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The European Academy of Cancer Sciences (EACS) is an independent advisory body of well‐recognised medical specialists and researchers striving to create a compelling interactive continuum of cancer research, from innovative basic research to implementation of state‐of‐the‐art evidence‐based cancer care and prevention. Achieving the above will entail bridging high‐quality basic and preclinical cancer research to research on prevention, early detection and therapeutics as well as improving coordination of translational research efforts across Europe. The latter is expected to be expedited through quality assuring translational cancer research in Comprehensive Cancer Centres – entities that link research with the healthcare system – and networks of cancer research centres. Achieving a critical mass of expertise, resources and patients is crucial. Improving late translational research, which involves clinical studies to assess effectiveness, and added value for the health care is also a high priority. Both high‐quality Big Data collections and the intelligent use of these data will promote innovation in cancer research and support outcomes research to assess clinical utility, quality of cancer care and long‐term follow‐up of treated patients. The EACS supports the mission‐oriented approach recently proposed by the European Commission in Horizon Europe to deal with major challenges and would like to persuade the EU and its member states to formally launch a mission in cancer to boost and streamline the cancer research continuum in Europe. Building a coherent translational cancer research continuum with a focus on patients and individuals at risk will require, however, foresight as well as the extensive and continuous provision of evidence‐based advice to inform policy. The European Academy of Cancer Sciences (EACS), an independent advisory body of medical specialists and researchers, has issued a position paper encouraging the European Union and its member states to formally launch a mission to boost and streamline cancer research. [ABSTRACT FROM AUTHOR]

RETRACTION: H. Zhang, T. Liu, S. Yi, L. Gu, and M. Zhou, “Targeting MYCN IRES in MYCN‐amplified Neuroblastoma With Mir‐375 Inhibits Tumor Growth and Sensitizes Tumor Cells to Radiation,” Molecular Oncology 9, no. 7 (2015): 1301–1311, https://doi.org/10.1016/j.molonc.2015.03.005The above article, published online on 24 March 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Kevin Ryan; FEBS Press; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image section duplications within the article (Figure 5B) and between this (Figures 3B and 4B) and another article published by the same group of authors in a different scientific context. The authors were unable to provide a satisfactory explanation and the original raw data, which has led the editors to lose confidence in the data presented. Therefore, the editors consider the conclusions substantially compromised and are retracting the paper. [ABSTRACT FROM AUTHOR]

RETRACTION: T. Liu, H. Zhang, S. Yi, L. Gu, and M. Zhou, “Mutual Regulation of MDM4 and TOP2A in Cancer Cell Proliferation,” Molecular Oncology 13, no. 5 (2019): 1047–1058, https://doi.org/10.1002/1878-0261.12457The above article, published online on 04 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Kevin Ryan; FEBS Press; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image panel duplications between this (Figures 3B, 4C, and 5C) and other articles published previously by an overlapping group of authors in a different scientific context. The authors were unable to provide a satisfactory explanation and the original raw data, which has led the editors to lose confidence in the data presented. Therefore, the editors consider the conclusions substantially compromised and are retracting the paper. [ABSTRACT FROM AUTHOR]

In this paper, we have modified the workflow of the traditional light transmission aggregometry (LTA) protocol to characterize tumor cell clusters in vitro in a quantifiable and multifaceted manner. Circulating tumor cell (CTC) clusters have high metastatic potential compared to single tumor cells traveling in the bloodstream. Thus, engineering new therapeutic strategies that specifically target this CTC population is essential. To accomplish this, quantifiable methods to characterize their therapeutic effect on tumor cell clusters is a prerequisite. The method presented here enables the user to precisely quantify the dissociation of cancer cell clusters in the presence of clinically relevant fibrinolytic agents, such as alteplase and tenecteplase. The efficacy of the fibrinolytic agents can be quantified using this in vitro assay, prior to conducting preclinical studies. Here, we have obtained the fibrinolytic activity data in terms of lag time to the initiation of tumor cell dissociation, time to 25% dissociation, and trend of dissociation over time. To validate the assay, cell counts and phase‐contrast microscopy images were recorded over time. Further, we explored an LTA‐assisted preparation of platelet–tumor‐cell clusters of calibrated size for potential downstream testing/applications. To assess whether the assay is applicable to characterize the dissociation of cancer cell clusters in the presence of platelets, we added low (50 000 platelets·μL−1), normal (200 000 platelets·μL−1) and high (450 000 platelets·μL−1) concentrations of platelets to the tumor cell clusters. In addition to dissociation parameters, microcopy images were recorded over time to validate the assay and enabled the enumeration of clusters and single cells. The correlative light electron microscopy (CLEM) technique was utilized to visualize the morphology and composition of platelet–tumor cell clusters. [ABSTRACT FROM AUTHOR]

Abstract: Nanotechnology is expected to play an increasingly important role in the diagnostics, prognostics, and management of targeted cancer treatments. While papers have described promising results for nanotechnology in experimental settings, the translation of fundamental research into clinical applications has yet to be widely adopted. In future, policy makers will need to anticipate new developments for clinical implementation and introduce technology assessments. Here we present an overview of the literature on the technology assessments that have already been undertaken on early stage nanotechnology in cancer care, with particular emphasis placed on clinical efficacy, efficiency, logistics, patient-related features and technology dynamics. Owing to the current stage of development of most nanotechnologies, we found only a limited number of publications describing the application of either Health Technology Assessment (HTA) or Constructive Technology Assessment (CTA). In spite of the promising conclusions of most papers concerning the benefits of clinical implementation, actual clinically relevant applications were rarely encountered, and so far only a few publications report application of systematic forms of technology assessment. Most articles consider aspects of environmental safety, regulation and ethics, often mentioning the need to investigate such issues more thoroughly. Evaluation of financial and organizational aspects is often missing. In order to obtain a realistic perspective on the translation and implementation process there is a need for a broad and systematic evaluation of nanotechnologies at early stages of development. Assessment methods taking technology dynamics into account, such as Constructive Technology Assessment (CTA) should be considered for evaluation purposes. [Copyright &y& Elsevier]

In this issue, Kresovich and colleagues have published a hallmark paper in Molecular, Environmental, Genetic and Analytic Epidemiology. By applying artificial intelligence to the Sister Study they created a new methylation‐based breast cancer risk score (mBCRS) based on blood DNA methylation. Using a prospective design and after accounting for age and questionnaire‐based breast cancer risk factors, the Odds PER Adjusted standard deviation (OPERA) for mBCRS and polygenic risk score (PRS) was 1.58 (95% CI: 1.38, 1.81) and 1.58 (95% CI: 1.36, 1.83), respectively, and the corresponding area under the receiver operating curve was 0.63 for both. Therefore, mBCRS could be as powerful as the current best PRS in differentiating women of the same age in terms of their breast cancer risk. These risk scores are among the strongest known breast cancer risk‐stratifiers, shaded only by new mammogram risk scores based on measures other than conventional mammographic density, such as Cirrocumulus and Cirrus, which when combined have an OPERA as high as 2.3. The combination of PRS and mBCRS with the other measured risk factors gave an OPERA of 2.2. OPERA has many advantages over changes in areas under the receiver operator curve because the latter depend on the order in which risk factors are considered. Although more replication is needed using prospective data to protect against reverse causation, there are many novel molecular and analytic aspects to this paper which uncovers a potential mechanism for how genetic and environmental factors combine to cause breast cancer. [ABSTRACT FROM AUTHOR]

Retraction: Li Y‐J, Yang Z, Wang Y‐Y, Wang Y. Long noncoding RNA ZNF667‐AS1 reduces tumor invasion and metastasis in cervical cancer by counteracting microRNA‐93‐3p‐dependent PEG3 downregulation. Mol Oncol. 2019;13(11):2375–2392. https://doi.org/10.1002/1878-0261.12565The above article, published online on 17 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Kevin Ryan; FEBS Press; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed implausible Western blot data (Fig. 5B,L,G,Q), and an image duplication in Fig. 6B. The authors' failure to respond with the original raw data has led the editors to lose confidence in the data presented. Therefore, the editors consider the conclusions substantially compromised and are retracting the paper. [ABSTRACT FROM AUTHOR]

RETRACTION: K. Liu, J.‐D. Ni, W.‐Z. Li, B.‐Q. Pan, Y.‐T. Yang, Q. Xia and J. Huang, "The Sp1/FOXC1/HOTTIP/LATS2/YAP/β‐Catenin Cascade Promotes Malignant and Metastatic Progression of Osteosarcoma," Molecular Oncology 14, no. 10 (2020): 2678–2695, https://doi.org/10.1002/1878-0261.12760. The above article, version of record published online on 29 August 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor in Chief, Kevin Ryan and John Wiley and Sons Ltd. The decision to retract the manuscript has been made due to insufficient explanation or provision of appropriate raw data to justify the duplicated ruler, which have appeared in other publications, along with overlap between different panels of Figs. 2E, 3F, and 4F. The editors consider the conclusions substantially compromised and are therefore retracting the paper. [ABSTRACT FROM AUTHOR]

RETRACTION: L. Wang, Y. Gao, D. Tong, X. Wang, C. Guo, B. Guo, Y. Yang, L. Zhao, J. Zhang, J. Yang, Y. Qin, L. Liu, and C. Huang, "MeCP2 Drives Hepatocellular Carcinoma Progression Via Enforcing HOXD3 Promoter Methylation and Expression Through the HB‐EGF/EGFR Pathway," Molecular Oncology 15, no. 11 (2021): 3147‐3163, https://doi.org/10.1002/1878-0261.13019. The above article, published online on 24 May 2021 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Kevin Ryan; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party regarding an image duplication between Figures 2C (MeCP2 panel) and 4G (left panel). The investigation also revealed inconsistencies in the gel blots of Figures 2J and 3N. The partial raw data shared by the authors was deemed insufficient to address these concerns. Therefore, the editors have lost confidence in the presented data, consider the conclusions substantially compromised and are retracting the paper. The authors were informed of the decision to retract but did not agree to the retraction or the retraction wording. [ABSTRACT FROM AUTHOR]

RETRACTION: M. Lagadari, N. R. Zgajnar, L. I. Gallo and M. D. Galigniana, 'Hsp90‐binding immunophilin FKBP51 forms complexes with hTERT enhancing telomerase activity', Molecular Oncology 10, no. 7 (2016): 1086–1098, https://doi.org/10.1016/j.molonc.2016.05.002. The above article, published online on 17 May 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor in Chief, Kevin Ryan and John Wiley and Sons Ltd. The retraction has been agreed due to several instances of image manipulation in figures 1C, 5B, 4A and 5A. The available raw data were not compelling. Based on the number of inappropriate duplications, the editors consider the conclusions substantially compromised and are therefore retracting the paper. The author, Mario D. Galigniana, disagrees with the retraction; acknowledgement of the retraction could not be obtained from the remaining co‐authors. [ABSTRACT FROM AUTHOR]

Abstract: There is increasing evidence that glioblastoma possess ‘stem-like’ cells, low concentrations of which can initiate a tumour. It has been proposed that these cells are radioresistant, and that this property contributes to the poor treatment outcomes of these tumours. In this paper we propose that radioresistance is not simply an intrinsic characteristic of glioma stem cells but a result of interactions between these cells and microenvironmental factors, i.e. the ‘microenvironment – stem cell unit’. The critical role of the microenvironment, along with glioma stem cells, is supported directly or indirectly by the following observations: glioma stem cells have been shown to reside preferentially in specific niches, the characteristics of which are known to influence cellular responses to radiation; radiation modifies environmental factors; and, contrarily to the consistency of clinical data, in vitro experiments have reported a wide variety in the radiation response of these cells. The paper, therefore, focuses on the interaction between tumour stem cells and the microenvironment, analyzing how its various elements (endothelial cells, extracellular matrix, cytokines, nitric oxide, oxygen levels) are affected by radiation and how these might influence the response of tumour stem cells to radiation. Finally, we summarize the ongoing debate on the optimal culture conditions for glioma stem cells and the difficulties in designing assays that reliably characterize their radiation response. [Copyright &y& Elsevier]

The PI3K/Akt signaling pathway, the most frequently altered signaling system in human cancer, is a crucial inducer of dysregulated proliferation and neoplastic processes; however, few therapeutic strategies using PI3K/Akt inhibitors singly have been shown to be effective. The purpose of this paper was to underline the potential benefit of pharmacological modulation of the PI3K/Akt pathway when combined with specific chemotherapeutic regimens. We have studied the ability of NVP‐BEZ235 (PI3K/mTOR inhibitor) and AZD5363 (Akt inhibitor) in the sensitization of cancer cells to cisplatin and doxorubicin. Our results show that NVP‐BEZ235 sensitizes cells preferentially to cisplatin while AZD5363 sensitizes cells to doxorubicin. At equal concentrations (5 μm), both inhibitors reduce ribosomal protein S6 phosphorylation, but AZD5363 is more effective in reducing GSK3β phosphorylation as well as S6 phosphorylation. Additionally, AZD5363 is capable of inducing FOXO1 and p53 nuclear localization and reduces BAD phosphorylation, which is generally increased by cisplatin and doxorubicin. Finally, the combination of AZD5363 and doxorubicin induces apoptosis in cells and robustly reduces cell ability to clonally replicate, which underlines a potential cooperative effect of the studied compounds. [ABSTRACT FROM AUTHOR]

The above article, published online on 29 April 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Kevin Ryan, FEBS Press, and John Wiley and Sons Ltd. The retraction has been agreed due to several image duplications in Figures 4B,E,G, and 5C,D, and inconsistencies between tumour luminescence images and the quantification in Figure 4K. Compelling raw data images were not available from the authors. The editors consider the conclusions substantially compromised and are therefore retracting the paper. Corresponding author Pritha Ray agrees to this retraction, since the raw data are no longer available for analysis and validation. Reference 1 Thakur B, Ray P. p53 loses grip on PIK3CA expression leading to enhanced cell survival during platinum resistance. Mol Oncol. 2016;10(8):1283–1295. https://doi.org/10.1016/j.molonc.2016.06.006 [ABSTRACT FROM AUTHOR]