FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2154586812> ?p ?o ?g. }

• W2154586812 endingPage "738" @default.
• W2154586812 startingPage "719" @default.
• W2154586812 abstract "The risk of ductal adenocarcinoma is greatly increased in patients with hereditary pancreatitis (HP). Analysis of the biggest series of HP patients studied to date resulted in an estimated lifetime risk for the development of ductal adenocarcinoma of 40%. Only patients in whom the disease was transmitted paternally contracted cancer, giving a lifetime risk for this subset of individuals of 70%.44 Lerch et al42 established that the risk of pancreatic cancer is also increased with maternal transmission of HP. Patients with sporadic chronic pancreatitis also have an increased risk of developing pancreatic cancer, which has been shown to be six times greater than that of unaffected individuals.43 Lowenfels et al44 showed that patients had chronic pancreatitis for at least 20 years before the development of pancreatic cancer. Patients who developed pancreatic cancer had more severe disease, manifested by increased complications of pancreatitis and increased calcification of the pancreas gland, compared with age-matched controls. This finding suggests that the relationship between the development of pancreatic cancer in patients with HP may be due to the duration and severity of the disease as a precursor to malignant pathogenesis, rather than the genetic predisposition of developing pancreatitis. Secondary screening for pancreatic ductal adenocarcinoma in patients with HP is desirable and feasible, given the high risk of cancer and the long lead time between the development of pancreatitis and pancreatic cancer. Conventional methods of diagnosis of pancreatic ductal adenocarcinoma are limited. Tumor markers are falsely elevated in 10% of patients with chronic pancreatitis,47 in cigarette smokers, and in the presence of jaundice.68 They are of little use in the diagnosis of lesions suitable for curative surgery because the sensitivity for detection in early tumors is less than 50%.29, 48 The sensitivity of CA19-9 for the detection of early pancreatic cancer (< 20 mm and confined to the pancreas) is only 43% in pure pancreatic juice and 0% in the serum.50 Other tumor markers, such as CEA, SPAN-1, and CA50, used alone or in combination, have been assessed and have a lower sensitivity than CA19-9.59 The accuracy of imaging early pancreatic lesions is disappointing. The sensitivity of detecting pancreatic ductal adenocarcinoma using computed tomography (CT) scan alone is approximately 33% for tumors less than 2 cm and 50% for tumors less than 3 cm.27 Muller et al56 found similar rates of detection in early pancreatic lesions, with 4 of 10 (40%) lesions less than 2 cm and 8 of 15 (67%) lesions less than 3 cm being visible on dynamic helical CT scan. Midwinter et al51 performed spiral CT scan on 24 patients with histologically proven ductal adenocarcinoma of the pancreas, who were being assessed for surgical resection. Mass lesions were detected in 23 of 26 pancreatic tumors of all stages; the remaining 3 tumors, which were missed, had a mean size of 22 mm. In another study, Phoa et al61 used spiral CT scan for the preoperative staging of potentially resectable pancreatic cancer. CT scan showed a mass lesion in 54 of 56 cases, with a mean diameter of 28 mm. Only half of these patients, however, were suitable for resection because of undiagnosed metastatic disease or understaged local invasion. In five of the patients with pancreatic cancer, distinction from chronic pancreatitis by CT scan criteria alone was not possible, suggesting that the sensitivity for the detection of pancreatic cancer in a background of chronic pancreatitis is likely to be even less. Johnson and Outwater37 used dynamic magnetic resonance (MR) imaging with gadolinium to differentiate chronic pancreatitis from ductal adenocarcinoma of the pancreas. Both groups showed abnormal pancreatic enhancement indicative of disease; however, there was considerable overlap between the two groups, precluding distinction of the two entities. The similar appearance of chronic pancreatitis and pancreatic cancer on imaging may be explained, in part, by the abundant fibrosis that occurs in both conditions. Endoscopic techniques for the diagnosis of pancreatic cancer are well established. Endoluminal ultrasound for the detection of malignancy on a background of chronic pancreatitis may be more sensitive than CT scan and MR imaging51 but because of poor specificity gives a positive predictive value of only 60%.1, 5, 65 Endoscopic retrograde cholangiopancreatography (ERCP) used in isolation is not sufficiently sensitive to detect subtle pancreatic ductal changes associated with early neoplastic lesions. Bakkevold et al4 prospectively examined stage I ductal adenocarcinomas and ampullary lesions and found that ERCP was 78% sensitive for diagnosing these lesions. Diagnosis of pancreatic cancer by using cytology alone on pancreatic juice obtained at ERCP has a sensitivity of 30% to 70% for the diagnosis of pancreatic cancer at all stages.21, 74 Studies that have correlated the stage of the pancreatic cancer have found that the sensitivity for detecting stage I and II pancreatic cancers using this method is only 56%.50 The sensitivity of conventional methods for diagnosing early pancreatic cancer, particularly in the presence of chronic pancreatitis, is disappointing. Advances in understanding of the molecular biology of chronic pancreatitis and pancreatic cancer have enabled the development of new strategies for the early diagnosis of pancreatic cancer, which are potentially more sensitive and specific than existing conventional modalities." @default.
• W2154586812 created "2016-06-24" @default.
• W2154586812 creator A5030627781 @default.
• W2154586812 creator A5052825850 @default.
• W2154586812 creator A5053841277 @default.
• W2154586812 date "2000-05-01" @default.
• W2154586812 modified "2023-09-25" @default.
• W2154586812 title "SCREENING FOR EARLY PANCREATIC DUCTAL ADENOCARCINOMA IN HEREDITARY PANCREATITIS" @default.
• W2154586812 cites W1501253762 @default.
• W2154586812 cites W1893714953 @default.
• W2154586812 cites W1968331471 @default.
• W2154586812 cites W1968442371 @default.
• W2154586812 cites W1969969669 @default.
• W2154586812 cites W1984120233 @default.
• W2154586812 cites W1987787632 @default.
• W2154586812 cites W1994470514 @default.
• W2154586812 cites W1995134833 @default.
• W2154586812 cites W1995215542 @default.
• W2154586812 cites W1998531538 @default.
• W2154586812 cites W2000669435 @default.
• W2154586812 cites W2000972493 @default.
• W2154586812 cites W2001458398 @default.
• W2154586812 cites W2001802638 @default.
• W2154586812 cites W2007278613 @default.
• W2154586812 cites W2009259264 @default.
• W2154586812 cites W2013856642 @default.
• W2154586812 cites W2030390835 @default.
• W2154586812 cites W2031725843 @default.
• W2154586812 cites W2032160180 @default.
• W2154586812 cites W2033997702 @default.
• W2154586812 cites W2038980248 @default.
• W2154586812 cites W2039470904 @default.
• W2154586812 cites W2040154556 @default.
• W2154586812 cites W2042316019 @default.
• W2154586812 cites W2043940574 @default.
• W2154586812 cites W2045348441 @default.
• W2154586812 cites W2046511270 @default.
• W2154586812 cites W2046577405 @default.
• W2154586812 cites W2047601328 @default.
• W2154586812 cites W2050164769 @default.
• W2154586812 cites W2053750242 @default.
• W2154586812 cites W2054207355 @default.
• W2154586812 cites W2056306761 @default.
• W2154586812 cites W2057917544 @default.
• W2154586812 cites W2058218248 @default.
• W2154586812 cites W2059250716 @default.
• W2154586812 cites W2059560004 @default.
• W2154586812 cites W2062056369 @default.
• W2154586812 cites W2064027311 @default.
• W2154586812 cites W2065991491 @default.
• W2154586812 cites W2066609521 @default.
• W2154586812 cites W2069786312 @default.
• W2154586812 cites W2072199705 @default.
• W2154586812 cites W2073336864 @default.
• W2154586812 cites W2075865556 @default.
• W2154586812 cites W2076097510 @default.
• W2154586812 cites W2076334056 @default.
• W2154586812 cites W2079422014 @default.
• W2154586812 cites W2080413696 @default.
• W2154586812 cites W2087302527 @default.
• W2154586812 cites W2088500030 @default.
• W2154586812 cites W2092748692 @default.
• W2154586812 cites W2092979002 @default.
• W2154586812 cites W2102245227 @default.
• W2154586812 cites W2105808730 @default.
• W2154586812 cites W2109884831 @default.
• W2154586812 cites W2116690382 @default.
• W2154586812 cites W2122652033 @default.
• W2154586812 cites W2139224474 @default.
• W2154586812 cites W2147833211 @default.
• W2154586812 cites W2154162092 @default.
• W2154586812 cites W2165899299 @default.
• W2154586812 cites W2167276102 @default.
• W2154586812 cites W2245672559 @default.
• W2154586812 cites W2318156113 @default.
• W2154586812 cites W23581992 @default.
• W2154586812 cites W2413781593 @default.
• W2154586812 doi "https://doi.org/10.1016/s0025-7125(05)70254-6" @default.
• W2154586812 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10872428" @default.
• W2154586812 hasPublicationYear "2000" @default.
• W2154586812 type Work @default.
• W2154586812 sameAs 2154586812 @default.
• W2154586812 citedByCount "25" @default.
• W2154586812 countsByYear W21545868122012 @default.
• W2154586812 countsByYear W21545868122016 @default.
• W2154586812 countsByYear W21545868122019 @default.
• W2154586812 countsByYear W21545868122020 @default.
• W2154586812 crossrefType "journal-article" @default.
• W2154586812 hasAuthorship W2154586812A5030627781 @default.
• W2154586812 hasAuthorship W2154586812A5052825850 @default.
• W2154586812 hasAuthorship W2154586812A5053841277 @default.
• W2154586812 hasConcept C121608353 @default.
• W2154586812 hasConcept C126322002 @default.
• W2154586812 hasConcept C181199279 @default.
• W2154586812 hasConcept C2775967933 @default.
• W2154586812 hasConcept C2776382852 @default.
• W2154586812 hasConcept C2776737053 @default.
• W2154586812 hasConcept C2778764654 @default.

• next