Relevant bibliographies by topics / Pancreatic cancer

Academic literature on the topic 'Pancreatic cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Pancreatic cancer"

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Li, Yumin, and Xiaohui Wang. "PET Imaging in Pancreatic Cancer." SDRP Journal of Food Science & Technology 4, no. 3 (2019): 659–69. http://dx.doi.org/10.25177/jfst.4.3.ra.493.

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Kashyap, Monika. "Pancreatic Cancer: A Silent Killer." International Journal of Science and Research (IJSR) 13, no. 5 (May 5, 2024): 136–38. http://dx.doi.org/10.21275/mr24430192939.

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Shi, Chanjuan, Ralph H. Hruban, and Alison P. Klein. "Familial Pancreatic Cancer." Archives of Pathology & Laboratory Medicine 133, no. 3 (March 1, 2009): 365–74. http://dx.doi.org/10.5858/133.3.365.

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Abstract Context.—Approximately 5% to 10% of individuals with pancreatic cancer report a history of pancreatic cancer in a close family member. In addition, several known genetic syndromes, such as familial breast cancer (BRCA2), the Peutz-Jeghers syndrome, and the familial atypical multiple mole melanoma syndrome, have been shown to be associated with an increased risk of pancreatic cancer. The known genes associated with these conditions can explain only a portion of the clustering of pancreatic cancer in families, and research to identify additional susceptibility genes is ongoing. Objective.—To provide an understanding of familial pancreatic cancer and the pathology of familial exocrine pancreatic cancers. Data Sources.—Published literature on familial aggregation of pancreatic cancer and familial exocrine pancreatic tumors. Conclusions.—Even in the absence of predictive genetic testing, the collection of a careful, detailed family history is an important step in the management of all patients with pancreatic cancer. While most pancreatic cancers that arise in patients with a family history are ductal adenocarcinomas, certain subtypes of pancreatic cancer have been associated with familial syndromes. Therefore, the histologic appearance of the pancreatic cancer itself, and/or the presence and appearance of precancerous changes in the pancreas, may increase the clinical index of suspicion for a genetic syndrome.
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Gubergrits, N. B., N. V. Byelyayeva, A. A. Suprun, and I. A. Kozinskaya. "Pancreatic syphilis mimicking cancer." Herald of Pancreatic Club 59, no. 2 (May 15, 2023): 35–38. http://dx.doi.org/10.33149/vkp.2023.02.06.

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Since the incidence of syphilis is increasing, the number of pancreatic lesions is expected to increase too. Pancreatic syphilis can be congenital or acquired. The pancreas is affected in 10–80% of patients with congenital syphilis. Infection of the pancreas occurs most often during the second half of pregnancy. Morphologically, there are five types of congenital pancreatic syphilis: gummy; diffuse interstitial pancreatitis, which can be combined with multiple miliary gummas and atrophy of the pancreatic parenchyma; indurative fibrous type; with atrophy of the lobules (atrophic type); and with a predominant lesion of the pancreatic ducts —sialangitis pancreatica. In congenital syphilis, the pancreatic head is mostly affected. Early and severe damage to the islets of Langerhans is typical. Acquired pancreatic syphilis is less common than congenital syphilis. Morphologically, it has three types: the edematous-infiltrative type, in secondary syphilis; the gummy type (pancreatitis gummosa), in tertiary syphilis; and sclerotic pancreatitis, or pancreatitis sclerotica, or “syphilitic cirrhosis of the pancreas”. The latter type is usually the outcome of the first two morphological types. Clinically acquired pancreatic syphilis proceeds according to the type of recurrent chronic pancreatitis, i.e., with periodic exacerbations (pancreatic attacks), but the pain is rarely intense, and the phenomenon of “deviation” of enzymes into the blood is rarely observed. This clinical type more often corresponds to the edematous-infiltrative morphological type of syphilitic organ damage, and less often to the gummy type. It should be noted that acquired pancreatic syphilis occurs against the background of specific damage to the liver, heart, aorta, kidneys, skin, stomach, central nervous system, etc. The differential diagnosis of gummy pancreatic lesions and pancreatic cancer is especially complicated. Antisyphilitic treatment should be administered. Due to a toxic-allergic reaction, the symptoms of pancreatitis may exacerbate at the start of a specific therapy.
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VG, Zaitsev. "Risks of Pancreatic Cancer and Dietary Glucosinolates." Gastroenterology & Hepatology International Journal 6, no. 2 (July 1, 2021): 1–3. http://dx.doi.org/10.23880/ghij-16000186.

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Pancreatic cancer has poor prognosis and is detected in the late stages usually. There is no way for specific prevention of pancreatic cancer. Brassicaceae vegetable-produced glucosinolates and isothiocyanates are known as anticancer substances. Aim of this mini-review was to estimate opportunities of pancreatic cancer prevention by glucosinolates and their derivatives. Results of ten clinical and epidemiologic studies were discussed. It was shown no clear and solid evidence for positive effects of glucosinolates, isothiocyanates or plants containing these substances in pancreatic cancer prevention or treatment have been observed
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Krishnamoorthy, Mithunah, John G. Lenehan, Jeremy P. Burton, and Saman Maleki Vareki. "Immunomodulation in Pancreatic Cancer." Cancers 12, no. 11 (November 12, 2020): 3340. http://dx.doi.org/10.3390/cancers12113340.

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Pancreatic cancer has a high mortality rate, and its incidence is increasing worldwide. The almost universal poor prognosis of pancreatic cancer is partly due to symptoms presenting only at late stages and limited effective treatments. Recently, immune checkpoint blockade inhibitors have drastically improved patient survival in metastatic and advanced settings in certain cancers. Unfortunately, these therapies are ineffective in pancreatic cancer. However, tumor biopsies from long-term survivors of pancreatic cancer are more likely to be infiltrated by cytotoxic T-cells and certain species of bacteria that activate T-cells. These observations suggest that T-cell activation is essential for anti-tumor immunity in pancreatic cancers. This review discusses the immunological mechanisms responsible for effective anti-tumor immunity and how immune-based strategies can be exploited to develop new pancreatic cancer treatments.
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Jeekel, J. "Pancreatic Cancer: Surgery of pancreatic cancer." Annals of Oncology 5 (1994): S73—S74. http://dx.doi.org/10.1093/annonc/5.suppl_3.s73.

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Shaeir, Sayed Shaker, Mohamed Atef ElKordy, Mohamed Emam Sobeih, Rasha Mahmoud Allam, and Ayman Hanafy. "Pancreatico-jejunostomy versus pancreatico-gasrostomy after pancreatico-duodenectomy in decreasing postoperative pancreatic fistula." Egyptian Journal of Surgery 42, no. 2 (April 2023): 473–81. http://dx.doi.org/10.4103/ejs.ejs_91_23.

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Background Pancreatico-duodenectomy is still the cornerstone in curating pancreatic and periampullary cancers. Many techniques for pancreatic anastomosis were described. Pancreatico-gastrostomy (PG) may be a suitable technique, especially in small pancreatic ducts where the stitching of duct to mucosa may be difficult. Still, the results of pancreatico-gastrostomy compared to pancreatico-jejunostomy (PJ) in terms of morbidity are not well studied; hence, this study was designed to investigate. Objective To compare pancreatico-gastrostomy versus pancreatico-jejunostomy post pancreatico-duodenectomy from points of operative techniques and characteristics, and postoperative morbidity and mortality. Patients and methods The Cohort study included all cases diagnosed with either pancreatic head or periampullary cancers and underwent pancreatico-duodenectomy at National Cancer Institute (NCI), Cairo University, between January 2021 and February 2023. Cases were enrolled into one of the two groups, group 1: underwent pancreatico-gastrostomy, while group 2 underwent pancreatico-jejunostomy. The two groups were compared by: Demographic characteristics, preoperative investigations results, operative, postoperative data and histopathological results of the specimens resected. Results Incidence of the pancreatic leak was not significantly different in both groups (17.6% versus 15.8% for PG and PJ respectively, P=0.833), operative time was shorter in a pancreatico-gastrostomy group (310, 355 min, P=0.001), Delayed gastric emptying (DGE) was less occurred in cases of pancreatico-gastrostomy (5.9%, 31.6%, P=0.006). Postoperative mortality was not different in both groups (8.8%, 2.6% for PG and PJ respectively, P=0.338). Conclusion Regarding the incidence of postoperative pancreatic fistula, both reconstruction methods produce comparable postoperative results. Pancreatico-gastrostomy is a good alternative technique to the standard pancreatico-jejunostomy.
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Kasuga, Akiyoshi, Takeshi Okamoto, Shohei Udagawa, Chinatsu Mori, Takafumi Mie, Takaaki Furukawa, Yuto Yamada, et al. "Molecular Features and Clinical Management of Hereditary Pancreatic Cancer Syndromes and Familial Pancreatic Cancer." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1205. http://dx.doi.org/10.3390/ijms23031205.

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Hereditary pancreatic cancers are caused by several inherited genes. Familial pancreatic cancer is defined as pancreatic cancer arising in a patient with at least two first-degree relatives with pancreatic cancer in the absence of an identified genetic cause. Hereditary pancreatic cancer syndromes and familial pancreatic cancers account for about 10% of pancreatic cancer cases. Germline mutations in BRCA1, BRCA2, ATM, PALB2, CDKN2A, STK11, and TP53 and mismatch repair genes (MLH1, MSH2, MSH6, PMS2, and EPCAM) are among the well-known inherited susceptibility genes. Currently available targeted medications include poly (ADP-ribose) polymerase inhibitors (PARP) for cases with mutant BRCA and immune checkpoint inhibitors for cases with mismatch repair deficiency. Loss of heterozygosity of hereditary pancreatic cancer susceptibility genes such as BRCA1/2 plays a key role in carcinogenesis and sensitivity to PARP inhibitors. Signature 3 identified by whole genome sequencing is also associated with homologous recombination deficiency and sensitivity to targeted therapies. In this review, we summarize molecular features and treatments of hereditary pancreatic cancer syndromes and surveillance procedures for unaffected high-risk cases. We also review transgenic murine models to gain a better understanding of carcinogenesis in hereditary pancreatic cancer.
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Ahn, Daniel H., and Tanios Bekaii-Saab. "Ampullary Cancer: An Overview." American Society of Clinical Oncology Educational Book, no. 34 (May 2014): 112–15. http://dx.doi.org/10.14694/edbook_am.2014.34.112.

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Ampullary cancers are rare, accounting for only 0.2% of gastrointestinal cancers and approximately 7% of all periampullary cancers.1They arise from the ampullary complex, distal to the confluence of the common bile and pancreatic duct ( Fig. 1 ). In contrast to other periampullary malignancies, true ampullary cancers present earlier in their disease course with symptoms that result from biliary obstruction. It is often difficult to distinguish primary ampullary cancers from other periampullary cancers preoperatively. In early stages, ampullary cancers are surgically treated, similar to pancreatic cancers, and typically with a pancreatico-duodenoectomy (or Whipple procedure). Because of their earlier presentation, resection rates for all patients are much higher than other periampullary carcinomas. Moreover, their prognosis tends to be better than those with other periampullary- and pancreatic-originating cancers. In patients with true ampullary cancer, there is very limited data to guide physicians on the choice of therapy, largely because of the rarity of the disease and the paucity of related research. Herein, we provide an overview of the biology, histology, current therapeutic strategies, and potential future therapies for carcinomas arising from the ampulla of Vater.
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Dissertations / Theses on the topic "Pancreatic cancer"

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Sirivatanauksorn, Vorapan. "Molecular analysis of pancreatic cancer." Thesis, Imperial College London, 1999. http://hdl.handle.net/10044/1/7489.

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Isaksson, Bengt. "Insulin resistance in pancreatic cancer /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-493-3/.

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Shehata, Fady Fouad Amin. "Pancreatic cancer : a developmental quest." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101742.

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Pancreatic cancer is considered the fifth leading cause of cancer deaths in Canada and one of the most fatal diseases in the world. Its definite underlying cause is still unidentified, and its actual cell of origin remains unclear. Unfortunately, most of the current research on the pancreas is focused on one disease only, namely diabetes with much less consideration for other pancreatic diseases. Diabetes has been extensively studied from a developmental aspect, and continues to attract the interest of numerous researchers. On the contrary, few accomplishments have been done to decode the developmental errors occurring in pancreatic cancer. It is therefore necessary to allocate more research resources to address this disease from a developmental aspect.
This study provides a literature review of the pancreas concerning its anatomy and function, transcription factors and signaling pathways controlling its development, and the role of these signaling pathways in pancreatic cancer. The review provides distinct emphasis on three important aspects. First, a review of pancreas development is provided, with a focus on different transcription factors and signaling pathways involved in this process. Second, it addresses how the signaling pathways which play a role in pancreas development are the same signaling pathways that play a role in pancreatic cancer, additional emphasis is placed on describing the genetic alterations occurring in pancreatic cancer. Third, a methodology of approaching pancreatic cancer research from a developmental aspect is presented. Using an example of one gene, Anterior gradient 2 (Agr2), is highly expressed in pancreatic cancer in ductal cells only, and might play a role in ductal cell development of the pancreas. Thus, the main objective of this review is to provide a developmental framework for the analysis of pancreatic cancer.
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Nakao, Akimasa. "Oncological problems in pancreatic cancer surgery." Nagoya University School of Medicine, 2000. http://hdl.handle.net/2237/5352.

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Wang, Lei. "Molecular Probes for Pancreatic Cancer Imaging." PDXScholar, 2016. http://pdxscholar.library.pdx.edu/open_access_etds/3108.

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Pancreatic ductal adenocarcinoma (PDAC) has the poorest five-year survival rate of any cancer. Currently, there are no effective diagnostics or chemotherapeutics. Surgical resection is the only curative therapy. However, most patients experience recurrence due largely to challenges in assessing tumor margin status in the operating room. Molecular probes that selectively highlight pancreatic cancer tissue, having the potential to improve PDAC margin assessment intraoperatively, are urgently needed. In this work, a series of red and near-infrared fluorescent probes is reported. Two were found to distribute to normal pancreas following systemic administration. One selectively accumulates in genetically modified mouse models of PDAC, providing cancer-specific fluorescence. In contrast to the small molecule probes reported previously, it possesses inherent affinity for PDAC cells and tissue, and thus does not require conjugation to targeting agents. Moreover, the probe exhibits intracellular accumulation and enables visualization of four levels of structure including the whole organ, tissue, individual cells and subcellular organelles. It can thus promote new strategies for precision image-guided surgery, pancreatic cancer detection, the monitoring of therapeutic outcomes and basic research.
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Mesenhöller, Maike. "Endogenous photosensitisation of pancreatic cancer cells." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343044.

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Lunardi, Serena. "Tumour-stroma interaction in pancreatic cancer." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:8cb21185-38ab-40ae-8f12-2b52cc61a988.

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Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant desmoplastic reaction driven by pancreatic stellate cells (PSCs). There is accumulating evidence that PSCs influence the malignant phenotype of PDAC. The aim of this study was to analyse the tumour response to radiation treatment in the presence of PSCs and to investigate the cytokine network in the coculture of PSCs and pancreatic cancer cells (PCCs). PSCs were used in coculture with different PCC lines. Clonogenic survival assays of several PCC lines cocultured with PSCs showed decreased radiosensitivity. This effect was abrogated by inhibition of the β1-integrin/FAK signalling pathway. Furthermore, tumour regrowth experiments after irradiation showed that coinjected PSCs were radioprotective for PCCs after single-dose and fractionated irradiation in xenografts. In addition, we examined the expression of 50 proteins in the supernatants of PCCs and PSCs in mono- and coculture conditions. The detected cytokine expression profile of PSCs included many proinflammatory factors. Also, we identified IP-10 as the chemokine with the highest differential upregulation in PSCs by paracrine stimuli from five different PCC lines. Human PDAC with a high stroma component had elevated IP-10 mRNA expression. IP-10 did not stimulate tumour cell growth and migration in our conditions even though several PCCs expressed its cognate receptor CXCR3. Nevertheless, we discovered that in human PDAC samples IP-10 and CXCR3 mRNA levels correlated with the presence of CD3ε, CD4, FoxP3, CTLA4 and CD39 used as surrogate markers for T regulatory cells (Tregs), known to exert an immunosuppressive effect. In conclusion, these data demonstrate that PSCs enhance survival of PCCs to radiation by activating β1-integrin/FAK signalling. Furthermore, the interaction between the tumour stroma in pancreatic cancer may support an immunosuppression by chemoattraction of Tregs following upregulation of IP-10. Further characterisation of the paracrine signalling between PCCs, PSCs and immune cells will improve the understanding of pancreatic cancer biology and could lead to the identification of new targets for multimodal therapy.
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Quinn, Bridget A. "Novel Therapeutic Strategies for Pancreatic Cancer." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/4671.

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Pancreatic cancer is a devastating disease that leaves patients with a very poor prognosis and few therapeutic options. Many of the treatment options available are the same that have been used for almost 2 decades. There is a dire need for both novel treatments for this disease as well as novel strategies of treatment. This body of work will introduce and provide evidence in support of a novel combination therapy for pancreatic cancer treatment, a novel strategy of modifying currently used chemotherapeutics for pancreatic cancer therapy, and a novel transgenic preclinical mouse model of pancreatic cancer. Sabutoclax, an antagonist of the anti-apoptotic Bcl-2 proteins, and Minocycline, a commonly used antibiotic, show potent synergy when used in combination in both pancreatic cancer cells and in multiple immune-deficient and immune-competent mouse models of pancreatic cancer. Sabutoclax alone is capable of inducing cell cycle arrest and apoptosis in cells and its cytotoxicity is enhanced significantly when combined with Minocycline. This combination results in the loss of Stat3 activation both in vitro and in vivo, which is essential for its toxicity. It also inhibits tumor growth and prolongs survival in the KPC transgenic mouse model of pancreatic cancer. Also presented here are studies that demonstrate efficacy in vivo of modified versions of Gemcitabine and Paclitaxel. These drugs are linked to a peptide that shows specificity for the EphA2 receptor, which is overexpressed on the surface of pancreatic cancer cells and only minimally on normal cells. This peptide results in increased cellular uptake of drug, as it is bypassing its normal mechanism of entry. These normal mechanisms are often dysregulated in cancer, leading to decreased uptake and drug resistance. The use of these modified drugs show significantly increased tumor growth inhibition as compared to the parent drug alone. Finally, we provide data on the characterization of a novel transgenic mouse model of pancreatic cancer. This model, the Pan Met View (PMV) mouse, combines the commonly used KPC transgenic mouse model of pancreatic cancer and a mouse that expresses a Luciferase reporter gene under the control of the cancer-specific promoter, CCN1. Our data shows that double transgenic PMV mice can now be used to follow primary tumor and metastasis development in real time by Bioluminescent imaging (BLI) through disease progression and potentially therapy. This strategy will enhance the use of genetically engineered mouse models (GEMMS) to study cancer initiation and progression with potential to non-invasively monitor therapy. These chapters present novel and exciting data that have the potential to open multiple avenues of translational study and result in significant advances in pancreatic cancer therapy.
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Fesinmeyer, Megan Dann. "Pancreatic cancer risk and prevention : association with PPARG gene and policy analysis of tabacco-related pancreatic cancer /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8440.

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Kottabi, Zahra. "Statistical Modeling and Analysis of Breast Cancer and Pancreatic Cancer." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4350.

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Abstract The object of the present study is to apply statistical modeling and estimate the mean of optimism of breast cancer patients as function of attribute variables; delay, education and age for each race of breast cancer patients. Moreover, to investigate the nonlinear association between optimism, education, age and delay with respect to each race and both. Furthermore, to develop differential equations that will characterize the behavior of the pancreatic cancer tumor size as a function of time. Having such differential equations, the mean solution of which once plotted will identify the rate of change of tumor size as a function of age. The structures of the differential equations characterize the growth of pancreatic cancer tumor. Once we have developed the differential equations and their solutions, and the object of the present study is to probabilistically evaluate commonly used methods to perform survival analysis of medical patients to validate the quality of the differential system and discuss its usefulness. In the last study, a comparison of parametric, semi-parametric and nonparametric analysis of probability survival time models. The first part of the evaluation of survival time by applying the statistical tests will guide us to how precede the actual cancer data and second part, identifying the parametric survival time function for each race and both. Moreover, we will evaluate the Kernel density, the popular Kaplan-Meier (KM) and the Cox Proportional Hazard (Cox PH) models by using actual pancreatic cancer data. As expected, the parametric survival analysis when applicable gives the best results followed by the not commonly used nonparametric Kernel density approach for evaluations actual cancer data.
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Books on the topic "Pancreatic cancer"

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Su, Gloria H. Pancreatic Cancer. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592597807.

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Cameron, John L. Pancreatic cancer. Hamilton, Ont: BC Decker, 2001.

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Neoptolemos, John P., Raul Urrutia, James Abbruzzese, and Markus W. Büchler, eds. Pancreatic Cancer. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6631-8.

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Su, Gloria H., ed. Pancreatic Cancer. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-287-2.

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Lowy, Andrew M., Steven D. Leach, and Philip A. Philip, eds. Pancreatic Cancer. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-69252-4.

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Riess, Hanno, Andrea Goerke, and Helmut Oettle. Pancreatic Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-71279-4.

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Reber, Howard A., ed. Pancreatic Cancer. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1810-4.

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Heiken, Jay, ed. Pancreatic Cancer. Cambridge: Cambridge University Press, 2008. http://dx.doi.org/10.1017/cbo9780511575440.

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Su, Gloria H., ed. Pancreatic Cancer. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8879-2.

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Evans, Douglas B., Peter W. T. Pisters, and James L. Abbruzzese, eds. Pancreatic Cancer. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/b97317.

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Book chapters on the topic "Pancreatic cancer"

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Arellano, Ronald S., and Ryan Nipp. "Pancreatic Cancer." In Image-Guided Interventions in Oncology, 287–98. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48767-6_17.

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Yamada, Shigeu, Kohtaro Terashima, Makoto Shinoto, Shigeo Yasuda, Miho Shiomi, and Tetsuro Isozaki. "Pancreatic Cancer." In Carbon-Ion Radiotherapy, 221–28. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54457-9_26.

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Pek, Chulja J. "Pancreatic Cancer." In Principles of Specialty Nursing, 261–76. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-76457-3_17.

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Chang, Jennifer S., and Mekhail Anwar. "Pancreatic Cancer." In Handbook of Evidence-Based Radiation Oncology, 441–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_20.

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Brunner, Thomas, and Daniel Schanne. "Pancreatic Cancer." In Target Volume Definition in Radiation Oncology, 131–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45934-8_7.

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Granov, Anatoliy, Leonid Tiutin, and Thomas Schwarz. "Pancreatic Cancer." In Positron Emission Tomography, 127–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21120-1_10.

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Aggarwal, Gaurav, and Suresh T. Chari. "Pancreatic Cancer." In Geriatric Gastroenterology, 581–85. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-1623-5_62.

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Calvo, Felipe A., Ignacio Azinovic, Gerardo Zornoza, Juan Voltas, Fernando Pardo, and Javier Alvarez-Cienfuegos. "Pancreatic Cancer." In Intraoperative Radiotherapy, 57–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84183-5_8.

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Daugherty, Larry C., Brandon J. Fisher, Christin A. Knowlton, Michelle Kolton Mackay, David E. Wazer, Anthony E. Dragun, James H. Brashears, et al. "Pancreatic Cancer." In Encyclopedia of Radiation Oncology, 609. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1213.

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Li, Peiwen. "Pancreatic Cancer." In Alternative and Complementary Therapies for Cancer, 185–204. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-0020-3_8.

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Conference papers on the topic "Pancreatic cancer"

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Babu, V. Kiran, and Praveen Mathew. "Primary Pancreatic Tuberculosis Mimicking Pancreatic Body Cancer." In ENDOCON 2024. Thieme Medical and Scientific Publishers Pvt. Ltd., 2024. http://dx.doi.org/10.1055/s-0044-1786265.

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Rinja, E., V. Sandru, R. Plescuta, A. Butuc, D. Vascu, V. Ionescu, R. Bala, et al. "PANCREATIC CYSTIC LESIONS: DOCTOR, DO I HAVE PANCREATIC CANCER!?" In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705027.

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Garon, Adam, Suresh Venkatachalapathy, Ricardo Correia, Sergiy Korposh, Steve Morgan, Seung-Woo Lee, George Gordon, et al. "Fabrication of an Optical Fibre Biosensor towards Endoscopic Ultrasound Guided Pancreatic Cancer Detection." In Optical Fiber Sensors. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/ofs.2023.th4.3.

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Mucin in pancreatic cyst fluid is linked to later development of pancreatic cancer. A fibre-tip surface plasmon resonance biosensor was fabricated to identify the presence and concentration of mucin in solution (sensitivity = 0.175 nm/(μg/ml)).
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Zhuk, L. A., and Y. V. Malinovskaya. "ANALYSIS OF INCIDENCE IN THE REPUBLIC OF BELARUS AND MINSK. CYTOLOGICAL FEATURES OF THE DIAGNOSTICS OF PANCREAS CANCER." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-48-52.

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The paper presents indicators of morbidity and survival of patients with pancreatic cancer, taking into account the age, as well as the prevalence of the process: local stages; the presence of regional or distant metastasis. The analysis of the incidence of pancreatic cancer in the Republic of Belarus for 2006-18 was carried out.
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Bobes-Bascarán, José, Ángel Fernández-Leal, E. Mosqueira-Rey, David Alonso Ríos, Elena Hernández-Pereira, and Vicente Moret-Bonillo. "Understanding Machine Learning Explainability Models in the context of Pancreatic Cancer Treatment." In Congreso XoveTIC: impulsando el talento científico (6º. 2023. A Coruña). Servizo de Publicacions. Universidade da Coruña, 2023. http://dx.doi.org/10.17979/spudc.000024.28.

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The increasing adoption of artificial intelligent systems at sensitive domains where humans are particularly, such as medicine, has provided the context to deeply explore ways of making machine learning models (ML) understandable for their final users. The success of such systems require the trust of their users, and thus there is a need to design and provide methods to understand the decisions made by such systems. We start from a public Pancreatic Cancer dataset and experiment with different ML models on a diagnosis scenario with the goal to decide whether a patient should be prescribed with a chemotherapy treatment. To validate the diagnosis results we explore different explainability approaches: Decision Tree, Random Forest, and model agnostic ad-hoc models, and compare them against a standard Pancreatic Cancer treatment set of rules. The increasing adoption of artificial intelligent systems at sensitive domains where humans are particularly, such as medicine, has provided the context to deeply explore ways of making machine learning models (ML) understandable for their final users. The success of such systems require the trust of their users, and thus there is a need to design and provide methods to understand the decisions made by such systems. We start from a public Pancreatic Cancer dataset and experiment with different ML models. To validate the diagnostic results we explore different explainability approaches: Decision Tree based approach, Random Forest based approach, and different model agnostic ad-hoc approaches, and we compare them against a standard Pancreatic Cancer treatment set of rules
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Takano, Shigetsugu, Maximilian Reichert, Hideyuki Yoshitomi, Basil Bakir, Koushik K. Das, Steffen Heeg, Shingo Kagawa, et al. "Abstract B30: Prrx1 isoforms regulate pancreatic cancer stem cell functions during pancreatic cancer progression." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; May 12-15, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.panca16-b30.

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Fehringer, Gordon, Steven Gallinger, Ayelet Borgida, Li Rita Zhang, Geoffrey Liu, and Rayjean J. Hung. "Abstract 4810: Family history of cancers, medical history, and pancreatic cancer risk in the Ontario Pancreatic Cancer Case-Control Study." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4810.

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Gonzalez-Villasana, Vianey, Cristian Rodriguez-Aguayo, Thiru Arumugam, Zobeida Cruz-Monserrate, Defeng Deng, Enrique Fuentes-Mattei, Rosa F. Hwang, et al. "Abstract 4959: Targeting pancreatic stellate cells (PSC) to treat pancreatic cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4959.

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Zhou, Feifan. "Laser immunotherapy for metastatic pancreatic cancer." In Optics in Health Care and Biomedical Optics X, edited by Qingming Luo, Xingde Li, Ying Gu, and Dan Zhu. SPIE, 2020. http://dx.doi.org/10.1117/12.2575415.

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Rapoport, N., K. H. Nam, D. A. Christensen, A. M. Kennedy, J. E. Shea, C. L. Scaife, Kullervo Hynynen, and Jacques Souquet. "Ultrasound-enhanced nanotherapy of pancreatic cancer." In 9TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND: ISTU—2009. AIP, 2010. http://dx.doi.org/10.1063/1.3367120.

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Reports on the topic "Pancreatic cancer"

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Beatty, Gregory, Patrick Guirnalda, and Santiago L. Luque. Listeria Vaccines for Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada600605.

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Wang, Lei. Molecular Probes for Pancreatic Cancer Imaging. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.3105.

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Yu, David. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599228.

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Yu, Davis S. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada621841.

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Mellenthin, Claudia, Vasile Balaban, Ana Dugic, Stephane Cullati, and Bernhard Egger. Risk factors for pancreatic cancer in patients with new onset diabetes - Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0065.

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Review question / Objective: Which additional risk factors raise the incidence of pancreatic cancer in the population of new onset diabetics? Condition being studied: Pancreatic cancer, new onset diabetes. Eligibility criteria: Inclusion criteria are:• English abstract available• The population of newly onset diabetics is examined, at least as a subgroup. Newly diagnosed is defined as onset of maximal 3 years ago.• Information on other risk factors of patients is available in the study.
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Munhenzva, Ian. Optimized Xanthene-based Probes for Pancreatic Cancer Imaging. Portland State University Library, May 2020. http://dx.doi.org/10.15760/etd.7333.

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Houchen, Courtney W. Tuft Cell Regulation of miRNAs in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada602496.

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Houchen, Courtney W. Tuft Cell Regulation of miRNAs in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada621275.

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Ting, David T., and Daniel A. Haber. Impact of Noncoding Satellite Repeats on Pancreatic Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613242.

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Myers, Richard M., Katherine E. Varley, and Marie K. Cross. Global Genomic Analysis of Prostate, Breast and Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada601853.

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You might also be interested in the extended bibliographies on the topic 'Pancreatic cancer' for particular source types:
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