Prevalence of venous thromboembolism at diagnosis of upper gastrointestinal cancer

Larsen, Anders Christian; Dąbrowski, Tomasz; Frøkjær, Jens Brøndum; Fisker, Rune Vincents; Iyer, Victor Vishwanath; Møller, Bjarne Kuno; Kristensen, Søren Risom; Thorlacius-Ussing, Ole

doi:10.1002/bjs.9353

Cited by 20 publications

(21 citation statements)

References 29 publications

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“…This study was conducted as an observational predictive study of patients with pancreatic adenocarcinoma who were admitted to the Department of Gastrointestinal Surgery, Aalborg University Hospital, from February 2008 until February 2011 . All participants gave written informed consent.…”

Section: Methodsmentioning

confidence: 99%

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Promoter hypermethylation in plasma‐derived cell‐free DNA as a prognostic marker for pancreatic adenocarcinoma staging

Henriksen

Madsen

Larsen

et al. 2017

Intl Journal of Cancer

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Correct staging of pancreatic cancer is paramount, as treatment is stage specific. However, minimally invasive tools to facilitate staging are lacking. DNA promoter hypermethylation is a hallmark of cancer. The aim of this study is to evaluate promoter hypermethylation in cell-free DNA as a prognostic marker for stage classification of pancreatic adenocarcinoma. Consecutive patients with pancreatic adenocarcinoma were prospectively included. Plasma samples were obtained before diagnostic work-up and treatment. Patients were staged according to the TNM classification. Methylation-specific PCR of 28 genes was performed. Prognostic prediction models for staging of pancreatic adenocarcinoma were developed by multivariable logistic regression analysis using stepwise backwards elimination. Ninety-five patients with pancreatic adenocarcinoma were included. The mean number of hypermethylated genes was identical for stage I, II and III disease (7.09 (95% CI; 5.51-8.66), 7.00 (95% CI; 5.93-8.07) and 6.77 (95% CI; 5.08-8.46)), respectively, and highly significantly different from stage IV disease (10.24 (95% CI; 8.88-11.60)). The prediction model (SEPT9v2, SST, ALX4, CDKN2B, HIC1, MLH1, NEUROG1, and BNC1) enabled the differentiation of stage IV from stage I-III disease (AUC of 0.87 (cut point 0.55; sensitivity 74%, specificity 87%)). Model (MLH1, SEPT9v2, BNC1, ALX4, CDKN2B, NEUROG1, WNT5A, and TFPI2) enabled the differentiation of stage I-II from stage III-IV disease (AUC of 0.82 (cut point 0.66; sensitivity 73%, specificity 80%)). Cell-free DNA promoter hypermethylation has the potential to be blood-based prognostic markers for pancreatic adenocarcinoma, as panels of hypermethylated genes enables the differentiation according to cancer stage. However, further validation is required.

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Section: Methodsmentioning

confidence: 99%

“…If surgery was not performed, the final clinical decision determined the T and N categories. All patients were discussed at a multidisciplinary team conference, where consensus was reached on staging and treatment …”

Section: Methodsmentioning

confidence: 99%

Promoter hypermethylation in plasma‐derived cell‐free DNA as a prognostic marker for pancreatic adenocarcinoma staging

Henriksen

Madsen

Larsen

et al. 2017

Intl Journal of Cancer

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“…This study was conducted as a prospective observational cohort study of patients with suspected or biopsy-verified pancreatic cancer admitted to the Department of Gastrointestinal Surgery, Aalborg University Hospital between February 2008 and February 2011 [18]. Additional benign control groups were patients with chronic pancreatitis treated at the hospital or at the outpatient clinic at Aalborg University Hospital between August 2013 and August 2014 and patients admitted with acute pancreatitis at the Department of Gastrointestinal Surgery, Aalborg University Hospital or the Department of General Surgery, Hospital of Vendsyssel between November 2013 and May 2015.…”

Section: Methodsmentioning

confidence: 99%

“…Consecutive patients with suspected or biopsy-verified upper gastrointestinal cancer were included prospectively in a study on gastrointestinal cancer and venous thromboembolism [18]. Patients had blood drawn on admission before diagnostic work-up and before any treatment.…”

Section: Methodsmentioning

confidence: 99%

Cell-free DNA promoter hypermethylation in plasma as a diagnostic marker for pancreatic adenocarcinoma

et al. 2016

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BackgroundPancreatic cancer has a 5-year survival rate of only 5–7%. Difficulties in detecting pancreatic cancer at early stages results in the high mortality and substantiates the need for additional diagnostic tools. Surgery is the only curative treatment and unfortunately only possible in localized tumours. A diagnostic biomarker for pancreatic cancer will have a major impact on patient survival by facilitating early detection and the possibility for curative treatment. DNA promoter hypermethylation is a mechanism of early carcinogenesis, which can cause inactivation of tumour suppressor genes. The aim of this study was to examine promoter hypermethylation in a panel of selected genes from cell-free DNA, as a diagnostic marker for pancreatic adenocarcinoma.MethodsPatients with suspected or biopsy-verified pancreatic cancer were included prospectively and consecutively. Patients with chronic/acute pancreatitis were included as additional benign control groups. Based on an optimized accelerated bisulfite treatment protocol, methylation-specific PCR of a 28 gene panel was performed on plasma samples. A diagnostic prediction model was developed by multivariable logistic regression analysis using backward stepwise elimination.ResultsPatients with pancreatic adenocarcinoma (n = 95), chronic pancreatitis (n = 97) and acute pancreatitis (n = 59) and patients screened, but negative for pancreatic adenocarcinoma (n = 27), were included. The difference in mean number of methylated genes in the cancer group (8.41 (95% CI 7.62–9.20)) vs the total control group (4.74 (95% CI 4.40–5.08)) was highly significant (p < 0.001). A diagnostic prediction model (age >65, BMP3, RASSF1A, BNC1, MESTv2, TFPI2, APC, SFRP1 and SFRP2) had an area under the curve of 0.86 (sensitivity 76%, specificity 83%). The model performance was independent of cancer stage.ConclusionsCell-free DNA promoter hypermethylation has the potential to be a diagnostic marker for pancreatic adenocarcinoma and differentiate between malignant and benign pancreatic disease. This study brings us closer to a clinical useful diagnostic marker for pancreatic cancer, which is urgently needed. External validation is, however, required before the test can be applied in the clinic.Trial registrationClinicalTrials.gov, NCT02079363 Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0286-2) contains supplementary material, which is available to authorized users.

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“…In cancer patients, the only study available that has assessed incidental PE in 385 chest-CT scans using a 4-row CT scanner reported an incidence frequency of 2.6% (95% confidence interval [CI] 1.2-4.7) [24]. Pooled analyses of eight studies covering 8491 cancer patients suggest that the frequency is slightly higher (3.6%, 95% CI 2.6-4.6) when using modern multi-slice CT scan machines (figure 2) [25][26][27][28][29][30][31]. This difference is more notable when comparing the older CT-scans with modern CT-scans in a more general population referred for chest CT, with frequencies of 1.8% (3 studies, 3253 patients; 95% CI 00.64-2.9) and 3.3% (3 studies, 3465 patients; 95% CI 1.6-5.0), respectively (figure 2) [32][33][34][35][36][37].…”

Section: Frequency Of Incidental Pementioning

confidence: 99%

Management of incidental pulmonary embolism

Klok

Huisman

2017

Eur Respir J

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Incidental pulmonary embolism (PE) is a frequent finding on routine computed tomography (CT) scans of the chest, occurring in 1.1% of coronary CT scans and 3.6% of oncological CT scans. Despite this high frequency, optimal management of incidental PE has not been addressed in clinical trials and remains the subject of debate. Although these CT scans have not been performed with a dedicated PE protocol and have suboptimal contrast enhancement, diagnosis of incidental PE has been shown to be accurate up to the segmental and subsegmental arteries. The embolic load in incidental PE is lower than that in symptomatic PE. Even so, observational studies suggest that the natural course of incidental PE is similar to that of symptomatic PE with regard to the risk of recurrent venous thrombotic disease and mortality. Interestingly, the increased use of more advanced CT technology has coincided with an increase in the rate of incidental subsegmental PE, as is the case for symptomatic subsegmental PE. Although clinical trials are lacking, and observational data are limited to cancer-associated incidental PE, the consensus is that the management of incidental PE is identical to that of symptomatic PE, including the choice of optimal drug class, outpatient treatment and total duration of treatment.

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Prevalence of venous thromboembolism at diagnosis of upper gastrointestinal cancer

Abstract: The prevalence of VTE at cancer diagnosis was significantly higher in patients with pancreaticobiliary tract cancer than in those with other forms of upper GI cancer, and in patients with advanced cancer stage.

Cited by 20 publications

References 29 publications

Promoter hypermethylation in plasma‐derived cell‐free DNA as a prognostic marker for pancreatic adenocarcinoma staging

Promoter hypermethylation in plasma‐derived cell‐free DNA as a prognostic marker for pancreatic adenocarcinoma staging

Cell-free DNA promoter hypermethylation in plasma as a diagnostic marker for pancreatic adenocarcinoma

Management of incidental pulmonary embolism

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