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Supplementary Table S3 from Down-Regulation of hsa-miR-10a in Chronic Myeloid Leukemia CD34+ Cells Increases USF2-Mediated Cell Growth

PDF - 124K, Supplementary Table 1. Clinical and molecular characteristics of the 21 patients with CRC included in the study. Supplementary Table 2. Analysis of PP2A activity levels using 1D6 or FL-309 antibodies, SET overexpression, CIP2A overexpression, PPP2R2A downregulation and PPP2R5E downregulation in 21 CRC patients. Supplementary Table 3. Primer sequences used for PPP2R1B mutation analysis.

Supplementary Figure S1. MKP-1 protein abundance levels in MDA-MB-231 cells treated with docetaxel at progressively increasing times. Supplementary Figure S2. Cell growth in the presence of the docetaxel or doxorubicin of breast cancer cell lines overexpressing MKP-1. Supplementary Table S1. Clinical and molecular characteristics of a series of 350 patients with early breast cancer. Supplementary Figure S3. IHC detection of MKP-1 and p-JNK1/2 in a representative normal tissue sample. Supplementary Table S2. Univariate and multivariate Cox analyses in the cohort of 350 breast cancer patients (disease-free survival analysis). Supplementary Table S3. Clinical and molecular characteristics of 64 locally advanced breast cancer patients who received neoadjuvant taxane-based chemotherapy.Supplementary Table S4. MKP-1 and p-JNK1/2 marker determinations in locally advanced breast cancer patients who received neoadjuvant taxane-based chemotherapy.

MAPK phosphatase-1 (MKP-1) is overexpressed during malignant transformation of the breast in many patients, and it is usually associated with chemoresistance through interference with JNK-driven apoptotic pathways. Although the molecular settings of the mechanism have been documented, details about the contribution of MKP-1 to the failure of chemotherapeutic interventions are unclear. Transient overexpression of MKP-1 and treatment with JNK-modulating agents in breast carcinoma cells confirmed the mediation of MKP-1 in the resistance to taxanes and anthracyclines in breast cancer, through the inactivation of JNK1/2. We next assessed MKP-1 expression and JNK1/2 phosphorylation status in a large cohort of samples from 350 early breast cancer patients treated with adjuvant anthracycline–based chemotherapy. We detected that MKP-1 overexpression is a recurrent event predominantly linked to dephosphorylation of JNK1/2 with an adverse impact on relapse of the tumor and overall and disease-free survival. Moreover, MKP-1 and p-JNK1/2 determinations in 64 locally advanced breast cancer patients treated with neoadjuvant taxane–based chemotherapy showed an inverse correlation between MKP-1 overexpression (together with JNK1/2 inhibition) and the pathologic response of the tumors. Our results emphasize the importance of MKP-1 as a potential predictive biomarker for a subset of breast cancer patients with worse outcome and less susceptibility to treatment. Mol Cancer Ther; 15(11); 2780–90. ©2016 AACR.

PDF - 2988K, Supplementary Figure 1. Levels of immunoprecipitated PP2A from lysates of 21 CRC patients used in PP2A phosphatase assays (1D6 antibody). Supplementary Figure 2. Quantification of PP2A activity in CRC patients with normal mucosa and tumor samples (FL-309 antibody); * P < 0.05; ** P < 0.01; N: normal mucosa; T: tumor sample. Supplementary Figure 3. Levels of immunoprecipitated PP2A from lysates of 21 CRC patients used in PP2A phosphatase assays (FL-309 antibody). Supplementary Figure 4. Comparison between normal PPP2R1B sequence and silent alterations at codons 72 (A) and 391 (B) found in two CRC patients. The position altered is indicated by an arrow. Supplementary Figure 5. Western blot analysis of PPP2R2A and PPP2R5E in 21 CRC patients. Supplementary Figure 6. Quantification of PP2A activity using the 1D6 and FL-309 antibodies and western blot analysis of PP2A, CIP2A and SET in 7 CRC cell lines; * P < 0.05; ** P < 0.01; N1-2, normal tissue. Supplementary Figure 7. FTY720 treatment induces a PP2A activation. (A) Treatment with OA inhibits the FTY720-induced PP2A activity in RKO and LoVo cells. (B) Levels of immunoprecipitated PP2A (FL-309 antibody) from the RKO and LoVo lysates used in the phosphatase assays. Supplementary Figure 8. Analysis of cell viability in SW480, HT-29 and DLD-1 cells after FTY720 treatment. Supplementary Figure 9. Optical microscope images showing changes in morphology and cell viability after FTY720 treatment in RKO and DLD-1 cells. Supplementary Figure 10. Colony forming ability of HT-29 and DLD-1 cells untreated or FTY720-treated alone or in combination with okadaic acid. Supplementary Figure 11. Western blot showing PP2A, AKT and ERK1/2 phosphorylation and expression after FTY720 treatment in HT-29 and SW480 cells. Supplementary Figure 12. Western blot analysis of CIP2A, c-MYC, SET and PP2A expression after FTY720 treatment in RKO and LoVo cells. Supplementary Figure 13. MTS assays showing the effect of FTY720 and 5-FU (A), SN-38 (B) or LOHP (C) alone or in combination in DLD-1 cells. Supplementary Figure 14. MTS assays showing the effect of FTY720 and 5-FU (A), SN-38 (B) or LOHP (C) alone or in combination in HT-29 cells. Supplementary Figure 15. Effects of FTY720 on proliferation and apoptosis in a total of 5 sets of human samples, including normal mucosa and colorectal tumor. Each row represents an effect on expression of the paired control and FTY720 treated samples, and each column, a single IHC marker, including Ki-67 and cleaved caspase 3. Downregulation of expression is displayed in green, upregulation in red, and no effect in black.

Supplementary Figures S1-S6 from Down-Regulation of hsa-miR-10a in Chronic Myeloid Leukemia CD34+ Cells Increases USF2-Mediated Cell Growth

Supplementary Figure S5. Immunohistochemical detection of SET expression in patients with metastatic colorectal cancer showing SET negative (A) and positive (B) stainings.

Supplementary Figure 2 from Inhibitor of Differentiation-1 as a Novel Prognostic Factor in NSCLC Patients with Adenocarcinoma Histology and Its Potential Contribution to Therapy Resistance

Supplementary Figure 3 from Inhibitor of Differentiation-1 as a Novel Prognostic Factor in NSCLC Patients with Adenocarcinoma Histology and Its Potential Contribution to Therapy Resistance

Purpose: High inhibitor of differentiation-1 (Id1) levels have been found in some tumor types. We aimed to study Id1 levels and their prognostic impact in a large series of stages I to IV non-small cell lung cancer (NSCLC) patients. Experiments in cell lines and cells derived from malignant pleural effusions (MPE) were also carried out.Experimental Design: A total of 346 NSCLC samples (three different cohorts), including 65 matched nonmalignant tissues, were evaluated for Id1 expression by using immunohistochemistry. Additional data from a fourth cohort including 111 patients were obtained for Id1 mRNA expression analysis by using publicly available microarrays. In vitro proliferation assays were conducted to characterize the impact of Id1 on growth and treatment sensitivity.Results: Significantly higher Id1 protein levels were found in tumors compared with normal tissues (P < 0.001) and in squamous carcinomas compared with adenocarcinomas (P < 0.001). In radically treated stages I to III patients and stage IV patients treated with chemotherapy, higher Id1 levels were associated with a shorter disease-free survival and overall survival in adenocarcinoma patients in a log-rank test. A Cox model confirmed the independent prognostic value of Id1 levels for both stages I to III and stage IV patients. In silico analysis confirmed a correlation between higher Id1 mRNA levels and poor prognosis for adenocarcinoma subjects. In vitro Id1 silencing in radio/chemotherapy-resistant adenocarcinoma cells from MPEs restored sensitivity to both therapies.Conclusions: In our series, Id1 levels showed an independent prognostic value in patients with adenocarcinoma, regardless of the stage. Id1 silencing may sensitize adenocarcinoma cells to radiotherapy and chemotherapy. Clin Cancer Res; 17(12); 4155–66. ©2011 AACR.

Supplementary Figures S1-S4 and Supplementary Tables S1-S4

Supplementary Figure 4 from Inhibitor of Differentiation-1 as a Novel Prognostic Factor in NSCLC Patients with Adenocarcinoma Histology and Its Potential Contribution to Therapy Resistance

Supplementary Figure 1 from Inhibitor of Differentiation-1 as a Novel Prognostic Factor in NSCLC Patients with Adenocarcinoma Histology and Its Potential Contribution to Therapy Resistance

Supplementary Figure Legends

Supplementary Table S1. Clinical and molecular characteristics of a series of 242 patients with metastatic CRC.

Supplementary Figure 5 from Inhibitor of Differentiation-1 as a Novel Prognostic Factor in NSCLC Patients with Adenocarcinoma Histology and Its Potential Contribution to Therapy Resistance

Purpose: SET is an endogenous PP2A inhibitor that might represent a novel molecular target for antitumor therapy. The aim of this study was to evaluate the molecular effects of SET deregulation and its potential clinical significance in metastatic colorectal cancer (mCRC).Experimental Design: We studied the biologic effects of SET on cell growth, colonosphere formation, caspase activity, PP2A activation status, and sensitivity to oxaliplatin and FTY720 treatments. Moreover, we analyzed SET expression by immunostaining in 242 patients with mCRC.Results: SET deregulation promotes cell growth and colonosphere formation and inhibits PP2A, thereby impairing its antitumor effects. Moreover, SET reduces sensitivity to oxaliplatin in colorectal cancer cell lines, which is restored after FTY720 treatment. SET overexpression was detected in 24.8% (60 of 242) of patients with mCRC and determined significantly shorter overall (8.6 vs. 27 months; P < 0.001) and progression-free survival (7.1 vs. 13.7 months; P < 0.001), and poor response to oxaliplatin-based chemotherapy (P = 0.004). Interestingly, its prognostic value was particularly evident in patients younger than 70 years and in those harboring KRAS mutations.Conclusions: SET overexpression is a frequent event in mCRC that plays a potential oncogenic role associated with worse outcome and resistance to oxaliplatin. Moreover, this alteration defines a subgroup of patients who could benefit from therapies containing PP2A activators such as FTY720. Clin Cancer Res; 21(2); 347–56. ©2014 AACR.

Purpose:OncoBEAM™ is a circulating tumor DNA (ctDNA) test that uses the BEAMing digital PCR technology. We clarified the association between the baseline tumor burden and discordance in the RAS status by metastatic sites in patients with a single metastatic site.Experimental Design:Data from previous Spanish and Japanese studies investigating the concordance of the RAS status between OncoBEAM™ and tissue biopsy in 221 patients with metastatic colorectal cancer (mCRC) were used. We collected data from patients with liver, peritoneal, or lung metastases and evaluated the concordance rates according to the metastatic site and the association between the concordance rate and tumor burden.Results:Patients had metastases in the liver (n = 151), peritoneum (n = 25), or lung (n = 45) with concordance rates of 91% (95% confidence interval, 85%–95%), 88% (68%–97%), and 64% (49%–78%), respectively. Factors associated with concordance included the baseline longest diameter and lesion number (P = 0.004), and sample collection interval (P = 0.036). Concordance rates ≥90% were observed in the following groups: liver metastases alone, regardless of the baseline longest diameter and lesion number; peritoneal metastases alone in patients with a baseline longest diameter ≥20 mm; and lung metastases alone in patients with a baseline longest diameter ≥20 mm and/or number of lesions ≥10.Conclusions:Plasma ctDNA-based liquid biopsy in patients with mCRC may be useful depending on the metastatic site. The maximum diameter and lesion number should be carefully considered when determining patients' RAS status with only peritoneal or lung metastases.

small-cell lung cancer (SCLC) is one of the most lethal malignancies. Its management is complex due to the lack of biomarkers and limited therapies. Galectin-1 (Gal-1) plays a major role in cancer development and progression. The aim of this study is to assess whether Gal-1 has a predictive role in the disease evolution and its therapeutic potential.The expression level of Gal-1 was examined by using a public RNA-sequencing (77 SCLC patients) and in-house immunohistochemistry (IHC) performed on biopsies from 81 patients. Survival curves and Cox regression analysis were used to assess the prognostic potential of Gal-1. In addition, a SCLC-PDX model was carried out and treated with either OTX008, an inhibitor of Gal-1, or vehicle to assess the effects of Gal-1 inhibition on this disease in vivo.Galectin-1 gene (LGALS1) expression showed a strong negative correlation with outcome in SCLC patients with advanced disease (p = 0.007). IHC unveiled that overall survival (OS) was significantly lower among extensive-stage SCLC (ES-SCLC) patient group with increased level of Gal-1 and platelet-to-lymphocyte ratio (PLR) (HR=3.07, 95% CI: 1.62, 5.79, p 0.001). The SCLC-PDX model showed a significant reduction in tumor size (tumor growth inhibition [TGI] index 73%) without side effects.in this study, high levels of Gal-1 and PLR were associated with poorer OS in SCLC patients, supporting their utility as clinical prognostic biomarkers. Moreover, the in vivo model suggests the inhibition of Gal-1 as a novel potential therapy for this disease with very poor prognosis.

Purpose: OncoBEAM™ is a circulating tumor DNA (ctDNA) test that uses the BEAMing digital PCR technology. We clarified the association between the baseline tumor burden and discordance in the RAS status by metastatic sites in patients with a single metastatic site. Experimental Design: Data from previous Spanish and Japanese studies investigating the concordance of the RAS status between OncoBEAM™ and tissue biopsy in 221 patients with metastatic colorectal cancer (mCRC) were used. We collected data from patients with liver, peritoneal, or lung metastases and evaluated the concordance rates according to the metastatic site and the association between the concordance rate and tumor burden. Results: Patients had metastases in the liver (n = 151), peritoneum (n = 25), or lung (n = 45) with concordance rates of 91% (95% confidence interval, 85%–95%), 88% (68%–97%), and 64% (49%–78%), respectively. Factors associated with concordance included the baseline longest diameter and lesion number (P = 0.004), and sample collection interval (P = 0.036). Concordance rates ≥90% were observed in the following groups: liver metastases alone, regardless of the baseline longest diameter and lesion number; peritoneal metastases alone in patients with a baseline longest diameter ≥20 mm; and lung metastases alone in patients with a baseline longest diameter ≥20 mm and/or number of lesions ≥10. Conclusions: Plasma ctDNA-based liquid biopsy in patients with mCRC may be useful depending on the metastatic site. The maximum diameter and lesion number should be carefully considered when determining patients' RAS status with only peritoneal or lung metastases.

Background: Galectin-1 (Gal-1) plays major roles in cancer by modulating different processes leading to tumor development and progression. In the last years, it has been suggested as a promising target for anticancer therapy. Recently, aflibercept has shown high affinity for Gal-1. Here, we investigated how aflibercept could exert its antitumor activity via Gal-1-driven pathways in neuroendocrine carcinomas (NECs). Methods and Results: NEC tumor xenografts were used to assess the effect of aflibercept on Gal-1 functions. Aflibercept induced a significant reduction of Gal-1 at epithelial, stromal, and extracellular localizations in lung NEC, whereas this was not observed in colon NECs, which displayed low expression of Gal-1. Additionally, aflibercept significantly reduced p-VEGFR2 protein, extracellular matrix remodeling, epithelial-mesenchymal transition, and activation of cancer-associated fibroblast hampering cell invasion in lung NEC but not in colon NEC. Gal-1 screening in human NECs confirmed that pulmonary and pancreatic tumors displayed higher levels of Gal-1 than colon NECs, becoming good candidates to benefit from aflibercept treatment. Conclusions: The lack of validated predictive markers of aflibercept is a weakness for guaranteeing the best treatment management with this drug. This work provides new mechanistic insight of aflibercept depending on Gal-1. Thus, in tumors overexpressing Gal-1, aflibercept has not only an antiangiogenic effect but also prevents Gal-1-mediated tumor-stroma cross talk. The stronger aflibercept effect in tumors with high levels of Gal-1 points out this protein as a molecular marker to predict the efficacy of this agent not only for NECs but also for other tumors with high levels of this protein.

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer, the incidence of which has risen over the last years. Although cSCC rarely metastasizes, early detection and treatment of primary tumours are critical to limit progression and local invasion. Several prognostic factors related to patients’ clinicopathologic profile and tumour features have been identified as high-risk markers and included in the stratification scales, but their association with regional control or survival is uncertain. Therefore, decision-making on the diagnosis and management of cSCC should be made based on each individual patient’s characteristics. Recent advances in non-invasive imaging techniques and molecular testing have enhanced clinical diagnostic accuracy. Surgical excision is the mainstay of local treatment, whereas radiotherapy (RT) is recommended for patients with inoperable disease or in specific circumstances. Novel systemic treatments including immunotherapies and targeted therapies have changed the therapeutic landscape for cSCC. The anti-PD-1 agent cemiplimab is currently the only FDA/EMA-approved first-line therapy for patients with locally advanced or metastatic cSCC who are not candidates for curative surgery or RT. Given the likelihood of recurrence and the increased risk of developing multiple cSCC, close follow-up should be performed during the first years of treatment and continued long-term surveillance is warranted, This work was supported by Sanofi

Peritoneal metastases from gastric cancer play a key role in the fatal prognosis of the disease. The lack of efficacy of actual therapeutic approaches together with the outcomes achieved with checkpoint inhibitors in gastric cancer compel us to address the current state-of-the-art immunotherapy treatment of peritoneal dissemination. The immunogenicity of the peritoneum has been described to be particularly active at omentum and peritoneal lymph nodes. Also, both innate and acquired immunity seems to be involved at different molecular levels. Recent works show PDL1 expression being less present at the peritoneal level; however, some clinical trials have begun to yield results. For example, the ATTRACTION-2 trial has demonstrated the activity of Nivolumab in heavily pretreated patients even though peritoneal metastases were diagnosed in a 30% of them. Despite positive results in the metastatic setting, peritoneal responses to systemic checkpoint inhibitors remains unclear, therefore, new strategies for intraperitoneal immunotherapy are being proposed for different ongoing clinical trials.

Molecular characterization of tumors has shifted cancer treatment strategies away from nonspecific cytotoxic treatment of histology-specific tumors toward targeting of actionable mutations that can be found across multiple cancer types. The development of high-throughput technologies such as next-generation sequencing, combined with decision support applications and availability of patient databases, has provided tools that optimize disease management. Precision oncology has proven success in improving outcomes and quality of life, as well as identifying and overcoming mechanisms of drug resistance and relapse. Addressing challenges that impede its use will improve matching of therapies to patients. Here we review the current status of precision oncology medicine, emphasizing its impact on patients - what they understand about precision oncology medicine and their hopes for the future.Lay abstract Precision oncology offers individualized treatment of cancer on a per-patient basis, based on the unique DNA fingerprint of a patient’s cancer. New, advanced technologies for DNA sequencing have led to rapid advancement in developing novel therapies. Decision-making tools have followed pace, leading to improved matching of therapy to patient, ultimately improving outcomes (including quality of life), building trust between patient and physician, and increasing hope for the future.

Objective To assess the economic impact of introducing biosimilars of bevacizumab for the management of cancer patients receiving systemic bevacizumab in the National Health System (SNHS) of Spain. Methods A 3-year budget impact analysis model was adapted to estimate the cost of introducing biosimilars of bevacizumab in the SNHS for the adult population who were candidates to receive treatment with bevacizumab. Values for the estimation of the population were obtained from the literature and were validated by an expert panel. In this analysis only pharmaceutical costs (euro, year 2021) obtained from official databases were considered. A sensitivity analysis was performed to examine the robustness of the model. Results The introduction of bevacizumab biosimilars would generate an annual cost saving of euro11 558 268 (-5.1%) for the first year with a penetration share of biosimilars from 30.0%, euro29 126 373 (-8.5%) for the second year with a share of 50.0% and euro52 361 778 (-13.6%) for the third year with a share of 80.0%. The total pharmaceutical costs of the scenario without biosimilars are euro227 033 352 for the first year, euro342 663 209 for the second year and euro385 013 076 for the third year. In contrast, the pharmaceutical costs of the scenario with bevacizumab biosimilars are euro215 475 084, euro313 536 836 and euro332 651 297 for years 1, 2 and 3, respectively. Conclusions The introduction of biosimilars in the Spanish Health System would generate saving costs in the pharmacological budget to boost biological drugs from the first year.

Gestational trophoblastic disease can result in serious complications and disease progression. Therefore, follow‐up of such patients is essential for early detection of malignant trophoblastic tumors and to reduce mortality rate. Primary treatment is chemotherapy but hysterectomy should be considered in patients who have uncontrollable hemorrhage and hemodynamic instability.

Purpose There is a lack of standards for the diagnosis, assessment and management of breakthrough cancer pain (BTcP). La Fundacion ECO (the Foundation for Excellence and Quality in Oncology) commissioned a study to establish a consensus and lay the foundations for the appropriate management of BTcP in oncology patients. Patients and methods A modified Delphi survey comprising two rounds was used to gather and analyze data, which was conducted over the Internet. Each statement that reached a consensus with the respondents was defined as a median consensus score (MED) of ≥7, and agreement among panelists as an interquartile range (IQR) of ≤3. Results In total, 69 medical oncologists responded, with a broad consensus that BTcP implied exacerbations of high-intensity pain, as opposed to moderate pain. Furthermore, they concurred that appropriate diagnostic equipment is needed, and that rapid-onset fentanyl formulations should be the preferred treatment for BTcP management. The panelists agreed that a lack of appropriate information and training to attend to patients, as well as limited patient visitation rights, were barriers to effective BTcP management. Regarding gaps in detected knowledge, the panelists were unsure of the measures necessary to assess the burden of the disease on the patient's quality of life and associated medication costs. Alongside this, there was a lack of awareness of the technical specifics of the different formulations of rapid-onset fentanyl. Conclusion These results represent the current status of BTcP management. They may inform recommendations and provide a framework for future research.

Background: Neuroendocrine carcinoma (NEC) is a rare and very aggressive tumor. It has been greatly understudied, and very little is known about optimal treatment strategy for patients with this disease. The purpose of this study was to evaluate in vivo whether anti-vascular endothelial growth factor (VEGF) drugs could be a therapeutic alternative for these tumors with a poor prognosis. Methods: We have developed 2 xenograft models using either human cell line derived from lung (H460) or from colon (COLO320) NEC to assess the effect of 2 antiangiogenic drugs, aflibercept and bevacizumab, on tumor growth and their pathological characteristics. Additionally, tumors were subjected to immunohistochemistry staining and proteins were measured with Western blot and ELISA. Results: Both aflibercept and bevacizumab showed significant antitumor activity (p < 0.001). In the H460 model, aflibercept resulted in 94% tumor growth inhibition (TGI) and bevacizumab treatment resulted in 72.2% TGI. Similarly, in the COLO320 model, aflibercept and bevacizumab resulted in 89.3 and 84% TGI, respectively. Moreover, antitumor activity occurs early after treatment initiation. Using Tumor Control Index score, which address the kinetics of tumor growth in a way comparable to the methods used in human clinical studies, we confirmed that both drugs inhibit significantly tumor growth. When tumor stabilization was evaluated, aflibercept shows higher ability to stabilize NEC tumors than bevacizumab. Conclusion: Results derived from this study strongly support anti-VEGF therapies, especially aflibercept, as a novel therapeutic option in NECs. Further studies are necessary, but our observations encourage the evaluation of antiangiogenics in clinical trials combined with standard chemotherapy.

Background: Patient quality care is a discipline that has acquired enormous relevance in today’s healthcare. The Quality Oncology Practice Initiative (QOPI) is a referral worldwide in terms of quality for oncology practices. The ECO Foundation is a foundation of experts representing the major Spanish hospitals involved in the treatment of cancer patients. ECO reached an agreement with ASCO to involve Spanish hospitals in the QOPI program. Methods: 6 rounds of data collection have taken place (Fall 2015 to Round 1 2018). Practices had to register online and submit data into the QOPI platform, and the ECO Foundation offered all centers the necessary support. 17 Spanish hospitals have participated in the 6 rounds, and 7 of them have repeated participation. Core and lung cancer modules were completed. Results: During the 6 rounds, 1,877 charts were submitted by the Spanish practices. In most of the rounds, the highest scores were: pathology report confirming malignancy; number of chemotherapy cycles documented; patient consent for chemotherapy; and 5 measures of the lung cancer module. The lowest scores were: chemotherapy treatment summary provided to patient within 3 months of chemotherapy end; chemotherapy treatment summary provided or communicated to practitioner(s) within 3 months of chemotherapy end; smoking/tobacco use cessation counselling recommended to smokers/tobacco users in past year; and tobacco cessation counselling administered or patient referred in past year. The percentage of participating practices that presented results higher than 70% was successively 64%, 50%, 75%, and 100% in the last 3 rounds. For the 7 hospitals that repeated participation, 3 reported an improvement of their global scores. Regarding QOPI Certification, 3 Spanish hospitals received this accreditation in September 2017 and one in June 2018. Conclusions: These preliminary results are a good starting point for the continued implementation of the QOPI program in Spain, thus providing a well-structured approach to analyze cancer care. The ECO Foundation will continue pursuing excellence and quality with further activities like the QOPI Certification program and Quality Training Program, these being performed for the first time in Spain in 2017 and 2018, respectively.