Relevant bibliographies by topics / PanIN

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Academic literature on the topic 'PanIN'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "PanIN"

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Zińczuk, Justyna, Konrad Zaręba, E. Konarzewska-Duchnowska, K. Guzińska-Ustymowicz, B. Kędra, A. Kemona, and A. Pryczynicz. "Assessment of the presence of pancreatic intraepithelial neoplasia in various diseases of this organ." Progress in Health Sciences 7, no. 2 (September 22, 2017): 43–49. http://dx.doi.org/10.5604/01.3001.0010.5718.

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<b>Purpose</b>: Pancreatic intraepithelial neoplasia (PanIN) is one of the most commonly occurring precancerous lesion in pancreas which leads to development of pancreatic ductal adenocarcinoma (PDAC). We assessed the presence and grade of pancreatic intraepithelial neoplasia in the course of various diseases of the pancreas and its correlations with chosen clinicopathological parameters. null <b>Results</b>: A total of 276 foci of PanIN were identified in 94 patients. The most common lesions were PanIN 1a and PanIN 1b which together constituted 68.2 % of all lesions, whereas the PanIN 2 was present in 21.7% and PanIN 3 in 10.1% of patients. No statistical differences were observed in gender tendency for the development of PanINs. There was correlation between age of patients and degree of PanIN (p=0.034). There is no statistical difference in PanIN frequency among patients with pancreatic ductal adenocarcinomas, neuroendocrine tumors, chronic pancreatitis and pancreatic cysts (p=0.592). <b>Conclusions</b>: Our study showed that important factor in development of pancreatic intraepithelial neoplasia is age and the presence of PanIN in nonneoplastic diseases in older people should be included to the group with increased risk of cancer development.
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Lin, Pei-Yu, Shih-Jung Peng, Chia-Ning Shen, Pankaj J. Pasricha, and Shiue-Cheng Tang. "PanIN-associated pericyte, glial, and islet remodeling in mice revealed by 3D pancreatic duct lesion histology." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 3 (September 1, 2016): G412—G422. http://dx.doi.org/10.1152/ajpgi.00071.2016.

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Pericytes and glial cells are accessory cells of neurovascular networks, which have been reported to participate in scar formation after tissue injury. However, it remains unclear whether similar reactive cellular responses occur in pancreatic intraepithelial neoplasia (PanIN). In this study we developed three-dimensional (3D) duct lesion histology to investigate PanIN and the associated pericyte, glial, and islet remodeling. Transparent mouse pancreata with a KrasG12D mutation were used to develop 3D duct lesion histology. Deep-tissue, tile-scanning microscopy was performed to generate panoramic views of the diseased pancreas for global examination of early stage and advanced duct lesion formation. Fluorescence signals of ductal and neurovascular networks were simultaneously detected to reveal associated remodeling. Significantly, in KrasG12D-mutant mice, when the low-grade PanINs emerge, duct lesions appear as epithelial buds with perilesional pericyte and glial activation. When PanINs occur in large scale (induced by cerulein injections to the mutant mice), the 3D image data identifies 1) aggregation of PanINs in clusters in space; 2) overexpression of the pericyte marker NG2 in the PanIN microenvironment; and 3) epithelial in-growth to islets, forming the PanIN-islet complexes. Particularly, the PanIN-islet complexes associate with proliferating epithelial and stromal cells and receive substantial neurovascular supplies, making them landmarks in the atrophic lobe. Overall, perilesional pericyte and glial activation and formation of the PanIN-islet complex underline cellular heterogeneity in the duct lesion microenvironment. The results also illustrate the advantage of using 3D histology to reveal previously unknown details of neurovascular and endocrine links to the disease.
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McGinnis, Timothy, Leonidas Bantis, Rashna Madan, Prasad Dandawate, Sean Kumer, Timothy Schmitt, Ravi Kumar Paluri, Anwaar Saeed, and Anup Kasi. "Survival outcomes of pancreatic intraepithelial neoplasm (PanIN) versus intraductal papillary mucinous neoplasm (IPMN) associated pancreatic adenocarcinoma." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 766. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.766.

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766 Background: Pancreatic intraepithelial neoplasms (PanINs) and intraductal papillary mucinous neoplasms (IPMNs) are common pancreatic adenocarcinoma precursor lesions. However, data regarding their respective associations with prognosis is lacking. Methods: We retrospectively evaluated 72 resected pancreatic adenocarcinoma cases at the KU Cancer Center between Aug 2009 and March 2019. Patients were divided into either one of two groups, PanIN or IPMN, based on the results of the surgical path report. We compared baseline characteristics, overall and progression free survival between the two groups, as well as OS and PFS based on local or distant tumor recurrence. Results: 52 patients had PanIN and 20 patients had IPMN. Demographic and baseline characteristics are as follows (PanIN/IPMN): Median age 62.5/69; Gender (male) 63%/65%; ECOG status (0-1) 98%/85%; pancreatic head tumors 87%/70%; pancreatic body tumors 6%/15%; pancreatic tail tumors 7%/15%; Abnormal CA19-9 at diagnosis 79%/67%; Comorbidity Index 5/5 respectively. Median PFS was 26.2 months (95% CI: 21.4-31.0) for PanIN and 74.3 months (95% CI: 15.7-132.9) for IPMN [p = 0.004]. Median OS was 70.3 months (95% CI: 35.4-105.2) for PanIN and 78.8 months (95% CI: 33.2-124.4) for IPMN [p = 0.013]. Within the PanIN group, median OS after recurrence was 71.3 months (95% CI: 68.8.-73.4) for local recurrence and 46.7 months (95% CI: 39.2-54.2) for distant recurrence [p = 0.330]. Conclusions: Patients who had a IPMN associated pancreatic cancer had better PFS and OS when compared to patients with PanIN associated pancreatic cancer. In patients with PanIN associated cancer that recurred, OS was better with local recurrence compared to distant recurrence but did not meet statistical significance. The results need to be validated in a larger cohort. [Table: see text]
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McGinnis, Timothy, Leonidas E. Bantis, Rashna Madan, Prasad Dandawate, Sean Kumer, Timothy Schmitt, Ravi Kumar Paluri, and Anup Kasi. "Survival Outcomes of Pancreatic Intraepithelial Neoplasm (PanIN) versus Intraductal Papillary Mucinous Neoplasm (IPMN) Associated Pancreatic Adenocarcinoma." Journal of Clinical Medicine 9, no. 10 (September 25, 2020): 3102. http://dx.doi.org/10.3390/jcm9103102.

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Pancreatic intraepithelial neoplasms (PanINs) and intraductal papillary mucinous neoplasms (IPMNs) are common pancreatic adenocarcinoma precursor lesions. However, data regarding their respective associations with survival rate and prognosis are lacking. We retrospectively evaluated 72 pancreatic adenocarcinoma tumor resection patients at the University of Kansas Hospital between August 2009 and March 2019. Patients were divided into one of two groups, PanIN or IPMN, based on the results of the surgical pathology report. We compared baseline characteristics, overall survival (OS), and progression free survival (PFS) between the two groups, as well as OS and PFS based on local or distant tumor recurrence for both groups combined. 52 patients had PanINs and 20 patients had IPMNs. Patients who had an IPMN precursor lesion had better median PFS and OS when compared to patients with PanIN precursor lesions. However, the location of tumor recurrence (local or distant) did not show a statistically significant difference in OS.
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Sagami, Ryota, Kentaro Yamao, Jun Nakahodo, Ryuki Minami, Masakatsu Tsurusaki, Kazunari Murakami, and Yuji Amano. "Pre-Operative Imaging and Pathological Diagnosis of Localized High-Grade Pancreatic Intra-Epithelial Neoplasia without Invasive Carcinoma." Cancers 13, no. 5 (February 24, 2021): 945. http://dx.doi.org/10.3390/cancers13050945.

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Pancreatic ductal adenocarcinoma (PDAC) arises from precursor lesions, such as pancreatic intra-epithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN). The prognosis of high-grade precancerous lesions, including high-grade PanIN and high-grade IPMN, without invasive carcinoma is good, despite the overall poor prognosis of PDAC. High-grade PanIN, as a lesion preceding invasive PDAC, is therefore a primary target for intervention. However, detection of localized high-grade PanIN is difficult when using standard radiological approaches. Therefore, most studies of high-grade PanIN have been conducted using specimens that harbor invasive PDAC. Recently, imaging characteristics of high-grade PanIN have been revealed. Obstruction of the pancreatic duct due to high-grade PanIN may induce a loss of acinar cells replaced by fibrosis and lobular parenchymal atrophy. These changes and additional inflammation around the branch pancreatic ducts (BPDs) result in main pancreatic duct (MPD) stenosis, dilation, retention cysts (BPD dilation), focal pancreatic parenchymal atrophy, and/or hypoechoic changes around the MPD. These indirect imaging findings have become important clues for localized, high-grade PanIN detection. To obtain pre-operative histopathological confirmation of suspected cases, serial pancreatic-juice aspiration cytologic examination is effective. In this review, we outline current knowledge on imaging characteristics of high-grade PanIN.
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Hwang, In kyeom, Bong Kyun Kang, Yoon Suk Lee, Jaihwan Kim, and Jin-Hyeok Hwang. "Prognostic impact of pancreatic intraepithelial neoplasia (PanIN)-III accompanying chronic pancreatitis in patients who underwent R0 resection for pancreatic adenocarcinoma." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 246. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.246.

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246 Background: The clinical significance of pancreatic intraepithelial neoplasia (PanIN)-III, known as carcinoma in situ of pancreatic ductal adenocarcinoma (PDAC), remains unclear yet. Recent research showed inflammation enhanced early cellular invasion of PanIN-III by facilitating epithelial to mesenchymal transition (EMT), even before frank malignancy in experimental model. Therefore we decided to investigate whether PanIN-III accompanying chronic pancreatitis (CP) might have an important prognostic impact in patient who underwent curative resection for PDAC. Methods: Medical records of 199 PDAC patients with R0 resection were reviewed. Presence and grade of PanIN and CP in resected specimen were determined based on College of American Pathologists protocol. Overall survival (OS) and disease free survival (DFS) were analyzed according to PanIN-III and CP. Results: CP was observed in 19.6% (39/199) of resected specimen and PanIN-III in 21.1% (42/199). In the group with CP, PanIN-III was associated with poor prognosis in univariate analysis (16.6 months vs. 32.0 months, P=0.001 for OS and 7.5 months vs. 15.1 months, p=0.012 for DFS), whereas PanIN-III was not a prognostic factor in the group without CP. When we divided into two groups [PanIN-III accompanying CP (n=12) vs. the others (n=187)], it showed that median DFS and OS were significantly shorter in PanIN-III and CP group than those of the others (7.5 months and 16.6 months vs. 12.4 months and 26.0 months, p=0.017 and p=0.003, respectively). In multivariate analysis, PanIN-III accompanying CP remained a statistically significant poor prognostic factor (HR: 2.06; 95% CI: 1.008 to 4.221; p=0.048 for OS, HR: 2.6; 95% CI: 1.267 to 5.462; P=0.009 for DFS using Cox proportional hazard ratio). Conclusions: PanIN-III accompanying CP might influence on poor long-term outcomes in patients who underwent R0 resection for PDAC. Therefore, it would support that chronic inflammation could enhance the dissemination of carcinoma in situ.
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Andriani, Andriani, and Indah Permatasari. "Analisis Tingkat Kesehatan Bank dengan Metode RGEC Pada BCA Syariah dan Panin Dubai Syariah." IQTISHODUNA 17, no. 1 (April 27, 2021): 65–80. http://dx.doi.org/10.18860/iq.v17i1.11521.

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This research is motivated by the development of increasingly rapid Islamic banking and increasing public trust in banks. Bank health services are one of the management controls because bank health is a reflection of the bank's performance. This study aims to see, describe and compare the soundness level of banks at BCA Syariah and Panin Dubai Syariah using the RGEC method (Risk Profile, GCG, Earning, Capital) with new SEOJK Number 10 / SEOJK.03 / 2014. The results show that the NPF BCA Syariah and Panin Dubai Syariah are in a very healthy position. FDR BCA Syariah is in a fairly healthy position and Panin Dubai Syariah is in an unhealthy position. ROA BCA Syariah and Panin Dubai Syariah are in a fairly healthy position. NOM BCA Syariah and Panin Dubai Syariah are in a healthy position. CAR BCA Syariah and Panin Dubai Syariah are in a very healthy position. The BCA Syariah GCG Report is in a very healthy position and the Panin Dubai Syariah GCG Report is in a healthy position. The analysis results show a significant difference between the performance of BCA Syariah and Panin Dubai Syariah, especially in the NPF, FDR, NOM and CAR variables, while there is no difference in the ROA variable.
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Wendt, Luiz Roberto, Alessandro Bersch Osvaldt, Vivian Pierre Bersch, Rita de Cássia Schumacher, Maria Isabel Albano Edelweiss, and Luiz Rohde. "Pancreatic intraepithelial neoplasia and ductal adenocarcinoma induced by DMBA in mice: effects of alcohol and caffeine." Acta Cirurgica Brasileira 22, no. 3 (June 2007): 202–9. http://dx.doi.org/10.1590/s0102-86502007000300008.

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PURPOSE: To evaluate the effects of alcohol and caffeine in a pancreatic carcinogenesis mouse model induced by 7,12-dimethylbenzantracene (DMBA), according to the PanIN classification system. METHODS: 120 male, Mus musculus, CF-1 mice were divided into four groups. Animals received either water or caffeine or alcohol or alcohol + caffeine in their drinking water. In all animals, 1 mg of DMBA was implanted into the head of the pancreas. After 30 days, euthanasia was performed; excised pancreata were then fixed in formalin, stained with hematoxylin-eosin and categorized as follows: normal ducts, reactive hyperplasia, PanIN-1A, PanIN-1B, PanIN-2, PanIN-3 or adenocarcinoma. RESULTS: PanIN lesions were verified in all groups. Adenocarcinoma was detected in 15% of animals in the caffeine group, 16.6% in the water group, 23.8% in the alcohol + caffeine group and 52.9% in the alcohol group (P<0.05). CONCLUSIONS: The experimental pancreatic carcinogenesis mouse model using DMBA effectively induces PanIN lesions and pancreatic adenocarcinoma. This study verified the association between alcohol use and pancreatic adenocarcinoma; caffeine did not present the same effect.
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Sato, Yasunori, Kenichi Harada, Motoko Sasaki, and Yasuni Nakanuma. "Histological Characterization of Biliary Intraepithelial Neoplasia with respect to Pancreatic Intraepithelial Neoplasia." International Journal of Hepatology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/678260.

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Biliary intraepithelial neoplasia (BilIN) is a precursor lesion of hilar/perihilar and extrahepatic cholangiocarcinoma. BilIN represents the process of multistep cholangiocarcinogenesis and is the biliary counterpart of pancreatic intraepithelial neoplasia (PanIN). This study was performed to clarify the histological characteristics of BilIN in relation to PanIN. Using paraffin-embedded tissue sections of surgically resected specimens of cholangiocarcinoma associated with BilIN and pancreatic ductal adenocarcinoma associated with PanIN, immunohistochemical staining was performed using primary antibodies against MUC1, MUC2, MUC5AC, cyclin D1, p21, p53, and S100P. For mucin staining, Alcian blue pH 2.5 was used. Most of the molecules examined here showed similar expression patterns in BilIN and PanIN, in which their expression tended to increase along with the increase in atypia of the epithelial lesions. Significant differences were observed in the increase in mucin production and the expression of S100P in PanIN-1 and the expression of p53 in PanIN-3, when compared with those in BilIN of a corresponding grade. These results suggest that cholangiocarcinoma and pancreatic ductal adenocarcinoma share, at least in part, a common carcinogenic process and further confirm that BilIN can be regarded as the biliary counterpart of PanIN.
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McAllister, Florencia, Jennifer M. Bailey, Janivette Alsina, Christopher Nirschl, Jeffrey Roeser, Danielle Blake, Rachana Lankapali, et al. "TH17 cells and early pancreatic tumorigenesis." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 144. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.144.

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144 Background: Chronic pancreatitis increases the risk of developing pancreatic ductal adenocarcinoma (PDAC), one of the deadliest human cancers. Activating Kras mutations have been detected in 30% of early pancreatic intraepithelial neoplasias (PanINs), increasing to 100% in PDAC. We hypothesized that inflammatory cells recruited to the pancreas in response to chronic injury can interact with epithelial cells harboring activated KrasG12D and affect the progression of PanIN lesions. Methods: We used the the transgenic Mist1:CreERT2; LSL-KrasG12D (KCiMist1) adult mice in which the LSL KrasG12Dallele is activated specifically in the acinar compartment. This model leads to the formation of PanINs with a classic "ductal" phenotype and the progression of lesions is accelerated by the induction of chronic pancreatitis with recurrent cerulein injections. Results: We have found that TH17 cells, a subtype of CD4+ T-helper cells known to play an active role in inflammation, are recruited to the pancreas during chronic pancreatitis and further increased upon KrasG12Dactivation. The differentiation of CD4+T cells into TH17 requires IL-6 and TGF-B, factors that are increased in the pancreatic tumor microenvironment. Stat3, a key transcription factor that determines the differentiation of TH17 lineage, is activated in the pancreatic dysplastic epithelium and in the stroma. We have discovered that PanINs from KCiMist1 mice overexpress the IL-17 Receptor (IL-17RA) by immunofluorescence and furthermore we confirmed this finding on human PanIN tissue arrays. Intrapancreatic injections of adenovirus encoding IL-17A, the main cytokine produced by TH17 cells, into KCiMist1 mice led to an increase in the progression of PanIN lesions by 6 weeks when compared with mice injected with control adenovirus. Finally, we transplanted IL-17-/- bone marrow into KCiMist1 mice and showed a significant decrease in metaplasia and PanINs formation when compared with mice transplanted with WT bone marrow. Conclusions: We found that TH17 cells, recruited to the pancreas in the presence of chronic pancreatitis, can accelerate the progression of early pancreatic tumorigenesis, setting the basis for future translational studies targeting TH17 cells.
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Dissertations / Theses on the topic "PanIN"

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Distler, Marius, Daniela E. Aust, Jürgen Weitz, Christian Pilarsky, and Robert Grützmann. "Precursor Lesions for Sporadic Pancreatic Cancer: PanIN, IPMN, and MCN." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-147337.

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Pancreatic cancer is still a dismal disease. The high mortality rate is mainly caused by the lack of highly sensitive and specific diagnostic tools, and most of the patients are diagnosed in an advanced and incurable stage. Knowledge about precursor lesions for pancreatic cancer has grown significantly over the last decade, and nowadays we know that mainly three lesions (PanIN, and IPMN, MCN) are responsible for the development of pancreatic cancer. The early detection of these lesions is still challenging but provides the chance to cure patients before they might get an invasive pancreatic carcinoma. This paper focuses on PanIN, IPMN, and MCN lesions and reviews the current level of knowledge and clinical measures.
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Hamidi, Tewfik. "La protéine de stress p8 permet l'adaptation des cellules cancéreuses pancréatiques aux conditions microenvironnementales extrêmes. : Etude de ses mécanismes d'action." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4100.

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La protéine de stress p8 fut découverte et caractérisée dans notre laboratoire. Cette protéine est surexprimée dans l'adénocarcinome pancréatique et possède un rôle dans la progression tumorale. Pendant ce travail de thèse, nous nous sommes focalisé sur le rôle de p8 dans les phases initiales de la tumorigénèse pancréatique et sur ses mécanismes d'action, impliqués dans la progression tumorale. Nous avons montré que p8 joue un rôle essentiel dans l'apparition des lésions PanINs suite à l'activation de l'oncogène Kras. Au niveau cellulaire, nous avons montré que la protéine p8 protège les cellules tumorales pancréatiques contre le stress de la privation en nutriments via la régulation de l'expression de RelB et IER3. La voie p8, RelB et IER3 est impliquée dans l'inhibition de l'apoptose suite au stress. De plus, nous avons observé que ces trois protéines sont co-exprimées dans les adénocarcinomes humains et leur expression corrèle avec l'évolution de la maladie. Dans un second lieu, nous avons démontré le rôle essentiel de la protéine p8 dans la résistance des cellules tumorales pancréatiques à l'hypoxie et à la privation en glucose. Nous avons identifié la voie p8/Aurora KinaseA, qui en réponse au stress métabolique, réduit l'apparition des dommages à l'ADN en contrôlant l'expression des gènes liés au cycle cellulaire et à la réparation de l'ADN. De plus, nos recherches ont montré que p8 protège les cellules tumorales du stress métabolique en inhibant la mort cellulaire dépendante de l'autophagie. Nous espérons que nos résultats aideront à mieux cibler les cellules tumorales pancréatiques et leur caractère résistant au stress micro-environnemental extrême
The stress protein p8 was discovered and characterized in our laboratory. Over expressed in pancreatic adenocarcinoma, p8 is involved in tumor progression. During my PhD studies, we focused on the role of p8 in pancreatic cancer development and on its mechanisms of action. First, we demonstrated that p8 is essential for PanIN development following Kras oncogene activation. At the cellular level, we found that p8 protects pancreatic cancer cells upon nutrient starvation stress through the regulation of RelB and IER3 expression. p8, RelB and IER3-dependent cascade inhibits apoptosis after the starvation stress. Furthermore, we showed that these tree proteins are co expressed in human pancreatic adenocarcinoma. One the other hand, our study showed that p8 is involved in pancreatic cancer cells resistance to hypoxia and glucose starvation. We identified a p8/Aurora KinaseA pathway which, in response to such metabolic stress, reduces DNA damage by regulating cell cycle and DNA repair genes expression. Moreover, our studies demonstrated that p8/AURKA path protects cancer cells against metabolic stress by inhibiting autophagy-associated cell death. We expect that our data will help to get new therapeutics against pancreatic cancer
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Serwaah-Panin, Amma [Verfasser], Dorothea [Gutachter] Kübler, and Ferdinand [Gutachter] Vieider. "Experiments in risk, insurance and development / Amma Serwaah-Panin ; Gutachter: Dorothea Kübler, Ferdinand Vieider." Berlin : Technische Universität Berlin, 2018. http://d-nb.info/1164076337/34.

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Tsuda, Motoyuki. "The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis." Kyoto University, 2019. http://hdl.handle.net/2433/242378.

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Salcedo, Allende Maria Teresa. "Neoplasia intraepitelial pancreática y adenocarcinoma ductal de pancreas: estudio de factores de las vías de señalización celular y su correlación con la clínica." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/377763.

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El adenocarcinoma ductal pancreático (ADP) constituye aproximadamente el 85% de los tumores del páncreas. Es el tumor en el que menos avances clínicos se han producido en los últimos 50 años y sigue teniendo un pronóstico muy malo. Por ello, es necesaria la identificación de factores de riesgo y la caracterización del proceso de progresión tumoral, así como la identificación de nuevas dianas terapéuticas. En esta Tesis Doctoral estudiamos el estado de las vías de señalización celular en una serie de ADP convencionales, así como en ductos de pancreatitis crónicas (PC) y las lesiones precursoras asociadas (PanIN). El objetivo principal del presente trabajo es el estudio inmunohistoquímico y molecular de diversos factores implicados en las vías de señalización celular y de transición epitelio-mesénquima (PI-3K-AKT-mTOR, Ras-Raf-MAPK, Hippo, p53, N-cadherina y p16), con el objetivo de poder definir un modelo de progresión desde lesiones de PanIN en PC a ADP infiltrante , así como demostrar la relación de los niveles de expresión de dichos factores con una serie de parámetros clínico-patológicos con valor pronóstico, estado mutacional y supervivencias, en el ADP. Los resultados del estudio de nuestra serie validan, por una parte, los criterios establecidos como factores con valor pronóstico: tamaño tumoral, margen quirúrgico afecto (R1), invasión vascular, invasión linfática, invasión perineural, metástasi hepáticas y estadios avanzados. En relación al modelo de progresión PanIN-ADP, demostramos que existe un aumento en la expresión de la gran mayoría de proteínas estudiadas desde su expresión en ductos de PC y la expresión en ADP. Asimismo, porponemos un valor de Ki67 ≥ a 20% como biomarcador útil a la hora de discernir entre proliferación ductular reactiva o ADP bien diferenciado en las biopsias pequeñas o en los márgenes quirúrgicos de piezas de resección. En relación al estudio genético de RAS, confirmamos que ningún caso presenta mutación para NRAS, a diferencia del 89% de los ADP, que presentan mutaciones de KRAS, y que la presencia de dicha mutación implica peor pronóstico. En cuanto a los factores de señalización celular en ADP, se confirma que la expresión de algunas proteínas (p4E-BP1, eIF4E y YAP1) se asocia a factores de mal pronóstico y peor supervivencia. No evidenciamos en el estudio relación significativa entre la expresión de las proteínas estudiadas con parámetros clínico-patológicos relacionados con estroma peritumoral (p16, desmoplasia, inflamación). Nuestros resultados concluyen que el estudio de los factores de las vías de señalización celular complementan el estudio anatomopatológico de los ADP. La determinación de Ki67 con un valor superior a 20% permite discernir entre una proliferación ductular reactiva/metaplasia acinar ductal y ADP bien diferenciado y lo proponemos como marcador a la hora de valorar margen quirúrgico de piezas de resección y biopsias pequeñas. La sobreexpresión de YAP1 nuclear, eIF4E citoplasmático y p4E-BP1 nuclear definen un perfil molecular de ADP de peor pronóstico. Finalmente, resaltar la relevancia de caracterizar factores asociados al microambiente que rodea al ADP e influyan en el comportamiento biológico de los mismos. El grupo de tumores sin mutaciones de KRAS y NRAS es muy interesante de cara a identificar otras eventuales alteraciones moleculares, con incidencia en el desarrollo de los ADP. La intención en un futuro es ampliar la serie para conseguir resultados significativos que permitan obtener más conclusiones.
Pancreatic ductal adenocarcinoma (ADP) constitutes approximately 85% of pancreatic tumors. It is the tumor in which fewer clinical developments have occurred in the last 50 years and continues to have a very poor prognosis. Therefore, the identification of risk factors and characterization of tumor progression, as well as the identification of new therapeutic targets is necessary. In this Thesis we studied the state of the cell signaling pathways in a number of conventional ADP as well as ducts of chronic pancreatitis (CP) and the associated precursor lesions (PanIN). The main objective of this paper is the study of various factors involved in cell signaling pathways and epitelio-mesenchymal transition (PI-3K-AKT-mTOR, Ras-Raf-MAPK, Hippo, p53, N-cadherin and p16) by immunohistochemical and molecular study, with the aim to define a model of progression from precursor lesions of PanIN in PC to infiltrating ADP; and to demonstrate the relationship of the expression levels of these factors with a series of pathological parameters with prognostic value, mutational state and survival in the ADP. The survey results of our series validate the established prognostic criteria factors: tumor size, surgical margin affection (R1), vascular invasion, lymphatic invasion, perineural invasion, progression to liver metastasis and advanced stages. Regarding the progression model PanIN-ADP show an increased expression of the vast majority of proteins studied since its expression in ducts of PC to ADP expression. Also, we propose a value of Ki67 ≥ 20% as useful biomarker to discern between a benign reactive ductular proliferation/acinar ductal metaplasia and a well differentiated ADP in small biopsies or in surgical margins of resected specimens. In relation to genetic study of RAS, we confirm that no event has mutation to NRAS, unlike the 89% of ADP showing KRAS mutations, and the presence of said mutation confers decreased survival. As for cell signaling factors in ADP, it is confirmed that the expression of some proteins (p4E-BP1, eIF4E and YAP1) factors associated with poor prognosis and shorter survival. No we show in the study significant relationship between the expression of the proteins with pathological parameters related to peritumoral stroma (p16, desmoplasia, inflammation). Our results conclude that the study of the factors of cellular signaling pathways complement the pathological report of the ADP. Ki67 determining a value greater than 20% can discern between a benign reactive ductular proliferation and a well differentiated ADP and propose it as a marker in assessing surgical resection margin and small biopsies. Overexpression of YAP1 nuclear, eIF4E cytoplasmic and p4E-BP1 nuclear define a molecular profile of ADP with worse prognosis. Finally, highlight the importance of characterizing factors associated with ADP microenvironment and their influence on biological behavior. The group of tumors without KRAS mutations and NRAS is very interesting in order to identify other molecular alterations, with impact on the development of ADP. The intention in the future is to expand the series to achieve significant results that allow more conclusions.
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Panin, Valerii [Verfasser], Thomas [Akademischer Betreuer] Aumann, and Joachim [Akademischer Betreuer] Enders. "Fully exclusive measurements of quasi-free single-nucleon knockout reactions in inverse kinematics. / Valerii Panin. Betreuer: Thomas Aumann ; Joachim Enders." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2012. http://d-nb.info/1106257030/34.

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DeVeaugh-Geiss, Angela Marie West Suzanne L. "Depression and comorbid panic and pain in primary care patients." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1734.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the Doctor of Philosophy of Epidemiology in the School of Public Health." Discipline: Epidemiology; Department/School: Public Health.
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Schmahl, Michelle Jordan. "Metabolic Profiling of Urine, Fecal, and Serum Samples and Pancreatic Tumors and Evaluation of HMGA1 Expression Levels in Pancreatic Intraepithelial Neoplasia Cells in the Ptf1a-Cre; LSL-KrasG12D Transgenic Mouse Model of Pancreatic Cancer." Miami University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=miami1523977530802748.

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Martínez, Romero Carles. "Polycomb group proteins Bmi1 and Ring1B are involved in cell plasticity and tumorigenesis of the pancreas." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7190.

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L'adenocarcinoma ductal pancreàtic (PDAC) és un dels càncers més letals. Per tal de millorar el diagnòstic precoç, s'estan investigant les etapes inicials de la formació del càncer, com és el cas de les lesions preneoplàstiques, i es vol desxifrar l'origen cel·lular de la malaltia. Les proteïnes Polycomb constitueixen una família de silenciadors epigenètics que es troben en una varietat de tumors sòlids. La hipòtesi principal és que Polycomb pot estar participant en els processos preneoplàstics del pàncreas i en l'aparició i progressió del tumor. La expressió de Bmi1 i Ring1B fou analitzada durant el desenvolupament del pàncreas, en teixit pancreàtic de diferents models murins de la malaltia i en mostres humans de teixit pancreàtic. Es va dur a terme l'anàlisi del mecanisme de Bmi1 mitjançant models in vitro i induint la depleció de Bmi1. Bmi1 i Ring1B s'expressaren en precursors pancreàtics durant etapes primerenques del desenvolupament i en cèl·lules ductals i dels illots,
però no en els acins, en el pàncrees adult. Bmi1 s'induí en cèl·lules acinars durant lesió aguda, en lesions metaplàstiques acinoductals, en neoplàsies intraepitelials pancreàtiques (PanIN) i en PDAC. Ring1B s'incrementà significativament en PanINs de grau alt i en PDAC. La disminució dels nivells de Bmi1 en la línia cel·lular acinar canvià l'expressió dels enzims digestius pancreàtics. Aquests resultats suggereixen que Bmi1 i Ring1B podrien estar contribuint de diferent manera en la progressió tumoral.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers. To improve early diagnosis, research efforts are focused in characterising early events of cancer formation like preneoplastic lesions and deciphering the cell origin of the malignancy. Polycomb proteins constitute a family of epigenetic silencers found in a variety of solid tumours. The main hypothesis is that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development and progression. The expression of Bmi1 and RingB was analysed during pancreatic development, in pancreatic tissue from mouse models of disease and in human pancreatic tissue samples. Mechanistic insights of Bmi1 were performed using in vitro models and with induced Bmi1 depletion. Bmi1 and Ring1B were expressed in pancreatic exocrine precursors during early development and in ductal and islet cells, but not in acinar cells, in the adult pancreas. Bmi1 was induced in acinar cells during acute injury, in acinar-ductal metaplastic lesions, in pancreatic intraepithelial neoplasia (PanIN) and PDAC. In contrast, Ring1B was significantly increased in high-grade PanINs and in PDAC. Bmi1 knockdown in acinar cell line changed the expression of pancreatic digestive enzymes. These results suggest that Bmi1 and Ring1B could contribute differently to tumour development.
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Bustamante, Mirayo Antonio. "Pain Diary : Pain Management Platform." Thesis, Uppsala universitet, Institutionen för informationsteknologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-177259.

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In the context of current human diseases and conditions, chronic pain is among the most typical reasons for seeking medical attention and is seen in 20 to 50 percent of patients attending primary care (Bajwa Z. H., 2012). With those figures in hand, the medical specialty of pain is of increasing interest to the scientific community and other parties involved in the management of chronic diseases. In the practical sense, chronic pain patients usually have, as of now, regular check-up appointments with their pain specialist, where medication is modified or maintained depending on the frequency and intensity of the patient’s pain episodes. As a matter of fact, between appointments, patients are usually encouraged to write a comprehensive account of their pain episodes and their characteristics in the form of a pain diary. In such diary, they write the intensity of their pain in a relative scale from 1 to 10, the location of the pain in their body, and other relevant comments, namely medication side-effects or the activity they were performing when pain appeared. This set of data is then used by pain specialists to calibrate the patient’s medication and follow their treatment. Pain Diary, the project developed and described in the present document, seeks a more flexible, precise approach for patients to record their pain diaries. The project emphasizes on the interaction between the patient and an electronic pain diary, in the form of an application for the iOS platform. This document discusses the human-computer interaction analysis, usability tests, accessibility tests, and prototypes created to develop a comprehensive user-oriented  solution for patients of cancer and other chronic diseases. Finally, the paper will present a functional prototype  created for iOS, taking into account UX (user experience) design and interaction, as well as a RESTful back-end to consider in a future large scale implementation of the project.
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Books on the topic "PanIN"

1

Go, Khup Za. Leivui panin. Guwahati: Christian Literature Centre, 2004.

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Forsblom, Enzio. Panin huilu: Kirjoituksia, esitelmiä, puheenvuoroja neljän vuosikymmenen ajalta. [Helsinki]: Organum-Seura, 1990.

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Gavri͡ushkin, A. V. Graf Nikita Panin: Iz istorii russkoĭ diplomatii XVIII veka. Moskva: Mezhdunar. otnoshenii͡a, 1989.

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Li thûk lam panin: Nepal ramah lo kai la, min pui rawh. Aizawl: Upa David Biswa, 2014.

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1981-, Weeks Joshua, ed. Panic x panic. New York: Del Rey/Ballantine Books, 2010.

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1981-, Weeks Joshua, ed. Panic X panic. New York: Del Rey/Ballantine Books, 2010.

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Aho, Juhani. Papin tytär ; Papin rouva. Helsinki: Suomalaisen Kirjallisuuden Seura, 2000.

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Panini. Montréal: Modus Vivendi, 2009.

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Panic. Abingdon, Oxon: Routledge, 2013.

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Marr, David. Panic. Collingwood, Vic: Black Inc., 2011.

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Book chapters on the topic "PanIN"

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Habbe, Nils, R. A. Meguid, V. Fendrich, G. Feldmann, R. H. Hruban, S. D. Leach, and A. Maitra. "Die Überexpression der onkogenen Kras-Mutation G12D im adulten Pankreas führt zur Entstehung von highgrade PanIN-Läsionen in Ela-CreERT2;LSL-KrasG12D-Mäusen." In Chirurgisches Forum 2008, 27–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78833-1_8.

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Chytil, Michal P., and Jiří Demner. "Panic mode without panic." In Automata, Languages and Programming, 260–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/3-540-18088-5_21.

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Alcock, Lara. "Panik." In Wie man erfolgreich Mathematik studiert, 229–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-50385-0_12.

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Gasch, B. "Panik." In Notfallpsychologie, 435–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-15308-2_32.

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McAllister-Williams, R. Hamish, Daniel Bertrand, Hans Rollema, Raymond S. Hurst, Linda P. Spear, Tim C. Kirkham, Thomas Steckler, et al. "Panic." In Encyclopedia of Psychopharmacology, 948–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_324.

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Talkovsky, Alexander M., and Peter J. Norton. "Panic." In Encyclopedia of Personality and Individual Differences, 3404–6. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_543.

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Johnsen, Gudrun. "Panic." In Bringing Down the Banking System, 19–46. New York: Palgrave Macmillan US, 2014. http://dx.doi.org/10.1057/9781137347350_3.

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Capdevielle, Delphine, and Jean-Philippe Boulenger. "Panic." In Encyclopedia of Psychopharmacology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_324-2.

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Talkovsky, Alexander M., and Peter J. Norton. "Panic." In Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_543-1.

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Sucharov, Mira. "Panic." In Borders and Belonging: A Memoir, 131–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53732-6_11.

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Conference papers on the topic "PanIN"

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Lafaro, Kelly J., Audrey Hendley, Jennifer Bailey, and Steven Leach. "Abstract PR04: Clonal composition and clonal selection during PanIN progression." 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-pr04.

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Collins, Meredith A., Yaqing Zhang, Sabita Rakshit, Judith S. Sebolt-Leopold, and Marina Pasca di Magliano. "Abstract B66: MAPK signaling mediates Kras-driven PanIN formation and maintenance." 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-b66.

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Tsuda, Motoyuki, Akihisa Fukuda, Satoshi Ogawa, Kenji Masuo, Norihiro Goto, Yukiko Hiramatsu, Yu Muta, et al. "Abstract 3518: Brg1 plays a critical role in PanIN formation through regulating Sox9 expression." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3518.

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Shen, Xiaoming, Jianming Lu, Stefanie Christopher, Andrew Lowy, and Joseph Kim. "Abstract 4024: Single-allele K-rasmutation mediates CXCR4 signaling in PanIN and pancreatic cancer cells." 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.am10-4024.

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Gunawan, Barbara, and Khairunisa Maynora Arvianda. "Bank Health Level Analysis Using CAMELS and RGEC Methods on PT Bank Panin Dubai Syariah Ltd." In Proceedings of the 5th International Conference on Accounting and Finance (ICAF 2019). Paris, France: Atlantis Press, 2019. http://dx.doi.org/10.2991/icaf-19.2019.4.

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Hendley, Audrey M., Jennifer M. Bailey, Janivette Alsina, Christine Iacobuzio-Donahue, Anirban Maitra, Albert Reynolds, and Steven D. Leach. "Abstract 66: p120 catenin: A novel regulator of PanIN epithelial cell delamination in preinvasive pancreatic cancer." 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.am2014-66.

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Bailey, Jennifer M., Janivette Alsina, Zeshaan Rasheed, Ya-Yuan Fu, Florencia McAllister, Pankaj Pasricha, William Matsui, Anirban Maitra, and Steven Leach. "Abstract 5008: A morphologically distinct cancer initiating cell in human and murine PanIN and 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.am2013-5008.

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Husain, Kazim, Barbara Centeno, Marta Perez, Guo Lee, Sabiha Kazim, Dung-Tsa Chen, Said Sebti, and Mokenge Malafa. "Abstract 1613: Delta-tocotrienol delays the progression of pancreatic intraepithelial neoplasia (PanIN) lesions in a conditional KrasG12D mouse model." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1613.

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Liou, Geou-Yarh, Heike Doeppler, Ligia Bastea, and Peter Storz. "Abstract A59: Crosstalk of different macrophage populations with pancreatic acinar or PanIN cells and contribution to development of pancreatic cancer." 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-a59.

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Mathison, Angela, Ann Salmonson, Brooke Paradise, Mckenna Missfeldt, Juan Iovanna, Daniel Billadeau, Raul Urrutia, and Gwen Lomberk. "Abstract 1391: The epigenetic regulator, G9a, is a KRAS-inducible protein and its inactivation inhibits PanIN formation by this oncogene." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1391.

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Reports on the topic "PanIN"

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Ellen McGinnis, Ellen McGinnis. The Panic Button!: A Biofeedback App for Panic Attacks. Experiment, March 2016. http://dx.doi.org/10.18258/6872.

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Gorton, Gary. The Subprime Panic. Cambridge, MA: National Bureau of Economic Research, October 2008. http://dx.doi.org/10.3386/w14398.

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Morton, Simon, and Victoria Lavin. Understanding of chronic pelvic pain and bladder pain. BJUI Knowledge, September 2020. http://dx.doi.org/10.18591/bjuik.0068.

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Gorton, Gary. The Panic of 2007. Cambridge, MA: National Bureau of Economic Research, September 2008. http://dx.doi.org/10.3386/w14358.

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Amtmann, Dagmar, Mark Jensen, Dennis Turk, Danielle Lavallee, Kendra Liljenquist, Alyssa Bamer, and Rana Salem. Developing Measures of Pain Appraisal and Pain-Related Self-Efficacy for People Living with Chronic Pain. Patient-Centered Outcomes Research Institute (PCORI), July 2019. http://dx.doi.org/10.25302/7.2019.me.140312550.

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Schmitt-Grohé, Stephanie, and Martin Uríbe. Pegs and Pain. Cambridge, MA: National Bureau of Economic Research, March 2011. http://dx.doi.org/10.3386/w16847.

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Hawkins, James M. Body Pain Reporting in Tricare Eligible Beneficiaries with Orofacial Pain. Fort Belvoir, VA: Defense Technical Information Center, May 2015. http://dx.doi.org/10.21236/ad1012704.

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Winch, Nicola M., Amanda Christine Madden, Matthew James Marcath, Eric Waggoner Nelius, and Douglas R. Mayo. PAIN Schubert Review: Experiment. Office of Scientific and Technical Information (OSTI), May 2020. http://dx.doi.org/10.2172/1618307.

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Chou, Roger, Jesse Wagner, Azrah Y. Ahmed, Ian Blazina, Erika Brodt, David I. Buckley, Tamara P. Cheney, et al. Treatments for Acute Pain: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer240.

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Objectives. To evaluate the effectiveness and comparative effectiveness of opioid, nonopioid pharmacologic, and nonpharmacologic therapy in patients with specific types of acute pain, including effects on pain, function, quality of life, adverse events, and long-term use of opioids. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, Embase®, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews) to August 2020, reference lists, and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) of outpatient therapies for eight acute pain conditions: low back pain, neck pain, other musculoskeletal pain, neuropathic pain, postoperative pain following discharge, dental pain (surgical or nonsurgical), pain due to kidney stones, and pain due to sickle cell disease. Meta-analyses were conducted on pharmacologic therapy for dental pain and kidney stone pain, and likelihood of repeat or rescue medication use and adverse events. The magnitude of effects was classified as small, moderate, or large using previously defined criteria, and strength of evidence was assessed. Results. One hundred eighty-three RCTs on the comparative effectiveness of therapies for acute pain were included. Opioid therapy was probably less effective than nonsteroidal anti-inflammatory drugs (NSAIDs) for surgical dental pain and kidney stones, and might be similarly effective as NSAIDs for low back pain. Opioids and NSAIDs were more effective than acetaminophen for surgical dental pain, but opioids were less effective than acetaminophen for kidney stone pain. For postoperative pain, opioids were associated with increased likelihood of repeat or rescue analgesic use, but effects on pain intensity were inconsistent. Being prescribed an opioid for acute low back pain or postoperative pain was associated with increased likelihood of use of opioids at long-term followup versus not being prescribed, based on observational studies. Heat therapy was probably effective for acute low back pain, spinal manipulation might be effective for acute back pain with radiculopathy, acupressure might be effective for acute musculoskeletal pain, an opioid might be effective for acute neuropathic pain, massage might be effective for some types of postoperative pain, and a cervical collar or exercise might be effective for acute neck pain with radiculopathy. Most studies had methodological limitations. Effect sizes were primarily small to moderate for pain, the most commonly evaluated outcome. Opioids were associated with increased risk of short-term adverse events versus NSAIDs or acetaminophen, including any adverse event, nausea, dizziness, and somnolence. Serious adverse events were uncommon for all interventions, but studies were not designed to assess risk of overdose, opioid use disorder, or long-term harms. Evidence on how benefits or harms varied in subgroups was lacking. Conclusions. Opioid therapy was associated with decreased or similar effectiveness as an NSAID for some acute pain conditions, but with increased risk of short-term adverse events. Evidence on nonpharmacological therapies was limited, but heat therapy, spinal manipulation, massage, acupuncture, acupressure, a cervical collar, and exercise were effective for specific acute pain conditions. Research is needed to determine the comparative effectiveness of therapies for sickle cell pain, acute neuropathic pain, neck pain, and management of postoperative pain following discharge; effects of therapies for acute pain on non-pain outcomes; effects of therapies on long-term outcomes, including long-term opioid use; and how benefits and harms of therapies vary in subgroups.
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Chou, Roger, Daniel Hartung, Judith Turner, Ian Blazina, Brian Chan, Ximena Levander, Marian McDonagh, Shelley Selph, Rongwei Fu, and Miranda Pappas. Opioid Treatments for Chronic Pain. Agency for Healthcare Research and Quality (AHRQ), April 2020. http://dx.doi.org/10.23970/ahrqepccer229.

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