JOP: Journal of the pancreas (J Pancreas )

Description

  • Impact factor
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  • 5-year impact
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  • Cited half-life
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  • Eigenfactor
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  • Website
    Journal of the Pancreas website
  • Other titles
    JOP. Journal of the Pancreas, Journal of the pancreas
  • ISSN
    1590-8577
  • OCLC
    46677991
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • JOP: Journal of the pancreas 09/2014; 15(5):2657.
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    ABSTRACT: To evaluate the safety and survival benefit of combined curative resection (CR) of the pancreas and major venous resection in the management of borderline resectable pancreatic adenocarcinoma.
    JOP: Journal of the pancreas 09/2014; 15(5):433-41.
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    ABSTRACT: EUS with fine-needle aspiration and cyst fluid analysis is routinely used to evaluate pancreatic cysts; however, the clinical course of these lesions is often not well defined.
    JOP: Journal of the pancreas 05/2014; 15(5):427-32.
  • JOP: Journal of the pancreas 01/2014; 15(4):411-2.
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    ABSTRACT: Cigarette smoking is a known risk factor of pancreatic disease. Nicotine - a major cigarette tobacco component - can traffic through the circulatory system and may induce fibrosis and metastasis, hallmarks of chronic pancreatitis and pancreatic adenocarcinoma, respectively. However, at the biomolecular level, particularly in pancreatic research, the effects of nicotine remain unresolved.
    JOP: Journal of the pancreas 01/2014; 15(5):465-74.
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    ABSTRACT: Cells in the interior of pancreatic tumors are believed to undergo continual autophagy to maintain homeostasis during unregulated growth in hypoxia caused by impaired vascularity. We hypothesize that treating metastatic cells with chloroquine, an inhibitor of autophagy, in hypoxia will decrease cell viability and induce cell death. MiaPaCa2 (non-metastatic) and S2VP10 (metastatic) cell lines were treated with 25 and 50 µM chloroquine for 24 and 48 hours in normoxia and hypoxia (5-10% O2). Viability was measured using ATPliteTM. After treatment, the cell stress was analyzed, and protein was lysed and quantified using the Bradford assay. Autophagy-associated protein levels were determined by Western blot. S2VP10 cells treated for 48 hours with 50 μM chloroquine in hypoxia had 24% viability compared to normoxia control, with loss of 10% viability caused by low O2 alone. MiaPaCa2 cells under these conditions had 60% viability compared to normoxia control, with loss of 25% viability caused by low O2 alone. Analysis of cell stress pathways and dosimetry of Western blot data suggest that chloroquine inhibits the autophagy pathway in the metastatic S2VP10 cells. Autophagy blockage with chloroquine or similar-acting drugs may serve as a viable therapy for highly metastatic pancreatic cancers.
    JOP: Journal of the pancreas 01/2014; 15(2):189-97.
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    ABSTRACT: Surgery remains the only curative treatment for pancreatic cancer; however, majority of patients present with advanced unresectable disease upon diagnosis. Treatment of nonmetastatic, locally advanced pancreatic cancer (LAPC) continues to require multidisciplinary bimodality or trimodality approach. Neoadjuvant therapies have been investigated for LAPC given its established role in other solid cancers such as breast cancer, gastric cancer, and rectal cancer. This strategy is now moving forward to management of potentially resectable disease as well. This meeting highlight focuses on recent updates on neoadjuvant therapy for both borderline resectable disease and potentially resectable disease, Abstracts #4120, #e15189, #e15226 and #TPS4158 will be discussed.
    JOP: Journal of the pancreas 01/2014; 15(4):354-7.
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    ABSTRACT: Several epidemiology studies have observed that there is a higher than expected association between diabetes mellitus (DM) and pancreatic ductal adenocarcinoma (PDAC). However, because no plausible mechanistic link exists between high glucose levels and carcinogenesis, additional risk factors are likely involved. Evaluating these epidemiologic data has been confounded by difficulty in identifying appropriate control populations and in replicating the demographics and risk found in previous studies. Furthermore, a significant subset of patients developed DM up to 2 years before the detection of cancer, suggesting that the glucose intolerance in these patients is a paraneoplastic syndrome linked to factors released from the tumor rather than typical type 1 or type 2 DM. Indeed, DM is a major co-morbidity of PDAC and is often reversed following resection of the cancer and a major part of the pancreas, while in other cases, pancreatic resection leads to DM. Finally, the DM may be associated with previous acute pancreatitis and/or subclinical chronic pancreatitis, so that the diagnosis of pancreatitis is often missed. The pancreatitis factor is important since the link between pancreatitis and pancreatic cancer is well established and a close temporal link between pancreatitis and diabetes in known. In these cases the primary epidemiology association is between DM and pancreatitis rather, and secondarily, there is a mechanistic association between pancreatitis and PDAC. To date, though, pancreatitis and pancreatogenic DM (Type 3c) has not been adequately assessed in a major epidemiology study. These observations indicate that glucose intolerance is non-specific, that PDAC can cause DM, and that pancreatitis may be an important missing link between DM and PDAC. Thus, new carefully controlled studies are needed to better understand the underlying cause of the association of PDAC with DM.
    JOP: Journal of the pancreas 01/2014; 15(5):2772.
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    ABSTRACT: About half of all patients with chronic pancreatitis (CP) develop diabetes mellitus (DM) due to the loss of islet cell mass, not just beta cells as in Type 1 DM (T1DM), or due to insulin resistance, as in Type 2 DM (T2DM). Patients with DM from loss of islets due to pancreatic disease or resection are diagnosed with pancreatogenic or Type 3c DM (T3cDM). Patients with T3cDM also lose counter-regulatory hormones, such as glucagon and pancreatic polypeptide, and experience maldigestion associated with pancreatic exocrine insufficiency. Patients with T3cDM are therefore more susceptible to hypoglycemia and a mismatch (asynchrony) between food ingestion and nutrient absorption. At the same time, the use of incretin therapy is likely useless, since maldigestion leads to the release of higher levels of hind gut hormones, including GLP1. Thus, T3cDM caused by CP or destruction of the islets involves a special class of potential risks and comorbidity that may be overlooked if the CP has not been diagnosed. Further, because CP is also associated with pancreatic ductal adenocarcinoma, better classification of patients with DM is needed to determine if PDAC is associated with DM or with undetected CP that gave rise to T3cDM that was previously misclassified as T1DM to T2DM.
    JOP: Journal of the pancreas 01/2014; 15(5):2773.
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    ABSTRACT: The natural history of incidental branch-duct intraductal papillary mucinous neoplasm of the pancreas is still unknown.
    JOP: Journal of the pancreas 01/2014; 15(4):391-3.
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    ABSTRACT: Pancreatic neuroendocrine tumors account for only 1-3% of all pancreatic neoplasms and the intraductal invasion of the main pancreatic duct (MPD) is rare.
    JOP: Journal of the pancreas 01/2014; 15(5):497-500.
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    ABSTRACT: Pancreatic cancer is the tenth most common cancer diagnosis; however, it is the fourth most common cause of death due to cancer. Recent estimates suggest that by 2020 pancreatic cancer will become the second most common cause of cancer death in the US. The 5-year survival rate in all patients is only ~5% and has not changed significantly over the past five decades. Though the relationship between diabetes mellitus and pancreatic cancer has been known for over 125 years, it still remains to be fully understood. The complex relationship between the two diseases has been the subject of numerous clinical, epidemiological, laboratory and experimental studies. Epidemiologic studies suggest that long-standing type 2 diabetes is a modest risk factor for the development of pancreatic cancer. Meta-analysis of multiple cohort and case-control studies show that the risk of pancreatic cancer in those with diabetes for >5 years is 1.5 to 2.0 fold higher. This s not fully explained by shared risk factors between the two diseases such as obesity. There is also strong clinical, epidemiological and experimental evidence to show that pancreatic cancer causes diabetes. Hyperglycemia and diabetes mellitus occur in ~85% of pancreatic cancer subjects, with diabetes being present in 45% to 67% of pancreatic cancer patients depending on how diabetes is ascertained. Majority (~75%) of diabetes in pancreatic cancer is new-onset, i.e., less than 3 years in duration. The new-onset diabetes often resolves with resection of cancer. The notion that new-onset diabetes in pancreatic cancer is a paraneoplastic phenomenon caused by tumor secreted products was strengthened by a recent study that proposed adrenomedullin, a 52 amino-acid polypeptide, as a strong candidate for mediator of diabetes in pancreatic cancer. In previous studies adrenomedullin has been shown not only to promote pancreatic cancer aggressiveness, but also inhibits insulin exocytosis from beta cells. In the aforementioned study pancreatic cancer cell lines overexpressing adrenomedullin were shown to inhibit insulin secretion, an effect that was reversed by silencing adrenomedullin. Adrenomedullin was also shown to be overexpressed in human pancreatic cancer and plasma levels of adrenomedullin were also increased in pancreatic cancer patients, especially those with diabetes. New-onset diabetes appears to be the only clue to the presence of asymptomatic sporadic pancreatic cancer. Nearly 25% of patients with pancreatic cancer are diagnosed with diabetes 6 months to 36 months before the diagnosis of pancreatic cancer. Conversely, subjects with new-onset diabetes over age 50 years have an 8-fold higher risk for having pancreatic cancer. Thus new-onset diabetes may be a clue to the early diagnosis of the cancer. However, the success of the strategy to use new-onset diabetes as a marker of pancreatic cancer will depend on our ability to distinguish pancreatic cancer-associate diabetes from the more common type 2 diabetes. This strategy provides for diagnosis of early, asymptomatic pancreatic cancer.
    JOP: Journal of the pancreas 01/2014; 15(5):2778.
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    ABSTRACT: Indication of surgery for branch duct intraductal papillary mucinous neoplasm (BD-IPMN) proposed by the consensus guidelines revised in 2012 was too complex to refer to in clinical practice. This study aimed to identify simple predictors of malignancy in BD-IPMN.
    JOP: Journal of the pancreas 01/2014; 15(5):459-64.
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    ABSTRACT: Despite incredible effort on understanding and awareness of diabetes, management procedure is becoming more challenging since the complications of the disease as well as the newly discovered or yet put on market drugs that may have a suspicious association with cancer. This metabolic disorder itself does already have high prevalence of cancer such as pancreas and colon. Thyroid cancer itself is also increasing and thyroid disorders associated with diabetes is well known endocrinological problem. Rise in thyroid cancer patients in diabetics are also emphasized in meta-analyses. Obesity does seem to be another factor for thyroid cancer; however, it is also commonly associated with patients who have type 2 diabetes. GLP-1 based therapy does not only help diminish blood glucose but help satiety and lose weight as well which is a desired effect of diabetes therapy since losing weight corrects many other cardiovascular risk factors. Thyroid cancer and its connectivity to GLP-1 analogue therapy is a concern, yet not proven; although may diminish the rate of prescription by some diabetologists, although some suggest outweigh the clinical positive effect.
    JOP: Journal of the pancreas 01/2014; 15(5):2788.