Carcinoma esophagus is an aggressive malignancy with high recurrence rates even after curative resection. This study aimed to evaluate recurrence patterns-both locoregional and systemic-after curative esophagectomy and to identify clinical and pathological predictors of recurrence to guide post-treatment surveillance and therapeutic strategies.

Amino acids are fundamental biomolecules that constitute the building blocks of proteins. Monitoring their dysregulation and fluctuations serves as an important indicator of human health. The aim of this study is to explore the role of exogenous amino acids metabolism in colon cancer development. Raman spectroscopy and Raman imaging were employed to investigate biochemical changes in normal human colon cells (CCD-18Co) and cancerous colon cells (Caco-2), both untreated and supplemented with leucine, threonine, and arginine. Spectroscopic data were analyzed using chemometric methods, specifically Partial Least Squares Discriminant Analysis (PLS-DA). Raman spectroscopy, combined with chemometric approach, identified unique Raman biomarkers - 1088/1262, 1444/1660, 1580/1004, and 1630/1444 - that correspond to changes in nucleic acids, lipids/lipids+Amide I, proteins, and lipids, respectively, in both normal and cancer cells supplemented with amino acids. These findings underscore the significant potential of Raman spectroscopy and Raman imaging as powerful tools for investigating the role of exogenous amino acids in colon cancer progression. We have also shown that the S₁-state lifetime of tetra-sulphonated aluminum phthalocyanine remains unaffected by amino acid supplementation, as confirmed by femtosecond transient absorption spectroscopy, supporting its stability as a photosensitizer for photodynamic therapy.

Gains of chromosome 12p11.21, encoding for the cancer-specific lncRNA LISRR, correlate with poor survival across different cancers. In melanoma, LISRR is upregulated in immunotherapy-resistant patients to contribute to the generation of drug-tolerant cells by activating an immune-suppressive translational program, affecting the synthesis of PD-L1 and of the glycocalyx. Accordingly, downregulation of LISRR initiates robust immune responses and resensitizes to immunotherapy ex vivo and in vivo. The use of glycans to evade immunity exhibits shared characteristics with the testis, where defects in the glycocalyx cause infertility. Mechanistically, we showed that LISRR affects the ribosome core composition and recruits deleted in azoospermia-associated protein 1 to polysomes to prime the integrated stress response. Our study reveals the contribution of lncRNAs to the generation of cancer-specific ribosomes and identifies an RNA-based strategy to overcome resistance to immune checkpoint blockade.

Decreased tobacco use has resulted in substantial declines in the prevalence of upper aerodigestive tract malignancies. However, the prevalence of oral cavity squamous cell carcinomas has been steadily increasing despite decreases in tobacco-related malignancies both within the United States and worldwide. The cause driving the increasing prevalence is unknown and may reflect a combination of viral, environmental, and genetic mechanisms. Radiologists must be familiar with the imaging appearance of oral cavity carcinomas to achieve proper staging and to guide surgical and/or radiation therapy management. This article will review the emerging trends in oral cavity carcinoma, the basics of oral cavity anatomy relevant to subsites of cancer involvement, the imaging appearance of this entity, and the information critical for appropriate staging to direct surgical management, medical treatment, and/or radiation therapy. Keywords: Ear/Nose/Throat, Head/Neck, Tongue, Neoplasms-Primary, Oncology, CT, MR Imaging, Diagnosis, PET/CT, PET/MRI © RSNA, 2025.

Glioblastoma multiforme (GBM), the most invasive primary malignant tumor of the central nervous system, is characterized by an extremely poor prognosis and a high recurrence rate. Its significant molecular heterogeneity challenges precise diagnosis and treatment. Recently, with the rapid development of molecular pathology, the combination of histological and molecular typing has become the mainstream method for GBM diagnosis. Here, we review the impact of classic molecular markers on patient prognosis in GBM, as well as the different values of traditional and novel molecular markers in prognosis assessment. We initially discuss the correlation between molecular markers and recurrence, as well as the research progress of molecular markers in emerging technological fields. Moreover, we propose the challenges currently faced by molecular markers in glioblastoma and discuss future research directions in this field.

The divergent loop structures of nicotinic acetylcholine receptor (nAChR) α3, α5, and α7 subunits (encoded by CHRNA3, CHRNA5, and CHRNA7) are involved in kinase phosphorylation and signal transduction, potentially affecting oral squamous cell carcinoma (OSCC), the most common head and neck cancer (HNC). However, their specific roles in OSCC remain unclear.

Lung and small cell neuroendocrine carcinomas (SCCs) are the most common sites and histological types of high-grade neuroendocrine carcinoma (NEC). Comprehensive epidemiological information on NECs is limited. We used the Taiwan Cancer Registry database to analyze the nationwide epidemiology and clinical outcomes of NECs in Taiwan.

Treatment for metastatic colorectal cancer (mCRC) has seen great advances but may not be equally available for all patients.

Gastric cancer (GC) has a high incidence, resistance to chemotherapeutic drugs and a bleak prognosis. Helicobacter pylori (H. pylori) 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 H. pylori‑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.

The thioredoxin (Trx) system comprises four core components: Trx‑interacting protein (TXNIP), Trx, Trx reductase (TrxR) and NADPH. TrxR utilizes NADPH to reduce Trx, reducing target proteins through its conserved thiol groups, thereby maintaining cellular redox balance. TXNIP inhibits Trx activity by forming a disulfide exchange reaction with Trx. Beyond its role in redox regulation, the Trx system interacts with various cellular regulators and participates in intracellular signaling networks. The Trx system exhibits dual regulatory roles in autophagy, with Trx primarily exerting an inhibitory effect on ferroptosis and apoptosis, whereas TXNIP promotes these processes. Multiple molecular mechanisms are implicated in these regulatory functions. Furthermore, the Trx system mediates cross‑regulation between autophagy and ferroptosis, as well as autophagy and apoptosis, thereby influencing cellular responses to stress conditions. The present review examines the structural components of the Trx system and the cellular translocation of TXNIP. Additionally, it explores the involvement of the Trx system in various diseases, including neurodegenerative disorders, cardiovascular diseases and cancer, highlighting its potential as a therapeutic target. By analyzing the molecular mechanisms through which the Trx system modulates cell death pathways, including ferroptosis, autophagy and apoptosis, the present review may provide novel research perspectives and theoretical foundations for developing disease treatment strategies.

The present study aimed to investigate the effect of microRNA (miR)-199a-3p on the biological function of non-small cell lung cancer (NSCLC) adenocarcinoma cells by targeting the fat mass and obesity‑associated protein (FTO)/myeloid zinc finger 1 (MZF1)/claudin domain‑containing 1 (CLDND1) axis. Human NSCLC cell lines, primarily A549 cells, were used for in vitro assays. Reverse transcription‑quantitative PCR and western blotting were performed to assess the expression of relevant genes and proteins. Dual‑luciferase reporter assays were used to verify the relationship between miR‑199a‑3p and FTO, as well as the transcriptional regulation of CLDND1 by MZF1. Methylated RNA immunoprecipitation was used to evaluate the N6‑methyladenosine (m6A) modification levels of MZF1, whereas photoactivatable ribonucleoside‑enhanced crosslinking and immunoprecipitation supported the binding of FTO to MZF1 mRNA. Cell proliferation, migration, invasion and apoptosis were assessed using Cell Counting Kit‑8, Transwell and flow cytometry assays. miR‑199a‑3p was downregulated in NSCLC tissues and cells. Overexpression of miR‑199a‑3p inhibited A549 cell proliferation, invasion and migration. Mechanistically, miR‑199a‑3p directly targeted and suppressed FTO, an m6A demethylase, leading to enhanced m6A modification of MZF1 mRNA and a subsequent decrease in MZF1 expression. Knockdown of MZF1 attenuated the oncogenic effects mediated by FTO, confirming that MZF1 served as a downstream effector of the miR‑199a‑3p/FTO axis. Moreover, MZF1 transcriptionally activated CLDND1, thereby facilitating the malignant phenotype of NSCLC cells. Collectively, these findings demonstrate that miR‑199a‑3p suppresses NSCLC progression by targeting FTO, promoting m6A methylation‑dependent downregulation of MZF1, and consequently decreasing CLDND1 expression. Thus, the miR‑199a‑3p/FTO/MZF1/CLDND1 axis may serve as a promising therapeutic target in NSCLC.

Amino acid (AA) sensing plays an important role in maintaining cellular metabolic homeostasis as well as tumorigenesis and progression. Studies on classic AA sensing pathways such as rapamycin complex 1 (mTORC1) and general control nonderepressible 2 (GCN2) have revealed their central position in cancer metabolic reprogramming. AA sensing pathways are often hijacked in tumors to adapt to the nutrient‑deprived microenvironment, promoting cell proliferation, anti‑apoptosis and treatment tolerance. In addition, the regulation of AA sensing and transport plays a crucial role in maintaining the metabolic flexibility of tumor cells. By targeting the AA sensing mechanism, it is expected to disrupt the metabolic homeostasis of cancer cells, providing new strategies for precision therapy. The present review summarized the latest advances in the research on the role of the mTORC1 and GCN2 AA sensing pathways in tumor metabolism, emphasizing their potential and the challenges faced in cancer diagnosis and treatment. Additionally, it provided novel insights into the therapeutic targeting of AA sensing pathways and proposes future research directions aimed at overcoming current limitations in cancer metabolism therapy.

The present study investigated the effects of Notoginsenoside R1 (NG‑R1) on human non‑small cell lung cancer (NSCLC) A549 cells and explored its potential mechanisms. Cell viability was assessed using the MTT assay after 72 h of treatment with varying concentrations of NG‑R1 (0.1, 0.2, 0.4, 0.8, 1.6 and 2 mg/ml), which inhibited A549 cell viability in a dose‑dependent manner. Cell proliferation, migration and invasion were evaluated using the BeyoClick™ EdU‑594 proliferation assay, wound healing assay and Matrigel®‑coated Transwell invasion assay, respectively. NG‑R1 at concentrations of 0.4, 0.8 and 1.6 mg/ml significantly suppressed proliferation, migration and invasion of A549 cells compared with the control. In addition, these doses of NG‑R1 increased intracellular reactive oxygen species (ROS) levels as measured using the fluorescent probe 2',7'‑dichlorofluorescein diacetate. Western blot analysis revealed that treatment with NG‑R1 (0.4, 0.8 and 1.6 mg/ml) upregulated the expression of the ferroptosis‑related protein transferrin receptor 1, and downregulated solute carrier family 7 member 11, glutathione peroxidase 4 and ferritin heavy chain 1. Collectively, these findings indicate that NG‑R1 inhibited the proliferation of NSCLC A549 cells, likely through the induction of ROS accumulation and ferroptosis.

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 Tumor Biology 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 (BC) ranks among the most prevalent malignant tumors in female patients. It represents a longstanding challenge to medical professionals in terms of diagnosis and treatment. Exploring BC pathogenesis offers insight into its complexity and facilitates the exploration of more effective treatment strategies. The present review aimed to describe the involvement of the immune system, inflammatory response and regulated cell death in BC development, offering avenues for novel therapeutic strategies against BC. Identifying novel treatment methods is key for enhancing the prognosis of patients with BC.

Schisantherin A (Sch A), a compound derived from Schisandra chinensis, has anti‑inflammatory, antitumor, neuroprotective and antifibrotic properties. However, to the best of our knowledge, the role of Sch A in non‑small cell lung cancer (NSCLC) has not yet been reported. The purpose of the present study was to determine whether Sch A can prevent the development of NSCLC and to elucidate the underlying mechanisms involved. The results of the present study demonstrated that Sch A inhibited the viability of A549 and HCC827 cells. Furthermore, Sch A increased the intracellular Fe2+ level, reduced the mitochondrial membrane potential and depleted the glutathione content in lung cancer cells. These effects were reversed by the ferroptosis inhibitors ferrostatin‑1 and deferoxamine. Bioinformatics analysis and reverse transcription‑quantitative PCR results suggested that Sch A increased the mRNA levels of the transcription factor yes‑associated protein (YAP). Additionally, Sch A upregulated the expression of YAP and ferroptosis‑related proteins, including acyl‑CoA synthase long‑chain family member 4 (ACSL4) and transferrin receptor (TfR), in lung cancer cells. Silencing of YAP led to the downregulation of its downstream targets, ACSL4 and TfR, even in the presence of Sch A. In vivo, Sch A significantly inhibited subcutaneous tumor growth in nude mice. In conclusion, Sch A may activate the YAP/ACSL4/TfR signaling axis to induce ferroptosis in NSCLC cells, positioning it as a potential small‑molecule therapeutic agent for NSCLC.

To assess whether miRNA expression can be a biomarker for distinguishing between hyperplastic and adenomatous polyps and colon cancer tissues.

Ovarian cancer is one of the most malignant tumors in women. Long noncoding RNAs have been demonstrated to regulate multiple biological processes, including cell proliferation, migration, apoptosis, and drug resistance, in various cancers. Small nucleolar RNA (snoRNA) host genes (SNHGs) are a group of long noncoding RNAs. Studies have reported that SNHGs are aberrantly expressed in many kinds of cancers and are associated with poor patient prognosis. In ovarian cancer, SNHGs play critical roles in the development and progression of ovarian cancer via different pathways. However, there is a lack of systematic reports on the research progress of SNHGs in ovarian cancer. Therefore, we reviewed the studies on the roles of SNHGs in the early diagnosis, development, and treatment of ovarian cancer and explored the underlying mechanisms to provide new insights into the treatment of ovarian cancer.

Breast cancer is the leading cause of cancer-related mortality in women, with triple-negative breast cancer (TNBC) being an aggressive subtype associated with poor prognosis and limited treatment options. TNBC is known for its immunogenic characteristics, including high genetic instability and elevated tumor-infiltrating lymphocytes (TILs). Immune checkpoint inhibitors (ICIs) have shown efficacy in TNBC treatment, but the optimal treatment duration in case of prolonged response remains unclear.

Regulatory T cells (Tregs) are highly enriched in the metabolic dysfunction-associated steatotic liver disease (MASLD) microenvironment, but their role in driving metabolic dysfunction-associated steatohepatitis (MASH) progression to hepatocellular carcinoma (HCC) remains unclear. Here, it is demonstrated that integrin β1 (ITGβ1, CD29) expression is upregulated by Tregs, enhancing cell adhesion and driving the malignant transformation of MASLD.