Serum levels of tissue factor in colorectal cancer patients

1998 ◽  
Vol 3 (5) ◽  
pp. 287-290
Author(s):  
Chika Shigemori
PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107470 ◽  
Author(s):  
Loretta De Chiara ◽  
Ana M. Rodríguez-Piñeiro ◽  
Oscar J. Cordero ◽  
Lidia Vázquez-Tuñas ◽  
Daniel Ayude ◽  
...  

2018 ◽  
Vol 37 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Jolanta Bugajska ◽  
Joanna Berska ◽  
Diana Hodorowicz-Zaniewska ◽  
Krystyna Sztefko

SummaryBackground: Polyunsaturated fatty acids (PUFAs) play a role in the development/progression of colon cancer. The aim of the study was to assess the relation between serum phospholipids PUFAs, colorectal tumour localization and disease progression. Methods: A total of 67 patients (18 with proximal colon, 17 with distal colon and 32 with rectal tumour localization) as well as 16 controls were studied. One year after surgery, 33 patients had disease progression. Serum levels of C16:1(n-7), C18:1(n-9), C18:3(n-3), C20:5(n-3), C22:6(n- 3), C18:2(n-6), C20:2(n-6), C20:4(n-6) fatty acids of se - rum phospholipids were quantitatively measured before surgery by gas-chromatography. Results: Significantly higher mean value of C18:2, as compared to control, has been noted only for patients with proximal (p<0.05) and distal tumour (p<0.03) localization. The lower mean level of C20:5 and unsaturation index (UI) were observed in colorectal cancer patients regardless the tumour localization, but the statistical difference was noted only for patients with proximal tumours (p<0.05, p<0.03). In patients with proximal tumours, significantly lower mean level of C20:4 and UI were noted in patients with disease progression, as compared to patients with proximal tumours without disease progression (p<0.05). Conclusion: The evaluation of PUFAs as a risk/prognostic factor in colorectal cancer patients should take into account tumour localization as a dependent variable.


Tumor Biology ◽  
2020 ◽  
Vol 42 (6) ◽  
pp. 101042832092523 ◽  
Author(s):  
Mouadh Barbirou ◽  
Ikram Sghaier ◽  
Sinda Bedoui ◽  
Rahma Ben Abderrazek ◽  
Hazar Kraiem ◽  
...  

The KCNB1 gene variants were differentially associated with cancers. However, their association with colorectal cancer has not yet been explored. We investigated the contribution of the KCNB1 gene variants rs3331, rs1051295, and indel (insertion/deletion) rs11468831 Polymorphism as predictors of the treatment response in colorectal cancer patients. A retrospective study, which involved 291 Tunisian colorectal cancer patients (aged 60.0 ± 13.1 years), who were stratified into responder and non-responder groups, according to TNM stages and their responsiveness to chemotherapy based on fluorouracil. KCNB1 genotyping was performed with amplification-refractory mutation system–polymerase chain reaction, and was confirmed by Sanger sequencing. Sex-specific response was found and colorectal cancer females are less likely to achieve a positive response during the chemotherapy strategy, compared to males. Weight and body mass index, tumor size, and tumor localization are considered as predictive factors to treatment responsiveness. Carriage of rs11468831 Ins allele was significantly associated with successful therapy achievement ( p adjusted < 0.001). Stratification of colorectal cancer patients’ response according to tumor localization and TNM stages reveals negative association of rs3331 Major allele to treatment response among the patients with advanced cancer stages (subgroup G2). The presence of rs3331 (homozygous minor) C/C genotype was positively associated with decline in carcino-embryonic antigen ( p = 0.043) and CA19-9 ( p = 0.014) serum levels. On the other hand, the presence of rs1051295 (homozygous minor) A/A genotype was correlated with marked decline in CA19-9 serum levels. KCNB1 haplotype did not reveal any association between haplotypes and treatment response. The results obtained suggest that gender-specific strategies for screening treatment and prevention protocols as well as KCNB1 variants may constitute an effective model for ongoing personalization medicine.


Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1425-1425
Author(s):  
Ludwig Traby ◽  
Hannah C. Puhr ◽  
Marietta Kollars ◽  
Kammer Michael ◽  
Gerald Prager ◽  
...  

Abstract Introduction Venous thromboembolism is a frequent complication in cancer patients and results in a considerable morbidity and mortality. The underlying mechanisms leading to the increased thrombotic risk are yet poorly understood. We have previously shown that levels of extracellular vesicles (EV) are elevated in patients with colorectal cancer compared to healthy control individuals (Hron et al, Thromb Haemost 2007;97:119-123). EV originate from blood or endothelial cells, or from the underlying tumor itself. They may contribute to coagulation activation and propagation by exposing tissue factor and by providing a surface for the interaction of coagulation factors. In that study, the number of EV was also positively correlated with levels of D-dimer, a fibrin split product and marker of coagulation activation. We hypothesize that number of EV and levels of D-dimer decline with decreasing tumor load during antineoplastic treatment. Therefore, the study aims at evaluating the long-term effect of chemotherapy on hemostatic system activation in patients with advanced colorectal cancer. Methods We conducted a pilot study including patients receiving chemotherapy because of advanced colorectal cancer. All chemotherapy regimens were based on 5-fluorouracilcombined with either oxaliplatin or irinotecan without or with an antibody (bevacizumab in 72%, cetuximab in 11%, and ramucirumab in 5% of patients, respectively). Patients were followed for 3 chemotherapy cycles. The study was approved by the local ethics committee, was conducted according to the Declaration of Helsinki and informed consent was obtained from all study patients. Venous blood was sampled at each cycle immediately before chemotherapy and was centrifuged at 2600 g for 15 minutes. The number of EV was assessed by flow cytometry using a FACSCalibur® flow cytometer with CellQuest™ software (Becton Dickinson) immediately after blood collection and centrifugation in fresh plasma. EV were defined by size (forward scatter, <1 µm) and annexin V binding. Tissue factor positive EV were characterized by an anti-CD142 antibody. Plasma was then frozen and stored at -80°C and was used for determination of markers of coagulation activation (D-dimer, prothrombin fragment f1.2) by commercially available ELISA kits. All outcome variables were log-transformed due to skewed distributions. The paired t-test was used to compare baseline (before the 1st chemotherapy) levels with measurements obtained from the 2nd and 3rd blood sampling. In order to provide a clearer legibility, all data is presented in absolute numbers and all values are given as median (quartiles) if not otherwise stated. Results 18 patients completed 3 cycles of chemotherapy. Their mean (± SD) age was 60.5 (± 12.2) years and 14 (78%) were men. None of the patients developed venous thromboembolism. Table 1 shows the levels of coagulation activation markers and the number of EV at baseline and before the 2nd and 3rd cycle of chemotherapy, respectively. D-dimer levels were 1.22 (0.42-2.31) µg mL-1 at baseline and significantly decreased over the course of treatment. D-dimer levels did not correlate with the number of EV either at baseline or at later time points. The number of EV decreased from 474 (312-617) x 103 mL-1 at baseline to 359 (239-474) x 103 mL-1 before the 3rd cycle. The proportion of tissue factor positive EV was small at baseline and throughout treatment. Levels of prothrombin fragment f1.2 did not change during treatment and did not correlate with number of EV at any time point. Conclusions In patients with advanced colorectal cancer chemotherapy attenuates coagulation activation as indicated by a decline of D-dimer levels and number of EV. These findings warrant further studies in a larger patient population and longer observation time. Table 1 Number of extracellular vesicles (EV) and markers of coagulation activation in plasma of colorectal cancer patients before and during chemotherapy Table 1. Number of extracellular vesicles (EV) and markers of coagulation activation in plasma of colorectal cancer patients before and during chemotherapy Disclosures No relevant conflicts of interest to declare.


2010 ◽  
Vol 32 (1) ◽  
pp. 160-164 ◽  
Author(s):  
Palma A. Iacovazzi ◽  
Maria Notarnicola ◽  
Maria G. Caruso ◽  
Vito Guerra ◽  
Silvia Frisullo ◽  
...  

2002 ◽  
Vol 17 (1) ◽  
pp. 63-66 ◽  
Author(s):  
R.A. Merendino ◽  
A. Ruello ◽  
S. Cascinu ◽  
B. Ferlazzo ◽  
A. Bene ◽  
...  

Aims and Background This study was carried out to evaluate the IL-18 blood concentrations of operated colorectal cancer patients and their possible variation in response to combination chemotherapy with 5-fluorouracil (5-FU) and folinic acid. Methods IL-18 levels were assayed in sera of 18 healthy donors and 18 surgical colorectal cancer patients before and after adjuvant chemotherapy with 5-fluorouracil and folinic acid. An ELISA kit for human IL-18 was used for the assay. Results Colorectal cancer patients showed significantly higher baseline levels of IL-18 than healthy donors (p<0.005). Furthermore, serum IL-18 levels increased significantly with respect to baseline in patients receiving adjuvant chemotherapy (p<0.005). Conclusions This study suggests that treatment with 5-fluorouracil and folinic acid may provoke an increase in IL-18 serum levels in colorectal cancer patients. This increase may help to explain the efficacy of adjuvant chemotherapy with 5-FU in colorectal cancer.


2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 497-497 ◽  
Author(s):  
Michela Del Prete ◽  
Mario Scartozzi ◽  
Tiziana Prochilo ◽  
Luca Faloppi ◽  
Riccardo Giampieri ◽  
...  

497 Background: Although a demonstrated clinical efficacy, a non negligible proportion of colorectal cancer patients does not seem to benefit from regorafenib and are consequently exposed to unnecessary toxicity. LDH serum levels represent an indirect marker of tumour hypoxia, neo-angiogenesis and worse prognosis in many tumour types. In colorectal cancer LDH showed a correlation with treatment outcome for patients receiving antiangiogenetic treatment, thus suggesting a possible interaction with the activity profile of these drugs. We analyzed the role of LDH serum levels in predicting clinical outcome for pre-treated metastatic colorectal cancer patients receiving regorafenib. The final aim was to individuate a potentially reliable and easy to use marker for patients stratification. Methods: 118 colorectal cancer patients treated with regorafenib were available for our analysis. For all patients, LDH values were collected within one month before the procedure and after treatment end. LDH cutoff value was determined by ROC curve analysis, patients were then divided into two groups (A and B, below and above cut-off level respectively). Patients were also classified according to the variation in LDH serum levels pre- and post-treatment (increased patients vs. decreased patients). Results: Patients in group A and B proved homogeneous for all clinical characteristics analyzed. In group A patients median progression free survival (PFS) was 3.18 months, whereas it was 1.87 months in group B patients (p = 0.0018). Median overall survival (OS) was 6.23 months and 3.28 months in group A and B respectively (p = 0.048). Significant differences were not noted among the 2 groups for response rate. All the other clinical variables analyzed failed to show any correlation with patients outcome. Conclusions: Our observations seem to suggest a role of LDH as a marker of clinical outcome in colorectal cancer patients receiving regorafenib. We can then speculate that high LDH patients may not be optimal candidates for regorafenib. After further confirmation in larger trial, these findings may be relevant for a better patients stratification and selection.


Sign in / Sign up

Export Citation Format

Share Document