Oncology reports最新文献

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the cell invasion assay data featured in Figs. 2G and H, 5M and N, and 9K and L, and the tumor images shown in Fig. 6B, were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to Oncology Reports, or were under consideration for publication at around the same time (some of which have been retracted). In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 117, 2021; DOI: 10.3892/or.2021.8068].

B‑cell lymphoma is difficult to cure because of its biological and clinical heterogeneity, and due to native chemoresistance. Immunotherapies that overcome cancer‑induced immune evasion have been the center of recent developments in oncology. This is emphasized by the accomplishment of various agents that disrupt programmed cell death protein 1 (PD‑1)‑mediated immune suppression in diverse tumors. However, while PD‑1 blockade has been effective in numerous malignancies, a significant proportion of cancers, including B‑cell lymphoma, show certain rates of primary resistance to these therapeutic strategies. Histone deacetylase inhibitors (HDACis) have exhibited anticancer activity though suppressing cell proliferation, inducing differentiation and triggering apoptosis. The present study aimed to explore a therapeutic strategy combining a HDACi (romidepsin) and PD‑1 blockade (BMS‑1) in B‑cell lymphoma, utilizing a constructed mouse model of B‑cell lymphoma. The IC₅₀ of the two inhibitors was confirmed by MTT assay, and their inhibitory effects were revealed to be dose‑ and time‑dependent. The data demonstrated that the combined treatment of romidepsin and BMS‑1 synergistically inhibited the growth of B‑cell lymphoma. Furthermore, it was revealed that romidepsin and BMS‑1 synergistically triggered apoptosis in mouse B‑cell lymphoma. The synergistic effect of these agents was capable of activating tumor‑infiltrating lymphocytes, particularly CD3⁺CD4⁺ and CD3⁺CD8⁺ T cells. The results of the present study underscore the potential of HDAC inhibition in conjunction with PD‑1 blockade as a novel therapeutic approach for B‑cell lymphoma, highlighting the synergistic effects of these two mechanisms in enhancing antitumor immunity.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blotting data shown in Fig. 4B and C on p. 1952, and the Transwell invasion assay data in Fig. 2F and 4I, had already appeared in previously published articles written by different authors at different research institutes (a number of which have been retracted). Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 42: 1946‑1956, 2019; DOI: 10.3892/or.2019.7302].

Following the publication of this article, an interested reader drew to the authors' attention that the flow cytometric (FCM) plots in Fig. 2A on p. 2278 showing the 'Dasatinib' and 'CA‑4' experiments were duplicates of each other. After having re‑examined their original data, and due to the overall similarity of the data, the authors have realized that these data were inadvertently assembled incorrectly in the figure. They realize that they also made a further mistake regarding the writing of the ratios of mitochondrial membrane‑depolarized HO‑8910 cells for these FCM plots (essentially, these were written the wrong way around): The percentage of mitochondrial membrane‑depolarized HO‑8910 cells should have been written as 22.50% for the dasatinib‑treated cells (the centre‑left FCM plot) and 15.71% for the CA‑4‑treated cells (centre‑right plot). A revised version of Fig. 2 now showing alternative data for the FCM experiments shown in Fig. 2A, is shown on the next page. Note that the errors made in terms of assembling the data in Fig. 2A did not greatly affect either the results or the conclusions reported in this paper, and all the authors agree with the publication of this corrigendum. The authors regret that these errors went unnoticed prior to the publication of their article, and are grateful to the Editor of Oncology Reports for granting them this opportunity to publish a corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 29: 2275‑2282, 2013; DOI: 10.3892/or.2013.2405].

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, with the cell migration assay data shown in Fig. 7 on p. 901, the "TPA" and "TPA + U0126" panels were strikingly similar, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. In addition, it was noted that the "TPA + hispolon" and "TPA + NAC" data panels in Fig. 4B on p. 899 contained overlapping sections. Thirdly, a data panel was shared between Figs. 1 and 4, although this was intentional on the part of the authors as the same experiment was being portrayed in these figures.  The authors were able to re‑examine their original data files, and realized that errors were made in asssembling Figs. 4B and 7. The revised versions of Figs. 4 and 7, now containing the correct data for the "TPA + NAC" experiment in Fig. 4B and the Control ("Ctrl") experiment in Fig. 7, are shown on the next two pages. The authors wish to emphasize that the corrections made to these figures do not affect the overall conclusions reported in the paper, and they are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this corrigendum. All the authors agree to the publication of this corrigendum, and also apologize to the readership for any inconvenience caused. [Oncology Reports 35: 896‑904, 2016; DOI: 10.3892/or.2015.4445].

Head and neck squamous cell carcinomas (HNSCCs), a heterogeneous group of cancers that arise from the mucosal epithelia cells in the head and neck areas, present great challenges in diagnosis, treatment and prognosis due to their complex aetiology and various clinical manifestations. Several factors, including smoking, alcohol consumption, oncogenic genes, growth factors, Epstein‑Barr virus and human papillomavirus infections can contribute to HNSCC development. The unpredictable tumour microenvironment adds to the complexity of managing HNSCC. Despite significant advances in therapies, the prediction of outcome after treatment for patients with HNSCC remains poor, and the 5‑year overall survival rate is low due to late diagnosis. Early detection greatly increases the chances of successful treatment. The present review aimed to bring together the latest findings related to the molecular mechanisms of HNSCC carcinogenesis and progression. Comprehensive genomic, transcriptomic, metabolomic, microbiome and proteomic analyses allow researchers to identify important biological markers such as genetic alterations, gene expression signatures and protein markers that drive HNSCC tumours. These biomarkers associated with the stages of initiation, progression and metastasis of cancer are useful in the management of patients with cancer in order to improve their life expectancy and quality of life.

In recent years, microRNAs (miRNAs or miRs) have been increasingly studied for their role in cancer and have shown potential as cancer biomarkers. miR‑143‑3p and miR‑143‑5p are the mature miRNAs derived from pre‑miRNA‑143. At present, there are numerous studies on the function of miR‑143‑3p in cancer progression, but there are no systematic reviews describing the function of miR‑143‑3p in cancer. It is widely considered that miR‑143‑3p is downregulated in most malignant tumors and that upstream regulators can act on this gene, which in turn regulates the corresponding target to act on the tumor. In addition, miRNA‑143‑3p can regulate target genes to affect the biological process of tumors through various signaling pathways, such as the PI3K/Akt, Wnt/β‑catenin, AKT/STAT3 and Ras‑Raf‑MEK‑ERK pathways. The present review comprehensively described the biogenesis of miR‑143‑3p, the biological functions of miR‑143‑3p and the related roles and mechanisms in different cancer types. The potential of miR‑143‑3p as a biomarker for cancer was also highlighted and valuable future research directions were discussed.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the 'Control' data panel shown for the EdU assay experiment in Fig. 6D on p. 1209 was strikingly similar to a data panel featured in Fig. 7 that had already been submitted to the journal Cancer Management and Research by different authors at different research institutes [Chen T‑J, Gao F, Yang T, Li H, Li Y, Ren H and Chen M‑W: Knockdown of linc‑POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer. Cancer Manag Res 12: 4379‑4390, 2020]. Owing to the fact that contentious data in the above article had already been submitted for publication prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 1202‑1212, 2021; DOI: 10.3892/or.2021.7949].

Cribriform morular thyroid carcinoma (CMTC) has been included within the group of thyroid tumors of uncertain histogenesis in the recent World Health Organization classification of endocrine tumors. Most CMTCs occur in young euthyroid women with multiple (and bilateral) thyroid nodules in cases associated with familial adenomatous polyposis (FAP) or as single nodules in sporadic cases. CMTC generally behaves indolently, while aggressiveness and mortality are associated with high‑grade CMTC. This tumor histologically displays a distinctive combination of growth patterns with morular structures. Strong diffuse nuclear and cytoplasmic immunostaining for β‑catenin is the hallmark of CMTC. Tumor cells are also positive for thyroid transcription factor‑1 and for estrogen and progesterone receptors, but negative for thyroglobulin and calcitonin. It is possible that the CMTC phenotype could result from blockage in the terminal/follicular differentiation of follicular cells (or their precursor cells) secondary to the permanent activation of the Wnt/β‑catenin pathway. In CMTC, the activation of the Wnt/β‑catenin pathway is the central pathogenetic event, which in FAP‑associated cases results from germline mutations of the APC regulator of WNT signaling pathway (APC) gene, and in sporadic cases from somatic inactivating mutations in the APC, AXIN1 and CTNNB1 genes. Estrogens appear to play a tumor‑promoting role by stimulating both the PI3K/AKT/mTOR and the RAS/RAF/MAPK signaling pathways. Additional somatic mutations (i.e. RET rearrangements, or KRAS, phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α, telomerase reverse transcriptase or tumor protein 53 mutations) may further potentiate the development and progression of CMTC. While hemithyroidectomy would be the treatment of choice for sporadic cases without high‑risk data, total thyroidectomy would be indicated in FAP‑associated cases. There is insufficient clinical data to propose therapies targeting the Wnt/β‑catenin pathway, but multikinase or selective inhibitors could be used in a manner analogous to that of conventional thyroid tumors. It is also unknown whether adjuvant antiestrogenic therapy could be useful in the subgroup of women undergoing surgery with high‑risk CMTC, as well as when there is tumor recurrence and/or metastasis.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a matching data panel comparing between one of the Transwell invasion assay experiments (the 'SW620/si‑NC' data panel) shown in Fig. 2F and Fig 6D in the following paper, written by different authors at different research institutes, that had already been published at the time of this paper's submission: Wang D, Yang T, Liu J, Liu Y, Xing N, He J, Yang J and Ai Y: Propofol inhibits the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through miR‑206/ROCK1 axis. Onco Targets Ther 13: 361‑370, 2020. In addition, a potential problem regarding the design of the experiment was noted with the selection of the primers for the amplification of the miRNA miR‑485‑5p. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 44: 2009‑2020, 2020; DOI: 10.3892/or.2020.7758].