Serum adenosine deaminase, catalase and carbonic anhydrase activities in patients with bladder cancer

Pirinççi, Necip; Geçit, İlhan; Güneş, Mustafa; Yüksel, Mehmet Bilgehan; Kaba, Mehmet; Tanık, Serhat; Demır, Halit; Aslan, Mehmet

doi:10.6061/clinics/2012(12)15

Cited by 30 publications

(19 citation statements)

References 31 publications

(49 reference statements)

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“…[4] Pathological invasion of blood vessels and lymphatic tissue are also considered to be independent prognostic factors. [8][9][10] More recently, a number of molecular markers with possible prognostic significance have been discussed in the literature. [11] Currently, the gold standard for diagnosing of bladder cancer is conventional white-light cystoscopy and biopsy.…”

Section: Introductionmentioning

confidence: 99%

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What are the currently available and in development molecular markers for bladder cancer? Will they prove to be useful in the future?

Abdulmajed

Sancak

Reşorlu

et al. 2014

Turkish Journal of Urology

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Urothelial carcinoma is the 9 th most common cancer worldwide. Most urothelial tumors are non-muscle invasive on presentation. However, two-thirds of non-invasive bladder cancers will eventually recur with a 25% risk of progression to muscle-invasive bladder cancer. Tumor stage, histological grade and pathological invasion of blood vessels and lymphatic tissue are the main indicators for urothelial cancer prognosis. The gold standard for diagnosing bladder cancer is conventional white-light cystoscopy and biopsy. Urine cytology is a highly specific, sensitive test for high-grade tumors or carcinoma in situ (CIS). Urinary NMP22 has an overall sensitivity and specificity for detecting bladder cancer of 49% and 87%, respectively. However, there are falsepositive results in the presence of urinary tract infection or hematuria. The detection of specific gene mutations related to urothelial cancers has been studied and employed to reproduce markers helpful for diagnosis. According to current studies, molecular markers can be used to predict tumor recurrence. From a prognostic point of view, new molecular markers have yet to be established as reliable indicators of tumor aggressiveness. We aimed to review the molecular markers with possible prognostic significance that have been discussed in the literature. This review examined the literature for various molecular markers under development for bladder cancer in an attempt to optimize patient care and reduce the costs of treating these patients.

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Section: Introductionmentioning

confidence: 99%

“…In contrast, the more expensive fluorescence-guided cystoscopy is more sensitive in diagnosing non-muscle invasive tumors (96%) and CIS (93%). [10] Approximately one-third of the deaths related to bladder cancer are potentially avoidable. Thus, the recommendation is to provide more timely care and aggressive management for such patients.…”

Section: Introductionmentioning

confidence: 99%

What are the currently available and in development molecular markers for bladder cancer? Will they prove to be useful in the future?

Abdulmajed

Sancak

Reşorlu

et al. 2014

Turkish Journal of Urology

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“…Total ADA (tADA) activity can be increased in serum in those diseases in which the number of T lymphocytes increases [9,10] and due to this fact it has been used as a marker of cell-mediated immunity [11,12] and inflammation [13]. Several diseases have been reported to increase serum ADA activity in humans, including inflammation such as chronic tonsillitis, rhinosinusitis or otitis media [3], immunomediated disorders such as systemic lupus erythematosus [14,15] or rheumatoid arthritis [16], and malignancies such as chronic lymphocytic leukemia [17], breast cancer [18] or bladder cancer [19]. Serum ADA has been also measured in veterinary species being higher in inflammation in dogs [20] and cows [21].…”

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confidence: 99%

Adenosine deaminase (ADA) characterization in saliva and serum samples of different animal species

Contreras-Aguilar¹,

Tvarijonaviciute²,

Monkevičienė³

et al. 2020

Preprint

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Background The enzymatic activity of total adenosine deaminase (tADA) and its isoenzymes ADA1 and ADA2 were studied in canine, equine, porcine and bovine serum and saliva. Erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) was used as a specific ADA1 inhibitor at different concentrations, and the distribution of the isoenzymes in serum and saliva was studied in different inflammatory situations in each species.Results Total ADA was present in serum and saliva of healthy animals of the four species. EHNA concentration of 0.47mM was needed for ADA1 inhibition in canine and porcine samples (serum and saliva) and bovine saliva, whereas for equine saliva 0.94mM was needed. ADA2 activity was not detected in bovine serum and was very low or absent in equine serum and bovine saliva. An automated procedure to measure ADA2 consisting of adding EHNA to a commercial reagent for tADA measurement provided repetitive (coefficients of variation <8.8% in serum and <10% in saliva) and accurate (linearity under dilution approaches gave R 2 >0.90) results, being equivalent to a manual incubation of the sample with EHNA at a similar concentration. Salivary tADA, as well as ADA1 and ADA2, were higher in dogs with leishmaniosis, horses with acute abdominal disease and pigs with lameness than in healthy animals. ADA showed significant correlation with serum ferritin in dogs ( r = 0.602, P < 0.01; r = 0.555, P < 0.05; and r = 0.632, P < 0.01; respectively for tADA, ADA1 and ADA2) and serum C-reactive protein in pigs ( r = 0.700, P < 0.01, for both tADA and ADA1; r = 0.770, P < 0.001, for ADA2), whereas salivary ADA2 significantly correlated with serum amyloid A in the horse ( r = 0.649, P < 0.01). In the cow, salivary tADA and ADA1 significantly increased after calving, being correlated with total white blood cell count ( r = 0.487, P < 0.05, both).Conclusions ADA activity, as well as its isoenzymes, can be measured in serum and saliva of different animal species, and the salivary levels of these analytes could potentially be inflammatory biomarkers in these species. BackgroundAdenosine deaminase (ADA, EC number 3.5.4.4) is an enzyme that can be found in several tissues and fluids and it has two different isoenzymes. The isoenzyme ADA1 is mainly present in lymphoid

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“…Evidence suggests that an increase in ADA activity can cause a reduction in the concentration of ADO in the extracellular medium, thus reducing tumour‐promoting functions . However, serum ADA has been shown to be increased in patients with bladder , breast and lung cancer . ADA serum levels in patients with melanoma have never been evaluated, and a full study of the effects of its metabolic product (INO) in human melanoma cells is still lacking.…”

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confidence: 99%

Inosine Strongly Enhances Proliferation of Human C32 Melanoma Cells through PLC‐PKC‐MEK1/2‐ERK1/2 and PI3K Pathways

Soares

Costa

Diniz

et al. 2014

Basic Clin Pharma Tox

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Malignant melanoma is the most deadly type of skin cancer. The lack of effective pharmacological approaches for this tumour can be related to the incomplete understanding of the pathophysiological mechanisms involved in melanoma cell proliferation. Adenosine has growth-promoting and growth inhibitory effects on tumour cells. We aimed to investigate effects of adenosine and its metabolic product, inosine, on human C32 melanoma cells and the signalling pathways involved. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction and bromodeoxyuridine (BrdU) proliferation assays were used to evaluate adenosine, adenosine deaminase and inosine effects, in the absence or presence of adenosine receptor (AR), A 3 AR and P2Y 1 R antagonists and PLC, PKC, MEK1/2 and PI3K inhibitors. ERK1/2 levels were determined using an ELISA kit. Adenosine and inosine levels were quantified using an enzyme-coupled assay. Adenosine caused cell proliferation through AR activation. Adenosine deaminase increased inosine levels (nanomolar concentrations) on the extracellular space, in a time-dependent manner, inducing proliferation through A 3 AR activation. Micromolar concentrations of inosine enhanced proliferation through A 3 AR activation, causing an increase in ERK1/2 levels, and P2Y 1 R activation via ENT-dependent mechanisms. We propose the simultaneous activation of PLC-PKC-MEK1/2-ERK1/2 and PI3K pathways as the main mechanism responsible for the proliferative effect elicited by inosine and its significant role in melanoma cancer progression.

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Serum adenosine deaminase, catalase and carbonic anhydrase activities in patients with bladder cancer

Cited by 30 publications

References 31 publications

What are the currently available and in development molecular markers for bladder cancer? Will they prove to be useful in the future?

What are the currently available and in development molecular markers for bladder cancer? Will they prove to be useful in the future?

Adenosine deaminase (ADA) characterization in saliva and serum samples of different animal species

Inosine Strongly Enhances Proliferation of Human C32 Melanoma Cells through PLC‐PKC‐MEK1/2‐ERK1/2 and PI3K Pathways

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