Pancreatic ductal adenocarcinoma (PDAC) resistance to oxaliplatin is associated with diminished drug uptake and a poor molecular apoptotic response; however, the relative contribution of each of these modes of resistance remains unclear. Accordingly, PDAC cell lines (AsPC‑1 and BxPC‑3) and human patient‑derived organoids (hPDOs; h08 and h19) were assessed in the present study, with proliferation assays, atomic absorption spectroscopy‑based quantification of intracellular oxaliplatin, luminogenic caspase 3/7 assays, PCR array‑based transcriptomic analysis and RNA sequencing performed to scrutinize the oxaliplatin resistance phenotype. Notably, AsPC‑1 cells [half maximal inhibitory concentration (IC50), 88.8±45 µM were 4.2‑fold more oxaliplatin resistant than BxPC‑3 cells (IC50, 21±0.7 µM; P=0.02)]. In addition, when normalized to intracellular platinum levels, AsPC‑1 cells remained 2.5‑fold more resistant than BxPC‑3 (the fold difference was decreased by 40% from 4.2‑fold to 2.5‑fold; P=0.21). In hPDOs, resistant h19 took up oxaliplatin 22% less efficiently than sensitive h08, and the nominal resistance difference was 3.5‑fold, and it remained at 2.8‑fold after controlling for drug accumulation (the fold difference was decreased by 20% from 3.5‑fold to 2.8‑fold; P=0.34). These findings indicated that diminished drug uptake non‑significantly contributed to oxaliplatin resistance, which was in agreement with the rather minor differences in drug transporter expression levels (including ATP7A and ATP7B). Furthermore, when challenged with identical intracellular oxaliplatin levels, AsPC‑1 cells exhibited delayed caspase 3/7 activity initiation, weaker induction of pro‑apoptotic genes BBC3 (1.7‑fold vs. 5‑fold) and PMAIP (2.5‑fold vs. 6‑fold), but stronger enhancement of anti‑apoptotic Jun expression (7‑fold vs. 3‑fold) than BxPC‑3 cells. Taken together, oxaliplatin resistance in PDAC models may be highly linked to a poor apoptotic response, whereas drug uptake seems to be of minor relevance.

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].

Glioblastoma (GBM), the most common type of primary malignant brain tumor, is characterized by aggressive cancer cells that contribute to infiltrative growth, thus resulting in therapeutic challenges and a poor prognosis. To explore the molecular mechanisms underlying cell motility and to identify therapeutic targets that may intervene in tumor invasion, public databases were used to investigate the S100B expression profile and the prognosis of patients with tumors. The effects of S100B on a GBM cell line were assessed through lentiviral transduction, as well as cell viability, colony formation, 5‑ethynyl‑2'‑deoxyuridine‑based cell proliferation, cross‑scratch, and Transwell migration and invasion assays. In addition, a tumor xenograft model was constructed to analyze tumor growth in vivo. Reverse transcription-quantitative PCR, western blotting and immunofluorescence staining were utilized to explore the molecular biological mechanisms of the TGF‑β2‑induced epithelial‑mesenchymal transition (EMT) in the S100B‑downregulated group. The findings demonstrated that S100B was significantly upregulated in GBM samples and was strongly associated with patient prognosis. In vitro and in vivo experiments confirmed that downregulation of S100B effectively suppressed the proliferation and tumorigenicity, as well as decreased the invasive and migratory capabilities of LN229 glioblastoma cells. Further investigation revealed that the inhibition of S100B resulted in downregulation of TGF‑β2 expression and reversal of the EMT process. Notably, recombinant TGF‑β2 restored the cell motility and EMT capacities attenuated by the downregulation of S100B. In conclusion, the present study revealed that S100B may induce the invasion and migration of GBM cells through TGF‑β2‑induced EMT, providing novel insights and potential therapeutic targets for GBM.

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 G0/G1 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 in vivo 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.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality, with limited curative options for advanced disease. Natural Killer (NK) cells are critical innate immune effectors, but their anti-tumor function is severely compromised by the immunosuppressive tumor immune microenvironment (TIME), particularly through transforming growth factor-beta (TGF-β). This study investigates the pivotal role of TGF-β signaling in modulating NK cell phenotypes and functions within the HCC TIME.

Human leukocyte antigen G (HLA-G) can induce tumor immune escape, facilitating tumor progression. Extracellular vesicles (EVs) are also involved in tumor progression, due to its activity on metastatic niche preparation and immune system modulation. However, the role of EVs bearing HLA-G, on its surface or cargo, is still few explored.

Tumor-associated macrophages (TAMs) shape the tumor microenvironment and drive hepatocellular carcinoma (HCC) progression. However, the prognostic significance of TAM polarity-related genes, particularly based on the CXCL9:SPP1 signature, remains unclear.

This study aimed to assess the value of preoperative [68Ga]Ga-FAPI-04 positron emission tomography (PET) for evaluating pathological complete response (pCR) in patients with gastrointestinal adenocarcinomas receiving neoadjuvant therapy (NAT).

Effective anti-tumor immunity critically depends on functional CD8+ T cells, yet in almost all solid tumors, these cells become dysfunctional, exhausted, or spatially excluded. This breakdown of immune surveillance arises not only from cell-intrinsic T cell exhaustion but also from multimodal communication among tumor, stromal, and immune cells within the tumor microenvironment (TME). This communication is mediated not only through direct receptor-ligand interactions but also through a suite of indirect mechanisms, such as metabolic competition, secretion of immunosuppressive metabolites and cytokines, extracellular vesicle exchange, and even mitochondrial transfer via tunneling nanotubes or membrane transfer through T cell trogocytosis. Together, these suppressive interactions impair CD8+ T cell metabolism, effector function, and persistence, thereby enabling tumor immune evasion. In this review, we summarize current understanding of how multimodal cell-cell communication, including immune checkpoints, metabolic reprogramming, and stromal crosstalk, cooperatively drive CD8+ T cell dysfunction. We also highlight emerging therapeutic strategies aimed at rewiring these suppressive networks, with emphasis on translational potential. A deeper understanding of the spatial, molecular, and metabolic context of CD8+ T cell suppression offers new avenues to enhance the efficacy of cancer immunotherapies.

Solute carrier family 2 member 3 (SLC2A3), a key glucose transporter, has been implicated in tumor metabolism and immune regulation, but its specific role in kidney renal clear cell carcinoma (KIRC) remains largely unclear.

By stabilizing actin filaments and recruiting non-muscle myosin II, the closely related tropomyosin (Tpm) isoforms Tpm3.1 and Tpm3.2 support actin-dependent processes including membrane dynamics, cell migration, and cytokinesis. Actin dynamics are essential for B cell function, but the roles of Tpm3.1 and 3.2 (collectively termed Tpm3.1/3.2) in B cells have not been explored. Moreover, new treatments are needed to limit the growth and dissemination of diffuse large B-cell lymphoma (DLBCL), the most prevalent B-cell malignancy.

Small cell lung cancer (SCLC) is challenging to manage due to its high malignancy and early metastatic spread. Although initial chemoradiotherapy responses are common, resistance rapidly develops, and long-term efficacy remains limited. Immune checkpoint inhibitors (ICIs) overcome previous survival barriers, extending overall survival (OS) and progression-free survival (PFS) in extensive-stage SCLC. Nevertheless, absolute clinical benefits remain modest. To address efficacy limitations, current research focuses on optimizing first-line strategies by exploring multimodal regimens (e.g., adding targeted therapy or radiotherapy to chemoimmunotherapy) and advancing molecular subtyping for precision oncology. Furthermore, emerging therapies such as DLL3-targeted agents, bispecific antibodies (bsAbs), antibody-drug conjugates (ADCs), and chimeric antigen receptor T-cell (CAR-T) therapy continue to demonstrate clinical progress. This review synthesizes advances in SCLC management, focusing on mechanisms and clinical applications of multimodal strategies and novel therapies. It provides guidance for clinical decisions, research directions, and survival improvement.

Conventional open thyroidectomy (COT) results in visible neck scarring. Transaxillary endoscopic thyroidectomy (TET) comprises gasless (suspension-assisted) and gas-inflated approaches, both of which offer superior scar concealment. This study aimed to compare the efficacy and safety of these two endoscopic techniques for treating papillary thyroid carcinoma (PTC).

This study investigates the relationship between the systemic immune-inflammation index (SII) and all-cause mortality (ACM) risk in individuals with stages IIIB-IV epidermal growth factor receptor (EGFR)-mutated lung adenocarcinoma.

Bone metastases (BM) are a frequent and clinically relevant manifestation in patients with metastatic pheochromocytomas and paragangliomas (mPPGL).

The prognosis for patients with hepatocellular carcinoma (HCC) remains suboptimal, despite the rapid advancement of anti-cancer immunotherapy. Chimeric antigen receptor (CAR) T cell therapy targeting glypican-3 (GPC3) has been developed for HCC; however, clinical trials have demonstrated heterogeneous responses among patients and limited CAR-T cell infiltration. Locoregional administration has emerged as a promising strategy for CAR-T therapy against solid tumours, yet its potential for HCC treatment has not been thoroughly explored.

Follicular dendritic cell sarcoma (FDCS) is an uncommon malignant neoplasm that arises from follicular dendritic cells (FDCs). The mediastinum is a more unusual site of FDCS. In this document, we detail a case involving the complete surgical removal of FDCS located in the mediastinum. A 28-year-old woman presented with symptoms of right chest pain. Accompanying symptoms include chest tightness, shortness of breath, and faintness. Chest computed tomography was performed and revealed abnormal enhancement in the mediastinal region. An excisional biopsy was carried out, and through the aid of immunohistochemistry (IHC), a diagnosis of FDCS was confirmed. Following surgery, the patient underwent radiotherapy for 27 sessions. The patient was followed up by the oncology service for 6 years and was still alive at the time of drafting this report. This exceedingly uncommon case underscores the challenges in making a differential diagnosis and emphasizes the significance of diagnostic indicators, including histopathology and IHC, in establishing a diagnosis. Clinicians should be alert to the possibility of encountering this disease and take into consideration various characteristics to avoid misdiagnosis.

Non Hodgkin's Lymphoma (NHL) consists of heterogeneous group of malignant lymphoid neoplasms that are closely related, but present a gamut of morphological, genetic and clinical features. In India, age adjusted incidence rate for NHL was found out to be 2.9/100000 in men and 1.5/100000 in women.

Despite guideline-directed therapies, most patients with advanced oesophageal squamous cell carcinoma (ESCC) derive limited benefit and are unable to tolerate iterative treatment modifications. Therefore, timely identification of resistant cases and the provision of alternative therapeutic options are urgently needed.

Cell death is a fundamental process essential to all living organisms, with apoptosis serving as one of the most crucial pathways across various stages of life. Dysregulation of apoptosis is closely associated with numerous diseases, particularly cancer. PUMA (p53 upregulated modulator of apoptosis) is a key mediator of apoptotic cell death. It is activated in response to a wide range of internal and external signals. Beyond its established role in apoptosis, PUMA also regulates other forms of cell death, including necroptosis, autophagy, and ferroptosis, underscoring its critical role in cancer cell death, especially during chemotherapy. However, PUMA activation is frequently impaired in many cancers, leading to resistance to cell death and treatment failure. This review highlights recent advancements in understanding the regulation of PUMA expression at multiple levels, including epigenetic, transcriptional, post-transcriptional, and post-translational mechanisms. It also examines the influence of diverse cellular regulators, such as epigenetic modifiers, transcription factors, non-coding RNAs, kinases, and ubiquitin ligases in modulating PUMA activity. Additionally, we discuss PUMA's role in cancer progression, its impact on the effectiveness of anti-cancer therapies, and its potential as a prognostic biomarker for therapeutic resistance. Finally, we propose critical questions to inspire future research, aiming to deepen the understanding of PUMA regulation and its significance in cancer therapy.