Serum Adenosine Deaminase Levels in Pancreatic Diseases

İbi̇ş, Mehmet; Köklü, Seyfettin; Yılmaz, Fatma Meriç; Başar, Ömer; Yılmaz, Gülsen; Yüksel, Osman; Yıldırım, Emre; Öztürk, Zeynel Abidin

doi:10.1159/000108970

Cited by 33 publications

(22 citation statements)

References 33 publications

(29 reference statements)

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“…Other serum/plasma markers, including matrix metallopeptidase 7 (MMP-7) and adenosine deaminase, successfully distinguished pancreatic adenocarcinoma from chronic pancreatitis, but showed no improvement in accuracy over CA 19-9 alone. 68, 71 The only assay to satisfy both criterions was based on a new monoclonal antibody to mucin 1 (MUC1) 66 , a membrane associated glycoprotein that is over expressed in multiple cancers including pancreatic adenocarcinoma and from which the CA 19-9 antigen is derived. However, with a sensitivity of 77% and specificity of 95% in the study, this MUC1 immunoassay remains below desirable accuracy levels.…”

Section: Challenges In Creating An Effective Screening Testmentioning

confidence: 99%

Screening for Pancreatic Cancer

Poruk

Firpo²,

Adler³

et al. 2013

Annals of Surgery

219

174

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Pancreatic cancer is the fourth most common cause of cancer mortality in the United States, with 5 year survival rates for patients with resectable tumors ranging from 15 - 20%. However, most patients present with distant metastases, are not resectable, and have a 5-year survival of close to 0%. This demonstrates a need for improved screening to identify pancreatic cancer while the tumor is localized and amenable to surgical resection. Studies of patients with pancreatic tumors incidentally diagnosed demonstrate longer median survival as compared with tumors discovered only when the patient is symptomatic, suggesting that early detection may improve outcome. Recent evidence from genomic sequencing indicates a 15 year interval for genetic progression of pancreatic cancer from initiation to the metastatic stage, suggesting a sufficient window for early detection. Still, many challenges remain in implementing effective screening. Early diagnosis of pancreatic cancer relies on developing screening methodologies with highly sensitive and specific biomarkers and imaging modalities. It also depends on a better understanding of the risk factors and natural history of the disease in order to accurately identify high risk groups that would be best served by screening. This review summarizes our current understanding of the biology of pancreatic cancer relevant to methods available for screening. At this time, given the lack of proven benefit in this disease, screening efforts should probably be undertaken in the context of prospective trials.

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Section: Challenges In Creating An Effective Screening Testmentioning

confidence: 99%

Screening for Pancreatic Cancer

Poruk

Firpo²,

Adler³

et al. 2013

Annals of Surgery

219

174

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“…at ASPET Journals on May 11, 2018 jpet.aspetjournals.org increments of adenosine deaminase expression and activity in different models of inflammation, including sepsis, small bowel enteritis, and hypoxia (Cohen et al, 2002;Eltzschig et al, 2006) and in the serum of patients with rheumatoid arthritis (Sari et al, 2003) or pancreatitis (Ibiş et al, 2007). However, the cellular localization of adenosine deaminase in normal or inflamed colonic tissues was not investigated in the present study, and it remains to be established whether the induction of adenosine deaminase in the setting of colitis occurs at intracellular or extracellular sites and whether such an increment depends on its increased expression in resident cells and/or accumulating immune cells.…”

Section: Adenosine Deaminase and Bowel Inflammation 439mentioning

confidence: 99%

The Blockade of Adenosine Deaminase Ameliorates Chronic Experimental Colitis through the Recruitment of Adenosine A_2Aand A₃Receptors

Antonioli¹,

Fornai²,

Colucci³

et al. 2010

J Pharmacol Exp Ther

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Adenosine modulates immune/inflammatory reactions. This study investigates the expression of adenosine deaminase in the inflamed colon, the effects of adenosine deaminase inhibitors on established colitis, and the recruitment of adenosine receptors by endogenous adenosine after adenosine deaminase blockade. Adenosine deaminase expression was determined by Western blot. The effects of 4-amino-2-(2-hydroxy-1-decyl)pyrazole [3,4-d]pyrimidine (APP; a novel adenosine deaminase inhibitor), erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; a reference adenosine deaminase inhibitor), dexamethasone, and selective adenosine receptor antagonists were tested in rats with 2,4-dinitrobenzenesulfonic acid-induced colitis. Systemic (food intake, body and spleen weight) and colonic [macroscopic/microscopic damage, tumor necrosis factor-␣ (TNF-␣), interleukin-6 (IL-6), and malondialdehyde (MDA)] inflammatory parameters were assessed. Test drugs were administered intraperitoneally for 6 days, starting at day 5 from colitis induction. Adenosine deaminase was detected in normal colon, and its expression was increased in inflamed tissues. Colitis was associated with decreased food intake and body weight, augmented spleen weight, and increased levels of colonic TNF-␣, IL-6, and MDA. APP or EHNA, but not dexamethasone, improved food intake and body weight. APP, EHNA, and dexamethasone counteracted the increments of spleen weight, ameliorated macroscopic and microscopic indexes of inflammation, and reduced TNF-␣, IL-6, and MDA levels. The beneficial effects of APP and EHNA on inflammatory parameters were prevented by the pharmacological blockade of A 2A or A 3 receptors, but not A 1 or A 2B . The present results show that: 1) bowel inflammation is associated with an enhanced adenosine deaminase expression; and 2) the anti-inflammatory actions of adenosine deaminase inhibitors against chronic established colitis depend on the sparing of endogenous adenosine, leading to enhanced A 2A and A 3 receptor activation.

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“…Changes in normal levels of ADA have been reported in a wide variety of pathologies . For example, alterations in the amount of one or both isoenzymes have been observed in a number of diseases such as hereditary hemolytic and Diamond Blackfan anemias, tuberculosis, systemic lupus erythematosus, inflammatory responses, rheumatoid arthritis, heart diseases, acquired immunodeficiency syndrome, autoimmunological thyroid diseases, some types of carcinoma, and neurological disorders, such as multiple sclerosis, meningitis, fibromyalgia, depression, and panic disorder …”

Section: Introductionmentioning

confidence: 99%

Moonlighting Adenosine Deaminase: A Target Protein for Drug Development

Cortés

Gracia

Moreno

et al. 2014

Medicinal Research Reviews

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Interest in adenosine deaminase (ADA) in the context of medicine has mainly focused on its enzymatic activity. This is justified by the importance of the reaction catalyzed by ADA not only for the intracellular purine metabolism, but also for the extracellular purine metabolism as well, because of its capacity as a regulator of the concentration of extracellular adenosine that is able to activate adenosine receptors (ARs). In recent years, other important roles have been described for ADA. One of these, with special relevance in immunology, is the capacity of ADA to act as a costimulator, promoting T-cell proliferation and differentiation mainly by interacting with the differentiation cluster CD26. Another role is the ability of ADA to act as an allosteric modulator of ARs. These receptors have very general physiological implications, particularly in the neurological system where they play an important role. Thus, ADA, being a single chain protein, performs more than one function, consistent with the definition of a moonlighting protein. Although ADA has never been associated with moonlighting proteins, here we consider ADA as an example of this family of multifunctional proteins. In this review, we discuss the different roles of ADA and their pathological implications. We propose a mechanism by which some of their moonlighting functions can be coordinated. We also suggest that drugs modulating ADA properties may act as modulators of the moonlighting functions of ADA, giving them additional potential medical interest.

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Serum Adenosine Deaminase Levels in Pancreatic Diseases

Cited by 33 publications

References 33 publications

Screening for Pancreatic Cancer

Screening for Pancreatic Cancer

The Blockade of Adenosine Deaminase Ameliorates Chronic Experimental Colitis through the Recruitment of Adenosine A_2Aand A₃Receptors

Moonlighting Adenosine Deaminase: A Target Protein for Drug Development

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Serum Adenosine Deaminase Levels in Pancreatic Diseases

Cited by 33 publications

References 33 publications

Screening for Pancreatic Cancer

Screening for Pancreatic Cancer

The Blockade of Adenosine Deaminase Ameliorates Chronic Experimental Colitis through the Recruitment of Adenosine A2Aand A3Receptors

Moonlighting Adenosine Deaminase: A Target Protein for Drug Development

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The Blockade of Adenosine Deaminase Ameliorates Chronic Experimental Colitis through the Recruitment of Adenosine A_2Aand A₃Receptors