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Relevant bibliographies by topics / Pancreatic Ductal

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Academic literature on the topic 'Pancreatic Ductal'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Pancreatic Ductal"

1

Wachsmann, Megan B., Laurentiu M. Pop, and Ellen S. Vitetta. "Pancreatic Ductal Adenocarcinoma." Journal of Investigative Medicine 60, no. 4 (April 1, 2012): 643–63. http://dx.doi.org/10.2310/jim.0b013e31824a4d79.

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Habib, Joseph R., Lingdi Yin, and Jun Yu. "Pancreatic ductal adenocarcinoma." Journal of Pancreatology 2, no. 3 (September 2019): 72–75. http://dx.doi.org/10.1097/jp9.0000000000000021.

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Konstantinidis, Ioannis T., Andrew L. Warshaw, Jill N. Allen, Lawrence S. Blaszkowsky, Carlos Fernandez-del Castillo, Vikram Deshpande, Theodore S. Hong, et al. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 257, no. 4 (April 2013): 731–36. http://dx.doi.org/10.1097/sla.0b013e318263da2f.

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Erickson, Lori A. "Pancreatic Ductal Adenocarcinoma." Mayo Clinic Proceedings 92, no. 9 (September 2017): 1461–62. http://dx.doi.org/10.1016/j.mayocp.2017.07.002.

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Longnecker, Daniel S. "Pancreatic Ductal Adenocarcinoma." American Journal of Pathology 189, no. 1 (January 2019): 6–8. http://dx.doi.org/10.1016/j.ajpath.2018.10.006.

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Crippa, Stefano, Stefano Partelli, and Massimo Falconi. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 266, no. 6 (December 2017): e108-e109. http://dx.doi.org/10.1097/sla.0000000000001921.

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Strobel, Oliver, and Markus W. Büchler. "Pancreatic Ductal Adenocarcinoma." Annals of Surgery 266, no. 6 (December 2017): e109-e110. http://dx.doi.org/10.1097/sla.0000000000001927.

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Izumi, Motoyoshi, Koichi Suda, Akira Torii, and Eisuke Inadama. "Pancreatic ductal myofibroblasts." Virchows Archiv 438, no. 5 (February 8, 2001): 442–50. http://dx.doi.org/10.1007/s004280000359.

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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.

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Al-Hawary, Mahmoud M., and Isaac R. Francis. "Pancreatic ductal adenocarcinoma staging." Cancer Imaging 13, no. 3 (2013): 360–64. http://dx.doi.org/10.1102/1470-7330.2013.9020.

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Dissertations / Theses on the topic "Pancreatic Ductal"

1

Kimura, Yoshito. "ARID1A Maintains Differentiation of Pancreatic Ductal Cells and Inhibits Development of Pancreatic Ductal Adenocarcinoma in Mice." Kyoto University, 2018. http://hdl.handle.net/2433/235986.

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Koustoulidou, Sofia. "Imaging p53 in pancreatic ductal adenocarcinoma." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:5e8aab43-59ca-45d9-9944-48f106e2826e.

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Pancreatic ductal adenocarcinoma (PDAC) represents 90% of pancreatic cancer cases and is characterised by poor survival rates and resistance to current therapeutic regimes as the majority of patients present with an already advanced disease at the time of diagnosis. Mutations of the TP53 tumour suppressor gene are a frequent event in tumourigenesis and appear in around 75% of pancreatic cancer cases just before the full development of PDAC and metastasis into the surrounding tissues. Molecular imaging tools, such as SPECT, using monoclonal antibodies specific towards tumour associated antigens, could aid the in vivo characterisation of biological processes and provide a non-invasive method for early diagnosis of cancer. Toward this end, a commercially available mouse monoclonal antibody against total p53 protein (anti-p53 (1C12)) was selected. Anti-p53 (1C12) was first evaluated in vitro regarding its specificity and affinity in cell lines with variable p53 status, derived from a genetically engineered mouse model of PDAC (KPC mice). The subcellular localisation of the p53 protein in the cell lines used was also studied. Following the selection of the antibody, the anti-p53 (1C12) was conjugated to the cell penetrating peptide TAT to facilitate cellular and nuclear translocation and then to p-SCN-Bn-DTPA to allow labeling with ¹¹¹In. Further in vitro evaluation was performed on the conjugated antibody, conferring subcellular translocation in fixed cells, unaffected binding affinity, favourable radiochemical yield and purity, and stability of the radioconjugate in serum. Retention of the radioconjugates was also observed and was signicantly different when compared to radiolabeled non-specific IgG₁-TAT in cells harbouring mutant p53. The ability of ¹¹¹In-BnDTPA-p53 (1C12)-TAT to selectively target endogenously expressed p53 was assessed in vivo using mouse allograft tumour models of the cell lines evaluated in vitro, and in genetically engineered KPC mice. This provided a preliminary 'proof-of-principle' concept for diagnostic detection of PDAC. The knowledge acquired from the current study may be used to develop a first imaging tracer against p53 which could significantly improve the biological evaluation of cancer.

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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.

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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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Machado, de Morais Ferreira R. "Investigating the origins of pancreatic ductal adenocarcinoma." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1473228/.

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Pancreatic ductal adenocarcinoma (PDAC) comprises 85% of all pancreatic cancers and is characterised by an extremely poor prognosis. It is becoming increasingly obvious that attention has to be focused on early tumour development, when the disease is still manageable. Thus, in this study, I aimed to assess the contribution of adult acinar and duct cells to PDAC development and to identify PDAC tumour-initiating cells (TICs). Our laboratory had previously identified Fbw7 as a potent tumour suppressor in PDAC (unpublished data). Fbw7F/F; KRasLSL-G12D/wt; Pdx1-Cre mice exhibited accelerated PDAC onset compared with KRasLSL-G12D/wt; Pdx1-Cre mice. I confirmed this observation and demonstrated that Fbw7 loss in the pancreatic epithelium had a greater proliferative effect in ductal cells, in the presence and absence of KRasG12D, leading to increased numbers of duct cells positive for phosphorylated histone 3. The selective loss of Fbw7 in adult ductal cells with concomitant KRasG12D expression (Fbw7F/F; KRasLSLG12D/ wt; Ck19-CreER mice) led to PDAC development, which was not preceded by mucinous lesions. These results were confirmed with the loss of p53 with simultaneous KRasG12D expression in adults duct cells (p53F/F; KRasLSL-G12D/wt; Ck19-CreER mice). The absence of mucinous PDAC precursors was not dependent on the genotype, as loss of Fbw7 in KRasG12D-expressing acinar cells allowed the development of mucinous murine pancreatic intraepithelial neoplasia (PanIN). Additionally, I induced bystander PanINs using orthotopic transplantation of PDAC cells. These results provide evidence that ductal cells can originate PDAC and that different pancreatic cells types might adopt different routes to PDAC development. Additionally, the observation of bystander PanINs questioned the sole pre-neoplastic nature of these lesions highlighting the need for a deeper understanding of PDAC biology. In the present work, I have also described a new marker of TICs within PDAC derived from pancreatic progenitors and adult ductal cells. Marker-high PDAC cells exhibited higher in vitro organoid-forming capacity, compared with marker-low cells, isolated from the primary tumour and after long-term cultures. Contrasting with marker-low tumour cells, marker-high cells were capable of forming secondary tumours at low numbers, demonstrating efficient tumour-initiating capacity and recapitulating the histology of the primary tumour source. These results could provide useful information for the development of PDAC targeted therapies.

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Lee, Alex Y. L. "Cell of origin in pancreatic ductal adenocarcinoma." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61174.

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Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a ductal morphology. Prior research has identified both pancreatic acinar and ductal cells as possible cells of origin for histologically similar PDAC. However, because different mutations were induced in acinar and ductal cells, apt comparisons could not be made to address whether the tumor cell of origin influences PDAC initiation, development, and other tumor differences. To address this open question, I induced oncogenic Ras expression (KrasG¹²D) with concomitant homozgyous Trp53 deletion at 4 weeks of age in a ductal cell specific (Sox9CreER; KrasLSL-G12D; Trp53flox/flox (“Duct:KPcKO”)) and an acinar cell specific (Ptf1aCreER; KrasLSL-G12D; Trp53flox/flox (“Acinar:KPcKO”)) mouse model. I found that Duct:KPcKO mice met their humane endpoints earlier (82 days post injection, p.i.) than the Acinar:KPcKO mice (128 days p.i.), for reasons associated with differences in the timing of PDAC onset. While tumors from both cells of origin were similarly proliferative and shared many physical characteristics, Duct:KPcKO mice developed tumors much earlier than Acinar:KPcKO mice and this was further associated with a difference in precursor lesion initiation. Specifically, ductal cells only formed high-grade lesions while acinar cells formed precursor lesions of all grades. These findings suggest that cell type intrinsic differences may allow ductal cells to rapidly form PDAC under genetically favorable conditions. In comparison, acinar cells likely require additional steps to alter cell identity and become duct-like – thus delaying PDAC initiation and extending survival. Taken together, I have demonstrated, by using cell type specific mouse models, that cell of origin can alter disease initiation, progression and impact PDAC phenotype.
Medicine, Faculty of
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Gall, Tamara. "Predicting disease recurrence in pancreatic ductal adenocarcinoma." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/41847.

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Pancreatic cancer (pancreatic ductal adenocarcinoma, PDAC) is one of the most lethal tumour types worldwide. The majority of patients present late with locally advanced or metastatic disease. Therefore, despite advances in operative techniques, perioperative management and oncological treatments, the overall 5-year survival remains < 5%. The reason for poor survival is due to disease recurrence even after curative surgical resection for small tumours. Determining factors that lead to disease recurrence may help in identifying those with a poor prognosis so that treatment options can be tailored to each patient. We investigated whether operative technique, clinicopathological factors or specific genetic mutations could influence disease recurrence. Further, we sought to identify a biomarker in the peripheral circulation that could be used as a prognostic marker. We confirmed that a positive medial resection margin and a high frequency of KRAS mutation in the tumour tissue result in early disease recurrence. Further, that the altered expression of five microRNAs may be useful as a blood-based prognostic predictor.

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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.

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Isohookana, J. (Joel). "Emerging novel prognostic markers in pancreatic ductal adenocarcinoma." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526220352.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive cancers, the 5-year survival rate being less than 5%. At the time of diagnosis, 90% of PDACs extend beyond the pancreas and distant metastases are often present. Due to aggressive growth, local expansion and early appearance of metastasis, primary PDAC tumours are local enough for curative surgical resection in only 10–20% of the cases. Adjuvant chemotherapy is indicated in these curative-treated cases, with slight improvement in survival. PDAC is considered to represent a heterogeneous group of biologically and prognostically different malignancies. Characterization of these subgroups is essential and there is an urgent need for more accurate biomarkers and targeted treatments in PDAC. In the current work, we immunohistochemically investigated the expression levels and prognostic values of oxidative stress markers (8-OHdG, Keap1, Prx I, II, III, V and VI), epigenetic histone modifiers (KDM4A, KDM4B, KDM4D and SIRT1–4), and cell-cycle regulators (p16, Rb, CDK4) and DNA-repair enzymes (FEN1 and MGMT) in the cohort of surgically treated PDAC patients. We found that Keap1 expression was associated with better pancreatic cancer-specific survival. Expression of antioxidative peroxiredoxins I, III, V and VI was also connected with a more favourable tumour characteristics and Prx I and VI showed prognostic value. When considering the biology of PDAC, we noticed that pivotal epigenetic regulation also occurred in exocrine pancreatic tissue adjacent to resection margins. Overexpression of the cell-cycle regulator CDK4 and the DNA-repair enzyme FEN1 in the whole population, and elevated expression level of MGMT in the most high-risk patients were connected with worse prognosis. The results of the study can be utilized in the future when individualized therapies are being designed for PDAC patients. Due to occurrence of the epigenetic regulation also in exocrine pancreatic tissue adjacent to resection margins, it could be evaluated in future for routine diagnostics and treatment optimization. The potential role of MGMT in the development of PDAC chemoresistance should be studied in the future
Tiivistelmä Haiman duktaalinen adenokarsinooma (PDAC) on yksi aggressiivisimmista syöpäsairauksista. Viiden vuoden elossaoloennuste on vain lähellä 5 prosenttia. Diagnoosihetkellä 90% haiman adenokarsinoomista yltää haiman ulkopuolelle ja usein kasvain on jo lähettänyt etäpesäkkeitä. Kasvutaipumuksen sekä metastasoinnin takia kuratiivinen kirurginen hoito on mahdollista vain 10–20% tapauksista. Liitännäissolunsalpaajahoito on aiheellista näissä kuratiivistavoitteisesti hoidetuissa tapauksissa. Kuitenkin vaikutus kokonaiselossaoloaikaan on melko vähäinen. Uusimman tutkimustiedon valossa PDAC:aa pidetäänkin heterogeenisenä ryhmänä biologisesti ja ennusteellisesti erilaisia tautiryhmiä. Näiden tautiryhmien tunteminen ja tunnistaminen riittävän tarkkojen merkkiaineiden avulla olisi ensiarvoisen tärkeää, jotta hoitoja voitaisiin kohdentaa niistä hyötyville potilaille. Väitöskirjatutkimuksessa selvitimme immunohistokemiallisin menetelmin oksidatiivisen stressin merkkiaineiden (8-OHdG, Keap1, Prx I, II, III, V ja VI), epigeneettisten histonimodifikaattorien (KDM4A, KDM4B, KDM4D ja SIRT1–4) sekä solusyklin säätelijöiden (p16, Rb, CDK4) ja DNA-korjausentsyymien (FEN1 ja MGMT) ilmentymistä ja ennusteellista arvoa kirurgisesti hoidetuilla PDAC-potilailla. Tutkimuksessamme totesimme, että kasvainkudoksen Keap1-ilmentymä yhdistyi parempiennusteiseen taudinkuvaan. Antioksidatiivisten peroksiredoksiinien I, III, V ja VI ilmentyminen yhdistyi niin ikään suotuisampaan kasvaimen fenotyyppiin ja Prx I ja VI osoittivat ennusteellista arvoa. Havaitsimme lisäksi, että PDAC:n biologiaan keskeistesti vaikuttavaa epigeneettistä säätelyä tapahtuu myös malignin haimakudoksen viereisessä eksokriinisessä haimakudoksessa. Solusyklin säätelijä CDK4:n ja DNA-korjausentsyymi FEN1:n voimakas ilmentyminen koko tutkimuspopulaatiossa sekä kohonnut MGMT:n ilmentyminen korkeimman riskin potilailla yhdistyivät huonompaan taudin ennusteeseen. Väitöskirjatyön tutkimustuloksia voidaan tulevaisuudessa hyödyntää, kun tutkitaan yksilöllisiä hoitomuotoja PDAC-potilailla. Koska epigeneettistä säätelyä tapahtuu myös syövän viereisessä eksokriinisessa haimakudoksessa, voidaan tulevaisuudessa tämän kudoksen arviointia mahdollisesti käyttää rutiinisti diagnostiikassa sekä hoidon optimoinnissa. MGMT:n mahdollinen rooli PDAC:n kemoresistenssin kehittymisessä tulisi tulevaisuudessa selvittää

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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

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Books on the topic "Pancreatic Ductal"

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Diagnostic pathology: Hepatobiliary and pancreatic. Salt Lake City: Amirsys, 2011.

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Lamps, Laura W. Diagnostic pathology: Normal histology. Salt Lake City, Utah: Amirsays, 2013.

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Guelrud, Moises. ERCP in pediatric practice: Diagnosis and treatment. Oxford: Isis Medical Media, 1997.

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L, Carr-Locke David, and Fox Victor L, eds. ERCP in pediatric practice: Diagnosis and treatment. Oxford: Isis Medical Media, 1997.

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Hoe, L. van. Atlas of cross-sectional and projective MR cholangiopancreatography. Berlin: Springer, 1999.

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G, Bohorfoush Anthony, ed. Interpretation of ERCP: With associated digital imaging correlation. Philadelphia: Lippincott-Raven, 1997.

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Carton, James. Pancreatic pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0009.

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This chapter discusses pancreatic pathology and covers pancreatic malformations, acute pancreatitis, chronic pancreatitis, pancreatic ductal carcinoma, pancreatic neuroendocrine tumours, pancreatic cystic tumours, and acinar cell carcinoma.

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Carton, James. Pancreatic pathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0008.

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Pancreatic malformations 132Acute pancreatitis 133Chronic pancreatitis 134Pancreatic ductal carcinoma 135Pancreatic endocrine tumours 136Pancreatic cystic tumours 138Acinar cell carcinoma 139• Common developmental anomaly in which pancreatic tissue is located outside the usual position of the pancreas.• The duodenum is the most common site, but it can be seen in the jejunum and ileum and within a Meckel's diverticulum (...

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Biliary and pancreatic ductal epithelia: Pathobiology and pathophysiology. New York: M. Dekker, 1997.

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

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Book chapters on the topic "Pancreatic Ductal"

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Izumi, Motoyoshi, and Koichi Suda. "Pancreatic Ductal Myofibroblasts." In Pancreas - Pathological Practice and Research, 56–66. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000100401.

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Matthews, Robert. "Pancreatic Ductal Adenocarcinoma." In PET/MR Imaging, 113–14. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65106-4_50.

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Pour, Parviz M., Yoichi Konishi, Günter Klöppel, and Daniel S. Longnecker. "Ductal Adenocarcinoma." In Atlas of Exocrine Pancreatic Tumors, 117–53. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68311-7_8.

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Porter, Kristin K. "Case 100: Pancreatic Ductal Disruption." In Pancreatic Imaging, 433–35. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_100.

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D’Onofrio, Mirko, Paola Capelli, Riccardo De Robertis, Paolo Tinazzi Martini, Emilo Barbi, Claudia Zampini, Stefano Crosara, Giovanni Morana, and Roberto Pozzi Mucelli. "Ductal Adenocarcinoma." In Imaging and Pathology of Pancreatic Neoplasms, 1–101. Milano: Springer Milan, 2014. http://dx.doi.org/10.1007/978-88-470-5678-7_1.

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Chhieng, David C., and Edward B. Stelow. "Pancreatic Ductal Adenocarcinoma and Its Variants." In Pancreatic Cytopathology, 35–66. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-68947-0_3.

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Schoenberg, M. H., K. H. Link, F. Gansauge, and H. G. Beger. "Multimodal Therapies for Pancreatic Ductal Adenocarcinoma." In Pancreatic Disease, 417–30. London: Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-0801-6_38.

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Rowe, Steven P. "Case 91: Chronic Pancreatitis Ductal Changes." In Pancreatic Imaging, 395–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_91.

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Rowe, Steven P. "Case 93: Chronic Pancreatitis, Ductal Stricture." In Pancreatic Imaging, 403–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_93.

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Levi, Joe U., Javier Casillas, Roberto Ruiz-Cordero, Monica T. Garcia-Buitrago, and Peter Hosein. "Pancreatic Ductal Adenocarcinoma (PDAC)." In Multidisciplinary Teaching Atlas of the Pancreas, 481–552. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46745-9_11.

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Conference papers on the topic "Pancreatic Ductal"

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Safi, SA, L. Haeberle, S. Babaei, L. Dizdar, WT Knoefel, and A. Krieg. "Survivin expression in the Pancreatic Ductal Adenocarcinoma." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695443.

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Arnold, F., J. Gout, L. Perkhofer, T. Seufferlein, P. Frappart, and A. Kleger. "RINT1 downregulation disrupts pancreatic ductal adenocarcinoma homeostasis." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716068.

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Veenstra, Veronique, Helene Damhofer, Tom van Leusden, Jan Kessler, Jan Paul Medema, Hanneke van Laarhoven, Louis Vermeulen, and Maarten Bijlsma. "Abstract 5177: Heterogeneity of pancreatic ductal adenocarcinoma visualized." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5177.

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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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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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Cao, Liwei, Chen Huang, Daniel Cui Zhou, Oliver F. Bathe, Daniel W. Chan, Ralph H. Hruban, Li Ding, Bing Zhang, and Hui Zhang. "Abstract 17: Proteogenomic characterization of pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-17.

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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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Sivakumar, Shivan, Enas Abu-Shah, David Ahern, Nagina Mangal, Srikanth Reddy, Aniko Rendek, Zahir Soonawalla, Michael Silva, Mark Middleton, and Michael L. Dustin. "Abstract A91: T-cell regulation in pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a91.

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Cho, Kyung Cho, Ralph Hruban, Hui Zhang, Chen Huang, Bing Zhang, Daniel Cui Zhou, Li Ding, and Emily Boja. "Abstract A60: Integrated proteogenomic characterization of pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-a60.

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Reports on the topic "Pancreatic Ductal"

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Betzler, Christopher. Differential Gene Expression in Pancreatic Ductal Adenocarcinoma and Stromal Tissue: Prognostic and Therapeutic Implications. Science Repository, June 2019. http://dx.doi.org/10.31487/j.jso.2019.02.11.

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