Expression of COX-2 is associated with accumulation of p53 in pancreatic cancer: analysis of COX-2 and p53 expression in premalignant and malignant ductal pancreatic lesions

Hermanová, Markéta; Trna, Jan; Nenutil, Rudolf; Dítě, Petr; Kala, Zdeněk

doi:10.1097/meg.0b013e3282f945fb

Cited by 40 publications

(17 citation statements)

References 36 publications

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“…It is inactivated largely via mutation, usually resulting in nuclear accumulation and positive IH stain [23][24][25] . The p53 abnormality is detected in 50% to 90% of pancreatic adenocarcinomas [23][24][25][26][27][28][29][30][31] , and in their precursor, PanIN, the positive stain ing is directly correlated to the grade [17,[29][30][31] . Our findings agree with previous studies on EUS-FNA of pancreas, which showed that the addition of p53 IH or DNA analysis resulted in a modest sensitivity gain [12][13][14] .…”

Section: Discussionmentioning

confidence: 99%

Staining for p53 and Ki-67 increases the sensitivity of EUS-FNA to detect pancreatic malignancy

Jahng

Reicher²,

Chung³

et al. 2010

WJGE

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AIM:To investigate whether tumor marker staining can improve the sensitivity of endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) to diagnose pancreatic malignancy. METHODS:Patients who underwent EUS-FNA were retrospectively identified. Each EUS-FNA specimen was evaluated by routine cytology and stained for tumor markers p53, Ki-67, carcinoembryonic antigen (CEA) and CA19-9. Sensitivity, specificity, positive and negative predictive values (PPV and NPV), and positive and negative likelihood ratios (PLR and NLR) were calculated in order to evaluate the performance of each test to detect malignancy. RESULTS:Sixty-one specimens had complete sets of stains, yielding 49 and 12 specimens from pancreatic adenocarcinomas and benign pancreatic lesions due to pancreatitis, respectively. Cytology alone had sensitivity and specificity of 41% and 100% to detect malignancy, respectively. In 46% of the specimens, routine cytology alone was deemed indeterminate. The addition of either p53 or Ki-67 increased the sensitivity to 51% and 53%, respectively, with perfect specificity, PPV and PLR (100%, 100% and infinite). Both stains in combination increased the sensitivity to 57%. While additional staining with CEA and CA19-9 further increased the sensitivity to 86%, the specificity, PPV and PLR were significantly reduced (at minimum 42%, 84% and 1, respectively). Markers in all combinations performed poorly as a negative test (NPV 26% to 47%, and NLR 0.27 and 0.70). CONCLUSION: Immunohistochemical staining for p53and Ki-67 can improve the sensitivity of EUS-FNA to diagnose pancreatic adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

Staining for p53 and Ki-67 increases the sensitivity of EUS-FNA to detect pancreatic malignancy

Jahng

Reicher²,

Chung³

et al. 2010

WJGE

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“…They supported the possible role of COX-2 in carcinogenesis of pancreatic ductal adenocarcinoma. It has been suggested that PanINs represent the possible link between chronic pancreatitis and pancreatic cancer and that COX-2 may represent a possible therapeutic target for potential chemoprevention in patients with chronic pancreatitis and pancreatic ductal adenocarcinoma using selective COX-2 inhibitors [35,36,37]. …”

Section: Introductionmentioning

confidence: 99%

The Role of Chronic Inflammation: Chronic Pancreatitis as a Risk Factor of Pancreatic Cancer

Dítě

Hermanová

Trna

et al. 2012

Dig Dis

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Pancreatic carcinoma is a condition with late diagnosis and one for which there is no effective screening method. One possible diagnostic approach of so-called early adenocarcinoma is the identification and systematic examination of individuals at risk for this condition. Between 1992 and 2005 we systematically observed 223 individuals diagnosed with chronic pancreatitis. In this 14-year period we performed classical biochemical tests, endoscopic ultrasound, CT scans and ERCP. We also asked about the number of cigarettes smoked per year and classified individuals consuming regularly more than 80 g of alcohol per day for 5 years for men and 50 g of alcohol per day for 5 years for women as having the alcoholic form of chronic pancreatitis. The remaining patients were classified according to the TIGARO classification. Alcohol-related etiology was detected in 73.1% of patients, 21.5% had the chronic obstructive form and only 5.4% were classified as idiopathic pancreatitis. Pancreatic carcinoma was detected in 13 patients with chronic pancreatitis (5.8%), 3 patients were diagnosed with gastric carcinoma and 1 with esophageal carcinoma. Pancreatic malignancy developed mainly in patients with the alcoholic form of pancreatitis (4.5%). In the 14-year period 11 subjects died, out of which 8 cases were related to pancreatic carcinoma. Pancreatic and extrapancreatic cancer localized in the gastrointestinal tract are serious complications of chronic nonhereditary pancreatitis. Systematic observation of patients with chronic pancreatitis must be performed with the aim of early diagnosis of pancreatic malignancies (but also including other types).

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“…A recent study identified that the COX-2 expression is significantly correlated with the tumor size in pancreatic cancer, which offers a new insight into the regulation of growth and development of metastases in pancreatic cancer [39] . A correlation between COX-2 and p53 expression levels in carcinomas was revealed, and an accumulation of p53 was associated with COX-2 overexpression in premalignant and malignant ductal lesions, which offers opportunities for targeted therapy and chemoprevention of pancreatic cancer using COX-2 inhibitors，especially in lesions with functional p53 [40] .…”

Section: Cox-2mentioning

confidence: 97%

Mutated genes in pancreatic cancer

2010

Chin. J. Cancer Res.

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Pancreatic cancer continues to be a deadly malignancy with still high mortality and poor survival. Little progress has been made on the treatment of advanced pancreatic cancer despite the significant advances in understanding, diagnosis, and access to conventional and novel treatments. Molecular pathology of the lesion is the key of our understanding of the mechanisms underlying the development of this cancer and will probably help us in earlier diagnosis and better therapeutic results. New treatment strategies and a more careful evaluation of innovative therapies are clearly needed for this disease. In view of many findings pancreatic cancer should be regarded as a systemic disease, and over the last several years, investigators have gained a better understanding of the molecular biology and events that lead to the development of malignancies. We here review the novel developments in the systemic exploring for commonly mutated genes in pancreatic cancer.

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Expression of COX-2 is associated with accumulation of p53 in pancreatic cancer: analysis of COX-2 and p53 expression in premalignant and malignant ductal pancreatic lesions

Cited by 40 publications

References 36 publications

Staining for p53 and Ki-67 increases the sensitivity of EUS-FNA to detect pancreatic malignancy

Staining for p53 and Ki-67 increases the sensitivity of EUS-FNA to detect pancreatic malignancy

The Role of Chronic Inflammation: Chronic Pancreatitis as a Risk Factor of Pancreatic Cancer

Mutated genes in pancreatic cancer

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