Discover Oncology

Our medical research library holds 13 studies published in Discover Oncology (2022–2026). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 13 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Springer
• Published: 2021 to the present, United States
• Language: English
• ISSN: 2730-6011 (electronic)
• Continues: Hormones and Cancer
• Its record in the NLM Catalog

2020s

• An analysis of succinate dehydrogenase B in pleural mesothelioma. C.J. Jennings, S.J. Marciniak, G. Pinton, et al. 2026;17(1). PubMed · Publisher · Free full text

  Abstract

  Aim: To investigate the expression of succinate dehydrogenase B and its potential as a therapeutic target in pleural mesothelioma (PM).

  Methods: The expression of succinate dehydrogenase B was examined in cell lines using PCR. The expression of succinate dehydrogenase B mRNA was subsequently examined in a series of fresh-frozen primary patient samples using reverse transcription polymerase chain reaction. The expression of succinate dehydrogenase B protein was examined by immunohistochemistry on a pleural mesothelioma tissue microarray derived from Formalin-Fixed and Paraffin-Embedded specimens to determine if succinate dehydrogenase B expression correlated with survival benefit. Using a resazurin-based assay we examined whether targeting the mitochondrial complex II (containing succinate dehydrogenase B) with a chemical inhibitor could have effects on cell proliferation.

  Results: Total ribonucleic acid was isolated from a panel of mesothelial-derived cell lines (both cancerous and non-cancerous), and expression of succinate dehydrogenase B messenger RNA was assessed by RT-PCR and found to be ubiquitously expressed. Total Ribonucleic acid was isolated from a panel of fresh-frozen surgical specimens, and succinate dehydrogenase B was significantly overexpressed in mesothelioma at the messenger RNA level. Immunohistochemical staining and analysis of a mesothelioma tissue microarray showed that expression did not correlate with any survival benefit, confirmed by in silico analyses of other datasets. However, links between DNA methylation at individual residues of the succinate dehydrogenase B gene and overall survival were identified, along with correlations to immune cell infiltrates. Targeting the mitochondrial complex II with oxaloacetic acid did not show any significant potential for higher efficacy in cell lines derived from malignant tumors compared to those derived from normal mesothelial cells.

  Conclusions: Our results demonstrate that succinate dehydrogenase B is overexpressed in PM but may not be a suitable candidate for therapeutic targeting in this disease.

  © 2026. The Author(s).

• Comprehensive pan-cancer analysis of FSCN1 as a marker for prognosis and immunity. R. Xu, W. Xu, C. Dong, et al. 2026;17(1). PubMed · Publisher · Free full text

  Abstract

  BACKGROUND: Fascin actin-bundling protein 1 (FSCN1), a member of actin cytoskeletal protein family genes, plays critical roles in cell migration, motility, adhesion, and other cellular interactions. It has shown its ascending importance in tumors of multiple systems, including the nervous system, respiratory system, digestive system and urinary system. Nevertheless, no systematic pan-cancer analysis has been carried out to investigate its function in diagnosis, prognosis, and immunological prediction. METHODS: We used UCSC Xena, The Cancer Genome Atlas (TCGA), Genotype Tissue Expression Project (GTEx), Human Protein Atlas (HPA), cBioPortal, STRING, Cancer single-cell state Atlas (CancerSEA), Genomics of Drug Sensitivity in Cancer (GDSC) and Xiantao Academic analysis tool websites and databases for the extraction of pan-cancer data on FSCN1. We adopted bioinformatics methods to explore the potential role of FSCN1 in pan-cancer, including analysis of the correlation between FSCN1 and clinicopathologic features, prognosis, genetic alteration, immune, DNA methylation, single cell function and drug sensitivity. Furthermore, a protein–protein interaction network was drawn, and gene set enrichment analysis was conducted to explore the functions of FSCN1. Finally, we validated the effects of FSCN1 on cell proliferation and apoptosis through experiments. RESULTS: The findings of the comprehensive pan-cancer analysis revealed that FSCN1 was highly expressed in most cancers, except in acute myeloid leukemia, prostate adenocarcinoma and thyroid carcinoma, and it has a certain diagnostic and prognosis value in many cancers. Furthermore, FSCN1 expression was found to correlate with immune cell infiltration, immune checkpoint (ICP) genes expression, DNA methylation and drug sensitivity in a variety of cancers. In addition, we discovered that FSCN1 participated in the proliferation and DNA repair at the single-cell level. Besides, Gene function enrichment analyses revealed that genes that were co-expressed with FSCN1 were enriched within the actin filament regulation pathways. CCK-8 assay and flow cytometry apoptosis assay results indicated that FSCN1 knockdown inhibited proliferation and induced apoptosis in mesothelioma (MESO). CONCLUSION: FSCN1 is a prospective marker for the diagnosis, prognosis, immunology, chemotherapy, and small molecular drugs targeted for pan-cancer treatment.

• Construction and validation of a prognostic risk score model for malignant mesothelioma. Q. An, F. Cui, G. Shi, et al. 2026;17(1). PubMed · Publisher · Free full text

  Abstract

  PURPOSE: Malignant mesothelioma is a rare, aggressive cancer. Although the World Health Organization (WHO) histologic subtypes–epithelioid (best prognosis), biphasic, and sarcomatoid (worst prognosis)—provide baseline stratification, architectural and molecular features (e.g., aneuploidy, immune infiltration) introduce heterogeneity not fully captured by histotype alone. METHODS: Using The Cancer Genome Atlas (TCGA) data and an independent validation cohort, we found that TNM stage was not independently prognostic after multivariable adjustment. We therefore developed a clinicomolecular model integrating transcriptomic and clinicopathological variables. Differential expression analysis of TCGA tumors identified 1,055 genes associated with poor prognosis (FDR < 0.05, |log2FC| > 1). Least absolute shrinkage and selection operator (LASSO) followed by multivariate Cox regression yielded five independent predictors: pathological subtype, receipt of pharmaceutical (systemic) therapy, and tumor expression of SPAG5, CORO1C, and SGCE. The final score was: RiskScore = 1.590 × (pathological type) − 2.258 × (pharmaceutical therapy) + 3.048 × SPAG5 + 1.652 × CORO1C + 0.908 × SGCE. RESULTS: In the TCGA cohort, high-risk patients had significantly shorter overall survival (log-rank p < 0.001), and time-dependent ROC AUCs exceeded 0.70 at 1–5 years. In the validation cohort, the RiskScore significantly stratified overall survival (log-rank p < 0.001) and demonstrated superior predictive accuracy over both TNM staging and the established European Organization for Research and Treatment of Cancer (EORTC) prognostic score. CONCLUSION: This clinicomolecular model provides prognostic discrimination superior to TNM stage and EORTC score, offering a robust tool for risk-stratified management of mesothelioma.

• Identification of disulfidptosis-related molecular subtypes in pleural mesothelioma demonstrates a correlation with the immune infiltration, prognosis and therapy efficacy. J. Ding, X. Huang, W. Yao, et al. 2026;17(1). PubMed · Publisher · Free full text

  Abstract

  Background: Pleural mesothelioma (PM) is a rare and aggressive malignancy with increasing incidence, high mortality, and limited treatment options. Disulfidptosis, a newly identified form of regulated cell death, may play an important role in cancer, but its relevance in PM remains unclear.

  Methods: Transcriptomic and clinical data of PM were obtained from public databases. PM was classified into molecular subtypes based on disulfidptosis-related genes (DRGs). We then compared prognosis, tumor microenvironment, metabolic features, predicted response to immune checkpoint blockade, and chemotherapy sensitivity between subtypes. In addition, a prognostic signature was established, and key genes were identified using random survival forest analysis.

  Results: Two novel DRG-defined molecular subtypes were identified in PM. The DRGs-high subtype (Cluster 2) was associated with significantly worse overall survival, an immunosuppressive microenvironment dominated by M2 macrophages, and a lower predicted likelihood of response to immune checkpoint blockade. In contrast, the DRGs-low subtype (Cluster 1) showed metabolic reprogramming toward glycolysis and fatty acid oxidation, increased NK cell infiltration, and reduced sensitivity to chemotherapy. An 11-gene prognostic signature demonstrated predictive performance, with an AUC of 0.95 for 5-year survival (95%CI 0.881-1.013). Random survival forest analysis identified LMNB2 and CDCA2 as key genes, both of which were highly expressed in tumor tissues.

  Conclusions: PM can be classified into two DRG-defined molecular subtypes with distinct prognostic, immune, and metabolic features. These findings provide insights into PM heterogeneity and may support future studies on therapeutic stratification. The prognostic signature remains exploratory and requires validation in independent external cohorts before clinical application.

  © 2026. The Author(s).

• Multi-omics integration reveals tumor and microenvironmental heterogeneity in malignant pleural mesothelioma. H. Hu, L. Li, W. Bian, et al. 2026;17(1). PubMed · Publisher · Free full text

  Abstract

  Malignant pleural mesothelioma (MPM) is a highly aggressive and molecularly heterogeneous malignancy with poor prognosis. Here, we performed an integrative multi-omic analysis combining bulk transcriptomics, copy number variation profiling, and single-cell RNA sequencing to systematically characterize MPM heterogeneity. Using non-negative matrix factorization, we identified three robust molecular subtypes (S-I, S-II, and S-III) with distinct transcriptional programs, genomic alterations, and tumor microenvironment compositions. Subtype S-I exhibited immune-inflamed signatures with abundant cytotoxic T cells and activated dendritic cells, suggesting potential responsiveness to immunotherapy. S-II was characterized by metabolic reprogramming and mTORC1 pathway activation, whereas S-III displayed stromal enrichment, extracellular matrix remodeling, and suppressed apoptotic signaling. Single-cell analysis revealed subtype-specific distributions of malignant and stromal cell subsets, corroborating bulk-level observations and highlighting intratumoral heterogeneity. Collectively, these findings refine the molecular classification of MPM, uncover subtype-specific regulatory programs, and identify potential therapeutic vulnerabilities, providing a framework for precision medicine strategies in this challenging malignancy.

• Pivotal role of long non-coding RNA in the development of new therapeutic approaches for plural mesothelioma. C.J. Kiriacos, D.M. Elkahwagy, M. Mansour. 2026;17(1). Review PubMed · Publisher · Free full text

  Abstract

  Pleural mesothelioma is a rare aggressive tumor that affects the parietal layer of the pleura. It constitutes 90% of mesotheliomas. Usually, the diagnosis takes place 30 to 40 years after asbestos exposure. Thus, patients are diagnosed at a very late stage, leading to a poor prognosis, with a low median survival rate of approximately one year and a 5-year survival rate of only 5%. The available treatment usually consists of a multimodal approach, including chemotherapy (platinum-based drugs and antifolates), surgery, and radiotherapy. Yet, new therapeutic approaches are still needed to achieve higher survival rates. Long non-coding RNAs are transcripts of more than 200 nucleotides and have been proven to participate in various cellular processes and biological mechanisms. Upon dysregulation, many biological pathways can be affected, initiating cancers or even promoting their aggressiveness. These non-coding RNAs have been studied for their therapeutic potential in various cancers. The role of long non-coding RNAs in PM, whether in regulating pathogenicity or as potential therapeutic targets, requires further investigation. This review highlights the role of lncRNAs in PM pathogenesis and their potential as therapeutic targets.

• The role of PCMT1 in prognosis tumor immune microenvironment and therapeutic responses across cancers. B. Wang, S. Huang, R. Ren, et al. 2026;17(1):257. PubMed · Publisher · Free full text

  Abstract

  Background: Emerging evidence highlights the overexpression of Protein-L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) in multiple malignancies. However, its pan-cancer prognostic significance, tumor immune microenvironment (TIME) interactions, and therapeutic implications remain underexplored.

  Methods: Multi-omics data were integrated from UCSC Xena, GTEx, UALCAN, and published cohorts. PCMT1 expression patterns were systematically analyzed across 33 cancer types. Associations between PCMT1 and clinical outcomes, immune infiltration, immune checkpoint genes (ICGs), tumor mutation burden (TMB), microsatellite instability (MSI), and drug sensitivity were evaluated using bioinformatics pipelines.

  Results: Our pan-cancer analysis revealed differential expression patterns of PCMT1 across various malignancies, with significant upregulation in 20 cancer types and downregulation in 3 cancer types. Notably, PCMT1 overexpression was predominantly observed in epithelial-origin tumors, such as ACC (adrenocortical carcinoma), BRCA (breast invasive carcinoma), COAD (colon adenocarcinoma), and LUAD (lung adenocarcinoma). Survival analysis demonstrated that elevated PCMT1 expression was significantly correlated with unfavorable prognosis in multiple epithelial tumors, particularly in BRCA, esophageal carcinoma (ESCA), head and neck squamous cell carcinoma (HNSC), liver hepatocellular carcinoma (LIHC), and mesothelioma (MESO). Furthermore, comprehensive analysis identified significant associations between PCMT1 expression and various tumor microenvironment features, including immune scores, six distinct immune cell types, four immunosuppressive cell populations, cancer-associated fibroblasts (CAFs)-related markers, and immunosuppressive factors. PCMT1 expression also showed significant correlations with tumor mutation burden (TMB), microsatellite instability (MSI), DNA stemness score (DNAss), and RNA stemness score (RNAss). Particularly noteworthy was the strong positive correlation between PCMT1 expression and CAFs infiltration, along with their associated factors. These findings were further validated in independent immunotherapy cohorts, where PCMT1 consistently demonstrated immunosuppressive characteristics.

  Conclusion: Multi-omics analysis suggests that PCMT1 may serve as a potential prognostic biomarker and a novel immunotherapy target for pan-cancer.

  © 2026. The Author(s).

• A pancancer analysis reveals the oncogenic role of glutaminase 1 (GLS1) in tumor metabolism and immune evasion: a bioinformatics analysis. J. Liu, S. Hong, K. Gu. 2025;16(1):2156. PubMed · Publisher · Free full text

  Abstract

  Background: Metabolic reprogramming is a significant factor that regulates the function and differentiation of immune cells, thereby influencing the progress of the immune response. The intricate interplay between glutamine metabolism and the immune microenvironment (TME) plays crucial roles in the pathogenesis of cancer. The initiation of glutamine metabolism is facilitated by the enzyme GLS1; however, its oncogenic role remains unclear.

  Methods: In this pancancer analysis, we aimed to investigate the potential oncogenic mechanism of GLS1 across various tumor types in The Cancer Genome Atlas (TCGA) dataset.

  Results: Our results revealed variable expression levels of GLS1 across different cancer types. Notably, higher expression levels of GLS1 were associated with worse prognosis in patients with kidney renal papillary cell carcinoma (KIRP, HR = 1.01; p < 0.01), liver hepatocellular carcinoma (LIHC, HR = 1.02; p < 0.01), and mesothelioma (MESO, HR = 1.01; p < 0.01). Additionally, we observed distinct associations between GLS1 expression levels and tumor methylation levels, tumor mutation burden (TMB), microsatellite instability (MSI), immune cell infiltration (IFL), and immune scores in several tumor types. We also detected the enrichment of GLS1 in key pathways, such as the mTOR, JAK, and KRAS pathways. Furthermore, we observed associations between GLS1 expression levels and a wide range of immune checkpoint genes, including both immunoinhibitors and immunostimulators, in most tumors.

  Conclusions: Our study provides initial insights into the oncogenic roles of GLS1 across different tumors. These findings suggest that GLS1 can serve as a potential biomarker for determining prognosis and designing therapeutic strategies for various tumor types.

  © 2025. The Author(s).

• Advancement in tumor treating fields of mechanism, clinical applications, and future directions. M. Zang, S. Zhu, Q. Niu. 2025;16(1):1049. Review PubMed · Publisher · Free full text

  Abstract

  Traditional cancer treatment modalities, such as surgical interventions, radiotherapy, and chemotherapy, persist as the cornerstone of standard care across a wide array of clinical settings. Despite their established effectiveness in combating cancer, these therapies are inherently invasive in nature and have great side effects, which seriously affect the quality of life of patients. Tumor Treating Fields is a low-intensity intermediate-frequency alternating electric field. Based on the current clinical study of Tumor Treating Fields in brain tumors, The U.S. Food and Drug Administration (FDA) initially approved Tumor Treating Fields in 2015 for the treatment of newly diagnosed or relapsed glioblastoma multiforme (GBM) and in 2019 for the treatment of malignant pleural mesothelioma (MPM). However, Tumor Treating Fields is still not widely appreciated in the treatment of high-mortality cancers, and although the therapeutic effect of Tumor Treating Fields has been validated in cell experiments and clinical trials, how to optimize its therapeutic effect remains to be studied. In this paper, the mechanism of Tumor Treating Fields treatment and its clinical progress were reviewed, and the dosimetry and numerical simulation of individualized treatment were comprehensively summarized, in order provide new ideas for further clinical research of this treatment model.

  © 2025. The Author(s).

• Epidemiological trends in laryngeal cancer burden: insights from GBD 2021 and SEER databases. J. Zhang, S. Yu, F. Wang, et al. 2025;16(1):1946. PubMed · Publisher · Free full text

  Abstract

  Background: The burden of laryngeal cancer (LC) warrants further exploration to better understand its current status and trends.

  Methods: Using data from the Global Burden of Disease (GBD) 2021, we assessed age-standardized incidence, mortality, and disability-adjusted life years (DALYs) rates for LC at the global, regional, and national levels. The LC burden was decomposed based on population size, age structure, and epidemiological changes, and cross-country inequalities were quantified using the World Health Organization's recommended standard health equity approach. Additionally, data from the Surveillance, Epidemiology, and End Results (SEER) database were combined with joinpoint regression analysis to determine the average annual percentage change (AAPC) in LC incidence and mortality trends in the United States.

  Results: GBD data showed a global decline in LC incidence and mortality rates from 1990 to 2021, with notable gender disparities and a higher burden in males. Key risk factors included smoking, alcohol use, asbestos, and sulfur exposure. Decomposition analysis identified population growth as the main driver of the LC burden, with regional and gender differences in aging and epidemiological trends. Inequality analysis revealed higher DALYs in low-SDI countries, with a widening gap over time. SEER data indicated a declining LC incidence in the US (1992-2021), and incidence-based mortality(IBM) increased until 2003 before declining.

  Conclusions: From 1990 to 2021, global LC incidence and mortality declined, with a higher burden in males. The gap in LC burden between high and low SDI countries has increased. These findings highlight the need for targeted public health strategies to address both epidemiological trends and socio-demographic inequalities.

  © 2025. The Author(s).

• Immunotherapy for pleural mesothelioma: from innovation to the frontlines of core clinical questions. T. Yoshida, K. Kuribayashi. 2025;17(1):43. Review PubMed · Publisher · Free full text

  Abstract

  In August 2018, Japan's Pharmaceuticals and Medical Devices Agency (PMDA) became the first in the world to approve immune checkpoint inhibitor (ICI) monotherapy with nivolumab for previously treated, unresectable, advanced, or recurrent pleural mesothelioma (PM), setting a global precedent. Subsequently, in October 2020, the U.S. Food and Drug Administration (FDA) approved the combination of nivolumab and ipilimumab (CheckMate 743 trial) as the first-line treatment for unresectable PM. This marked the first update to standard first-line therapy in approximately 15 years since the approval of cisplatin (CDDP) plus pemetrexed (PEM) based on the EMPHACIS trial in 2004. Most recently, in September 2024, the FDA approved pembrolizumab plus platinum and PEM (KEYNOTE-483 trial) as another first-line option for advanced or metastatic PM. These developments underscore the rapid evolution of systemic therapy for PM. However, several urgent clinical questions have emerged in real-world practice. This article aims to address these issues based on the latest evidence and expert insights.

  © 2025. The Author(s).

• The efficacy and safety of anlotinib combined with chemotherapy in treatment of advanced soft tissue sarcoma. Y. Ni, Y. Dong, A. Jiang, et al. 2024;15(1):598. PubMed · Publisher · Free full text

  Abstract

  Background: To evaluate the efficacy and safety of anlotinib combined with chemotherapy in the treatment of advanced soft tissue sarcoma (STS).

  Methods: A total of 14 patients with advanced STS consisting of 4 liposarcoma, 3 undifferentiated polymorphous sarcoma, 2 synovial sarcoma, 1 Extraosseous ewing sarcoma, 1 spindle cell sarcoma, 1 Sarcomatoid malignant mesothelioma, 1 hemangiosarcoma, and 1 fibrosarcoma, were treated with anlotinib plus chemotherapy. The anlotinib was combined with chemotherapy as the first-line treatment in 13 patients, and as second-line treatment in 1 patient. Chemotherapy regimens were based on anthracyclines and ifosfamide, and other drugs included paclitaxel, and so on. Efficacy and safety were evaluated every 2 treatment cycles.

  Results: According to the stage of AJCC, 9 patients were stage III and 5 patients were stage IV. The average cycle of treatment is 3.86. Among the 14 patients, 2 cases had received surgical treatment after neoadjuvant chemothrapy, 5 cases had partial response (PR), 7 cases had stable disease (SD), and 2 cases had progressive disease (PD). The overall response rate (ORR) was 35.7% (5/14). Patients who had not underwent surgical treatment were with a disease control rate (DCR) of 83.3% (10/12). The median progression free survival (PFS) was 8.25 months. The common treatment-related adverse effects included bone marrow suppression, nausea, vomiting and hypertension. Three patients had severe adverse effect, which was febrile neutropenia. No treatment-related death was found.

  Conclusions: Anlotinib combined with chemotherapy in the treatment of STS is effective and tolerable, which is a promising strategy. It is worthy of further clinical research.

  © 2024. The Author(s).

• BAP1 in cancer: epigenetic stability and genome integrity. S. Caporali, A. Butera, I. Amelio. 2022;13(1):117. Review PubMed · Publisher · Free full text

  Abstract

  Mutations in BAP1 have been identified in a hereditary cancer predisposition syndrome and in sporadic tumours. Individuals carrying familiar BAP1 monoallelic mutations display hypersusceptibility to exposure-associated cancers, such as asbestos-driven mesothelioma, thus BAP1 status has been postulated to participate in gene-environment interaction. Intriguingly, BAP1 functions display also a high degree of tissue dependency, associated to a peculiar cancer spectrum and cell types of specific functions. Mechanistically, BAP1 functions as an ubiquitin carboxy-terminal hydrolase (UCH) and controls regulatory ubiquitination of histones as well as degradative ubiquitination of a range of protein substrates. In this article we provide an overview of the most relevant findings on BAP1, underpinning its tissue specific tumour suppressor function. We also discuss the importance of its epigenetic role versus the control of protein stability in the regulation of genomic integrity.

  © 2022. The Author(s).

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