancer in males. The corresponding mortality ratios were 1.7 and 1.29. Among females, smoking, drinking and chewing areca were significant risks. Conclusions: The incidence and mortality rates of oral and esophageal cancers are increasing among males, and incidence rates of oral cancer is also increasing among females. Both diseases have associations with using tobacco, alcohol, and areca. It is necessary to modify life styles (i.e. cigarette smoking, alcohol consumption and areca chewing) in order to prevent oral and esophageal cancers in our population.
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