Evaluations of the combined use of blood- and tissue-based protein biomarkers for pancreatic cancer.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a low 5-year survival rate. Biomarkers may be of value for the early diagnosis of pancreatic cancer. This study assessed blood- and tumour tissue-based biomarkers associated with pancreatic cancer. METHODS: We studied 61 patients who underwent pancreatic resection. Of these 61 patients, 46 patients had PDAC, and 15 patients had inflammatory tumours. Blood and tumour tissue levels of VEGF, hypoxia-inducible factor 1α (HIF-1α) and glucose transporter 1 (GLUT1) were measured. RESULTS: Blood concentrations of VEGF (p < 0.000001) and HIF-1α (p = 0.000002) were significantly higher in the PDAC group than in the inflammatory tumour group. Tumour tissue concentrations of VEGF (p < 0.000001), HIF-1α (p = 0.000005) and GLUT1 (0.000002) were also significantly higher in the PDAC group. Univariate analyses revealed that age, BMI, and blood levels of CA19-9, VEGF, and HIF-1α were potential predictors of PDAC. Potential predictors of PDAC in tumour tissue were VEGF, HIF-1α and GLUT1. Multivariate analyses found that VEGF was the most powerful independent predictor of PDAC in blood (OR = 1.016; 95% CI: 1.007-1.025; 0.001) and tumour tissue (OR = 1.02; 95% CI: 1.008-1.032, p = 0.001). The cut-off point for blood VEGF was 134.56 pg/ml, with a sensitivity of 97.8%, specificity of 86.7%, PPV of 95.7%, and NPV of 92.9%. The cut-off point for tissue tumour VEGF in PDAC was 208.59 pg/mg, with a sensitivity, specificity, PPV and NPV of 97.7%, 92.9%, 97.7%, and 92.9%, respectively. CONCLUSIONS: There are significant differences in blood-based biomarkers for differentiating between PDAC and inflammatory tumours of the pancreas. VEGF was an independent predictor of PDAC independent of its addition to the routinely used tumour marker CA19-9 antigen.

Blood-based protein biomarkers and red blood cell aggregation in pancreatic cancer.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is highly malignant with a low 5-year survival rate. Blood biomarkers may be of value for the noninvasive diagnosis of pancreatic cancer. OBJECTIVE: This study assessed blood-based biomarkers and disturbances in red blood cell aggregation associated with pancreatic cancer. METHODS: We studied 61 patients who underwent pancreatic resection. Of these 61 patients, 46 patients had PDAC, and 15 patients had inflammatory tumours. Serum VEGF, hypoxia-inducible factor (HIF-1α), elastin-derived peptides (EDPs), total sialic acid (TSA) and resistin levels were measured. Red blood cell aggregation was assessed by a laser-assisted optical rotational cell analyser. RESULTS: VEGF (p < 0.000001), HIF-1α (p = 0.000002), resistin (p = 0.000349), EDP (p = 0.000089) and TSA (p = 0.000013) levels were significantly higher in the PDAC group than in the inflammatory tumour group. The aggregation index (AI), syllectogram amplitude (AMP) and threshold shear rate (γthr) were significantly higher in the PDAC group, whereas the aggregation half-time (t1/2) was lower than in the inflammatory tumour group. Multivariate analyses revealed that VEGF, TSA and EDP levels were variables that predicted PDAC. VEGF levels were the most powerful predictor of PDAC independent of CA 19-9 levels. The cut-off points for VEGF, TSA and EDP levels were 134.56 pg/ml, 109.11 mg/dl and 36.4 ng/ml, respectively, with sensitivities of 97.8%, 87% and 69.6%, respectively, and specificities of 86.7%, 86.7% and 93.3%, respectively. CONCLUSION: This study indicated that there are significant differences in blood-based biomarkers for differentiating between PDAC and inflammatory tumours of the pancreas. We also confirmed that PDAC is associated with the excessive aggregation of RBCs.

The Concentration of CMKLR1 Expression on Clinicopathological Parameters of Colorectal Cancer: A Preliminary Study.

Background and Objectives: Colorectal cancer (CRC) is the second-most common cause of cancer-related deaths worldwide. Angiogenesis is crucial for cancer growth, infiltration of surrounding tissues, and metastasis and plays a key role in the pathogenesis of CRC. Chemerin/chemokine-like receptor 1 (CMKLR1) is one of the biochemical pathways involved in the regulation of angiogenesis in solid tumors. The aim of the study was to assess the CMKLR1 level in tumor and margin tissues of CRC in relation to histopathological parameters: microvessel density (MVD), budding, tumor-infiltrating lymphocytes (TILs), TNM scale, and grading. Materials and Methods: The study involved 43 samples of tumor and margin tissues obtained from CRC patients. To assess the concentration of CMKLR1 a commercially available enzyme-linked immunosorbent assay kit was used. For 35 cases, we performed CD34 immunostaining. The MVD, budding, and TILs were assessed using a light microscope. Results: The levels of CMKLR1 in both tumor and margin were negatively correlated with MVD and budding. CMKLR1 concentration in margin was higher in tissues with lymphocytic infiltration. Conclusions: Low vascularity and low budding are associated with higher CMKLR1 expression. CMKLR1 might play a multifunctional role in CRC pathogenesis by influencing tumor budding and peritumoral lymphocytic infiltration.

Serum omentin-1 and chemerin concentrations in pancreatic cancer and chronic pancreatitis.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by very poor prognosis. It is caused by asymptomatic course of the disease at early stage. Symptomatic PDAC means usually advanced stage of the disease, making radical treatment impossible. Finding of biological PDAC marker could improve PDAC treatment through early diagnosis. In our study, we investigated two adipokines: omentin and chemerin concentration in PDAC, chronic pancreatitis (CP) and healthy individuals. We examined 27 PDAC patients, 10 CP patients and 36 controls. To determine concentration of adipokines we used ELISA immunoenzymatic assay. Level of both adipokines was increased when comparing control group to PDAC patients. Additionally, chemerin concentration in CP group was elevated comparing to control. To evaluate both adipokines as potential PDAC biomarkers we performed ROC analysis. Chemerin (AUC = 0.913) displayed better discriminant ability than omentin-1 (AUC = 0.73). Some authors believe that chemerin may promote tumour growth by stimulating angiogenesis and is supposed to be a factor recruiting mesenchymal stroma cells (MSC) in tumour regions. Omentin-1 can inhibit tumourigenesis by TP53 stimulation. On the other hand, according to some studies, omentin-1 may promote cancer proliferation via Akt signalling pathway. Results from our study showed significantly elevated level of chemerin and omentin-1 in PDAC patients. Therefore, we believe that both investigated adipokines may provide promising and novel pharmacological insights for oncological diagnosis in the near future.

Influence of Obesity on Anastomotic Leakage After Anterior Rectal Resectionperformed Due to Cancer.

UNLABELLED: Anterior resection for rectal cancer carries the risk of serious complications, especially fistulas at the site of anastomosis. Numerous factors have been shown to impact anastomotic leakage. The results of studies on the influence of obesity on the frequency of anastomotic leakage after rectal resection performed due to cancer have been contradictory. The aim of the study was to evaluate the relationship between body mass index (BMI) and frequency of anastomotic leakage after anterior rectal resection performed due to cancer. MATERIAL AND METHODS: This retrospective analysis included 222 subsequent patients who had undergone anterior resection due to cancer with an anastomosis formed with a mechanical suture. The patients were divided into 3 groups depending on their BMI quartile as follows: Group I, BMI < 23.8 kg/m2 (lower quartile); group II, BMI between 23.8 and 29.38 kg/m2 (middle quartile); and group III, BMI > 29.38 kg/m2 (upper quartile). RESULTS: Anastomotic leakage occurred in 8 (3.6%) patients. Fistulas occurred in 4 out of 61 patients (6.56%) in group I, which was the highest incidence of fistulas for all 3 groups. In group II, fistulas occurred in 2 out of 55 patients (3.63%), and similarly, in group III, they occurred in 2 out of 106 patients (1.87%). The differences found in the frequency of fistulas between groups were not statistically significant (p=0.31). The logistic regression analysis did not show any relationship between leakage and age (p = 0.55; OR = 1.02; 95% CI: 0.95 - 1.1), sex (p = 0.97; OR = 0.97; 95% CI: 0.22 - 4.25) or BMI (p = 0.27; OR = 0.58; 95% CI: 0.22 - 1.53). CONCLUSIONS: The results of our study show that BMI did not have any influence on the frequency of anastomotic leakage after anterior rectal resection performed due to cancer.

Mortality and anastomotic leakage after anterior resection for rectal cancer.

BACKGROUND/AIMS: The aim of the study was to analyze the mortality and symptomatic anastomotic leak following stapled anastomosis after anterior resection for rectal cancer. METHODOLOGY: We analyzed retrospectively 161 patients subjected to elective anterior resection of the rectum. There were 102 (63.3%) men and 59 (37.7%) women. The patients were divided into two groups according to tumor location: group I - 129 (80.1%) patients with tumor located >6 cm from the anal verge and group II - 32 (19.9%) patients with tumor located =6 cm. RESULTS: Anastomotic leak was found in 5 (3.1%) patients, three (2.3%) from group I and two (6.2%) from group II (p<0.26). Anastomotic leak was found more often in patients with renal failure (p<0.0023) and in those who had undergone RBC concentrate transfusion (p<0.0045). Seven (4.3%) patients died in the postoperative period. Deaths occurred more frequently in patients with valvular heart disease (p<0.00002), renal failure (p<0.0047) and in those given concentrates of RBC (p<0.045). CONCLUSIONS: Incidence of postoperative surgical complications after resection for rectal cancer is not high and is acceptable; however, there is an increased risk of leakage after low anterior resection. Renal failure as well as RBC concentrate transfusion have an influence on mortality and anastomotic leak.

[Iliac vessels malformations as a cause of gluteal varices]. / Malformacje naczyn biodrowych jako przyczyna zylaków posladków.

Gluteal varices are caused by different malformations (congenital or other disorders) within pelvic vessels. They are usually congenital, rarely acquired disorders. The rarity of incidence, diagnostic difficulties and sometimes ineffective methods of treatment made the authors of this article to present a case of 51-year-old patient with hemorrhoids with concomitant left gluteal varices caused by internal iliac artery-vein fistula.