• Biomarkers
• Cancer
• Liquid biopsy
• Platelets
• Tumor metastasis
• Tumor-educated platelets

• 172/20-23 INSTITUTO NACIONAL DE MEDICINA GENÓMICA, SECRETARIA DE EDUCACION CIENCIA Y TECNOLOGÍA E INNOVACIÓN
• 172/20-23 INSTITUTO NACIONAL DE MEDICINA GENÓMICA, SECRETARIA DE EDUCACION CIENCIA Y TECNOLOGÍA E INNOVACIÓN

• Cancer
• Coagulation
• PD-L1
• Platelets
• VTE

• Humans
• Blood Platelets/metabolism
• Blood Platelets/pathology
• Neoplasms/blood
• Neoplasms/pathology
• Neoplasms/complications
• Thrombophilia/blood
• Thrombophilia/etiology
• Disease Progression
• Blood Coagulation/physiology

• 82172776 National Natural Science Foundation of China
• 19ZXDBSY00060 Tianjin Science and Technology Plan Project

• Cancer
• drug discovery
• microphysiological systems
• organ-chips
• platelets
• tumor microenvironment

• Animals
• Mice
• Microphysiological Systems
• Neoplasms
• Blood Platelets
• Biological Transport
• Cross Reactions
• Tumor Microenvironment

• R01 HL157790 NHLBI NIH HHS

• cancer
• circulating tumor cells (CTCs)
• epithelial-to-mesenchymal transition (EMT)
• metastasis
• platelets
• tumor-educated platelets (TEPs)

• ADP
• Aspirin
• Atopaxar
• Clopidogrel
• cancer
• platelet
• thrombin
• thromboxane

• 87935 and 106926 National Research Foundation

• osteosarcoma
• p-crp
• prognosis

• Bone Neoplasms
• C-Reactive Protein/analysis
• China/epidemiology
• Humans
• Osteosarcoma/surgery
• Prognosis
• Retrospective Studies

Platelets play a critical role in coagulation and fibrinolysis processes, but recent literature also indicates their central involvement in immune response, cancer progression and metastasis. During platelet activation, small extracellular vesicles (EVs) are released. The ascites are a fluid developing in the peritoneum of ovarian cancer patients in an advanced stage. This study analysed the expression of platelet markers GPIIb/IIIa and PF4 in small-EVs populations isolated from the ascitic fluid of patients with advanced ovarian cancer. The percentage of platelet-derived small-EVs was positively correlated with platelet distribution width to platelet count in sera (PDW/PLT), a surrogate indicator of platelet activation. Overall, we presented a method that can be helpful in future studies to determine the correlation between the extent of platelet activation in ascites and disease status.

In ovarian cancer, ascites represent the microenvironment in which the platelets extravasate to play their role in the disease progression. We aimed to develop an assay to measure ascites’ platelet activation. We enriched small extracellular vesicles (EVs) (40–200 nm) from ascites of high-grade epithelial ovarian cancer patients (n = 12) using precipitation with polyethylene glycol, and we conducted single-particle phenotyping analysis by nano-flow cytometry after labelling and ultra-centrifugation. Atomic force microscopy single-particle nanomechanical analysis showed heterogeneous distributions in the size of the precipitated particles and their mechanical stiffness. Samples were fluorescently labelled with antibodies specific to the platelet markers GPIIb/IIIa and PF4, showing 2.6 to 18.16% of all particles stained positive for the biomarkers and, simultaneously, the EV membrane labelling. Single-particle phenotyping analysis allowed us to quantify the total number of non-EV particles, the number of small-EVs and the number of platelet-derived small-EVs, providing a platelet activation assessment independent of the ascites volume. The percentage of platelet-derived small-EVs was positively correlated with platelet distribution width to platelet count in sera (PDW/PLT). Overall, we presented a high-throughput method that can be helpful in future studies to determine the correlation between the extent of platelet activation in ascites and disease status.

The tumor microenvironment (TME) is the complex and heterogenous ecosystem of solid tumors known to influence their growth and their progression. Besides tumor cells, the TME comprises a variety of host-derived cell types, ranging from endothelial cells to fibroblasts and immune cells. Clinical and experimental data are converging to indicate that platelets, originally known for their fundamental hemostatic function, also participate in tumor development and shaping of the TME. Considering the abundance of antiplatelet drugs, understanding if and how platelets contribute to the TME may lead to new therapeutic tools for improved cancer prevention and treatments.

The tumor microenvironment (TME) has gained considerable interest because of its decisive impact on cancer progression, response to treatment, and disease recurrence. The TME can favor the proliferation, dissemination, and immune evasion of cancer cells. Likewise, there is accumulating evidence that intratumoral platelets could favor the development and aggressiveness of solid tumors, notably by influencing tumor cell phenotype and shaping the vascular and immune TME components. Yet, in contrast to other tumor-associated cell types like macrophages and fibroblasts, platelets are still often overlooked as components of the TME. This might be due, in part, to a deficit in investigating and reporting the presence of platelets in the TME and its relationships with cancer characteristics. This review summarizes available evidence from clinical and animal studies supporting the notion that tumor-associated platelets are not incidental bystanders but instead integral and active components of the TME. A particular emphasis is given to the description of intratumoral platelets, as well as to the functional consequences and possible mechanisms of intratumoral platelet accumulation.

• angiogenesis
• lymphangiogenesis
• platelets
• solid tumors
• tumor microenvironment
• tumor-associated platelets
• vascular integrity

Oral squamous cell carcinoma (OSCC) is mostly diagnosed at an advanced stage, with local and/or distal metastasis. Thus, locoregional and/or local control of the primary tumor is crucial for a better prognosis in patients with OSCC. Platelets have long been considered major players in cancer metastasis. Traditional antiplatelet agents, such as aspirin, are thought to be potential chemotherapeutics, but they need to be used with caution because of the increased bleeding risk. Podoplanin (PDPN)-expressing cancer cells can activate platelets and promote OSCC metastasis. However, the reciprocal effect of platelets on PDPN expression in OSCC has not been investigated. In this study, we found that direct contact with platelets upregulated PDPN and integrin β1 at the protein level and promoted invasiveness of human OSCC Ca9.22 cells that express low levels of PDPN. In another human OSCC HSC3 cell line that express PDPN at an abundant level, silencing of the PDPN gene reduced cell invasiveness. Analysis of the public database further supported the co-expression of PDPN and integrin β1 and their increased expression in metastatic tissues compared to normal and tumor tissues of the oral cavity. Taken together, these data suggest that PDPN is a potential target to regulate platelet-tumor interaction and metastasis for OSCC treatment, which can overcome the limitations of traditional antiplatelet drugs.

• Direct contact
• Metastasis
• Oral cancer
• Platelets
• Podoplanin

• ACP1
• Gastrointestinal cancer
• LMWPTP
• Platelets
• Tumor microenvironment
• Tyrosine phosphatases

• cancer cells
• cancer treatment
• cancer-platelet crosstalk
• platelets
• thrombosis

•

Platelet cancer cell interactions are a key factor in driving the pro-metastatic phenotype.

Tumour metastasis accounts for over 90% of cancer related deaths. The platelet is a key blood component, which facilitates efficient metastasis. This study aimed to understand the molecular mechanisms involved in tumour-platelet cell interactions.

The interaction between cancer cells and platelets was examined in 15 epithelial cell lines, representing 7 cancer types. Gene expression analysis of EMT-associated and cancer stemness genes was performed by RT-PCR. Whole transcriptome analysis (WTA) was performed using Affymetrix 2.0ST arrays on a platelet co-cultured ovarian model.

Platelet adhesion and activation occurred across all tumour types. WTA identified increases in cellular movement, migration, invasion, adhesion, development, differentiation and inflammation genes and decreases in processes associated with cell death and survival following platelet interaction. Increased invasive capacity was also observed in a subset of cell lines. A cross-comparison with a platelet co-cultured mouse model identified 5 common altered genes; PAI-1, PLEK2, CD73, TNC, and SDPR.

Platelet cancer cell interactions are a key factor in driving the pro-metastatic phenotype and appear to be mediated by 5 key genes which have established roles in metastasis. Targeting these metastasis mediators could improve cancer patient outcomes.

• 5-gene panel
• Cancer
• Metastasis
• PAI-1
• Platelets

• Blood Platelets
• Humans
• Ovarian Neoplasms/drug therapy
• Ovarian Neoplasms/pathology
• Platelet Aggregation Inhibitors
• Tumor Microenvironment

• P30 CA016672 NCI NIH HHS
• P50 CA217685 NCI NIH HHS
• R21 EB025945 NIBIB NIH HHS
• R01 CA177909 NCI NIH HHS
• R35 CA209904 NCI NIH HHS
• National Science Foundation
• National Institutes of Health
• National Institute of Biomedical Imaging and Bioengineering
• UVA Cancer Center
• National Science Foundation Graduate Research Fellowship

• Platelets
• anti-platelet drugs
• cancer
• cardiovascular diseases
• personalized medicine

• Colon cancer
• Computed tomography
• Survival
• Systemic inflammation
• Tumor staging
• Visceral obesity

• P-selectin
• P-selectin ligand
• metastasis
• platelet
• platelet-tumor crosstalk

• cell-based imaging
• extracellular vesicle
• leukocyte
• magnetic resonance imaging
• mesenchymal stromal cell
• microorganisms
• nanoparticle
• near-infrared
• nuclear imaging
• platelets

• Cell Tracking/methods
• Cell-Derived Microparticles/metabolism
• Contrast Media
• Humans
• Leukocytes/metabolism
• Magnetic Resonance Imaging/methods
• Mesenchymal Stem Cells/metabolism
• Nanoparticles/chemistry
• Positron-Emission Tomography/methods
• Surgery, Computer-Assisted/methods
• Surgery, Computer-Assisted/standards

• C25574/A24321 Cancer Research UK
• 24321 Cancer Research UK

Surgery combined with postoperative chemotherapy is an effective method for treating patients with gastric cancer (GC) in Asia. The important roles of systemic inflammatory response in chemotherapy have been gradually verified. The purpose of this study was to assess the difference in clinical effectiveness of FOLFOX (oxaliplatin + leucovorin + 5-fluorouracil) and XELOX (oxaliplatin + capecitabine), and the prognostic value of postoperative platelet–lymphocyte ratio (PLR) in the XELOX group.

Patients who received radical gastrectomy combined with postoperative chemotherapy between 2004 and 2014 were consecutively selected into the FOLFOX and XELOX groups. Group bias was reduced through propensity score matching, which resulted in 278 patients in each group. Cut-off values of systemic immune inflammation (SII) score and PLR were obtained by receiver operating characteristic curve. Kaplan–Meier and Log-rank tests were used to analyze overall survival. The chi-square test was used to analyze the association between clinical characteristics and inflammatory indexes. Univariate and multivariate analyses based on Cox regression analysis showed independent risk factors for prognosis. The nomogram was made by R studio.

Patients receiving XELOX postoperative chemotherapy had better survival than those receiving FOLFOX (P < 0.001), especially for stage III GC (P = 0.002). Preoperative SII was an independent risk factor for prognosis in the FOLFOX group, and PLR of the second postoperative chemotherapy regimen in the XELOX group, combined with tumor size and pTNM stage, could construct a nomogram for evaluating recurrence and prognosis.

XELOX is better than FOLFOX for treatment of GC in Chinese patients, and a nomogram constructed by PLR, tumor size and pTNM stage can predict recurrence and prognosis.

• gastric cancer
• nomogram
• oxaliplatin capecitabine
• platelet–lymphocyte ratio
• postoperative chemotherapy
• prognosis
• systemic immune inflammation

Breast cancer (BC) is a molecularly heterogeneous disease that encompasses five major molecular subtypes (luminal A (LA), luminal B HER2 negative (LB-), luminal B HER2 positive (LB+), HER2 positive (HER2+) and triple negative breast cancer (TNBC)). BC treatment mainly depends on the identification of the specific subtype. Despite the correct identification, therapies could fail in some patients. Thus, further insights into the genetic and molecular status of the different BC subtypes could be very useful to improve the response of BC patients to the range of available therapies. In this way, we used gold nanoparticles (AuNPs, 12.96 ± 0.72 nm) as a scavenging tool in combination with Sequential Window Acquisition of All Theoretical Mass Spectra (SWATH-MS) to quantitatively analyze the serum proteome alterations in the different breast cancer intrinsic subtypes. The differentially regulated proteins specific of each subtype were further analyzed with the bioinformatic tools STRING and PANTHER to identify the major molecular function, biological processes, cellular origin, protein class and biological pathways altered due to the heterogeneity in proteome of the different BC subtypes. Importantly, a profile of blood coagulation proteins was identified in the serum of HER2-overexpressing BC patients.

• HER2+
• SWATH-MS
• breast cancer (BC)
• fingerprinting
• gold nanoparticles (AuNPs)
• protein corona (PC)

• Biomarkers, Tumor/blood
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Blood Coagulation Factors/metabolism
• Breast Neoplasms/blood
• Breast Neoplasms/classification
• Breast Neoplasms/metabolism
• Case-Control Studies
• Female
• Genes, erbB-2
• Gold
• Humans
• Mass Spectrometry
• Metal Nanoparticles
• Peptide Mapping/methods
• Protein Corona
• Receptor, ErbB-2/genetics
• Receptor, ErbB-2/metabolism
• Triple Negative Breast Neoplasms/blood
• Triple Negative Breast Neoplasms/genetics
• Triple Negative Breast Neoplasms/metabolism

• Antidepressant
• brain-derived neurotrophic factor
• cancer
• megakaryocyte
• platelet

• Cancer
• Circular RNA
• Invasion
• Metastasis
• Tumor microenvironment

• epithelial-mesenchymal transition
• extravasated platelet aggregation
• gastric cancer
• myeloid-derived suppressor cell
• peritoneal metastasis

• platelet adhesion
• innate immune surveillance
• CD44 isoform
• infectious complication
• hematogenous distant metastasis

Platelets are one factor promoting tumor development. Conversely, lymphocytes are one factor for immune protection. The peripheral blood platelets–lymphocyte ratio (PLR) is useful as an inflammation/immune indicator to predict postoperative recurrence and prognosis of a variety of malignancies. The peripheral blood neutrophil–lymphocyte ratio (NLR) has also been reported as a useful inflammation/immune indicator. However, there are few studies evaluating the relationship between these peripheral blood indicators and the effectiveness of chemotherapy. Thus, we examined these relationships in gastric cancer patients.

Between 2005 and 2018, 41 gastric cancer patients treated with preoperative DCS therapy (docetaxel, cisplatin, and S-1) therapy followed by gastrectomy were evaluated. Data for peripheral blood tests prior to the initiation of chemotherapy were used. The effectiveness of chemotherapy was determined using Response Evaluation Criteria in Solid Tumors (RECIST) and the pathological response of primary lesions (Ef grade). The relationship between the blood test results and the effectiveness of chemotherapy was evaluated.

Each optimal cut-off value of peripheral inflammation/immune indicators was calculated through ROC curves. Although the pathological responder (Ef grade 2 or 3) revealed significantly better prognosis than the non-responder (Ef grade 0-1b), no relationship was found between responder according to RECIST and prognosis (P=0.014, P=0.992). In univariate analysis, a low PLR (<180, P=0.005), low NLR (<2.6, P=0.019), high lymphocyte (≥1.43, P=0.019) and high PNI (≥40, P=0.032) were identified as prognostic markers, whereas PLR was the only marker correlated with pathological response (P=0.031).

PLR obtained prior to chemotherapy might be a useful indicator for predicting chemosensitivity owing to the simplicity of its procedure.

• chemosensitivity
• gastric cancer
• platelet-lymphocyte ratio
• preoperative chemotherapy

The purpose of this retrospective study was to identify preoperative inflammatory biomarkers and clinical parameters and evaluate their prognostic significance in patients with spinal metastasis from clear cell renal cell carcinoma (CCRCC).

Correlations of overall survival (OS) with traditional clinical parameters and inflammatory indicators including the neutrophil–lymphocyte ratio (NLR), platelet–lymphocyte ratio (PLR), lymphocyte–monocyte ratio (LMR), albumin–globulin ratio (AGR), and C-reactive protein to albumin ratio (CRP/Alb ratio) were analyzed in 95 patients with spinal metastasis from CCRCA using the Kaplan–Meier method to identify potential prognostic factors. Factors with P values ≤ 0.1 were subjected to multivariate analysis by Cox regression analysis. P values ≤ 0.05 were considered statistically significant.

The 95 patients included in this study were followed up by a mean of 48.8 months (median 51 months; range 6–132 months), during which 21 patients died, with a death rate of 22.1%. The statistical results indicated that patients with total piecemeal spondylectomy (TPS), targeted therapy, NLR < 3.8 and PLR < 206.9 had a significantly longer OS rate.

TPS and targeted therapy could significantly prolong the OS of patients with spinal metastasis from CCRCC. In addition, NLR and PLR are robust and convenient prognostic indicators that have a discriminatory ability superior to other inflammatory biomarkers.

• clear cell renal cell carcinoma
• inflammatory biomarkers
• overall survival
• prognosis
• spinal metastasis

Integrin-mediated platelet-tumor cell contacting plays an important role in promoting epithelial-mesenchymal transition (EMT) transformation of tumor cells and cancer metastasis, but whether it occurs in breast cancer cells is not completely clear.

The purpose of this study was to investigate the role of integrin α2β1 in platelet contacting to human breast cancer cell line MCF-7 and its effect on the EMT and the invasion of MCF-7 cells.

Human platelets were activated by thrombin, and separated into pellets and releasates before the co-incubation with MCF-7 cells. Cell invasion was evaluated by transwell assay. The surface integrins on pellets and MCF-7 cells were inhibited by antibodies. The effect of integrin α2β1 on Wnt-β-catenin pathway was assessed by integrin α2β1-silencing and Wnt-β-catenin inhibitor XAV. The therapeutic effect of integrin α2β1-silencing was confirmed in the xenograft mouse model.

Pellets promote the invasion and EMT of MCF-7 cells via direct contacting of surface integrin α2β1. The integrin α2β1 contacting activates Wnt-β-catenin pathway and promotes the expression of EMT proteins in MCF-7 cells. The activated Wnt-β-catenin pathway also promotes the autocrine of TGF-β1 in MCF-7 cells. Both Wnt-β-catenin and TGF-β1/pSmad3 pathways promote the expression of EMT proteins. Integrin α2β1-silencing inhibits breast cancer metastasis in vivo.

The direct interaction between platelets and tumor cells exerts its pro-metastatic function via surface integrin α2β1 contacting and Wnt-β-catenin activation. Integrin α2β1-silencing has the potential effect of inhibiting breast cancer metastasis.

• Direct interaction
• Epithelial-mesenchymal transition
• MCF-7 cell
• Platelet
• TGF-β1
• Wnt-β-catenin

• Mean platelet volume
• Pancreatic neuroendocrine tumor
• Platelet count
• Platelet-to-lymphocyte ratio
• Recurrence
• Survival
• Tumor-infiltrating platelets

• Adult
• Aged
• Aged, 80 and over
• Biomarkers/blood
• Blood Platelets/cytology
• Disease-Free Survival
• Epithelial-Mesenchymal Transition
• Female
• Follow-Up Studies
• Humans
• Lymphocyte Count
• Lymphocytes/cytology
• Male
• Middle Aged
• Neoplasm Metastasis
• Neoplasm Recurrence, Local
• Neuroendocrine Tumors/blood
• Neuroendocrine Tumors/diagnosis
• Neuroendocrine Tumors/mortality
• Neuroendocrine Tumors/surgery
• Pancreatic Neoplasms/blood
• Pancreatic Neoplasms/diagnosis
• Pancreatic Neoplasms/mortality
• Pancreatic Neoplasms/surgery
• Platelet Count
• Postoperative Period
• Prognosis
• Proportional Hazards Models
• Retrospective Studies

• fibrosis
• hemostasis
• hepatic stellate cells
• hepatocellular carcinoma
• macrophages
• platelets
• tumor-stroma interactions

• Disease-free survival
• Inflammatory biomarkers
• Overall survival
• Prognosis
• Spinal chondrosarcoma

• angiogenesis
• cancer biomarker
• drug resistance
• metastasis
• platelet
• platelet-derived growth factor

• Blood Platelets/metabolism
• Blood Platelets/pathology
• Carcinoma, Pancreatic Ductal/pathology
• Carcinoma, Pancreatic Ductal/surgery
• Disease-Free Survival
• Female
• Humans
• Kaplan-Meier Estimate
• Male
• Middle Aged
• Neoplasm Staging/methods
• Pancreatic Neoplasms/pathology
• Pancreatic Neoplasms/surgery
• Platelet Count
• Platelet Glycoprotein GPIb-IX Complex/metabolism
• Preoperative Period
• Risk Assessment/methods
• Survival Rate

Gastric cancer is common in developing regions, and we hope to find out an economical but practical prognostic indicator. It was reported that pre-treatment peripheral neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR), as well as differentiation status, were associated with cancer progression. Hence, we introduced a novel combined Neutrophil/platelet/lymphocyte/differentiation Score (cNPLDS) to improve the prediction value of palliative chemotherapeutic response in advanced gastric cancer.

According to statistical sample size estimation, 136 primary diagnosed unresectable advanced ptaients were included for a retrospective study. The follow-up end-point was progression free survival (PFS) during the first-line palliative chemotherapy. Differentiation stratified patients into well, medium and poor groups by score 1 to 3, while patients with neither elevated NLR and PLR, only one elevated, or both elevated were of the combined NLR-PLR score (cNPS) 1 to 3, respectively. The cNPLDS was calculated by multiplying the tumor differentiation score and cNPS.

Determined by the receiver operating characteristic (ROC) curve, the optimal cut-off points for NLR and PLR were 3.04 and 223. Through univariate analysis and survival analysis, poor differentiation, high NLR, high PLR, high cNPS, and high cNPLDS respectively indicated inferior PFS during the first-line palliative chemotherapy. Patients were furhter classified into low to high risk groups by cNPLDS. Groups of elevated NLR, PLR, cNPS, and cNPLDS showed lower disease control rate. Compared to other parameters, cNPLDS significantly improved the accuracy in predicing the first-progression.

This study indicates that the novel parameter cNPLDS is superior to NLR or PLR alone, or even cNPS, in predicting the first-line chemosensitivity in advanced gastric cancer.

• Chemosensitivity
• Gastric cancer
• Neutrophil-to-lymphocyte ratio
• Platelet-to-lymphocyte ratio
• Tumor differentiation

Cancer patients experience a four-fold increase in thrombosis risk, indicating that cancer development and progression are associated with platelet activation. Xenograft experiments and transgenic mouse models further demonstrate that platelet activation and platelet-cancer cell interaction are crucial for cancer metastasis. Direct or indirect interaction of platelets induces cancer cell plasticity and enhances survival and extravasation of circulating cancer cells during dissemination. In vivo and in vitro experiments also demonstrate that cancer cells induce platelet aggregation, suggesting that platelet-cancer interaction is bidirectional. Therefore, understanding how platelets crosstalk with cancer cells may identify potential strategies to inhibit cancer metastasis and to reduce cancer-related thrombosis. Here, we discuss the potential function of platelets in regulating cancer progression and summarize the factors and signaling pathways that mediate the cancer cell-platelet interaction.

• biomarker
• cancer metastasis
• cancer therapy
• platelet

• Biomarkers, Tumor/metabolism
• Blood Platelets/physiology
• Humans
• Models, Biological
• Neoplasm Metastasis/pathology
• Neoplasm Metastasis/physiopathology
• Neoplasms/pathology
• Neoplasms/physiopathology
• Platelet Activation/physiology

• R01 CA207772 NCI NIH HHS
• R01 CA215095 NCI NIH HHS
• R21 CA209045 NCI NIH HHS

• Rectal prolapse
• laparoscopic surgery
• mesh
• peritoneal closure
• posterior wrap
• rectopexy

• CRP to albumin ratio
• osteosarcoma
• prognosis

Cancer-related systemic inflammation responses have been correlated with cancer development and progression. The prognostic significance of several inflammatory indicators, including neutrophil–lymphocyte ratio (NLR), platelet–lymphocyte ratio (PLR), Glasgow Prognostic Score (GPS), C-reactive protein to albumin ratio (CRP/Alb ratio), lymphocyte–monocyte ratio (LMR), and neutrophil–platelet score (NPS), were found to be correlated with prognosis in several cancers. However, the prognostic role of these inflammatory biomarkers in Ewing sarcoma has not been evaluated. This study enrolled 122 Ewing patients. Receiver operating characteristic (ROC) analysis was generated to determine optimal cutoff values; areas under the curves (AUCs) were assessed to show the discriminatory ability of the biomarkers; Kaplan–Meier analysis was conducted to plot the survival curves; and Cox multivariate survival analysis was performed to identify independent prognostic factors. The optimal cutoff values of CRP/Alb ratio, NLR, PLR, and LMR were 0.225, 2.38, 131, and 4.41, respectively. CRP/Alb ratio had a significantly larger AUC than NLR, PLR, LMR, and NPS. Higher levels of CRP/Alb ratio (hazard ratio [HR] 2.41, P=0.005), GPS (HR 2.27, P=0.006), NLR (HR 2.07, P=0.013), and PLR (HR 1.85, P=0.032) were significantly correlated with poor prognosis. As the biomarkers had internal correlations, only the CRP/Alb ratio was involved in the multivariate Cox analysis and remained an independent prognostic indicator. The study demonstrated that CRP/Alb ratio, GPS, and NLR were effective prognostic indicators for patients with Ewing sarcoma, and the CRP/Alb ratio was the most robust prognostic indicator with a discriminatory ability superior to that of the other indicators; however, PLR, LMR, and NPS may not be suitable as prognostic indicators in Ewing sarcoma.

• CRP/Alb ratio
• Ewing sarcoma
• inflammatory biomarkers
• prognosis
• survival

• antiplatelet
• cancer
• cancer therapy
• platelet

• Chemoresistance
• Gastric cancer
• Platelets
• Preoperative chemotherapy
• Surrogate marker