Prostate cancer remains one of the most prevalent malignancies and a major cause of cancer‑related mortality among men worldwide. Despite widespread use of prostate‑specific antigen testing, current diagnostic approaches suffer from low specificity and limited ability to distinguish between indolent and aggressive disease, resulting in overdiagnosis and overtreatment. Advances in molecular biology, genomics and metabolomics have led to the identification of novel biomarkers that have potential for improving the precision of prostate cancer diagnosis, prognosis and therapy. The present review provides a comprehensive overview of emerging prostate cancer biomarkers, including genetic (such as , and ), RNA‑based (such as PCA3 and miRNAs), metabolic (such as citric acid and polyamines) and methylation markers (such as , and ). These biomarkers not only enhance diagnostic accuracy but also facilitate risk stratification, prediction of therapeutic response and real‑time disease monitoring through liquid biopsy technologies. Moreover, integrating multi‑omics data with artificial intelligence and machine learning may further improve early detection and personalized treatment strategies. Overall, the development and clinical implementation of these biomarkers represent a transformative step toward precision medicine in prostate cancer, enabling earlier diagnosis, optimized therapy selection and improved patient outcomes.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the Bcl‑2 protein bands shown for the HCC827 cell line in the western blots in Fig. 3A on p. 342 were unexpectedly similar to the Akt protein bands shown for the A549 cell line in Fig. 3B. In addition, the Bcl‑2 protein bands shown for the H358 and HCC827 cell lines (the left‑hand and middle gels) possibly contained a pair of mutually overlapping protein bands, and the β‑actin control bands featured in the left‑hand and middle lanes of Fig. 3A for the H358 and HCC827 cell lines, and the β‑actin control bands featured in the middle and right‑hand lanes for the H358 and HCC827 cell lines in Fig. 1C on p. 340, were similarly more similar than might have been expected. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 35: 337‑345, 2009; DOI: 10.3892/ijo_00000345].

Gastric cancer (GC) is a major global health burden, ranking fifth in incidence and third in cancer‑related mortality. By 2040, there are expected to be ~1.8 million new cases and 1.3 million fatalities associated with GC. Spasmolytic polypeptide‑expressing metaplasia (SPEM) is a central component of gastric precancerous lesions, which remodels the gastric mucosa in response to injury through a lineage of mucus‑secreting cells. Interleukins (ILs) are the communication means for innate and adaptive immune cells as well as non‑immune cells and tissues. Their complex network regulation contributes to the development of SPEM and is a key driver in the transformation of SPEM to GC. The present review systematically described the IL‑related mechanisms underlying the formation and progression of SPEM and categorizes the roles of different ILs by family. In addition, the molecular association between IL dynamics and SPEM following infection is explored, and various SPEM experimental model characteristics and IL‑based therapeutic strategy advances and limitations are discussed. The clinical translation of IL‑targeted therapies is limited, but the development of therapies that target pathogenesis specifically and the enhancement of IL therapy combinations with other therapeutic options may improve efficacy and reduce side effects. Increased understanding of the causes of SPEM and the mechanisms underlying GC may open up new avenues for early detection and targeted therapy.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the transfection experiments shown in Fig. 3 on p. 760, two pairs of data panels showed a surprisingly high level of similarity, such that the data appeared to have been derived from the same original sources where the results from differently performed experiments were intended to have been shown. The authors responded to the reader's concern by providing replacement data for Fig. 3; however, upon performing an independent analysis of the data in this paper in the Editorial Office, it was also noted that western blot data were overlapping in Fig. 4, and for the cell invasion assay experiments shown in Fig. 5, Fig. 5A and B were also found to contain overlapping data, albeit the level of brightness of the images differed. Owing to the large number of duplications of data, and other potential anomalies, that were identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these additional concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 46: 757-763, 2015; DOI: 10.3892/ijo.2014.2748].

Ovarian cancer (OC) is the most lethal disease in women. Resistance to paclitaxel (PTX) is the main cause of treatment failure in patients with OC. The STAT1 protein is a transcription factor implicated in a variety of cellular processes. The present study explored the function and regulatory mechanism of STAT1 in the reversal of PTX resistance and . The OC cell lines SK‑OV‑3 and OVCAR‑3 and their counterpart PTX‑resistant OC cell lines SK3R‑PTX and OV3R‑PTX were applied. The Tet‑On STAT1‑overexpression plasmids were constructed using the technique of the Tet‑On gene expression system and were packaged by lentivirus. RNA and protein were detected by reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis, respectively. OC cell mRNA‑sequencing and subsequent RT‑qPCR verification revealed that STAT1 expression was downregulated in PTX‑resistant cells compared with their sensitive counterparts (P<0.01), except for STAT1β expression in SK3R cells (P>0.05). Cell viability was assessed using a CCK‑8 assay and PTX sensitivity was detected based on their IC values. Overexpression of STAT1 sensitized PTX responses and decreased the tumor volume in xenograft mice. Bioinformatics analysis indicated that STAT1 had favorable effects on the overall survival of patients with OC. Apoptotic cells were detected using flow cytometry. STAT1α overexpression increased the percentage of apoptotic cells to 53.20±0.92 and 36.74±0.77% in OV3R‑PTX and A2780‑PTX cells, respectively, after 1 µM PTX treatment for 24 h. Mechanistically, overexpression of STAT1, especially STAT1α, confirmed by western blot and immunofluorescence staining, induced apoptosis by increasing apoptotic molecules such as Fas cell surface death receptor (FAS) and caspase‑8 (CASP8), which was abolished in the presence of a caspase blocker (Z‑VAD‑FMK). Furthermore, the dual‑luciferase assay confirmed that STAT1 directly bound to the promoter regions of the FAS and CASP8 genes. Thus, the present data demonstrated that STAT1 was a key mediator of the PTX chemotherapy response. Low STAT1 expression was a marker of PTX resistance, whereas overexpression of STAT1 sensitized OC cells to PTX and promoted apoptosis via the FAS/CASP8 signaling pathway. These findings may provide a potential therapeutic strategy to reverse PTX resistance in OC patients by targeting STAT1.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the MTT assay experiments shown in Fig. 2A on p. 1655, the GDC‑0152/ANGPTL2 panel appeared to overlap with the ANGPTL2 panel, albeit the panel had been rotated through 180°; moreover, the magnification of the right‑hand panel was very different, creating an impression that the ANGPTL2 panel showed more cells. Upon analyzing the data independently in the Editorial Office, it came to light that that certain of the flow cytometric data in Fig. 2B and the nuclear staining experiments in Fig. 2C were strikingly similar to data in other articles written by different authors at different research institutes that had already been accepted for publication elsewhere. Owing to the fact that the contentious data in the above article had already been published prior to its submission to , 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. [International Journal of Oncology 46: 1651‑1658, 2015; DOI: 10.3892/ijo.2015.2872].

Cancer stem cells (CSCs), a small subpopulation of cancer cells that exhibit stem‑like properties, possess the ability to differentiate and self‑renew. These capabilities enable CSCs to act as tumor‑initiating cells, driving tumorigenesis and proliferation, leading to major clinical challenges. Specifically, CSCs play a crucial role in metastasis, recurrence and drug resistance, thereby leading to complications in therapeutic responses. The plasticity of CSCs leads to heterogeneity, allowing them to adopt diverse phenotypes in response to intrinsic genetic factors or extrinsic environmental cues. This adaptability may serve as a mechanism for CSCs to thrive in the tumor microenvironment (TME) and promote tumor progression. The present article aimed to review the multifaceted nature of CSCs, examining their functional diversity, biomarkers and interactions with the TME. Through elucidating the mechanisms that underlie this heterogeneity, researchers aim to develop targeted therapeutic interventions against CSCs, thereby enhancing the efficacy of cancer treatments and improving patient outcomes.

Biliary tract cancer (BTC) encompasses a group of aggressive malignancies arising from the bile duct epithelium, including gallbladder cancer and cholangiocarcinoma, which are characterized by aggressive progression, frequent metastases and poor prognoses. BTC accounts for ~3% of all digestive system tumors, with a 5‑year overall survival rate of <20%. BTC presents a clinical challenge. Despite multidisciplinary therapeutic approaches incorporating surgery, chemotherapy and radiotherapy, persistent obstacles, including high tumor recurrence rates (>50%) and the development of treatment resistance remains, underscoring the urgent need for novel treatment strategies such as targeted therapies and immunotherapies. Ferroptosis, a distinct mechanism of regulated cell death triggered by lipid peroxidation, serves critical roles in disease occurrence and progression. Increasing evidence supports the potential of ferroptosis as a targeted therapy in malignancies, with emerging implications for personalized BTC treatment. The present review investigated the molecular mechanisms and signaling pathways that govern ferroptosis, the advances in the understanding of ferroptosis during the initiation and progression of BTC, and the translation potential of ferroptosis for precision therapeutics. By integrating current knowledge, the present study aimed to provide theoretical suggestions for future mechanistic investigations and clinical studies of ferroptosis‑based interventions for patients with BTC.

Gastric cancer (GC) ranks among the most prevalent malignancies worldwide and is associated with high mortality rates. Ephrin‑B2 (EFNB2), a membrane‑bound ligand that interacts with Eph receptor tyrosine kinases, has been implicated in various cancer‑related biological processes; however, its precise role in GC remains poorly understood. By integrating data from multiple public databases with immunohistochemical analyses of tissue microarrays, significant upregulation of EFNB2 expression in GC specimens compared with paired adjacent normal tissue was demonstrated. Elevated EFNB2 levels were associated with the poor overall survival and disease‑free survival in patients with GC. EFNB2 knockdown inhibited cellular proliferation and viability, increased apoptosis, and induced cell cycle arrest at the G/G phase in GC cells. By contrast, EFNB2 overexpression resulted in the opposite oncogenic effects. Mechanistically, rescue experiments identified the Wnt/β‑catenin signaling cascade as the primary molecular pathway mediating EFNB2‑driven tumorigenic effects. These results were further validated using cell‑derived xenograft models, which confirmed the key role of Wnt/β‑catenin pathway activation in EFNB2‑induced tumor progression. Collectively, these results suggested that EFNB2 represents a promising molecular target for therapeutic intervention in GC.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the immunohistochemical data shown in Fig. 2B and C, the PBS/TUNEL panel in Fig. 2B appeared to be strikingly similar to the PBS/E1A panel shown in Fig. 2C. Furthermore, for the E1A experiments portrayed in Fig. 2C, portions of the data panels shown for the H101 and E1A groups also appeared to be strikingly similar, albeit with rotation of one of the panels. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 46: 1759‑1767, 2015; DOI: 10.3892/ijo.2015.2852].

Obesity is a global epidemic strongly associated with increased breast cancer (BC) risk and mortality, particularly in postmenopausal women. Obesity‑induced chronic breast inflammation drives carcinogenesis via dysregulated adipokine signaling (leptin and adiponectin), insulin resistance, hyperinsulinemia and pro‑inflammatory cytokines (TNF‑α and IL‑6). These factors activate oncogenic pathways (NF‑κB and PI3K/AKT/mTOR pathways), which promote DNA damage, cell proliferation and immunosuppression. Clinically, obesity is associated with advanced tumor presentation, reduced treatment efficacy and poorer survival compared with those of normal‑weight patients with BC. Despite progress, the molecular interactions between obesity‑related inflammation and BC remain incompletely understood, and diagnostic/prognostic tools for obese patients require refinement. The present review synthesizes current evidence on obesity‑BC mechanisms and their clinical translation to inform prevention and precision oncology strategies.

Following the publication of the above paper, a potential problem regarding the presentation of the co‑localization experiments shown in Fig. 5A and C was brought to the Editor's attention by a concerned reader. Specifically, the Flotillin/gp91 co‑localization panels (Fig. 5A) appeared to be unexpectedly similar to the Flotillin/p22 panels (Fig. 5C), even though, according to the Materials and methods section, the different antibody treatments that were reported might have precluded the possibility of these images looking so similar. The authors were contacted by the Editorial Office to offer an explanation for this potential anomaly in the presentation of the data in this paper (or to clarify how the experiments had been performed), although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 37: 1483‑1493, 2010; DOI: 10.3892/ijo_00000801].

Transition‑metal nanoparticles (NPs) have been extensively studied owing to their unique physical and chemical properties, ability to form a variety of nanostructures and targeting properties. After surgery, chemotherapy, radiotherapy and targeted therapy, immunotherapy has emerged as a major strategy for cancer treatment. In particular, immune checkpoint inhibition has attracted much attention in preclinical and clinical applications. The combination of transition‑metal NPs with tumor immunotherapy offers great potential. Therefore, the present review focused on four major transition‑metal NPs (Au, Ag, Cu and Fe NPs) and their respective categories, presented their characteristics and roles in the biomedical field and discussed their potential toxicities. In addition, the mechanisms of action of different tumor immunotherapies and the applications of transition‑metal NPs in tumor immunotherapy are discussed. The current status of, and challenges associated, with the clinical transformation of transition‑metal NPs in tumor immunotherapy are described to provide ideas for the subsequent development and clinical application of transition‑metal NPs.

Lung cancer remains a leading cause of cancer‑related death. Despite advances in targeted therapies and immunotherapy, treatment outcomes remain suboptimal due to tumor heterogeneity and therapeutic resistance. The tumor microenvironment (TME), a dynamic ecosystem comprising immune cells, stromal components, extracellular matrix and bioactive molecules, serves a critical role in promoting tumor progression and resistance. The present review comprehensively analyzes the molecular mechanisms underlying TME‑mediated immune evasion, and resistance to chemotherapy, radiotherapy and immunotherapy. In addition, emerging therapeutic strategies targeting the TME are highlighted, such as immune microenvironment modulation, metabolic and epigenetic interventions, and nanotechnology‑based drug delivery systems. By integrating multi‑omics datasets and spatial transcriptomics, TME‑directed interventions are moving toward biomarker‑guided, personalized regimens.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the westen blot data included in Fig. 4C and D looked strikingly similar, such that the same data may have been included more than once in these figure parts to show the results of differently performed experiments. Upon performing an independent analysis of the data in the Editorial Office, it also came to light that data featured in Fig. 3A of the above paper had been re‑used in a figure in a paper featuring some of the same authors that was published in the journal . The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 48: 1985‑1996, 2016; DOI: 10.3892/ijo.2016.3404].

Gastric cancer (GC) has a high incidence, resistance to chemotherapeutic drugs and a bleak prognosis. () can promote GC development through Correa's cascade by impacting various forms of programmed cell death (PCD). As an iron‑dependent form of PCD, ferroptosis has emerged as a major focus in biomedical research. Notably, there have been developments in elucidating the mechanisms underlying ferroptosis dysregulation throughout Correa's cascade. On one hand, targeting ferroptosis may provide a promising direction for the development of drugs for chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). On the other hand, targeting ferroptosis in GC may be a potential option to overcome the challenges in conventional therapies such as resistance to chemotherapy. Consequently, the present review aims to deliver a comprehensive understanding of the mechanisms underlying ferroptosis dysregulation in ‑associated GC and summarize the latest progress of ferroptosis‑related studies in CAG, IM and GC. The present study identifies key regulators of ferroptosis at distinct pathological stages, thereby providing insight of novel strategies for the management of precancerous lesion‑related diseases and GC.

Following the publication of the above paper, it was drawn to the Editor's attention by an interested reader that the middle and right‑hand protein blots shown for the RIPK4 data in Fig. 2B (relating to the PANC‑1‑Rsh1 and PANC‑1‑Rsh2 experiments) were strikingly similar to western blot data shown in Fig. 3B for the RAF‑1 data (and the same PANC‑1‑Rsh1 and PANC‑1‑Rsh2 experiments), albeit the bands were presented with different exposures/a change in contrast, also with apparent horizontal flipping and vertical resizing. Upon contacting the authors, they realized that errors had been made during the assembly of the experimental images presented in Fig. 3B. These errors were likely to have resulted from oversights made during the process of data consolidation and figure assembly; specifically, this led to the inadvertent use of incorrect images for the RAF‑1 western blot results in both the PANC‑1 cell line (as was correctly identified by the interested reader on PubPeer) and in the Capan‑1 cell line (which the authors identified themselves upon performing their own subsequent review). The authors were also able to present photos of the raw, unedited versions of the gels to the Editorial Office. A revised version of Fig. 3, now showing the correct data for the RAF‑1 blots for both the PANC‑1 and Capan‑1 cell lines, as specified above, is shown on the next page. The authors confirm that the errors made in assembling Fig. 3 did not have a major impact on the conclusions reported in the above article, and they thank the Editor of for allowing them the opportunity to publish a Corrigendum. Furthermore, all the authors agree to the publication of this Corrigendum, and apologize to the readers for any inconvenience caused. [International Journal of Oncology 52: 1105‑1116, 2018; DOI: 10.3892/ijo.2018.4269].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the first two lanes of the Actin blot in Fig. 1D looked strikingly similar to the Actin panels in Fig. 2E for the MDA‑MB‑231 cell line, In addition, the Actin panel in Fig. 4A (showing a time series) looked very similar to the Actin panel in Fig. 4B (showing different treatments). Upon analyzing the data independently in the Editorial Office, it came to light that there was an overlapping pair of data panels for the immunohistochemical data shown in Fig. 6C, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original source, and data featured in Fig. 6D had subsequently appeared in a paper published in the journal that was written by different authors at different research institutes. The authors were contacted by the Editorial Office to offer an explanation for these possible anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 48: 2479‑2487, 2016; DOI: 10.3892/ijo.2016.3483].

Breast cancer is characterized by notable heterogeneity and remains one of the leading causes of cancer‑related death among women. Autophagy, a process by which cells use lysosomes to degrade cytoplasmic proteins and damaged organelles, is not only associated with chemotherapy resistance, but is also involved in immune‑mediated tumor cell killing and immune evasion, making it a promising target for cancer therapy. Pharmacological inhibition of autophagy in breast cancer cells suppresses tumor progression. In the present study, the small molecular compound FZU‑0045‑053 (053) was identified, which exhibited autophagic and immunomodulatory effects. The effect of 053 on autophagy regulation in breast cancer cells was evaluated using transmission electron microscopy, an mRFP‑GFP‑ microtubule‑associated protein 1 light chain 3 (LC3) tandem fluorescent adenovirus, the CYTO‑ID Autophagy Detection Kit and western blot analysis. Cell viability was subsequently assessed with proliferation assay and ATP assay kits. Apoptosis induction and the expression of immune‑related molecules were measured by flow cytometry. Furthermore, a triple‑negative breast cancer mouse model was established to validate the antitumor and autophagy‑modulating effects of 053 using immunofluorescence and immunohistochemical staining. Finally, a 4T1 syngeneic mouse model was utilized to corroborate the immunomodulatory effects of 053 through immunohistochemistry and flow cytometric analysis. The findings indicated that 053 regulated autophagy in the breast cancer cell lines MDA‑MB‑231 and MCF‑7, similar to the late autophagy inhibitor chloroquine. This regulation resulted in the accumulation of autophagic substrates, specifically LC3‑II and sequestosome 1, by blocking autophagic flux. By blocking autophagy flux, 053 suppressed proliferation, induced apoptosis and ultimately restored chemosensitivity in MDA‑MB‑231 cells. In addition, the MDA‑MB‑231 xenograft model indicated that 053 inhibited autophagy by blocking autophagic flux, which lead to the accumulation of LC3 and sequestosome 1. 053 also negatively regulated the expression of programmed death‑ligand 1 (PD‑L1) in tumor cells. The 4T1 xenograft model showed that 053 had a notable immune‑promoting effect, whereby it not only negatively regulated the expression of PD‑L1 in tumor cells but also modulated T cell activation and proliferation by downregulating the expression of co‑inhibitory molecules (T‑cell immunoglobulin and mucin‑domain containing‑3 and programmed cell death protein 1) on T cells and upregulating co‑stimulatory molecules (4‑1BB, OX40 and inducible T‑cell co‑stimulator). xenograft models demonstrated that 053 had notable antitumor effects and high biosafety, with improved antitumor efficacy when combined with the chemotherapy drug gemcitabine. In summary, 053 can block autophagy and promote antitumor immune responses, showing promise as a new generation of adjuvant drugs for tumor chemotherapy and immunotherapy.

Hepatocellular carcinoma (HCC) continues to rank as a predominant contributor to cancer‑related mortality on a global scale, attributed to its insidious onset and unfavorable prognosis. The ribosomal protein lateral stalk subunit P0 (RPLP0) has recently gathered widespread attention as a crucial factor in the pathological progression of various neoplasms; however, its exact role in HCC remains inadequately defined. Consequently, the present study endeavored to shed light on the function and mechanistic underpinnings of RPLP0 in HCC and assess its clinical significance and potential as a therapeutic target. qPCR and western blot analyses indicated that RPLP0 was markedly upregulated in HCC, with its elevated levels correlating with poorer survival outcomes. Silencing RPLP0 expression suppressed the proliferative, invasive, migratory, and epithelial‑mesenchymal transition (EMT) abilities of HCC cells, while concurrently promoting apoptosis, autophagy, and G/M cell cycle arrest, as evidenced by CCK‑8, colony formation, Transwell assays and flow cytometry analysis, respectively. Moreover, the findings revealed that RPLP0 downregulation mediated the suppression of the JAK2/STAT3 pathway through reactive oxygen species (ROS) accumulation, which in turn downregulated c‑Myc expression. Furthermore, chromatin immunoprecipitation and dual luciferase assays demonstrated that c‑Myc directly bound to the promoter sequence of RPLP0, thereby augmenting its transcriptional activity. In summary, the current study highlighted that RPLP0 establishes a feedback circuit with c‑Myc by facilitating JAK2/STAT3 pathway activation through suppressing ROS levels, while c‑Myc reciprocally activates RPLP0, forming a regulatory circuit loop that drives HCC progression. Thus, targeting the c‑Myc/RPLP0/ROS/JAK2/STAT3 axis emerges as a promising therapeutic strategy for the management of HCC.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the cell invasion assay experiments shown in Fig. 4B, the 'Con' and 'LPA+HF' data panels contained an overlapping section, such that data which were intended to show the results of differently performed experiments appeared to have been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further.  [International Journal of Oncology 44: 309‑318, 2014; DOI: 10.3892/ijo.2013.2157].