scholarly journals Thrombin Generation As a Predictive Biomarker for Venous Thromboembolism in Patients with Pancreatic and Lung Cancer Undergoing Systemic Therapy

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 3226-3226
Author(s):  
Lukas P Emery ◽  
Michael Y. Cho ◽  
Aderonke Ajala ◽  
Lauren T. Salvatore ◽  
Deborah L. Ornstein ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Cancer Patients ◽  
Systemic Therapy ◽  
Thrombin Generation ◽  
Tumor Type ◽  
Coagulation Activation ◽  
Significant Difference ◽  
The Relationship ◽  
Initial Peak ◽  
Over Time

Abstract Introduction: Venous thromboembolism (VTE) is common in patients with active malignancy. While thromboprophylaxis can mitigate this risk, current guidelines do not support routine use as the benefit is modest and maybe negated by an increase in bleeding complications. However, there is significant variation in VTE risk within the cancer population, thus prophylaxis can be considered in high-risk patients. The Khorana score (KS) is validated to predict chemotherapy-associated VTE; however, it has several limitations including variable performance based on tumor type as well as a static risk categorization, based on pre-chemotherapy laboratory data, rather than a continuous assessment. Thrombin generation (TG) is an emerging biomarker that assesses global coagulation activation and predicted increased VTE risk in cancer patients in the Vienna Cancer and Thrombosis Study (PMID: 21464402). This study enrolled a heterogeneous cancer population, however, peak TG was not reported by tumor type nor were the TG levels monitored over time in response to systemic therapy. The primary aim of this study was to assess the relationship between TG (both peak TG and endogenous thrombin potential, ETP) and KS. Secondary outcomes were to evaluate the impact of systemic therapy on peak TG and ETP levels over time and to assess the relationship between TG and clinical outcomes. Methods: This was a prospective study that enrolled adults with newly diagnosed, locally advanced or metastatic adenocarcinoma of the lung or pancreas. All patients received their care at Dartmouth Hitchcock Medical Center. Those with a history of active VTE or use of full dose anticoagulant within 30 days prior to enrollment were excluded. After informed consent, KS was calculated and blood was collected in sodium citrate tubes at 3 different time points (at initiation of therapy, and at the beginning of the 2 nd and 3 rd cycles of systemic therapy). Platelet-poor plasma was prepared by centrifugation and stored at - 80°C until analysis by calibrated automated thrombogram (CAT; Thrombinoscope BV, Maastricht, Netherlands) using 1 pM tissue factor and 4 uM phospholipids to trigger coagulation reactions. Measurements were performed in triplicate for each specimen, and raw data were converted to peak TG and ETP. Information about VTE events, response to treatment and survival was obtained by chart review. Mean and standard deviation were calculated for continuous variables and unpaired T test was used for statistical analysis. Results: We report the results from 32 participants (17 lung, 15 pancreas). The majority of patients had metastatic disease (94%) and all received systemic therapy. The median age was 67 and 56% of participants were male. The KS breakdown for the cohort was: KS1, 25%; KS2, 53%; KS3, 19%; KS4, 3%. Mean peak TG was 279, 352, 487 and 325 nmole and mean ETP was 1320, 1653, 2252, 1726 nmole/min for KS 1, 2, 3 and 4, respectively. Initial peak TG and ETP levels were significantly higher in the KS ≥2 group compared to those with KS=1 (peak TG: 384 ±135 vs 279 ±82, p 0.047; Initial ETP: 1806 ±632 vs 1320 ±286, p 0.045). There were 8 VTE events (25%) with all but one occurring in the pancreatic cancercohort; all events occurred in KS 2 and 3 groups (75% and 25% respectively). No statistically significant difference was observed for initial peak TG or ETP in those with VTE vs those without (Peak TG: 342 ±171 vs 363 ±119, p 0.701; ETP: 1736 ±720 vs 1667 ±571, p 0.783). Both peak TG and ETP decreased in response to systemic therapy (initial peak TG vs final: 376 ±115 vs 225 ±125, p 0.0001; initial ETP vs final: 1799 ±498 vs 1254 ±423, p 0.0003). No significant difference in survival was noted based on initial ETP level of <1500 nmole/min vs ≥1500 nmole/min (574 ±620 vs 287 ±227, p 0.069). Conclusions: There appears to be an association between KS and peak TG and ETP. In addition, both peak TG and ETP declined in response to systemic therapy, suggesting that the degree of coagulation activation is related to tumor burden. Our findings in this small study support further investigation of TG for VTE risk assessment in cancer patients. Future strategies incorporating TG into risk stratification models may allow oncologists to better identify the population that may benefit most from pharmacologic thromboprophylaxis. Funding: Northern New England Clinical Oncology Disclosures No relevant conflicts of interest to declare.

Levels of Prothrombin Fragment F1+2 in Patients with Hyperhomocysteinemia and a History of Venous Thromboembolism

1997 ◽  
Vol 78 (05) ◽  
pp. 1327-1331 ◽  
Author(s):  
Paul A Kyrle ◽  
Andreas Stümpflen ◽  
Mirko Hirschl ◽  
Christine Bialonczyk ◽  
Kurt Herkner ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Thrombin Generation ◽  
Oral Anticoagulant Therapy ◽  
Oral Anticoagulants ◽  
Control Group ◽  
Prothrombin Fragment ◽  
Hemostatic System ◽  
Significant Difference ◽  
System Activation ◽  
One Year

SummaryIncreased thrombin generation occurs in many individuals with inherited defects in the antithrombin or protein C anticoagulant pathways and is also seen in patients with thrombosis without a defined clotting abnormality. Hyperhomocysteinemia (H-HC) is an important risk factor of venous thromboembolism (VTE). We prospectively followed 48 patients with H-HC (median age 62 years, range 26-83; 18 males) and 183 patients (median age 50 years, range 18-85; 83 males) without H-HC for a period of up to one year. Prothrombin fragment Fl+2 (Fl+2) was determined in the patient’s plasma as a measure of thrombin generation during and at several time points after discontinuation of secondary thromboprophylaxis with oral anticoagulants. While on anticoagulants, patients with H-HC had significantly higher Fl+2 levels than patients without H-HC (mean 0.52 ± 0.49 nmol/1, median 0.4, range 0.2-2.8, versus 0.36 ± 0.2 nmol/1, median 0.3, range 0.1-2.1; p = 0.02). Three weeks and 3,6,9 and 12 months after discontinuation of oral anticoagulants, up to 20% of the patients with H-HC and 5 to 6% without H-HC had higher Fl+2 levels than a corresponding age- and sex-matched control group. 16% of the patients with H-HC and 4% of the patients without H-HC had either Fl+2 levels above the upper limit of normal controls at least at 2 occasions or (an) elevated Fl+2 level(s) followed by recurrent VTE. No statistical significant difference in the Fl+2 levels was seen between patients with and without H-HC. We conclude that a permanent hemostatic system activation is detectable in a proportion of patients with H-HC after discontinuation of oral anticoagulant therapy following VTE. Furthermore, secondary thromboprophylaxis with conventional doses of oral anticoagulants may not be sufficient to suppress hemostatic system activation in patients with H-HC.

scholarly journals Venous thromboembolism in non-small cell lung cancer patients who underwent surgery after induction therapy

2020 ◽  
Vol 68 (10) ◽  
pp. 1156-1162
Author(s):  
Yasunori Kaminuma ◽  
Masayuki Tanahashi ◽  
Eriko Suzuki ◽  
Naoko Yoshii ◽  
Hiroshi Niwa
Keyword(s):  
Lung Cancer ◽  
Venous Thromboembolism ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Induction Therapy ◽  
Small Cell ◽  
Small Cell Lung ◽  
Free Survival ◽  
Lung Cancer Patients ◽  
Significant Difference

Abstract Objectives Lung cancer patients have been reported to have a high incidence of venous thromboembolism (VTE) and a high recurrence rate of VTE. However, there are no detailed reports of VTE in lung cancer patients who underwent surgery after induction therapy. We examined the incidence and clinical features of VTE in these patients. Methods We retrospectively evaluated 89 patients with non-small cell lung cancer who underwent surgery after induction therapy at our department between April 2009 and March 2018. The incidence of VTE, clinical features, and long-term prognosis were retrospectively examined. Results Among the 89 patients, 4 (4.5%) developed VTE, and there was no significant difference in the background characteristics between patients with and without VTE. All four patients developed VTE during preoperative treatment. In the patients with VTE, anticoagulant therapy with oral anticoagulants was administered after heparinization, and the median duration of anticoagulant therapy was 18.7 months. There were no cases of symptomatic VTE recurrence after surgery, regardless of lung cancer recurrence. Although the overall survival (OS) showed no significant difference between patients with and without VTE, the disease-free survival was significantly shorter in patients with VTE than in those without it (median 6.3 vs. 71.6 months, p < 0.01). Conclusions In induction cases, the incidence of VTE was 4.5%, and it can at least be stated that no symptomatic VTE developed or recurred after surgery. Patients with VTE in induction therapy had short progression-free survival and required careful follow-up after surgery.

The effects of low-molecular-weight heparin at two different dosages on thrombin generation in cancer patients.

2010 ◽  
Vol 104 (07) ◽  
pp. 92-99 ◽  
Author(s):  
Ludwig Traby ◽  
Alexandra Kaider ◽  
Rainer Schmid ◽  
Alexander Kranz ◽  
Peter Quehenberger ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cancer Patients ◽  
Low Molecular Weight Heparin ◽  
Thrombin Generation ◽  
Low Molecular Weight ◽  
Prothrombotic State ◽  
Coagulation Activation ◽  
Thrombotic Risk ◽  
Baseline Levels ◽  
D Dimer

SummaryNon-surgical cancer patients are at high thrombotic risk. We hypothesised that the prothrombotic state is reflected by elevated thrombin generation and can be mitigated by increasing the low-molecularweight heparin (LMWH) dose. Non-surgical cancer patients were randomised to enoxaparin 40 or 80 mg. D-dimer, prothrombin fragment F1+2 (F1+2) and peak thrombin (PT) were measured 2, 4, 6 hours (h) after LMWH (day 1) and daily for 4 days. A total of 22 and 27 patients received enoxaparin 40 and 80 mg, respectively. D-dimer and F1+2 moderately decreased after 6 h in both groups. After enoxaparin 80 mg, D-dimer baseline levels [median (quartiles)] decreased from day 1 to 4 [1054.9 (549.5, 2714.0) vs. 613.0 (441.1, 1793.5) ng/ml] (p<0.0001), while no difference was seen after 40 mg. Baseline PT levels [median (quartiles)] were 426.2 nM (347.3, 542.3) (40 mg) and 394.0 nM (357.1, 448.8) (80 mg). After 80 mg, PT significantly decreased to 112.4 nM (68.5, 202.4), 57.1 nM (38.0, 101.2) and 43.6 nM (23.4, 112.8) after 2, 4 and 6 h, which was lower than after 40 mg (p=0.003). After 80 mg, PT decreased from day 1 to 4 [358.6 nM (194.2, 436.6); p=0.06] while no difference was seen after 40 mg. In conclusion, in cancer patients coagulation activation and thrombin generation is substantially increased. Peak thrombin levels are sensitive to the anticoagulant effects of LMWH at different dosages. The prothrombotic state is substantially attenuated by higher LMWH doses.

The Effects of Hydroxyurea on the Thrombin Generation and Microparticles in Sickle Cell Anemia Patients

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2292-2292
Author(s):  
Patrick Van Dreden ◽  
Grigoris T Gerotziafas ◽  
Barry J Woodhams ◽  
Mourad Chaari ◽  
Robert Girot ◽  
...  
Keyword(s):  
Steady State ◽  
Sickle Cell ◽  
Thrombin Generation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
No Production ◽  
Generation Process ◽  
Coagulation Activation ◽  
Significant Difference ◽  
Hydroxyurea Therapy

Abstract Abstract 2292 Introduction: The clinical course of sickle cell disease (SCD) is punctuated by episodic vascular occlusive events. The possibility that activation of the clotting system plays a contributory role in these complications is supported by abundant clinical data during both steady-state disease and pain crisis. Hydroxyurea therapy induces fetal haemoglobin, improves laboratory parameters and reduces acute clinical complications of SCD, but despite an abundance of evidence for coagulation and platelet activation, it remains incompletely defined whether these changes contribute to the reduced thrombin generation. This study is designed to evaluate coagulation profiles of patients with SCA in steady state and to determine whether hypercoagulable state is modified or not in patients on hydroxyurea therapy. Patients and Methods: We studied erythrocyte derived microparticles (Ed-MP) and platelet derived microparticles (Pd-MP) expressing or not expressing phosphatidylserine (PS) in patients with steady state SCD and we evaluated their specific procoagulant activity and their impact on thrombin generation process. A total of 92 steady state SCD patients were included in the study, of which 19 were under treatment with hydroyurea. The control group consisted of 30 healthy age and sex matched controls. Microparticles in whole blood were assessed using flow cytometry. Ed-MP and Pd-MP were identified using an anti-CD235 and CD41 monoclonal antibodies and annexin V. Thrombin generation in platelet poor plasma (PPL) was measured by CAT assay using PPP-reagent 5pM (Thrombinoscope, The Netherlands). Procoagulant phospholipid dependent activity in plasma was assessed by the Procoag-PPL assay (Diagnostica Stago, France). Thrombomodulin (TM) levels were measured by enzyme-linked immunosorbent assay (Elisa) Asserachrom thrombomodulin (Diagnostica Stago, Asnieres, France). Results: Hydroxyurea treated patients had lower counts of leukocytes, reticulocytes and platelets and an increased mean hemoglobin concentration as compared to non treated patients. Leukocyte and reticulocytes counts of treated patients were higher than those of controls. Platelets counts did not differ between treated and untreated patients. Patients on treatment with hydroxyurea had significantly lower levels of Ed-MP/PS+ and Ed-MP compared to untreated patients. The concentration of Pd-MP/PS+ and Pd-MP were not significantly different between hydroxyurea treated and non treated patients. The Ed-MP/PS+ showed a significant inverse correlation with Hb F (p<0.05). Thrombogram parameters, lag-time, ttPeak, Peak and MRI were significantly different between hydroxyurea treated patients and non treated patients. In hydroxyurea treated patients in contrast to the untreated ones no correlation was found between Ed-MP/PS+ and Ed-MP and parameters of thrombin generation. Among hydroxyurea treated patients 68% showed MRI levels higher than the UNL. Stratification groups of treated patients according to the levels of microparticles with Ed-MP/PS+ or Pd-MP/PS+ concentration higher than the UNL showed non significant difference compared to entirely group of patients. The PPL concentration was significantly lower in the SCD-treated patient compared to untreated patients (p<0.05). In contrast to platelet-derived-microparticles, the numbers of erythrocyte-derived-microparticles differed between patients with and without hydroxyurea during steady state. In patients treated with hydoxyurea, platelets were correlated with Ed-MP, Pd-MP with and without PS+ (p<0.05), but any of the others parameters showed one association. Procoagulant phospholipids and thrombomodulin were increased in SCD with and without hydroxyurea compared with controls group (p<0.05). Conclusion: Treatment with hydroxyurea result in decreases in plasma markers of thrombin generation, and may decrease coagulation activation by reducing PS expression on the surface of both RBCs and platelets in addition to being a NO donor hydro may also decrese haemostatic activation by its effect in decreasing the white blood cell count and particularly monocytes that express TF, furthermore the beneficial effects of hydroxyurea may be due to vasodilatationand decressed platelet and coagulation activation following NO production. Disclosures: Van Dreden: Diagnostica Stago: Employment. Gerotziafas:APHP: Employment. Woodhams:Diagnostica Stago: Employment. Chaari:APHP: Employment. Girot:APHP: Employment. Kartechi:APHP: Employment. Galea:APHP: Employment. Lionnet:APHP: Employment. Elalamy:APHP: Employment.

Effects of Chemotherapy on Extracellular Vesicles and Coagulation Activation in Colorectal Cancer Patients: A Pilot Study

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1425-1425
Author(s):  
Ludwig Traby ◽  
Hannah C. Puhr ◽  
Marietta Kollars ◽  
Kammer Michael ◽  
Gerald Prager ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Venous Thromboembolism ◽  
Pilot Study ◽  
Cancer Patients ◽  
Tissue Factor ◽  
Extracellular Vesicles ◽  
Advanced Colorectal Cancer ◽  
Coagulation Activation ◽  
Colorectal Cancer Patients ◽  
D Dimer

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.

The influence of venous thromboembolism on prognosis of esophageal cancer patients.

2016 ◽  
Vol 34 (4_suppl) ◽  
pp. 29-29
Author(s):  
En Amada ◽  
Hiroya Takeuchi ◽  
Fumihiko Kato ◽  
Hirofumi Kawakubo ◽  
Kazumasa Fukuda ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Adjuvant Chemotherapy ◽  
Cancer Patients ◽  
Disease Free Survival ◽  
Secondary Outcome ◽  
Neck Lymph Node ◽  
Significant Difference ◽  
Neo Adjuvant Chemotherapy

29 Background: Venous thromboembolism (VTE) is sometimes found in esophageal cancer patients who underwent surgical treatment. VTE contains deep vein thrombosis, pulmonary embolism and catheter-related thrombosis. Our previous study revealed that pre-therapeutic plasma fibrinogen level, C-reactive protein level, adenocarcinoma histology and neck lymph node dissection are the risk factors for venous thromboembolism in patients[Surg Today, 2015]. However, the correlation between VTE and prognosis is not clear in esophageal cancer. We hypothesized that VTE may have an impact on prognosis of esophageal cancer patients. Methods: One hundred and seventy-two patients who underwent radical esophagectomy from March 2008 to December 2012 in our hospital were reviewed in this study. The existence of VTE was assessed from the neck to the pelvis with computed tomography at the initial visit and after neo-adjuvant chemotherapy (NAC) and 6thpostoperative day. The patient and tumor characteristics, neo-adjuvant chemotherapy were compared between patients with VTE (VTE group) and those without VTE (non-VTE group). The primary outcome is disease-free survival (DFS) and the secondary outcome is overall survival (OS). Results: Twenty-one VTE events among 172 patients (12%) were observed. Six of which occurred preoperatively and were considered to be associated with NAC, 14 were detected postoperatively and one occurred just after inserting a peripherally inserted central catheter preoperatively. The VTE group and the non-VTE group have homogenous characteristics in patients’ backgrounds and tumor features. We found no significant difference in median DFS and OS between two groups. However, in patients with pathologically N 0 or 1(7thedition of UICC TNM classification, n = 157), the median DFS was significantly shorter in VTE group compared with non-VTE group (41 months versus 64 months, p = 0.04). The recurrence risk increased 50.9% in VTE group in comparison with non VTE group (p = 0.048). By using logistic regression analysis, we found that existence of VTE is an independent risk factor with Odd’s ratio 2.964 (p = 0.026). Conclusions: Our study suggests that VTE may be the risk factor for recurrence in esophageal cancer patients.

scholarly journals Histopathologic Characteristics of Invasive and Non-invasive Ductal Tumors have Relationship with Different Phenotypes of ER / PR Receptors in Breast Cancer Patients

2021 ◽  
Vol 6 (3) ◽  
pp. 181-185
Author(s):  
Rahim Golmohammadi ◽  
Mohammad Reza Mohajeri ◽  
Alireza Mosavi Jarrahi ◽  
Ali Reza Moslem ◽  
Akbar Pejhan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Hormone Receptors ◽  
Ductal Carcinoma ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Tumor Type ◽  
Breast Cancer Patients ◽  
Non Invasive ◽  
Significant Difference

Objective: Contradictory reports have been published regarding the expression levels of the hormone receptors of estrogen and progesterone (ER / PR) and theirclinical importance in diagnosis of breast cancer. The aim of this study was to evaluate the relationship between pathological features of invasive and non-invasive ductal tumors by different ER / PR phenotypes. Methods: This descriptive-analytical study was performed on 74 specimens of breast cancer referred to Isfahan Hospitals for diagnosis between 2015 - 2018. After fixation of the specimens in formalin, tissue passage, cross section and H / E staining, the specimens were divided into two groups: non- invasive and Invasive ductal Carcinoma. After removing of mask, expression of different ER / PR phenotypes was performed using primary monoclonal antibody and immunohistochemically methods. Results: From 74 malignant specimens, 61 (82.4%) were in the category of invasive ductal tumors and 13 cases (17.6%) were in the category of non-invasive ductal tumors. Out of 73 patients with positive ER or PR phenotype 47 samples (63.5%) had ER + / PR +phenotypes, 6 samples had (8.1%) ER+ / PR –phenotype, 20 samples (27%) had ER- / PR + phenotype and only one sample (1.4%) had the ER- / PR- phenotype and was in the category of invasive ductal tumors. There was not detected ER- / PR- phenotype expression in non-invasive ductal tumor. Further analysis showed that there were not significant difference between ER / PR phenotype and tumor stage (p =0.36) or with tumor Grade (P=0.38), high age of menopause or post menopause (P> 0.05). Conclusion: Our data shows that expression of ER- / PR- phenotype only was detected in invasive ductal tumor. It is thought that the tumor type maybe affects the expression of different types of ER / PR hormone receptor phenotypes in breast cancer patients.

Prognosis and non-sentinel lymph node status of the breast cancer patients with micrometastatic sentinel lymph nodes.

2011 ◽  
Vol 29 (27_suppl) ◽  
pp. 140-140
Author(s):  
M. Takahashi ◽  
H. Jinno ◽  
T. Hayashida ◽  
S. Hirose ◽  
M. Mukai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lymph Node ◽  
Sentinel Lymph Node ◽  
Cancer Patients ◽  
Systemic Therapy ◽  
Axillary Lymph Node ◽  
Lymph Node Status ◽  
Axillary Lymph ◽  
Breast Cancer Patients ◽  
Significant Difference

140 Background: Sentinel lymph node biopsy (SLNB) is a more sensitive and accurate nodal staging procedure than axillary lymph node dissection (ALND). Because of detailed pathologic evaluation in SLNs, more nodal micrometastases have been identified. However, it remains controversial whether to perform ALND for patients with micrometastases in SLNs and their prognostic significance is also a matter of debate. The purpose of this study is to determine the non-sentinel lymph node (NSLN) status and prognosis of the patients with micrometastatic SLNs. Methods: A prospective database of 1,012 clinically node-negative, T1-T2 breast cancer patients, who underwent SLNB from January 2002 to Dec 2010 at Keio University Hospital was analyzed. SLNs were detected using a combined method of isosulfun blue dye and small-sized technetium-99m-labeled tin colloid. Intraoperative frozen examination was performed with hematoxylin and eosin (HE) staining. SLNs, fixed and embedded in paraffin, were additionally diagnosed with HE staining and immunohistochemical (IHC) analysis. Results: Micrometastases in SLNs were found in 69 (6.8%) of 1,012 patients. Thirty eight (55.1%) of 69 patients with micrometastatic SLNs underwent immediate or delayed ALND and revealed no NSLN metastasis. Among 31 (44.9%) patients with micrometastatic SLNs who omitted ALND and axillary radiation therapy, no axillary lymph node recurrence has been observed after a median follow-up of 50 months, although 29 patients (93.5%) in these 31 patients received adjuvant systemic therapy. There is no significant difference in recurrence free survival between the patients with micrometastatic and negative SLNs (98.0% vs. 95.7%, respectively). Conclusions: These date suggested that it may not be necessary to perform ALND for the patients with micrometastatic SLNs and the presence of micrometastases in SLNs may not worsen prognosis with proper systemic therapy.

Anticoagulants for the treatment of venous thromboembolism in patients with cancer: An updated pairwise and network meta-analysis of randomized trials.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e14692-e14692
Author(s):  
Shima Sidahmed ◽  
Ahmed Abdalla ◽  
Babikir Kheiri ◽  
Areeg Bala ◽  
Mohammed Salih ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Cancer Patients ◽  
Vitamin K ◽  
Major Bleeding ◽  
Metastatic Cancer ◽  
Meta Analysis ◽  
Number Needed To Treat ◽  
Cancer Type ◽  
Significant Difference ◽  
All Cause Mortality

e14692 Background: Cancer-associated venous thromboembolism (VTE) is common. Although low molecular weight heparin (LMWH) is the standard therapy in this setting, little is known with regard to non-vitamin K antagonist oral anticoagulants (NOACs). Therefore, we thought about evaluating the safety and efficacy of various anticoagulants in this vulnerable population. Methods: Electronic database search was conducted to identify randomized clinical trials (RCTs) that compared LMWH, NOACs, and/or vitamin-K-antagonists (VKA) in cancer patients. We performed frequentist direct and Bayesian network meta-analysis using random-effects model to calculate odds ratios (ORs), 95% confidence intervals (CIs), and 95% credible intervals (CrIs). The primary outcome was VTE (pulmonary embolism and deep-vein thrombosis) recurrence. Secondary outcomes were major bleeding and all-cause mortality. Results: We identified 13 RCTs with 6,595 total patients (mean age 62.4 ± 12.2; 50.4% female; 17.7% hematological malignancies; and 6 months median follow-up). The most common cancer type was colorectal and 48% of the population had metastatic cancer at baseline. NOACs were associated with significantly reduced VTE recurrence compared with VKA (OR = 0.58; 95% CI = 0.40-0.83; P < 0.01; number needed to treat [NNT] = 40) and LMWH (OR = 0.46; 95% CI = 0.25-0.85; P = 0.01; NNT = 20). LMHW was associated with significantly reduced VTE recurrence compared with VKA (OR = 0.52; 95% CI = 0.39-0.71; P < 0.01; NNT = 18). NOACs were associated with significantly reduced major bleeding compared with VKA (OR = 0.56; 95% CI = 0.35-0.91; P = 0.02; NNT = 64). There was no significant difference identified between the anticoagulant groups in regard to all-cause mortality. Conclusions: Among cancer patients with VTE, NOACs were associated with significantly reduced VTE recurrence compared to LMWH and VKA, and significantly reduced major bleeding compared with VKA. LMWH was associated with significantly reduced VTE recurrence compared with VKA.

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