Relevant bibliographies by topics / Pancreatic ductal cancer

Academic literature on the topic 'Pancreatic ductal cancer'

Author: Grafiati
Published: 7 July 2024
Last updated: 7 July 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Pancreatic ductal cancer":

1

Chen, Yan, Huiyun Zhu, Yuqiong Wang, Yingxiao Song, Pingping Zhang, Zhijie Wang, Jun Gao, Zhaoshen Li, and Yiqi Du. "MicroRNA-132 Plays an Independent Prognostic Role in Pancreatic Ductal Adenocarcinoma and Acts as a Tumor Suppressor." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381882431. http://dx.doi.org/10.1177/1533033818824314.

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The role of microRNA-132 in human pancreatic ductal adenocarcinomas is still ambiguous. We explored the association between microRNA-132 and pancreatic ductal adenocarcinoma prognosis. The expression of microRNA-132 in 50 pancreatic ductal adenocarcinoma tissue samples and pancreatic ductal adenocarcinoma cell lines was examined, and the association between its expression and pancreatic ductal adenocarcinoma prognosis was assessed. Functional analysis and factors downstream of microRNA-132 were investigated. Kaplan-Meier survival curves showed that high expression of microRNA-132 was a significant prognostic factor for 1-year survival of patients with pancreatic ductal adenocarcinoma ( P = .028). Multivariate analysis for overall survival indicated that high expression of microRNA-132 was an independent prognostic factor for patients with pancreatic ductal adenocarcinoma ( P = .044). Low expression of microRNA-132 was associated with poor prognosis in pancreatic ductal adenocarcinoma. Ectopic expression of microRNA-132 significantly inhibited proliferation and promoted apoptosis of 2 pancreatic ductal adenocarcinoma cell lines. Bioinformatic analysis revealed that microRNA-132 may exert its effects on pancreatic ductal adenocarcinoma through downregulating mitogen-activated protein kinase 3 and nuclear transcription factor Y subunit α. The results of this study further our understanding of the relationship between microRNA-132 and pancreatic ductal adenocarcinoma by showing that microRNA-132 might inhibit the progression of pancreatic ductal adenocarcinoma by regulating mitogen-activated protein kinase and nuclear transcription factor Y subunit alpha.
2

González-Boja, Iranzu, Antonio Viúdez, Saioa Goñi, Enrique Santamaria, Estefania Carrasco-García, Jairo Pérez-Sanz, Irene Hernández-García, et al. "Omics Approaches in Pancreatic Adenocarcinoma." Cancers 11, no. 8 (July 25, 2019): 1052. http://dx.doi.org/10.3390/cancers11081052.

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Pancreatic ductal adenocarcinoma, which represents 80% of pancreatic cancers, is mainly diagnosed when treatment with curative intent is not possible. Consequently, the overall five-year survival rate is extremely dismal—around 5% to 7%. In addition, pancreatic cancer is expected to become the second leading cause of cancer-related death by 2030. Therefore, advances in screening, prevention and treatment are urgently needed. Fortunately, a wide range of approaches could help shed light in this area. Beyond the use of cytological or histological samples focusing in diagnosis, a plethora of new approaches are currently being used for a deeper characterization of pancreatic ductal adenocarcinoma, including genetic, epigenetic, and/or proteo-transcriptomic techniques. Accordingly, the development of new analytical technologies using body fluids (blood, bile, urine, etc.) to analyze tumor derived molecules has become a priority in pancreatic ductal adenocarcinoma due to the hard accessibility to tumor samples. These types of technologies will lead us to improve the outcome of pancreatic ductal adenocarcinoma patients.
3

Rayn, V. U., M. A. Persidskiy, E. V. Malakhova, I. V. Anuchina, A. A. Khalikova, Ya E. Timofeeva, and L. V. Bereshkeeva. "Precursors of pancreatic cancer in background of chronic opisthorchiasis." Medical Science And Education Of Ural 22, no. 1 (March 31, 2021): 118–21. http://dx.doi.org/10.36361/1814-8999-2021-22-1-118-121.

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Aim. To establish the association between pancreatic cancer precursor lesions and chronic opisthorchiasis. Materials and methods. A single center case-control study was conducted at a low-volume pancreatic surgery center in Khanty-Mansiysk. We retrospectively collected morphological data from 47 pancreatoduodenectomies performed for pancreatic ductal adenocarcinoma. The study group included 23 cases of pancreatic ductal adenocarcinoma with concomitant chronic Opisthorchis felineus invasion which were compared to 24 controls consisting of “pure” cancer. Qualitative analysis was performed using χ2 Pearson criterion. Exact Fisher test was used for small samples. Time to progression and overall survival rates were calculated using Kaplan-Meier survival analysis. Data were collected and analyzed in Statistica 7.0. Results. PanINs were seen in 41,7% pancreata resected for ductal adenocarcinoma of the head and in 95,7% cases of pancreatic cancer in background of chronic opisthorchiasis (р = 0,000; 95% CI 3,5-268). PanIN high grade were observed only in opisthorchiasis group. In mixed pathology invasive cancer component tended to be more dedifferentiated and advanced when compared to pure cancer group (p = 0,029). Median disease free survival was 9 mo. in both groups and overall survival was 13 mo. in non-opisthorchiasis group and 15,3 mo. in opisthorchiasis group (р = 0,437). Conclusion. Chronic opisthorchiasis is associated with pancreatic intraepithelial neoplasia. Pancreatic ductal adenocarcinoma in background of opisthorchiasis with preneoplastic lesions tend to be more advanced in stage and poorly differentiated. Disease free and overall survival have no statistically significant differences in patients with and without Opisthorchis felineus invasion.
4

Melzer, Michael Karl, Frank Arnold, Katja Stifter, Friedemann Zengerling, Ninel Azoitei, Thomas Seufferlein, Christian Bolenz, and Alexander Kleger. "An Immunological Glance on Pancreatic Ductal Adenocarcinoma." International Journal of Molecular Sciences 21, no. 9 (May 8, 2020): 3345. http://dx.doi.org/10.3390/ijms21093345.

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Pancreatic ductal adenocarcinoma (PDAC) has still a dismal prognosis. Different factors such as mutational landscape, intra- and intertumoral heterogeneity, stroma, and immune cells impact carcinogenesis of PDAC associated with an immunosuppressive microenvironment. Different cell types with partly opposing roles contribute to this milieu. In recent years, immunotherapeutic approaches, including checkpoint inhibitors, were favored to treat cancers, albeit not every cancer entity exhibited benefits in a similar way. Indeed, immunotherapies rendered little success in pancreatic cancer. In this review, we describe the communication between the immune system and pancreatic cancer cells and propose some rationale why immunotherapies may fail in the context of pancreatic cancer. Moreover, we delineate putative strategies to sensitize PDAC towards immunological therapeutics and highlight the potential of targeting neoantigens.
5

Djanani, Angela, Andreas Schmiderer, Lukas Niederreiter, Markus Niederreiter, and Herbert Tilg. "Management of ductal pancreatic cancer." European Surgery 51, no. 3 (May 15, 2019): 135–38. http://dx.doi.org/10.1007/s10353-019-0583-z.

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6

Sun, Hongzhi, Bo Zhang, and Haijun Li. "The Roles of Frequently Mutated Genes of Pancreatic Cancer in Regulation of Tumor Microenvironment." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382092096. http://dx.doi.org/10.1177/1533033820920969.

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Pancreatic ductal adenocarcinoma has extremely high malignancy and patients with pancreatic ductal adenocarcinoma have dismal prognosis. The failure of pancreatic ductal adenocarcinoma treatment is largely due to the tumor microenvironment, which is featured by ample stromal cells and complicated extracellular matrix. Recent genomic analysis revealed that pancreatic ductal adenocarcinoma harbors frequently mutated genes including KRAS, TP53, CDKN2A, and SMAD4, which can widely alter cellular processes and behaviors. As shown by accumulating studies, these mutant genes may also change tumor microenvironment, which in turn affects pancreatic ductal adenocarcinoma progression. In this review, we summarize the role of such genetic mutations in tumor microenvironment regulation and potential mechanisms.
7

Hartl, Leonie, JanWillem Duitman, Hella L. Aberson, Kan Chen, Frederike Dijk, Joris J. T. H. Roelofs, Mark P. G. Dings, et al. "CCAAT/Enhancer-Binding Protein Delta (C/EBPδ): A Previously Unrecognized Tumor Suppressor that Limits the Oncogenic Potential of Pancreatic Ductal Adenocarcinoma Cells." Cancers 12, no. 9 (September 7, 2020): 2546. http://dx.doi.org/10.3390/cancers12092546.

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CCAAT/enhancer-binding protein δ (C/EBPδ) is a transcription factor involved in growth arrest and differentiation, which has consequently been suggested to harbor tumor suppressive activities. However, C/EBPδ over-expression correlates with poor prognosis in glioblastoma and promotes genomic instability in cervical cancer, hinting at an oncogenic role of C/EBPδ in these contexts. Here, we explore the role of C/EBPδ in pancreatic cancer. We determined C/EBPδ expression in biopsies from pancreatic cancer patients using public gene-expression datasets and in-house tissue microarrays. We found that C/EBPδ is highly expressed in healthy pancreatic ductal cells but lost in pancreatic ductal adenocarcinoma. Furthermore, loss of C/EBPδ correlated with increased lymph node involvement and shorter overall survival in pancreatic ductal adenocarcinoma patients. In accordance with this, in vitro experiments showed reduced clonogenic capacity and proliferation of pancreatic ductal adenocarcinoma cells following C/EBPδ re-expression, concurrent with decreased sphere formation capacity in soft agar assays. We thus report a previously unrecognized but important tumor suppressor role of C/EBPδ in pancreatic ductal adenocarcinoma. This is of particular interest since only few tumor suppressors have been identified in the context of pancreatic cancer. Moreover, our findings suggest that restoration of C/EBPδ activity could hold therapeutic value in pancreatic ductal adenocarcinoma, although the latter claim needs to be substantiated in future studies.
8

Perkins, Corey Melissa, Jinmai Jiang, Hesamedin Hakimjavadi, Julie K. Bray, Alyssa Gosling, Lais da Silva, Gamze Bulut, et al. "Abstract 780: Transcriptional profile of human pancreatic acinar ductal metaplasia." Cancer Research 82, no. 12_Supplement (June 15, 2022): 780. http://dx.doi.org/10.1158/1538-7445.am2022-780.

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Abstract Aberrant acinar to ductal metaplasia (ADM), one of the earliest events involved in exocrine pancreatic cancer development, is typically studied using pancreata from transgenic mouse models. We used primary, human pancreatic acinar cells to evaluate the transcriptional profile during the course of ADM. Following six days of culture on Matrigel, acinar cells underwent morphological and molecular changes reminiscent of ADM. RNA was sequenced from 14 donor’s paired pancreata (day 0 and 6 of culture). Unsupervised hierarchical clustering demonstrated complete separation of the gene expression profile between culture day 0 (acinar phenotype) and day 6 (ductal phenotype). By and large, acinar-specific genes were downregulated in the samples from day 6 ADM while ductal-specific genes were upregulated. Using a gene set enrichment approach, we identified regulons that are involved in regulating ADM including downregulated, acinar-associated transcription factors (including PTF1A, RBPJL, and XBP1) and upregulated, ductal- and progenitor-associated transcription factors (SOX11, SOX4, and YAP1). The expression of pancreatic cancer associated genes significantly correlated with the gene expression/regulon activity observed in normal pancreas undergoing ADM. We reported a detail analysis of the transcriptional profile during human ADM. Our findings confirm that many ADM-related transcription factors and signaling pathways discovered in transgenic mouse models are applicable to human ADM and highlights the relevancy of in vitro models of pancreas plasticity using human tissue. Citation Format: Corey Melissa Perkins, Jinmai Jiang, Hesamedin Hakimjavadi, Julie K. Bray, Alyssa Gosling, Lais da Silva, Gamze Bulut, Jamel Ali, Wendy Setiawan, Martha Campbell-Thompson, Srikar Chamala, Thomas D. Schmittgen. Transcriptional profile of human pancreatic acinar ductal metaplasia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 780.
9

Shabunin, A. A., A. A. Karpov, E. V. Kizhaev, V. V. Bedin, M. M. Tavobilov, O. V. Paklina, and G. R. Setdikova. "Combined surgical treatment of pancreatic head cancer." Annaly khirurgicheskoy gepatologii = Annals of HPB surgery 23, no. 3 (October 21, 2018): 8–13. http://dx.doi.org/10.16931/1995-5464.201838-13.

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Aim.To improve the outcomes in patients with pancreatic head cancer using intraoperative radiotherapy (IORT).Material and methods.Prospective trial included patients with ductal adenocarcinoma of the pancreatic head who underwent pancreatic surgery followed by IORT.Results.There were 63 patients with pancreatic ductal adenocarcinoma for the period from January 2013 till December 2016. IORT was applied in 31 cases. Annual, 3-year survival and disease-free survival were analyzed.Conclusion.Surgery followed by IORT is safe and current approach for pancreatic head cancer.
10

Jansen, Kristina, Franziska Büscheck, Katharina Moeller, Martina Kluth, Claudia Hube-Magg, Niclas Christian Blessin, Daniel Perez, et al. "DOG1 is commonly expressed in pancreatic adenocarcinoma but unrelated to cancer aggressiveness." PeerJ 9 (August 3, 2021): e11905. http://dx.doi.org/10.7717/peerj.11905.

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Background DOG1 (ANO1; TMEM16A) is a voltage-gated calcium-activated chloride and bicarbonate channel. DOG1 is physiologically expressed in Cajal cells, where it plays an important role in regulating intestinal motility and its expression is a diagnostic hallmark of gastrointestinal stromal tumors (GIST). Data on a possible role of DOG1 in pancreatic cancer are rare and controversial. The aim of our study was to clarify the prevalence of DOG1 expression in pancreatic cancer and to study its association with parameters of cancer aggressiveness. Methods DOG1 expression was analyzed by immunohistochemistry in 599 pancreatic cancers in a tissue microarray format and in 12 cases of pancreatitis on large tissue sections. Results DOG1 expression was always absent in normal pancreas but a focal weak expression was seen in four of 12 cases of pancreatitis. DOG1 expression was, however, common in pancreatic cancer. Membranous and cytoplasmic DOG1 expression in tumor cells was highest in pancreatic ductal adenocarcinomas (61% of 444 interpretable cases), followed by cancers of the ampulla Vateri (43% of 51 interpretable cases), and absent in 6 acinus cell carcinomas. DOG1 expression in tumor associated stroma cells was seen in 76 of 444 (17%) pancreatic ductal adenocarcinomas and in seven of 51 (14%) cancers of the ampulla Vateri. Both tumoral and stromal DOG1 expression were unrelated to tumor stage, grade, lymph node and distant metastasis, mismatch repair protein deficiency and the density of CD8 positive cytotoxic T-lymphocytes in the subgroups of ductal adenocarcinomas and cancers of ampulla Vateri. Overall, the results of our study indicate that DOG1 may represent a potential biomarker for pancreatic cancer diagnosis and a putative therapeutic target in pancreatic cancer. However, DOG1 expression is unrelated to pancreatic cancer aggressiveness.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Pancreatic ductal cancer":

1

Jacobetz, Michael. "Optimizing drug delivery in pancreatic ductal adenocarcinoma." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609438.

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2

Cardenas, Alex. "Sphingosine-1-Phosphate in Pancreatic Ductal Adenocarcinoma." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/306974.

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Pancreatic ductal adenocarcinoma is an extremely lethal cancer that is difficult to treat. A better understanding of the biology of pancreatic ductal cancer will help to develop targeted therapies that may improve clinical outcomes. Recently, the lipid signaling molecule sphingosine-1-phosphate (S1P) has emerged as a driver of malignant behavior in many types of cancer. Its role in pancreatic cancer remains unknown. Pancreatic cancer cells express high levels of the S1P receptor known as S1PR1, which is the receptor most important for mediating growth and migration through S1P signaling. In addition, the subcellular expression of the sphingosine kinases is altered in pancreatic cancer cells, which may contribute to their malignant behavior. Exogenous S1P increases pancreatic cancer cell migration, while inhibition of S1P signaling decreases the metabolic activity of pancreatic cancer cells as well as their ability to invade and migrate. Taken together, these results demonstrate the importance of S1P signaling in maintaining malignant behavior in pancreatic cancer cells. In addition, inhibition of S1P signaling represents a potential therapeutic target in pancreatic ductal cancer.
3

Kawesha, Anthony. "Prognostic molecular markers in resected ductal pancreatic carcinoma." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7596/.

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Previous studies of molecular prognostic markers following resection for exocrine pancreatic cancer have produced conflicting results. The aim of this study was to undertake a comprehensive analysis of potentially useful markers in a large multicentre patient population and compare these markers with standard pathological prognostic variables. Formalin fixed, paraffin-embedded specimens of pancreatic ductal adenocarcinoma were analysed from 157 patients (100 men and 57 women with a median [range] age of 60 [33-77] years) who had undergone pancreatectomy. Immunhistochemistry was used to detect expression of p16\(^{INK4}\), p53, p21\(^{WAF1}\), cyclin D1, c-erbB-2 and c-erbB-3. In a selected number of p53 positive and negative staining cases, mutational analysis was undertaken using DNA obtained from microdissected specimens. Mutations in codons 12 and 13 of the K-ras oncogene were detected by SSCP and sequencing following DNA extraction and amplification by PCR. The median [range] survival post-resection was 12.5 [3-83] months. Abnormalities of p16\(^{INK4}\), p53, p21\(^{WAF1}\), cyclin D1, c-erbB-2 and c-erbB-3 expression were found in 87%, 41%, 75%, 72%, 33% and 57% of cases, respectively. There was no significant correlation between expression of any of these markers and patient survival. K-ras mutations were found in 73 (75%) out of 97% cases with amplifiable DNA. The presence of K-ras mutation alone did not correlate with survival, but there were significant differences in survival according to the type of K-ras mutation (p=0.0007). Reduced survival was found in patients with GaT, cGT and GcT K-ras mutations compared to GtT, aGT and GaC mutations. In conclusion survival was associated with the type of K-ras mutation but not the expression of p16\(^{INK4}\), p53, p21\(^{WAF1}\), cyclinD1, c-erbB-2 and c-erbB3.
4

Naidoo, Kalnisha. "Molecular mechanisms of lymphatic invasion in pancreatic ductal adenocarcinoma." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8606.

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Pancreatic Ductal Adenocarcinoma (PDAC) is one of the five leading causes of cancer-related deaths in the West, and this, largely, is due to metastatic disease. In order to better understand PDAC metastatic spread and identify novel therapeutic targets, we analysed the proteome of primary tumours and matched lymph node (LN) metastases. As frozen specimens of metastatic lesions are scarce, we examined formalin-fixed paraffin-embedded (FFPE) tissues. Whilst such tissue is in routine diagnostic use, the cross-linkages induced by fixation have, in the past, precluded proteomic investigation for research purposes. Recent technological advances have, however, overcome this technical limitation. Using laser capture microdissection (P.A.L.M system), we isolated malignant epithelia from seven FFPE primary PDAC tumours and matched LN metastases. Following dissection, samples were analysed in duplicate using Multidimensional Protein Identification Technology (MudPIT); this resulted in the identification of 1504 proteins, 854 of which were common to all samples analysed. Comparison of the obtained proteins with data from previous proteomics studies on pancreatic tissue, pancreatic juice, serum and urine resulted in a less than 30 % overlap, indicating that our study has expanded the current database of proteins expressed in this malignancy substantially. Statistical analysis further showed that 115/854 proteins (13.5%) were significantly differentially expressed (g-value ≥ 3.8). Two proteins, S100P and 14-3-3 sigma, with highly significant g-values were confirmed to be significantly differentially expressed (S100P: p = 0.05 and 14-3-3 sigma: p < 0.001) 4 in a larger series of 55 cases of matched primary PDAC and LN metastases using immunohistochemistry. We chose to investigate further the roles of S100P in lymphatic invasion in vitro and in vivo. By co-culturing a Panc1 S100P-overexpressing clone (S5L), or a vector control clone (V3L), with human dermal lymphatic endothelial cells (HDLEC), we were able to show that different receptors mediate S5L adhesion to resting and activated HDLEC as opposed to V3L; and that the presence of S5L cells in these co-cultures significantly increased permeability at one (p = 0.02), four (p = 0.002) and eight (p = 0.007) hours post-seeding, and significantly increased translymphatic endothelial migration at 72 hours (p = 0.006). Using the V3L and S5L cell lines, which were transduced to express luciferase, we also created an orthotopic mouse model of PDAC, as well as experimental metastatic mouse models, in CD1 nude mice. These models were used to evaluate the effects of S100P on primary tumour growth, metastasis and site-specific growth. S100P was only found to significantly increase primary tumour growth in this model (n = 10 animals/group), both by bioluminescence (p = 0.002) and tumour weight (p = 0.01). No metastases (spontaneous and/or experimental) were seen however. Thus, this model can be used to evaluate the anti-tumour efficacy of novel therapies to S100P in the future.
5

Kadaba, Raghunandan. "Desmoplastic stromal cells modulate tumour cell behaviour in pancreatic cancer." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8825.

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Pancreatic ductal adenocarcinoma (PDAC) is characterised by an intense desmoplastic stromal response that can comprise 60 to 80% of tumour volume and has been implicated to be a factor in promoting tumour invasiveness and the poor prognosis associated with this cancer type. It is now well established that pancreatic stellate cells, which are vitamin A storing cells found in the periacinar spaces of the stroma in the normal gland, are primarily responsible for this desmoplastic reaction. Studying the interaction between stellate cells and cancer cells could provide for a better understanding of the disease process. During the evolution of PDAC, the stromal proportion increases from 4% in the normal gland to up to 80%. We hypothesised that there is an optimal proportion of stellate cells and cancer cells that modulates tumour behaviour and we attempted to dissect out this probable ‘tipping point’ for stromal composition upon cancer cell behaviour using a well-established in vitro organotypic culture model of pancreatic cancer. The cancer cell-stromal cell interaction led to extra-cellular matrix contraction and stiffening; and an increase in cancer cell number. The stromal stellate cells conferred a pro-survival and pro-invasive effect on cancer cells which was most pronounced at a stellate cell proportion of 0.66-0.83. The expression of key molecules involved in EMT and metastasis such as E-Cadherin and β-catenin showed a reduction and this was found to be most significant again at a stellate cell proportion of 0.66-0.83. Stellate cells altered the genetic profile of cancer cells leading to differential expression of genes involved in key cellular pathways such as cell-cycle and proliferation, cell movement and death, cell-cell signalling, and inflammatory response. qRT-PCR confirmed the differential expression of the top differentially expressed genes and protein validation by immunofluorescence staining using PIGR as a candidate molecule confirmed the experimental findings in human PDAC specimens. This study demonstrates that the progressive accumulation of desmoplastic stromal cells has a tumour progressive (pro-survival, pro-invasive) effect on cancer cells in addition to stiffening (contraction) of the extracellular matrix (maximum effect when the stromal cell proportion is 60-80%). This is mediated through a number of signalling cascades and molecular targets. Dampening this tumour-promoting interaction between cancer and stromal cells by ‘multi-targeting’ agents may allow traditional chemo- and/or radiotherapy to be effective.
6

Mohammad, Jiyan Mageed. "Therapeutic Potential of Piperlongumine for Pancreatic Ductal Adenocarcinoma." Diss., North Dakota State University, 2019. https://hdl.handle.net/10365/31347.

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Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies because it is often diagnosed at a late disease stage and has a poor response rate to currently available treatments. Therefore, it is critical to develop new therapeutic approaches that will enhance the efficacy and reduce the toxicity of currently used therapies. Here we aimed to evaluate the therapeutic potential and mechanisms of action for piperlongumine (PL), an alkaloid from long pepper, in PDAC models. We postulated that PL causes PDAC cell death through oxidative stress and complements the therapeutic efficacy of chemotherapeutic agents in PDAC cells. First, we determined that PL is one of the most abundant alkaloids with antitumor properties in the long pepper plant. We also showed PL in combination with gemcitabine, a chemotherapy agent used to treat advanced pancreatic cancer, reduced tumor weight and volume compared to vehicle-control and individual treatments. Further, biochemical analysis, including RNA sequencing and immunohistochemistry, suggested that the antitumor activity of PL was associated with decreased cell proliferation, induction of cell cycle arrest, and oxidative stress-induced cell death. Moreover, we identified that c-Jun N-terminal kinase (JNK) inhibition blocks PL-induced cell death, translocation of Nrf2, and transcriptional activation of HMOX1 in PDAC. Finally, high-throughput drug and CRISPR screenings identified potential targets that could be used in combination with PL to treat PDAC cells. Collectively, our data suggests that cell cycle regulators in combination with PL might be an effective approach to combat pancreatic cancer.
NIH
7

Puleo, Francesco. "Pancreatic ductal adenocarcinoma: From biomarkers discovery to personalized treatment." Doctoral thesis, Universite Libre de Bruxelles, 2018. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/271618.

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En 2016, environ 53 070 patients ont reçu un diagnostic d'adénocarcinome canalaire pancréatique (PDA) aux États-Unis et la plupart d'entre eux mourront de leur maladie dans les 5 ans. Le registre belge du cancer rapporte une incidence estimée à 1200 nouveaux cas par an. La survie globale à 5 ans pour toutes stades confondus a marginalement augmenté au cours des 50 dernières années, passant de 2 à 6%, malgré l'imagerie, les soins périopératoires et l'amélioration des techniques chirurgicales.La chirurgie reste la seule chance de guérison, cependant, seulement 10-15% des patients nouvellement diagnostiqués sont jugés éligibles pour une chirurgie. Même s'il existe peu d'autres modalités de traitement efficaces qui puissent considérablement prolonger la survie globale, la plupart des patients finiront par mourir de métastases au foie, au poumon et / ou au péritoine, les sites de propagation les plus courants. Les patients, les cliniciens et les chercheurs restent frustrés par le manqué d’outils thérapeutiques et des nouvelles stratégies sont nécessaires pour comprendre et mieux prendre en charge cette maladie.Le terme «cancer» engendre un sentiment de peur et colère, en particulier quand on est confronté au diagnostic dévastateur de cancer du pancréas. En plus, une réaction commune est de personnifier le cancer comme une entité maléfique qui doit être combattue pour sauver la vie du patient. Les armes pour cette bataille comprennent le scalpel d'un chirurgien, la chimiothérapie, la radiothérapie, les thérapies ciblées, les immunothérapies, les approches holistiques et la foi religieuse. Mais nous avons trop souvent oublié ou sous-estimé la contribution de la recherche translationnelle pour la médecine de précision, pour mieux adapter les thérapies et éviter les toxicités inutiles.Dans un sens biologique, qu'est-ce qu'un cancer du pancréas ou un cancer? Le cancer est une maladie génétique, soumise à un phénomène évolutif avec ses propres règles, contraintes et caractéristiques prévisibles qui mènent finalement à un phénotype unique.La stratégie "one size fits all" dans la PDA a souvent échoué dans les essais de nouveaux médicaments dans une population non sélectionnée.Cette thèse est une contribution modeste et authentique à une approche plus personnalisée du PDA, de l'acquisition tissulaire, à l'analyse de biomarqueurs tissulaires, à une analyse moléculaire plus profonde afin de mieux comprendre cette maladie mortelle et de proposer l'intégration de biomarqueurs dans le developpement d’etudes cliniques guides par les analyses moléculaires.
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
8

Chan, Derek Steven Hung Che. "Tumoral immune privilege in a murine model of pancreatic ductal adenocarcinoma." Thesis, University of Cambridge, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709503.

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9

Cook, Natalie. "The Notch pathway is a therapeutic target in pancreatic ductal adenocarcinoma." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609962.

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10

Roshan, Moniri Mani. "Pancreatic ductal-derived mesenchymal stem cells : their distribution, characterization and cytotoxic effect on pancreatic cancer cells." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43529.

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Mesenchymal stem cells (MSCs) have attracted significant attention in cancer research as a result of their accessibility, tumor-oriented homing capacity, and the feasibility of auto-transplantation. This study detected the sensitivity of pancreatic cancer cell lines (PCCs) to pancreatic-derived, engineered MSCs under different culture conditions. Pancreatic ductal tissue was extracted from adult human pancreas. MSCs were derived and expanded ex-vivo and verified to fulfil criteria for human MSCs according to the guidelines of the International Society for Cellular Therapy. MSCs were analyzed for distribution and migratory capacity to the site of pancreas and PCCs in in vivo and in vitro models, and found to have homing capacity to the pancreas and towards PCCs (MSCs were attracted to all PCCs compared to normal human A1F8 cells and they displayed significant attraction to the media obtained from cancer cells compared to normal media (p<0.05)). PCCs (BXPC3, ASPC1, Panc-1, TRM6 and HP62) were analyzed by FACS for TNF-α Related Apoptosis Inducing Ligand (TRAIL) receptors. MSCs engineered with non-secreting TRAIL (MSCnsTRAIL) and secreting TRAIL (MSCstTRAIL) and PTEN (MSCPTEN) were used for both direct and indirect co-cultures. TRAIL/PTEN expression was assessed by both ELISA and western blot analysis; higher molecular weight was observed in the MSCnsTRAIL (56kDA) compared with MSCstTRAIL (26kDa). The TRAIL content of supernanatats from MSCstTRAIL was significantly higher than MSCnsTRAIL (p<0.05). PTEN-RFP fusion protein showed a higher molecular weight of 74 kDa in comparison with endogenous PTEN (47 kDa). A real time detection of MSCs cytotoxicity on PCCs displayed proportional cancer cell death to the ratio of conditioned media used from MSCnsTRAIL, MSCstTRAIL, and MSCPTEN. Naive MSCs exhibit intrinsic cytotoxic effect on pancreatic cancer cells and this effect was potentiated by TRAIL/PTEN-engineering. This study provides a practical platform for the development of MSC-based therapy for pancreatic cancer.
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Books on the topic "Pancreatic ductal cancer":

1

E, Preece Paul, Cuschieri A, and Rosin R. David, eds. Cancer of the bile ducts and pancreas. Philadelphia, PA: Saunders, 1989.

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Tanaka, Masao. Intraductal Papillary Mucinous Neoplasm of the Pancreas. Springer, 2013.

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Tanaka, Masao. Intraductal Papillary Mucinous Neoplasm of the Pancreas. Springer, 2016.

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Tanaka, Masao. Intraductal Papillary Mucinous Neoplasm of the Pancreas. Springer London, Limited, 2013.

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Poterucha, John J. Hepatology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0211.

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The evaluation of patients who have abnormal liver test results includes many clinical factors: the chief complaints of the patient, patient age, risk factors for liver disease, personal or family history of liver disease, medications, and physical examination findings. Because of these many factors, designing a standard algorithm for the evaluation of abnormal liver test results is difficult and often inefficient. Nevertheless, with basic information, abnormalities can be evaluated in an efficient, cost-effective manner. Diseases that predominantly affect the biliary system are called cholestatic diseases. They can affect the microscopic ducts (eg, primary biliary cirrhosis) or the large bile ducts (eg, pancreatic cancer causing obstruction of the common bile duct), or both (eg, primary sclerosing cholangitis).

Book chapters on the topic "Pancreatic ductal cancer":

1

Sheel, Andrea, James Nicholson, Ioannis Sarantitis, John P. Neoptolemos, and William Greenhalf. "Secondary Screening for Inherited Pancreatic Ductal Adenocarcinoma." In Pancreatic Cancer, 1401–34. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7193-0_63.

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Sheel, Andrea, James Nicholson, Ioannis Sarantitis, John Neoptolemos, and William Greenhalf. "Secondary Screening for Inherited Pancreatic Ductal Adenocarcinoma." In Pancreatic Cancer, 1–34. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6631-8_63-1.

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Denbo, Jason W., and Jason B. Fleming. "Current Issues of Borderline Resectable Pancreatic Ductal Adenocarcinoma." In Pancreatic Cancer, 139–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-47181-4_11.

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Rösch, W. "Ductal Imaging in Pancreatic Cancer." In Diagnostic Procedures in Pancreatic Disease, 294–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71128-2_42.

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Hagland, Hanne R. "Cancer Cell Metabolism in Pancreatic Ductal Adenocarcinoma." In Textbook of Pancreatic Cancer, 219–34. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-53786-9_16.

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Roalsø, Marcus, Øyvind Holsbø Hald, Daniel Ansari, Roland Andersson, and Kjetil Søreide. "The Role of Epigenetics in Pancreatic Ductal Adenocarcinoma." In Textbook of Pancreatic Cancer, 321–36. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-53786-9_22.

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George, Ben. "Molecular Profiling in Pancreatic Ductal Adenocarcinoma." In Management of Localized Pancreatic Cancer, 133–41. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98944-0_12.

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Bednar, Filip, and Marina Pasca di Magliano. "Mouse Models of Pancreatic Ductal Adenocarcinoma." In Molecular Genetics of Pancreatic Cancer, 145–70. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6549-2_7.

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Wang, Liang, Dacheng Xie, and Daoyan Wei. "Pancreatic Acinar-to-Ductal Metaplasia and Pancreatic Cancer." In Methods in Molecular Biology, 299–308. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8879-2_26.

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Camelo, Felipe, and Anne Le. "The Intricate Metabolism of Pancreatic Cancers." In The Heterogeneity of Cancer Metabolism, 77–88. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_5.

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AbstractCurrently, approximately 95% of pancreatic cancers are pancreatic ductal adenocarcinomas (PDAC), which are the most aggressive form and the fourth leading cause of cancer death with extremely poor prognosis [1]. Poor prognosis is primarily attributed to the late diagnosis of the disease when patients are no longer candidates for surgical resection [2]. Cancer cells are dependent on the oncogenes that allow them to proliferate limitlessly. Thus, targeting the expression of known oncogenes in pancreatic cancer has been shown to lead to more effective treatment [3]. This chapter discusses the complexity of metabolic features in pancreatic cancers. In order to comprehend the heterogeneous nature of cancer metabolism fully, we need to take into account the close relationship between cancer metabolism and genetics. Gene expression varies tremendously, not only among different types of cancers but also within the same type of cancer among different patients. Cancer metabolism heterogeneity is often prompted and perpetuated not only by mutations in oncogenes and tumor-suppressor genes but also by the innate diversity of the tumor microenvironment. Much effort has been focused on elucidating the genetic alterations that correlate with disease progression and treatment response [4, 5]. However, the precise mechanisms by which tumor metabolism contributes to cancer growth, survival, mobility, and aggressiveness represent a functional readout of tumor progression (Fig. 1).

Conference papers on the topic "Pancreatic ductal cancer":

1

Capello, Michela, Michele Milella, Francesco Novelli, Paola Cappello, Sammy Ferri-Borgogno, Weidong Zhou, Giorgia Mandili, et al. "Abstract A2: Autoantibody signature in pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a2.

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Yung, Christina K., Christine Ouellete, Lee Timms, Michelle Sam, Kimberly Begley, Thomas J. Hudson, John D. McPherson, et al. "Abstract B18: Genomic analysis of pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-b18.

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Roy, Ishan, Noah P. Zimmerman, Susan Tsai, Douglas B. Evans, and Michael B. Dwinell. "Abstract A74: CXCL12 and CXCR4 are reciprocally expressed in normal pancreatic ducts and pancreatic ductal adenocarcinoma respectively." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a74.

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Tinsley, Samantha L., Rebecca A. Shelley, Mary C. Thoma, Goutham Narla, Rosalie C. Sears, and Brittany A. Allen-Petersen. "Abstract PR-008: The role of PP2A-B56α in acinar-to-ductal metaplasia and initiation of pancreatic ductal adenocarcinoma." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-pr-008.

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Cruz-Monserrate, Zobeida, Christina L. Roland, Defeng Deng, Thiruvengadam Arumugam, Anna Moshnikova, Oleg A. Andreev, Yana Reshetnyak, and Craig D. Logsdon. "Abstract B24: Targeting pancreatic ductal adenocarcinoma acidic microenvironment." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b24.

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Deng, Zijian, Xiangkun Xu, Juvenal Reyes, and Ken Kang-Hsin Wang. "Bioluminescence tomography-guided system for pre-clinical pancreatic cancer radiation research." In Clinical and Translational Biophotonics. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/translational.2024.jd6a.3.

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We innovated bioluminescence tomography(BLT)-guided system for orthotopic pancreatic ductal adenocarcinoma(PDAC) radiotherapy research. Our BLT localized PDAC with 1.25±0.19mm accuracy. BLT-guided conformal plan covered 100% of tumor with limited normal tissue involvement, consistent across inter-fraction case.
7

Perez-Mancera, Pedro A., David A. Tuveson, Alistair G. Rust, Andrew V. Biankin, Lodewyk F. A. Wessels, Stephen A. Wood, Christine A. Iacobuzio-Donahue, Christian Pilarsky, David A. Largaespada, and David J. Adams. "Abstract A64: The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a64.

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Valdez, Shannon M., Karam S. Takhar, Dorothy Leung, Allen Delaney, May Q. Wong, Karen K. Cham, David A. Owen, et al. "Abstract 1422: Cancer-associated fibroblasts influence the sensitivity of pancreatic cancer cells to gemcitabine in pancreatic ductal adenocarcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1422.

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Chen, Ru, Sheng Pan, Anirban Maitra, Diane Simeone, David Dawson, and Teresa Brentnall. "Abstract 2866: Proteins associated with pancreatic cancer survival in patients with resectable pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2866.

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Ungureanu, B. S., G. Claudia, D. Pirici, M. C. Irina, and S. Adrian. "Pancreatic Cancer Stem Cells Expression on Endoscopic Ultrasound Fine Needle Biopsy Pancreatic Ductal Adenocarcinoma Samples." In ESGE Days 2023. Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1766074.

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