Cancer[JOURNAL]
Sun
200 papers
Nano-silymarin combined with methylene blue photodynamic therapy versus monotherapies of head and neck squamous cell carcinoma: in-vitro study.
Hefzi D, Koopaie M, Hakimiha N … +1 more , Younespour S
BMC Cancer · 2026 Jun · PMID 42374269 · Full text
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) presents significant therapeutic challenges due to its aggressiveness and the morbidity of conventional treatments. Photodynamic therapy (PDT) offers a localized...
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) presents significant therapeutic challenges due to its aggressiveness and the morbidity of conventional treatments. Photodynamic therapy (PDT) offers a localized approach, but its efficacy can be limited. This study investigated the potential of nano-silymarin, a bioactive flavonolignan complex with known anticancer properties, in combination with methylene blue-mediated PDT (MB-PDT) in HNSCC cells. METHODS: The cytotoxic, apoptotic, and anti-migratory effects of various treatments were assessed in HN5 cells. Groups included controls, individual agents (nano-silymarin, MB, laser), dual therapies, and the triple combination (nano-silymarin + MB + laser). Cell viability was measured using the MTT assay, apoptosis by flow cytometry, and migration by the scratch assay. Results were analyzed using one-way ANOVA with Tukey's post hoc test. Synergy was quantified using the Bliss independence, Loewe additivity, and zero interaction potency models. RESULTS: The triple combination (nano-silymarin + MB-PDT) demonstrated the most potent effect, synergistically reducing cell viability to 40.63% (compared with 69.65% for nano-silymarin and 77.32% for MB-PDT). It induced the highest level of total apoptosis (42.93%) and nearly completely inhibited cell migration (97.2% wound openness at 72 h). This anti-migratory effect was significantly greater than the sum of the effects of the individual monotherapies, indicating a synergistic blockade of cellular invasion. Synergy analysis confirmed a strong synergistic interaction, with a Combination index of 0.682. CONCLUSION: Nano-silymarin significantly potentiates the anticancer efficacy of MB-PDT against HNSCC cells through strong synergistic interactions, thereby enhancing cytotoxicity, apoptosis, and migration inhibition. These findings support further development of nano-silymarin in combinatorial PDT regimens for HNSCC.
Targeted genomic DNA sequencing (506-gene panel) and whole-exome sequencing analysis of EBV-positive inflammatory follicular dendritic cell sarcoma.
You Z, Chen S, Chen X … +2 more , Chen X, Wang C
BMC Cancer · 2026 Jun · PMID 42374265 · Full text
INTRODUCTION: Epstein-Barr virus-positive inflammatory follicular dendritic cell sarcoma (EBV+ IFDCS), recently reclassified in the 5th edition of the WHO classification of lymphoid neoplasms, is a rare mesenchymal and d...
INTRODUCTION: Epstein-Barr virus-positive inflammatory follicular dendritic cell sarcoma (EBV+ IFDCS), recently reclassified in the 5th edition of the WHO classification of lymphoid neoplasms, is a rare mesenchymal and dendritic cell tumor distinct from conventional follicular dendritic cell sarcoma (FDCS) in cellular origin and clinicopathological features. To address this, we present the largest sequencing cohort of EBV+ IFDCS to date, combining targeted next-generation sequencing (NGS) of 12 cases and whole-exome sequencing (WES) of 3 cases. This study aims to elucidate the molecular characteristics of EBV+ IFDCS to better understand its pathogenesis and identify potential therapeutic targets. MATERIALS AND METHODS: 12 EBV+ IFDCS cases were analyzed using next-generation sequencing (NGS) with a 506-gene panel, and whole-exome sequencing (WES) was performed on 3 cases. The analysis focused on identifying copy number variations (CNVs), gene fusions, and pathogenic mutations. KEGG pathway analysis was conducted to explore enriched oncogenic pathways. RESULTS: CNV analysis via WES identified focal chromosomal deletions in 2 of 3 cases: 7p and 14q deletions in Case 1, and 17p deletion plus deep deletions in NPRL2 (chromosome 3) and STK11 (chromosome 19) in Case 6. While pathogenic/drug-sensitive SNVs varied across the 12 patients (Fig. 2). Only Patient 3 (48-year-old female, splenic classical subtype EBV+ IFDCS) was TMB-H (11.2 mutations/Mb, ≥ 10 mutations/Mb as threshold), harboring NQO1 p.P187S (VAF = 32.6%) and a germline PKHD1 Class 3 VUS. This case had no unique somatic mutations vs. low-TMB cases, with histological features (fascicular spindle cells, moderate lymphoplasmacytic infiltration) consistent with the classical subtype (Fig. 1A). KEGG pathway analysis revealed enrichment in PI3K-AKT, cell cycle, Notch, and EBV infection pathways. WES of Patients 1, 6, 10 showed TMB-L (1.8-3.5 mutations/Mb); Patient 3's TMB-H (11.2 mutations/Mb, ≥ 10 mutations/Mb as solid tumor threshold) was validated via targeted NGS (723× coverage). WES of TMB-L cases revealed predominant missense mutations/SNVs (C > T transitions: 50% of SNPs, Fig. 5C), with 3-9 somatic mutations per case and no shared mutations-highlighting potential potential high tumor heterogeneity, further supported by Patient 3's unique TMB-H phenotype. CONCLUSION: This study reveals the unique molecular landscape of EBV+ IFDCS, characterized by frequent NQO1 mutations and activation of key oncogenic pathways. These findings provide critical insights into the tumor's pathogenesis and suggest potential molecular targets for future therapeutic strategies.
Assessing the prognostic value of SIL1 in pan-cancer cohorts and its practical application as a biomarker in glioma practice.
Liu P, Peng Y, Sun Y … +3 more , Hu S, Lv D, Yan Y
BMC Cancer · 2026 Jun · PMID 42374254 · Full text
BACKGROUND: Gliomas are aggressive brain tumors associated with a poor prognosis. Although SIL1, an endoplasmic reticulum chaperone factor, is known to maintain protein homeostasis, its specific role in glioma pathogenes...
BACKGROUND: Gliomas are aggressive brain tumors associated with a poor prognosis. Although SIL1, an endoplasmic reticulum chaperone factor, is known to maintain protein homeostasis, its specific role in glioma pathogenesis remains poorly understood. This study aimed to investigate the clinical significance and biological functions of SIL1 in glioma. METHODS: We performed a pan-cancer multi-omics analysis using TCGA and GTEx datasets to evaluate SIL1 expression, its prognostic value, and its associations with genomic instability, tumor stemness, and immune infiltration. Gene set enrichment analysis (GSEA) was utilized to identify potentially involved signaling pathways. For in vitro functional validation, human glioma cell lines (U251 and A172) were subjected to siRNA-mediated knockdown and lentiviral rescue assays to assess cellular proliferation, migration, apoptosis, and epithelial-mesenchymal transition (EMT) dynamics. RESULTS: SIL1 was significantly upregulated in gliomas and correlated with poor patient survival. High SIL1 expression was associated with increased tumor heterogeneity (based on MATH scores), DNA methylation-derived stemness indices, and an immunosuppressive microenvironment characterized by the enrichment of M2 macrophages, regulatory T cells (Tregs), and immune checkpoint molecules. In vitro, SIL1 knockdown suppressed glioma cell proliferation and invasion, promoted mitochondrial apoptosis, and mitigated the EMT phenotype, potentially by impairing SNAIL nuclear translocation. Notably, these phenotypic changes were effectively rescued following lentiviral overexpression of SIL1. CONCLUSION: Our findings suggest that SIL1 is a potential prognostic biomarker in glioma. Its elevated expression correlates with increased malignancy, stemness features, EMT, and an immunosuppressive microenvironment, indicating that SIL1 may serve as a promising therapeutic target for glioma intervention.
Single-cell transcriptomics reveals MAFB-driven macrophage reprogramming and immune divergence in recurrent glioblastoma.
He Y, Yu J, Huang M … +4 more , Lu P, Liu B, Zhang C, Zhang C
BMC Cancer · 2026 Jun · PMID 42374253 · Full text
BACKGROUND: Glioblastoma (GBM) is the most aggressive and most common type of primary brain tumor, with poor prognosis despite standard therapies. The mechanisms driving recurrence remain poorly understood. Tumor-associa...
BACKGROUND: Glioblastoma (GBM) is the most aggressive and most common type of primary brain tumor, with poor prognosis despite standard therapies. The mechanisms driving recurrence remain poorly understood. Tumor-associated macrophages (TAM) dominate the GBM microenvironment and promote tumor growth, angiogenesis, and immune suppression, yet their activation states and transcriptional programs are not well defined. RESULTS: By integrating large-scale single-cell transcriptomic datasets, we delineate profound immune microenvironmental divergence in recurrent GBM, characterized by the emergence of a distinct CXCL3⁺ tumor-associated macrophage (TAM) population. These CXCL3⁺ TAMs exhibit a robust pro-inflammatory cytokine program, intensified interactions with malignant and immunosuppressive immune cells, and a strong association with poor patient survival. Regulatory network analysis identifies MAFB as the central transcriptional regulator of this TAM state. MAFB is selectively enriched in macrophages, markedly upregulated in recurrent tumors, and strongly correlated with pro-inflammatory gene signatures. Immunohistochemistry and multiplex immunofluorescence further demonstrate an expanded population of MAFB⁺ mesenchymal-like TAMs in recurrent GBM. Depletion of MAFB in patient-derived GBM cells suppresses intracranial tumor growth and prolongs survival in vivo. CONCLUSIONS: Our study highlights profound immune remodeling in primary and recurrent GBM. We further define a MAFB-driven CXCL3⁺ macrophage program that shapes the immune landscape of recurrent GBM and underscore this axis as a promising target for microenvironmental reprogramming.
Integrated multi-omics analysis reveals folate metabolism-related genes as prognostic markers and therapeutic targets in clear cell renal cell carcinoma.
Lin J, Li S, Zhou Y … +10 more , Han Z, Chen W, Zheng H, Liu S, Dai J, Cheng W, Fu C, Deng W, Xi H, Zeng J
BMC Cancer · 2026 Jun · PMID 42374231 · Full text
BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is an aggressive tumor with high metastatic potential and therapeutic resistance, yet the role of folate metabolism in its pathogenesis and immune evasion remains uncle...
BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is an aggressive tumor with high metastatic potential and therapeutic resistance, yet the role of folate metabolism in its pathogenesis and immune evasion remains unclear. This study aims to develop and validate a folate metabolism-related gene (FMRG) scoring system to stratify patients by prognostic risk and immune phenotypes, and to explore the functional role of key FMRGs in ccRCC progression. METHODS: Using transcriptomic and clinical data from The Cancer Genome Atlas (TCGA), we developed a folate metabolism-related gene (FMRG) scoring system via integrative machine learning and validated it in an external cohort. We analyzed associations of the FMRG score with clinicopathological features, biological pathways, immune infiltration, therapeutic responsiveness, and drug sensitivity. Single-cell RNA sequencing and spatial transcriptomics mapped candidate gene expression, and in vitro experiments validated the functional role of NGF. RESULTS: A ten-gene prognostic model based on the FMRG score stratified ccRCC patients into groups with distinct clinical outcomes, immune profiles, and therapeutic responses. NGF was upregulated in ccRCC, with heterogeneous spatial expression. Functional assays showed that NGF enhances proliferation, migration, and invasion. CONCLUSIONS: This folate metabolism-based scoring framework facilitates prognostic stratification, tumor microenvironment characterization, and prediction of immunotherapy response in ccRCC. NGF is identified as a functional mediator of tumor progression, offering potential therapeutic targets and insights into metabolic-immune crosstalk.
Imaging the hallmarks of cancer.
Grimm J, Kiessling F, Brindle KM … +9 more , Hanahan D, Jain SK, Lambin P, Lammers T, Li KC, de Vries IJM, Weber WA, Weigelin B, Pichler BJ
Nat Rev Cancer · 2026 Jun · PMID 42373751 · Publisher ↗
The hallmarks of cancer were introduced by Hanahan and Weinberg as a conceptual organizing framework to distil the complexity of tumours. This concept of cancer hallmarks has become an enduring theme in cancer research....
The hallmarks of cancer were introduced by Hanahan and Weinberg as a conceptual organizing framework to distil the complexity of tumours. This concept of cancer hallmarks has become an enduring theme in cancer research. Moreover, an increasing number of therapeutic strategies are being aimed at targeting these hallmarks. However, translating them into the clinic requires technologies to monitor their effectiveness and biomarkers that can stratify patients for the choice of specific therapies. Tumour heterogeneity and the ability of tumour cells to rapidly mutate and develop evasion strategies makes the development of non-invasive imaging capabilities to interrogate these hallmarks as biomarkers and monitor them longitudinally and quantitatively particularly important. This Review presents a holistic discussion of non-invasive diagnostic imaging capabilities related to the hallmarks of cancer; some hallmarks can be assessed with imaging probes that directly target biomolecules, whereas others can be interrogated indirectly by imaging pathophysiological processes. Additionally, visualizing the hallmarks of cancer can be addressed with artificial intelligence-assisted, multiparametric image analysis (for example, radiomics, radiogenomics and deep learning). The approaches discussed have been evaluated in a translational context, and some of them already have a substantial role in clinical practice, for example, to guide treatment strategies, including surgical resections, radiotherapy and molecularly targeted chemo-, immuno- and radiopharmaceutical therapies.
CLIM-TIME links tumour genetics to spatial immune architecture.
Hu W
Nat Rev Cancer · 2026 Jun · PMID 42373750 · Publisher ↗
Abstract loading — click title to view on PubMed.
Real-world safety, prognostic, and design considerations in ketogenic diet trials for pancreatic cancer.
Bruckner HW, Knopf E
Cancer · 2026 Jul · PMID 42371807 · Publisher ↗
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Proliferative ecotype determines lethal prognosis and therapeutic benefit in urothelial carcinoma.
Sun J, Jin K, Ding Y … +13 more , Wu Y, Zhang L, Su X, Shi J, Liu Z, Zeng H, Liu H, Chang Y, Zhu Y, Wang Z, Xu L, Zhang W, Xu J
Cancer · 2026 Jul · PMID 42367015 · Publisher ↗
BACKGROUND: Ki-67 is routinely used in clinical practice to quantify proliferative activity, yet proliferation has not been incorporated into current molecular classification systems for urothelial carcinoma (UC). This w...
BACKGROUND: Ki-67 is routinely used in clinical practice to quantify proliferative activity, yet proliferation has not been incorporated into current molecular classification systems for urothelial carcinoma (UC). This work studies the tumor microenvironment (TME), therapeutic vulnerabilities, and clinical implications of the proliferative ecotype in UC. METHODS: The authors assembled a multi-cohort data set of 1431 UC patients from four institutional cohorts and five publicly available data sets with comprehensive clinicopathological annotations. Through an integrated multi-omics framework coupled with experimental validation, they assessed how proliferative status shape lineage differentiation, clinical outcomes, treatment response, and TME architecture. RESULTS: High Ki-67 expression identified a proliferative ecotype associated with markedly worse prognosis but enhanced sensitivity to platinum-based chemotherapy and PD-1/PD-L1 blockade. This ecotype displayed elevated tumor purity and tumor mutation burden, with characteristic genomic alterations including enrichment of TP53, ERCC2, and ATM/RB1/FANCC mutations and reduced 9p21.3 loss. The proliferative ecotype orchestrated an immune-enriched TME dominated by CD8 T cells and B cells. Functional analyses revealed that CD8 T cells preferentially differentiated toward an exhausted state, and mechanistic interrogation identified a GDF-15-TGFBR2 signaling axis through which epithelial cells modulate CD8 T-cell dysfunction. CONCLUSIONS: This study identifies a proliferative ecotype of UC that is orthogonal to classical luminal/basal ecotypes. Despite its adverse prognosis, this ecotype confers superior responsiveness to chemotherapy and immunotherapy and features a distinct genomic and immune ecosystem. These findings position proliferative status as a clinically actionable axis that may refine molecular classification and guide precision therapy in UC.
Potential evaluation of SULT1A3 as an early diagnostic marker for nasopharyngeal carcinoma: a study based on serum proteomics screening and ELISA validation.
Lin Z, Song W, Liang W … +3 more , Liu J, Gan R, Wang Y
BMC Cancer · 2026 Jun · PMID 42365246 · Full text
BACKGROUND: Nasopharyngeal carcinoma (NPC) represents a highly prevalent and aggressive malignancy endemic to Southeast Asia. Early and accurate diagnosis is critical to improving survival outcomes; however, the absence...
BACKGROUND: Nasopharyngeal carcinoma (NPC) represents a highly prevalent and aggressive malignancy endemic to Southeast Asia. Early and accurate diagnosis is critical to improving survival outcomes; however, the absence of robust, stage-specific biomarkers remains a key obstacle to clinical implementation of early screening strategies. METHODS: We performed untargeted serum proteomic profiling using mass spectrometry in 15 treatment-naïve early-stage NPC patients and 15 VCA-IgA-positive healthy controls. Bioinformatics analyses were conducted to identify differentially expressed proteins (DEPs). Machine learning (random forest combined with recursive feature elimination) was employed to prioritize candidate biomarkers, which were subsequently verified using enzyme-linked immunosorbent assay (ELISA) in independent sample cohorts. RESULTS: In total, 1,428 serum proteins were identified, among which 1,410 were reliably quantified. We observed 31 upregulated and 189 downregulated proteins in NPC patients relative to controls. Spearman correlation analysis revealed significant associations: LTA4H (leukotriene A4 hydrolase) levels correlated with serum cell infiltration (r = 0.383, p = 0.032) and CD8 + T-cell abundance (r = 0.408, p = 0.021); both SULT1A3 (sulfotransferase family 1 A member 3) and FGL1 (fibrinogen-like protein 1) levels were positively associated with M1 macrophage infiltration (r = 0.510, p = 0.003 and r = 0.430, p = 0.015, respectively). In a preliminary validation cohort (n = 80), ELISA yielded AUC values of 0.631 (95% CI: 0.515-0.736, p = 0.04) for LTA4H, 0.787 (95% CI: 0.681-0.871, p < 0.001) for SULT1A3, and 0.688 (95% CI: 0.575-0.787, p = 0.002) for FGL1. In large-scale independent validation, SULT1A3 achieved an AUC of 0.826 (95% CI: 0.766-0.876; sensitivity = 78.89%, specificity = 75.47%) in cohort 1 (n = 196) and 0.796 (95% CI: 0.723-0.857; sensitivity = 76.67%, specificity = 76.67%) in cohort 2 (n = 150). CONCLUSIONS: Through an integrated workflow combining proteomic screening, machine learning prioritization, and multi-stage ELISA validation, we identified SULT1A3 as a candidate serum-based biomarker for early detection of NPC. Preliminary findings suggest that SULT1A3 may have potential utility in clinical screening, though further validation in independent, multi‑center cohorts is required.
Am80 (tamibarotene) and ATRA induce highly similar molecular responses and myeloid differentiation in non-APL AML, enhanced by LSD1/GCN5 inhibition and increased RARA expression.
Ghazvini Zadegan F, Stanko C, Fiedler F … +15 more , Ölsner L, Özcan SG, Schütt J, Schnöder TM, Sbirkov Y, Szymanski L, Stengel S, Dittrich P, Müller JP, Heidel FH, Hochhaus A, Scholl S, Schnetzke U, Brioli A, Schenk T
BMC Cancer · 2026 Jun · PMID 42365243 · Full text
BACKGROUND: Acute myeloid leukemia (AML) remains a challenging disease with a poor prognosis, necessitating more personalized therapeutic strategies. Retinoic acid receptor (RAR) activation is crucial for myeloid differe...
BACKGROUND: Acute myeloid leukemia (AML) remains a challenging disease with a poor prognosis, necessitating more personalized therapeutic strategies. Retinoic acid receptor (RAR) activation is crucial for myeloid differentiation, but non-APL AML cells resist differentiation induced by the pan-RAR agonist all-trans retinoic acid (ATRA). Am80 (tamibarotene), a specific RARA agonist, has been reported to partially overcome this resistance in AML with high RARA expression. However, its effects on myeloid differentiation, especially in comparison to ATRA, remain understudied. METHODS: In this study we compared the effects of Am80 and ATRA in non-APL AML samples, focusing on subsets with high RARA and/or RARG expression, using molecular and phenotypic differentiation assessments. RESULTS: In contrast to previous findings, Am80 showed no advantage over ATRA in inducing differentiation in AML cell lines or primary samples, regardless of RARA and RARG expression levels. Cotreatment with inhibitors of the epigenetic modifiers LSD1 and GCN5, which facilitates retinoid-induced myeloid differentiation, enhanced the effects of both Am80 and ATRA to the same extent, with more pronounced responses observed in RARA-high samples. Gene expression analysis revealed identical molecular responses to Am80 and ATRA. CONCLUSIONS: The study provides evidence that ATRA can be substituted by the more stable Am80 in retinoid-based AML therapies. It also identifies elevated RARA expression as a potential marker for sensitivity to combination therapy with retinoids and epigenetic inhibitors in AML.
Study protocol: targeted delivery of interleukin-12 in combination with hepatic artery infusion pump therapy for patients with adrenocortical carcinoma liver metastases.
Friedman LR, Smith EC, Sarvestani AL … +18 more , Eade AV, Ho J, Pu T, Larrain C, Hannah CE, Magee T, Smith KM, Satterwhite AA, Xiao S, Burke JF, Sinha S, Desai PP, Remmert K, Cavnar MJ, Gulley JL, Schlom J, Del Rivero J, Hernandez JM
BMC Cancer · 2026 Jun · PMID 42365236 · Full text
BACKGROUND: Adrenocortical carcinoma (ACC) is a rare, aggressive malignancy often detected at an advanced stage with limited effective treatment options beyond first-line chemotherapy. The liver is a common site of metas...
BACKGROUND: Adrenocortical carcinoma (ACC) is a rare, aggressive malignancy often detected at an advanced stage with limited effective treatment options beyond first-line chemotherapy. The liver is a common site of metastasis, and patients frequently present with substantial hepatic disease burden that precludes complete resection. Locoregional therapies, including hepatic artery infusion pump (HAIP) delivery of floxuridine, have not been thoroughly evaluated for treatment of ACC liver metastasis, likely due to its rare incidence and highly aggressive nature. PDS01ADC (previously referred to as NHS-IL12) is a novel antibody-drug conjugate designed to deliver the immunomodulatory cytokine interleukin-12 to areas of tumor necrosis and modulate the tumor microenvironment to support immune surveillance and cytotoxic tumor responses. Combination of PDS01ADC with HAIP therapy (HAIP-delivered floxuridine plus systemic chemotherapy) was recently found to be feasible for clinical evaluation by an interim analysis in patients with colorectal liver metastases. Patients who received PDS01ADC with HAIP therapy had extended overall survival compared to patients who received HAIP therapy alone in a nonrandomized prior sequential study. We discuss herein the rationale and initiation of a new clinical trial arm to evaluate HAIP therapy with PDS01ADC for patients with ACC liver metastasis who have failed standard of care therapy. METHODS: Patients with unresectable ACC liver metastasis and either resectable or no progressive extrahepatic disease will receive combination therapy including HAIP floxuridine and subcutaneous injection of PDS01ADC administered concurrently with systemic gemcitabine and oxaliplatin in 28-day cycles. The primary outcome measured is overall response rate as measured by Response Evaluation Criteria in Solid Tumors (RECIST v1.1) criteria. Secondary outcomes measured in this study include intrahepatic and extrahepatic progression-free survival, overall survival, and safety of PDS01ADC combination therapy with HAIP-delivered floxuridine. DISCUSSION: For select patients with ACC liver metastasis, HAIP therapy with PDS01ADC may improve disease control and thereby prolong survival. TRIAL REGISTRATION: Study ID NCT05286814 version 2026-05-04; https://clinicaltrials.gov/study/NCT05286814.
Doxorubicin-loaded chitosan/gold nanoparticles enhance anticancer effects and reduce CLMAT3 and ZNRD1-AS1 expression in colorectal cancer cells.
Alizadeh F, Rajabi A, Goharmomayez S … +2 more , Fathi M, Safaralizadeh R
BMC Cancer · 2026 Jun · PMID 42365229 · Full text
BACKGROUND: Globally, colorectal cancer (CRC) stands as the second most lethal malignancy. Chemotherapeutic drugs have shown some limitations, including systemic toxicity and non-specificity. Nanocarriers such as chitosa...
BACKGROUND: Globally, colorectal cancer (CRC) stands as the second most lethal malignancy. Chemotherapeutic drugs have shown some limitations, including systemic toxicity and non-specificity. Nanocarriers such as chitosan/gold nanoparticles (CS/Au NPs) facilitate drug localization at tumor sites, thereby reducing off-target adverse effects. METHODS: Doxorubicin-loaded CS/Au NPs were synthesized, and their physicochemical properties were analyzed using Fourier transform infrared (FT-IR) spectroscopy and dynamic light scattering (DLS). HCT116 cells were treated with both free doxorubicin and CS/Au-DOX NPs. In vitro cytotoxic effects were evaluated using the MTT assay. Additionally, apoptosis induction, cell cycle arrest, and cellular uptake assay were examined by flow cytometry. The scratch assay used to evaluate the effect of CS/Au-DOX NPs on the cell migration potential of HCT116, and the expression levels of CLMAT3 and ZNRD1-AS1 were determined by qRT-PCR. RESULTS: CS/Au-DOX NPs exhibited high encapsulation efficiency (78%) with favorable nanoscale properties, and were markedly more potent than free doxorubicin against HCT116 cells (IC 0.5 vs. 3 µM). Flow cytometry revealed significant apoptosis induction, G2/M arrest, and enhanced cellular uptake in HCT116 following treatment with CS/Au-DOX NPs. These NPs also reduced the migration potential of CRC cells. In CRC tissues, CLMAT3 and ZNRD1-AS1 were upregulated, with CLMAT3 overexpression associated with lymph node metastasis, while both lncRNAs showed limited diagnostic value. Notably, CS/Au-DOX NPs downregulated CLMAT3 and ZNRD1-AS1 expression in HCT116 cells. CONCLUSION: CS/Au-DOX NPs substantially enhanced the anticancer efficacy of DOX in the HCT116 cell line. Furthermore, CLMAT3 and ZNRD1-AS1 exhibited only limited utility as diagnostic biomarkers in CRC, suggesting that their clinical applicability in early detection may be restricted.
A phase II study of cabozantinib in metastatic or unresectable refractory gastrointestinal stromal tumour(GIST): a single-centre study from India.
Ventrapragada N, Rastogi S, Singh K … +5 more , Singh A, Shamim SA, Gamanagatti S, Yadav R, Dash NR
BMC Cancer · 2026 Jun · PMID 42363143 · Full text
BACKGROUND: Beyond third-line therapy, options for metastatic/advanced GIST are limited, especially in low- and middle-income countries (LMICs) where access to fourth-line ripretinib is often restricted. Cabozantinib, a...
BACKGROUND: Beyond third-line therapy, options for metastatic/advanced GIST are limited, especially in low- and middle-income countries (LMICs) where access to fourth-line ripretinib is often restricted. Cabozantinib, a multi-kinase inhibitor targeting KIT and related resistance pathways, could serve as a pragmatic alternative. This Phase II study evaluated the efficacy and safety of cabozantinib in patients with metastatic/advanced GIST who had progressed after ≥ 3 prior Tyrosine Kinase Inhibitors (TKIs). METHODS: This is a single-arm phase II trial that enrolled patients with advanced GIST who had progressed on ≥ 3 TKIs with ECOG PS 0-2. Cabozantinib was given orally at 60 mg daily (40 mg if < 40 kg and/or ECOG PS 2). The primary endpoint was 3-month Progression Free Rate (PFR) by RECIST v1.1. Overall Response Rate (ORR) was assessed by RECIST v1.1 and Choi Criteria. Quality of Life (QoL) was done by EORTC-QLQ-C30. Using Ahern's single-stage phase II design, the trial tested whether cabozantinib could achieve a 3-month PFR of at least 25% in the fourth-line setting versus a null PFR of 5% or less. With a one-sided alpha of 0.05 and 90% power, the required sample size for this single-arm study was 25 patients. RESULTS: Sixteen patients were enrolled. The cohort had a median age of 54.3 years, and most patients were male (75%). Median prior lines were 3 (range 3-5), and 44% had ECOG PS 2. Primary sites were stomach (50%) and small intestine (25%). Liver was the predominant side of metastases (81.3%). Primary mutations included KIT exon 11 (56%), exon 9 (25%), and SDH-deficient GIST (12.5%); the most common secondary mutation pattern was exon 11 + 17 (43%). The 3-month PFR was 62.5% by RECIST v1.1, with median PFS of 4.0 months. ORR was 6.2% by RECIST and 18.8% by Choi criteria. Common grade 3 adverse events were hand-foot skin reaction (18.8%), hypertension (18.8%), and diarrhoea (12.5%). Treatment interruptions and dose reductions occurred in 80% and 73.3%, respectively. Overall, QoL and Global Health Status remained stable. CONCLUSION: Cabozantinib demonstrated clinically meaningful activity with manageable toxicity in refractory metastatic/advanced GIST after ≥ 3 TKIs, supporting its role as a potential option in LMIC contexts where ripretinib access is limited. Larger, comparative phase III trials are warranted to confirm efficacy and better define optimal patient selection and dosing strategies. TRIAL REGISTRATION: Trial Registration Number-CTRI/2024/06/068636. Our trial was registered with Clinical Trials Registry - India (CTRI) on 10/06/2024.
Immuno-oncology in the perioperative setting: the next frontier in resectable head and neck cancers - a systematic review.
Kapoor A, Gupta A, Sansar B … +5 more , Mishra BK, Menon N, Shah M, Noronha V, Prabhash K
BMC Cancer · 2026 Jun · PMID 42363133 · Full text
Perioperative immunotherapy-particularly immune checkpoint inhibitors (ICIs)-has emerged as a promising strategy to reduce recurrence in resectable head and neck squamous cell carcinoma (HNSCC). Despite standard multimod...
Perioperative immunotherapy-particularly immune checkpoint inhibitors (ICIs)-has emerged as a promising strategy to reduce recurrence in resectable head and neck squamous cell carcinoma (HNSCC). Despite standard multimodal therapy, nearly half of patients experience relapse within five years. ICIs such as nivolumab and pembrolizumab have transformed recurrent/metastatic HNSCC, and their integration into curative settings is under active investigation.We conducted a PRISMA-compliant systematic review of PubMed, Embase, Cochrane Library, and major oncology conference proceedings (2018-2026) to identify clinical trials evaluating ICIs in the perioperative setting of HNSCC. Two reviewers independently screened and extracted data. Outcomes of interest included safety, pathological response, event-free or disease-free survival (EFS/DFS), and overall survival (OS). Meta-analysis was not performed due to heterogeneous study designs.Twenty-five studies (18 published, 7 conference abstracts) met inclusion criteria. Neoadjuvant ICI monotherapy was safe but showed modest major pathological response (MPR) rates (~ 6%). Combination strategies were more effective: the IMCISION trial reported 35% MPR with nivolumab plus ipilimumab vs. 17% with nivolumab alone. Neoadjuvant therapy did not delay surgery. In the adjuvant setting, the NIVOPOSTOP trial showed improved 3-year DFS with nivolumab plus postoperative chemoradiotherapy (63.1% vs. 52.5%). The KEYNOTE-689 trial showed perioperative pembrolizumab significantly improved EFS (51.8 vs. 30.4 months), leading to FDA approval in PD-L1 CPS ≥ 1 tumors.Pathologic response correlated with improved survival. Ongoing trials are refining biomarkers, combinations, and sequencing. Perioperative immunotherapy is reshaping curative-intent management of HNSCC, establishing a new multidisciplinary treatment paradigm.
Measurement of metabolic activity by telemetric temperature sensing after immunotherapy and chemotherapy on three different mouse tumor models.
Meisamy S, Brattain K, Shao Q … +4 more , Steinberger D, Moffitt C, Meisamy R, Nelson M
BMC Cancer · 2026 Jun · PMID 42363127 · Full text
This study evaluates within-subject temporal differences between tumor and body temperatures using three cancer models: melanoma, breast cancer, and colon cancer, to monitor the effects of immunotherapy and chemotherapy...
This study evaluates within-subject temporal differences between tumor and body temperatures using three cancer models: melanoma, breast cancer, and colon cancer, to monitor the effects of immunotherapy and chemotherapy on temperature differences. In the melanoma arm, TRP-2 immunotherapy led to increased tumor temperatures compared to the control group, with significant overall treatment separation observed at 58 h into the treatment protocol. For breast cancer, AC-Taxol chemotherapy resulted in a drop in body temperature for both treatment and control groups, with significant treatment group separation on tumor vs. body observed at 96 h. In colon cancer, anti-PD-1 immunotherapy showed an upward trend in tumor temperatures, with significant separation from the control group at 94 h. A series of statistical tests, including mixed-model repeated measures and non-parametric tests, revealed significant differences in temperature trends between treatment and control groups for all cancer types. Furthermore, examination of radial smoothing repeated measures models revealed how the clinical application of this technology could be applied. These results suggest that temperature-based monitoring may be an effective tool for assessing therapeutic responses in cancer treatments, highlighting the utility of thermal measurements in evaluating immunotherapy and chemotherapy efficacy.
Preparation, characterization and anticancer applications of HAase from Pedobacter heparinus.
Dou B, Wu R, Ma X … +2 more , Hu C, Duan X
BMC Cancer · 2026 Jun · PMID 42363124 · Full text
Hyaluronidase (HAase) is an enzyme capable of degrading hyaluronic acid (HA). In anti-tumor therapy, HAase can enhance the efficacy of anti-cancer drugs by regulating the tumor microenvironment and overcoming drug delive...
Hyaluronidase (HAase) is an enzyme capable of degrading hyaluronic acid (HA). In anti-tumor therapy, HAase can enhance the efficacy of anti-cancer drugs by regulating the tumor microenvironment and overcoming drug delivery barriers, and it can also be used directly to inhibit tumor growth. In this study, we identified a previously uncharacterized HAase (Ph-HAase) from Pedobacter heparinus. After purification, the enzyme was obtained with a 43.08% recovery, a 47.5-fold purification, and a specific activity of 32.32 IU/mg. SDS-PAGE and LC-MS analyses revealed that the molecular weight of Ph-HAase was 79.6 kDa. Ph-HAase exhibited excellent stability at temperatures below 30 °C and within the pH range of 6.5 to 7.5. The enzyme activity was found to be relatively high at pH 6.5 and 45℃. Although HA served as the preferred substrate, Ph-HAase also exhibited degradative activity toward Chondroitin Sulfate (CS) and Dermatan Sulfate (DS). Notably, we found that Ph-HAase induced apoptosis in melanoma B16F10 cells via the mitochondrial pathway, characterized by loss of membrane potential and ROS accumulation, and affected the expression of apoptosis-related genes and proteins. In vivo studies further confirmed its anti-melanoma effect. This study is the first to report HAase derived from P. heparinus and to demonstrate its potential for melanoma treatment.
Prehabilitation in cancer care: an evolving field.
Gaffney C, Gorzelitz J, Reeves J … +1 more , Steffens D
BMC Cancer · 2026 Jun · PMID 42363120 · Full text
Cancer treatment imposes significant physiological and psychological demands on patients whose reserves are already under strain. Prehabilitation, the systematic optimisation of physical, nutritional, and psychological c...
Cancer treatment imposes significant physiological and psychological demands on patients whose reserves are already under strain. Prehabilitation, the systematic optimisation of physical, nutritional, and psychological condition prior to cancer treatment, has emerged as a promising strategy to build reserve and accelerate recovery. Yet critical questions remain around patient selection, optimal dose and delivery, and equitable implementation. In this editorial, we outline the current state of evidence, key challenges, and emerging priorities, and invite contributions to BMC Cancer's "Prehabilitation in Cancer Care" Special Collection.
Epidemiology of pre-cancerous cervical lesions among women in Adama, Ethiopia.
Lema TF
BMC Cancer · 2026 Jun · PMID 42363111 · Full text
BACKGROUND: Cervical pre-cancer is a distinct change in the epithelial cells of the transformation zone of the cervix; the cells begin developing in an abnormal fashion in the presence of persistent or long-term high-ris...
BACKGROUND: Cervical pre-cancer is a distinct change in the epithelial cells of the transformation zone of the cervix; the cells begin developing in an abnormal fashion in the presence of persistent or long-term high-risk oncogenic human papillomavirus infection. It is estimated that out of women infected with human papillomavirus, 10% will develop pre-cancerous changes in their cervical tissue. About 8% of the women who develop these changes will develop pre-cancer limited to the outer layers of the cervical cells, and about 1.6% will develop invasive cancer. The main purpose of the study was to determine the epidemiology of pre-cancerous cervical lesions among women in Adama, Ethiopia. METHOD: A cross-sectional study was carried out from April to May 2023. Interviewer administered, structured questionnaire was employed, and visual inspection with acetic acid applied for screening of the cervix. Systematic sampling technique was used to collect data from 383 participants. Data was entered into Epi Info version 7, and analysed using Statistical Package for Social Science version 26. Binary logistic regression for bivariate and multivariable analyses with adjusted odds ratios and 95% CIs were used to identify factors associated with the development of pre-cancerous cervical lesions. The level of significance of association was determined as a p-value < 0.05. RESULTS: The overall prevalence of pre-cancerous cervical lesions was 12.5% (95% CI: 9.17%, 15.83%). Post-coital bleeding (AOR = 25.34: 95% CI: 6.22, 103.20), age at first sex (AOR = 3.96: 95% CI: 1.24, 12.69), lifetime sexual partner (AOR = 8.37: 95% CI: 1.00, 70.14) and HIV sero-status (AOR = 10.96: 95% CI: 2.25, 53.37) were identified as independent factors significantly associated with the development of pre-cancerous cervical lesions. CONCLUSIONS: There was high prevalence of pre-cancerous cervical lesions among participants compared to a study finding obtained in North Ethiopia [18]. Conduct health education to the public on avoidance of identified cervical cancer risk factors. Multiple factors (post-coital bleeding, age at first sex, lifetime sexual partner and HIV sero-status) were identified as independent factors significantly associated with the development of pre-cancerous cervical lesions. Awareness creation campaigns and educational programs about the prevention of pre-cancerous cervical lesions and associated risk factors need to be implemented in the community.
Prognostic significance of pretreatment pan-immune inflammation value in esophageal squamous cell carcinoma patients undergoing definitive chemoradiotherapy.
Cai Y, Wei N, Zhang J … +4 more , Lin R, Teng C, Yao Q, Lin Z
BMC Cancer · 2026 Jun · PMID 42363078 · Full text
BACKGROUND: The pan-immune inflammation value (PIV) reflects the balance between host immune and inflammatory status and is a commonly used indicator for evaluating cancer prognosis. However, to date, no studies have con...
BACKGROUND: The pan-immune inflammation value (PIV) reflects the balance between host immune and inflammatory status and is a commonly used indicator for evaluating cancer prognosis. However, to date, no studies have confirmed the prognostic value of pretreatment PIV in patients with locally advanced esophageal squamous cell carcinoma (ESCC) undergoing definitive chemoradiotherapy (dCRT). METHODS: The receiver operating characteristic (ROC) curve was used to determine the optimal cutoff value of the PIV for predicting prognosis. Univariate and multivariate Cox regression analyses were performed to identify independent prognostic factors. Restricted cubic spline (RCS) curve analysis was used to investigate the relationship between PIV and prognosis. A visual analysis was conducted using the SHAP method. Combined with TNM staging, a comprehensive risk stratification model was constructed through recursive partitioning analysis (RPA). Finally, the model was evaluated through decision curve analysis (DCA) and ROC curve. RESULTS: A total of 696 patients were included. The level of PIV before treatment was significantly correlated with a larger primary tumor burden. RCS analysis revealed a non-linear relationship between PIV and survival outcomes. Both univariate and multivariate Cox analyses confirmed that the pre-treatment PIV was an independent prognostic factor for overall survival (OS) and progression-free survival (PFS). Subgroup analysis showed that in all subgroups except those receiving ≥ 3 cycles of chemotherapy, high PIV was an adverse prognostic factor. Based on PIV and TNM stage, a new risk stratification model was constructed through RPA, which classified patients into three risk groups with significantly different OS and PFS. Compared with the traditional TNM stage, this RPA model showed significantly better predictive performance. CONCLUSION: Pretreatment PIV is an independent prognostic biomarker in locally advanced ESCC patients undergoing dCRT. The novel RPA model integrating PIV with TNM staging outperforms traditional staging, offering a refined "anatomical-biological" risk stratification tool to guide personalized treatment.
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