Journal Of Cancer Research And Clinical Oncology[JOURNAL]
Sun
200 papers
Insights into SUMOylation in gastric cancer: molecular mechanisms and emerging therapeutic opportunities.
Tabnak P, Ebrahimnezhad M
J Cancer Res Clin Oncol · 2025 Nov · PMID 41317288 · Full text
Gastric cancer remains a significant global health challenge due to its aggressive behavior, high mortality rates, and limited treatment success. Growing research underscores the critical role of SUMOylation, a reversibl...
Gastric cancer remains a significant global health challenge due to its aggressive behavior, high mortality rates, and limited treatment success. Growing research underscores the critical role of SUMOylation, a reversible post-translational modification, in regulating key cellular processes such as DNA repair, gene expression, genomic stability, and signaling pathways. Aberrant SUMOylation is closely linked to gastric cancer development, metastasis, and resistance to therapies, positioning it as a potential therapeutic target. This review consolidates current knowledge of the SUMOylation system, which involves activating (E1), conjugating (E2), and ligating (E3) enzymes, alongside SUMO-specific proteases (SENPs) that reverse the modification. We explore how SUMOylation influences cancer-promoting and tumor-suppressing pathways by stabilizing or degrading critical proteins, modulating immune responses, driving epithelial-mesenchymal transition, and contributing to chemoresistance. Furthermore, we discuss promising therapeutic approaches targeting SUMOylation, including small-molecule inhibitors, natural bioactive compounds, and synthetic lethal strategies that exploit SUMO pathway weaknesses. Preclinical studies suggest these approaches could enhance chemotherapy and immunotherapy effectiveness, offering new precision treatment options. Deepening our understanding of SUMOylation in gastric cancer is vital for developing innovative, mechanism-driven therapies to improve patient outcomes.
Research progress on ferroptosis in drug resistance and therapy of gastric cancer.
Liu Y, Jia L, Yang L … +2 more , Ning Z, Li Y
J Cancer Res Clin Oncol · 2025 Nov · PMID 41315060 · Full text
AIM: The clinical management of gastric cancer (GC) is frequently challenged by the development of drug resistance, leading to poor patient outcomes. This review aims to explore the role of ferroptosis, an iron-dependent...
AIM: The clinical management of gastric cancer (GC) is frequently challenged by the development of drug resistance, leading to poor patient outcomes. This review aims to explore the role of ferroptosis, an iron-dependent form of programmed cell death driven by lipid peroxidation, in overcoming this therapeutic hurdle. Our objective is to provide a theoretical foundation for developing novel strategies to reverse drug resistance in GC by targeting the ferroptosis pathway. METHODS: This review systematically elucidates the core regulatory mechanisms of ferroptosis and analyzes its key role in mediating drug resistance in GC. We synthesize current literature to explore potential therapeutic strategies that leverage ferroptosis induction to sensitize cancer cells. Furthermore, we critically examine the complex interplay between ferroptosis and the tumor microenvironment (TME) and discuss the challenges associated with translating these findings into personalized treatment approaches, integrating insights from emerging technologies. RESULTS: Our analysis confirms that ferroptosis is governed by a precise regulatory network involving glutathione metabolism, lipid peroxidation, and iron homeostasis, which is frequently dysregulated in GC. We identify that key mechanisms of conventional drug resistance are linked to the evasion of ferroptosis. Consequently, several potential therapeutic strategies, including the use of ferroptosis inducers (FINs) and combination therapies, show promise in resensitizing resistant GC cells. The review also highlights the dual role of the TME, which can either suppress or promote ferroptosis, adding a layer of complexity. Finally, we identify significant challenges in patient stratification and the need for reliable biomarkers to achieve personalized ferroptosis-based therapies. CONCLUSION: Targeting ferroptosis presents a promising and innovative research avenue for reversing drug resistance in gastric cancer. Strategies designed to induce ferroptosis effectively overcome common resistance mechanisms and hold significant therapeutic potential. Future research must focus on integrating multi-omics technologies and advanced drug delivery systems to decipher the complex regulatory networks of ferroptosis within the TME and to develop biomarkers for personalized treatment, thereby paving the way for improved clinical outcomes.
Knockdown of FOXD3-AS1 inhibits the progression of prostate cancer by targeting miR-491-5p/PEG10.
Yu Y, Liu Q, Wen Y
J Cancer Res Clin Oncol · 2025 Nov · PMID 41291383 · Full text
BACKGROUND: The lncRNA FOXD3-AS1 shows abnormal expression in various tumors, but its role in prostate cancer (PCa) remains unclear. OBJECTIVE: This study sought to examine FOXD3-AS1 expression patterns in PCa and its mo...
BACKGROUND: The lncRNA FOXD3-AS1 shows abnormal expression in various tumors, but its role in prostate cancer (PCa) remains unclear. OBJECTIVE: This study sought to examine FOXD3-AS1 expression patterns in PCa and its molecular role in regulating PEG10 through miR-491-5p. METHODS: The methodological approach involved the application of RT-qPCR to determine the expression profiles of FOXD3-AS1, miR-491-5p, and PEG10 across PCa tissues and in vitro cell systems; subcellular localization analysis determined the cytoplasmic distribution of FOXD3-AS1; Cell proliferation, migratory and invasive capacities, as well as apoptosis, were assessed using CCK-8, transwell, and flow cytometric assays, respectively; dual-luciferase reporter assays verified the targeting relationships between molecules; statistical software was used for data analysis. RESULTS: FOXD3-AS1 demonstrated substantial upregulation within prostate carcinoma tissues and cultured cells and was found to be predominantly localized within the cytoplasmic compartment. Functional experiments demonstrated that depleting FOXD3-AS1 strongly impeded cell multiplication, spread, and penetration, and enhanced apoptotic activity. Rescue assays demonstrated that co-intervention of miR-491-5p or its downstream target PEG10 could counteract the tumor-suppressive effects induced by FOXD3-AS1 silencing. Mechanistically, FOXD3-AS1 functions as a ceRNA, sequestering miR-491-5p to attenuate its repression of PEG10. CONCLUSION: FOXD3-AS1 influences PCa cell behavior via the miR-491-5p/PEG10 axis.
Surgical resection for pulmonary metastases from head and neck adenoid cystic carcinoma: a propensity-matched survival analysis.
Yu Z, Yang X, Wu J … +8 more , Yu X, Cui J, Gao X, Ma B, Ke J, Zhang B, Chen X, Yu L
J Cancer Res Clin Oncol · 2025 Nov · PMID 41291298 · Full text
OBJECTIVE: The management of pulmonary metastases (PM) from head and neck adenoid cystic carcinoma (ACC) remains controversial, with limited evidence guiding the choice between surgical and non-surgical strategies. This...
OBJECTIVE: The management of pulmonary metastases (PM) from head and neck adenoid cystic carcinoma (ACC) remains controversial, with limited evidence guiding the choice between surgical and non-surgical strategies. This study aimed to compare long-term survival outcomes between patients undergoing surgical resection and those receiving non-surgical management for ACC-derived PM. METHODS: We conducted a retrospective analysis of 204 patients with pulmonary metastases from head and neck ACC treated at our institution between January 2010 and December 2024. Patients were categorized into Surgery (n = 108) and Non-Surgery (n = 96) groups. To address selection bias and improve causal inference in this observational study, propensity score matching (PSM) was performed based on key clinical variables, generating 68 well-matched pairs. Overall survival (OS) and progression-free survival (PFS) were compared using Kaplan-Meier analysis and Cox proportional hazards models. RESULTS: Before matching, the Surgery group demonstrated significantly higher 5-year OS (97.73% vs. 84.2%, P = 0.0004) and PFS (89.39% vs. 74.66%, P = 0.021). After PSM, the survival advantage persisted, with the Surgery group showing improved 5-year OS (95.75% vs. 82.91%, P = 0.0063) and PFS (86.93% vs. 73.86%, P = 0.0039). Multivariate analysis confirmed surgical resection as an independent prognostic factor for improved OS (HR = 0.08, 95% CI: 0.01-0.42, P = 0.0032), alongside tumor grade, presence of pleural effusion, and International Registry of Lung Metastases (IRLM) stage. CONCLUSIONS: In this propensity-matched analysis, surgical metastasectomy was associated with significantly improved survival in selected patients with ACC lung metastases, supporting its consideration as a valuable therapeutic option for oligometastatic disease within a multidisciplinary framework.
Association of donor and recipient single-nucleotide polymorphisms of interleukin-1 gene with outcomes after allogeneic hematopoietic stem cell transplantation in childhood.
Kämpfner K, Wittig S, Gruhn B
J Cancer Res Clin Oncol · 2025 Nov · PMID 41291248 · Full text
PURPOSE: Complications such as graft-versus-host disease (GVHD), hepatic sinusoidal obstruction syndrome, and infections compromise the success of allogeneic hematopoietic stem cell transplantation (HSCT) as a treatment...
PURPOSE: Complications such as graft-versus-host disease (GVHD), hepatic sinusoidal obstruction syndrome, and infections compromise the success of allogeneic hematopoietic stem cell transplantation (HSCT) as a treatment modality for malignant or genetic diseases. Identification of beneficial non-human leukocyte antigens (HLA), such as cytokines, is one approach to reduce the rate of unintended events. This study investigated the association between single-nucleotide polymorphisms (SNPs) of the gene of the proinflammatory cytokine interleukin-1 (IL-1) and treatment outcomes after allogeneic HSCT in a pediatric population. METHODS: In our single-center study, we retrospectively analyzed a cohort of 270 children and their respective donors. They underwent allogeneic HSCT for the first time, and their conditioning regimen was myeloablative in all cases. We used polymerase chain reaction to genotype the SNPs of IL-1α rs1800587 (C > T), IL-1β rs16944 (C > T), and IL-1β rs1143627 (C > T). The outcome measures included overall survival (OS), event-free survival (EFS), relapse rate (RR), transplant-related mortality (TRM), and the occurrence of acute or chronic GVHD. RESULTS: The distribution of IL-1α rs1800587 genotype was as follows: we observed the CC genotype in 124 of 256 recipients (48.4%) and 132 of 270 donors (48.9%). We detected the CT genotype in 115 patients (44.9%) and 114 donors (42.2%) and found the homozygous TT genotype in 17 children (6.6%) and 24 of their donors (8.9%). The distribution of the SNP IL-1α rs1800587 is in Hardy-Weinberg equilibrium. The incidence of moderate or severe acute GVHD was significantly decreased in recipients receiving a donor transplant with the TT genotype (4% (TT) versus 25% (CC/CT); p = 0.028). We found no significant SNP IL-1α rs1800587 (C > T) associations for chronic GVHD, RR, TRM, EFS, and OS. For the other genotypes analyzed, IL-1β rs11644 (C > T) and IL-1β rs1143627 (C > T), we also found no significant associations for acute and chronic GVHD, RR, TRM, EFS, and OS, neither in donors nor in recipients. The results of the multivariate analysis revealed a hazard ratio of 0.17 (confidence interval 0.0229-1.27), and a trend that IL-1α rs1800587 could be an independent risk factor for acute GVHD (p = 0.084). CONCLUSION: Our study identified the donor IL-1α rs1800587 CC/CT genotype as a possible genetic risk factor for developing moderate to severe acute GVHD (grade II - IV) in pediatric patients who underwent allogeneic HSCT. Once confirmed in further studies, these results may influence the donor selection and prophylaxis to decrease the risk of acute GVHD in children.
The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.
Zheng Y, Jin Q
J Cancer Res Clin Oncol · 2025 Nov · PMID 41272363 · Full text
Chronic obstructive pulmonary disease (COPD) and lung cancer are highly correlated and frequently co-occur. Any degree of COPD significantly increases the risk of developing lung cancer, suggesting they may share common...
Chronic obstructive pulmonary disease (COPD) and lung cancer are highly correlated and frequently co-occur. Any degree of COPD significantly increases the risk of developing lung cancer, suggesting they may share common pathogenic mechanisms. The hypoxia-inducible factor 1 (HIF-1) signaling pathway, a complex regulatory network for cellular sensing and response to hypoxia, is abnormally activated in both COPD and lung cancer. Chronic inflammation, immune microenvironment imbalance, extracellular matrix remodeling, epithelial-mesenchymal transition, angiogenesis, and epithelial differentiation, all closely related to the HIF-1 pathway, lie at the intersection of both diseases. Consequently, the HIF-1 pathway is proposed as a potential molecular mechanism underpinning the occurrence, progression, and poor prognosis of lung cancer with COPD (LC-COPD). In this review, we focus on the role and mechanisms of HIF-1 in advancing LC-COPD, highlighting its promising potential as a therapeutic target.
Clinical application value of modified overlap anastomosis for Siewert type II and III adenocarcinoma of esophagogastric junction.
Fan Y, Hou L, Zhang H … +7 more , Zhang R, Shi G, Li Q, Wang X, Wang Y, Wei Q, Gao T
J Cancer Res Clin Oncol · 2025 Nov · PMID 41264122 · Full text
AIM: To explore the clinical application value of modified overlap anastomosis for Siewert type II and III adenocarcinoma of esophagogastric junction, and to further evaluate its feasibility and safety. METHODS: We retro...
AIM: To explore the clinical application value of modified overlap anastomosis for Siewert type II and III adenocarcinoma of esophagogastric junction, and to further evaluate its feasibility and safety. METHODS: We retrospectively analyzed clinical data from 222 patients with Siewert type II and III adenocarcinoma of the esophagogastric junction admitted to our hospital between January 2017 to October 2023. All patients underwent laparoscopic total gastrectomy with D2 lymph node dissection. 64 patients underwent esophagojejunostomy with modified overlap anastomosis, and 158 patients were operated using the circular stapled anastomosis. Variables that are statistically different were compared between groups using propensity score matching (PSM). The differences in surgical-related indicators and clinical outcomes for the two groups were compared. Finally, we analyzed the risk factors associated with esophagojejunostomy (EJ)-related complications. RESULTS: There was no statistically significant difference between the two groups of patients in terms of BMI, gender, age, and tumor-related information (P value > 0.05). However, there was then a difference in preoperative hemoglobin between the two groups. To eliminate heterogeneity, we combined patients with PSM. In terms of intraoperative conditions and postoperative recovery after PSM, compared with the circular stapled anastomosis group, the modified overlap group showed the shorter total operation time, shorter the length of the auxiliary incision, shorter time to the soft diet intake, milder postoperative pain. In terms of postoperative complications and overall survival after PSM, the modified overlap group can reduce the probability of abdominal infection and there was no difference in overall survival (OS) and postoperative late complications between the two groups. Multivariate analysis showed that the Siewert type [odds ratio (OR), 0.355; 95% confidence interval (CI) 0.189-0.639, P value = 0.005] was independent risk factors of EJ-related complications. CONCLUSION: Although the modified overlap group had slightly lower total protein after surgery, it had advantages in operation time, the length of the auxiliary incision, the soft diet intake time, postoperative pain, abdominal infection. General surgeons should exercise heightened vigilance in preventing EJ-related complications for patients classified as Siewert type II. In summary, modified Overlap anastomosis is safe and reliable. It has clinical application value.
Exploring the evolving role of apolipoproteins in oncology: global trends and emerging frontiers.
Tian D, Hu Z, Yang Z … +8 more , Zhao L, Zhao H, Sang X, Du S, Luo Y, Zhang L, Xu Y, Lu X
J Cancer Res Clin Oncol · 2025 Nov · PMID 41258938 · Full text
BACKGROUND: Metabolic reprogramming, especially lipid metabolism, is crucial in cancer progression and treatment resistance. Apolipoproteins are crucial targets for research as they regulate autophagy, oxidative stress,...
BACKGROUND: Metabolic reprogramming, especially lipid metabolism, is crucial in cancer progression and treatment resistance. Apolipoproteins are crucial targets for research as they regulate autophagy, oxidative stress, and chemoresistance. A systematic bibliometric and bioinformatics approach is necessary to identify trends and elucidate the molecular mechanisms linking apolipoproteins to cancer. METHODS: A systematic bibliometric analysis was conducted using the Web of Science Core Collection and PubMed. VOSviewer, CiteSpace, and the Bibliometrix R package were employed to analyze and visualize co-authorship networks, keyword trends, and other key metrics. Bioinformatics analysis integrated protein-protein interaction network construction, hub gene identification, and enrichment analysis using R-based pipelines. RESULTS: China has led the international research on apolipoproteins and cancer since 2015. Research has shifted from molecular studies to clinical applications, highlighting the roles of apolipoproteins in cancer risk, progression, and prognosis. Bioinformatic analysis identified key genes represented by APOA1 (apolipoprotein A1), APOE (apolipoprotein E), APOA2 (apolipoprotein A2), and ALB (Albumin) as central regulators in lipid localization, cholesterol metabolism, insulin resistance, and the peroxisome proliferator-activated receptors (PPARs) signaling pathways. CONCLUSIONS: This study combines bibliometric and bioinformatic approaches to explore apolipoprotein research in cancer. The research trend revealed apolipoproteins with the most research potential in a specific cancer type, as confirmed in the clinical trials. Bioinformatic research found the key genes regulating several essential lipid-related pathways. This article clearly outlined the research landscape and frontiers of this field by combining various databases and methods, highlighting the significant potential of apolipoproteins in the development of novel cancer medications.
Recent updates and future perspectives about ALDH1B1 as a potential anticancer target: a review.
Zhao T, Sun Z, Li Z … +3 more , Qu L, Li Y, Liu J
J Cancer Res Clin Oncol · 2025 Nov · PMID 41258925 · Full text
Aldehyde dehydrogenases (ALDHs) are responsible for the NAD(P)-dependent oxidation of aldehydes into carboxylic acids, fulfilling key roles in detoxification, antioxidant defense, biosynthesis, and regulatory processes....
Aldehyde dehydrogenases (ALDHs) are responsible for the NAD(P)-dependent oxidation of aldehydes into carboxylic acids, fulfilling key roles in detoxification, antioxidant defense, biosynthesis, and regulatory processes. Elevated expression and activity of ALDH isoenzymes have been documented in various human cancers, where they are linked to cancer recurrence. While the human genome encodes 19 functional ALDH genes, aldehyde dehydrogenase 1B1 (ALDH1B1) has emerged as a critical enzyme in diverse human pathologies. ALDH1B1 is a major mitochondrial enzyme involved in detoxifying lipid peroxidation by-products and metabolizing various aldehyde substrates. Notably, both low and high ALDH1B1 expression levels contribute to tumor progression and with marked variability observed across different tumor types. This review summarizes the essential functions and potential ALDH1B1 mechanisms in the tumor initiation, progression, metastasis, and therapeutic responses across cancer types. Our analysis indicates that ALDH1B1 is a potential therapeutic target for cancer therapy.
Constructing a novel MPT-driven necrosis-associated gene set for predicting prognosis and immune status in skin cutaneous melanoma.
Wenxian Y, Shuwen F
J Cancer Res Clin Oncol · 2025 Nov · PMID 41254408 · Full text
BACKGROUND: Skin cutaneous melanoma (SKCM) is an aggressive malignancy with limited prognostic markers. Mitochondrial permeability transition (MPT)-driven necrosis has been implicated in tumor progression and immune regu...
BACKGROUND: Skin cutaneous melanoma (SKCM) is an aggressive malignancy with limited prognostic markers. Mitochondrial permeability transition (MPT)-driven necrosis has been implicated in tumor progression and immune regulation, yet its role in SKCM remains unclear. METHODS: 39 MPT-driven necrosis-related genes (MPTDNRG) were retrieved from Molecular Signatures Database (MSigDB). Using TCGA-SKCM and GTEx datasets, differentially expressed genes (DEGs) were identified and incorporated into Cox and LASSO analyses. An MPT-driven necrosis-related gene signature (MPTDNRGS) was constructed. The signature was validated in GEO cohorts (GSE19234, GSE65904). A nomogram integrating clinical factors was established to assess predictive performance. Functional enrichment, immune infiltration, and checkpoint responsiveness were evaluated. Single-cell RNA-seq (scRNA-seq) datasets were further analyzed to map cell-type-specific expression and T-cell trajectories. RESULTS: A five gene signature (BIRC3, CASP7, ENDOG, PRF1, PRKCB) stratified patients into high and low risk groups with distinct survival outcomes. The nomogram achieved strong predictive accuracy (3-year AUC = 0.772). High risk patients exhibited suppressed immune activation, lower T-cell infiltration, and reduced predicted response to immune checkpoint inhibitors. Single cell analysis revealed higher MPTDNRGS scores in tumor-infiltrating T cells than in normal controls. Pseudotime trajectories showed cytotoxic T cells transitioning to immunosuppressive phenotypes, marked by progressive BIRC3 upregulation. Elevated BIRC3 correlated with immune inhibitory markers and enrichment of TGF-β and IL6/JAK/STAT3 pathways. CONCLUSION: We established and validated a novel MPT-driven necrosis-based prognostic model for SKCM. This model reliably predicted patient outcomes and immune status. BIRC3 emerged as a potential regulator of T-cell dysfunction and a promising therapeutic target in SKCM.
Integration of RASSF1A and TSPYL5 methylation and AFP protein as plasma biomarker for hepatocellular carcinoma diagnosis.
Chen H, Luo Y, Li L … +10 more , Xu F, Lai X, Li J, Li X, Song W, Liu Y, Bao D, Liu J, Zhou G, Wan S
J Cancer Res Clin Oncol · 2025 Nov · PMID 41254209 · Full text
BACKGROUND: Early detection of hepatocellular carcinoma (HCC) represents a significant clinical challenge due to the lack of effective biomarkers. Previous studies have revealed abnormal hypermethylation of RASSF1A and T...
BACKGROUND: Early detection of hepatocellular carcinoma (HCC) represents a significant clinical challenge due to the lack of effective biomarkers. Previous studies have revealed abnormal hypermethylation of RASSF1A and TSPYL5 in HCC tissues, prompting further investigation into their utility as potential biomarkers for HCC diagnosis. In this study, we explored the clinical value of RASSF1A/TSPYL5 methylation alone and in combination with AFP protein as diagnostic biomarkers for early HCC detection. METHODS: Bioinformatics analysis using MethSurv, LinkedOmics, and Wanderer was conducted to assess the methylation levels of RASSF1A and TSPYL5 in HCC tissue samples from the public database. The methylation status of these two genes was validated in cell lines and plasma samples from HCC patients. Furthermore, the ARTHCC model, comprising the measurement of RASSF1A and TSPYL5 methylation and AFP protein, was developed and validated using plasma samples from HCC patients. RESULTS: Our comprehensive bioinformatic analysis revealed that TSPYL5 CpG sites were hypermethylated in HCC tissue samples, particularly among CpG island and shore regions. Approximately 40% of CpG sites of RASSF1A also exhibited hypermethylation. The hypermethylation status of TSPYL5 may be associated with portal vein tumor thrombus (PVTT) in HCC patients. Combining analysis of RASSF1A and TSPYL5 methylation levels with AFP protein, the ARTHCC model demonstrates superior sensitivity and specificity for detecting HCC in both the discovery and validation cohorts. Notably, the ARTHCC model consistently exhibited robust performance across different subgroups. CONCLUSIONS: This study provides compelling evidence that the combination of RASSF1A/TSPYL5 methylation and AFP protein is a promising biomarker panel for the early detection of HCC. The ARTHCC model demonstrates remarkable sensitivity and specificity, outperforming AFP.
Primary hemangioblastoma of rectum: a rare case report and review of literature.
Zheng A, Zhang S, Ma Q … +3 more , Yang W, Xiao H, Liang X
J Cancer Res Clin Oncol · 2025 Nov · PMID 41240144 · Full text
PURPOSE: Hemangioblastoma is an uncommon tumor of uncertain histogenesis, primarily found in the central nervous system. However, extraneural cases have been reported in visceral organs such as the kidneys, pancreas, per...
PURPOSE: Hemangioblastoma is an uncommon tumor of uncertain histogenesis, primarily found in the central nervous system. However, extraneural cases have been reported in visceral organs such as the kidneys, pancreas, peritoneum, and liver. Hemangioblastoma occurring in the gastrointestinal tract is extremely rare, with only 4 cases can be retrieved. Here, we presented a case of rectal hemangioblastoma. METHODS: A 59-year-old woman sought medical attention for altered stool consistency and the colonoscopy revealed a submucosal lesion in the rectum. Subsequently, she underwent endoscopic submucosal dissection. Grossly, the excised lesion was a broad-based polypoid mass measuring 1.2 × 0.8 × 0.8 cm, with a grayish-white appearance and no signs of hemorrhage or necrosis. Histologically, the tumor consisted of a rich network of thin-walled blood vessels interspersed with vesicular neoplastic cells, with minimal mitotic activity. Immunohistochemistry found that neoplastic cells were positive for D2-40, and β-catenin showed normal membranous staining pattern. No pathogenic mutations in the VHL gene were detected by NGS in this sample. However, we found genetic alterations in other genes potentially associated with the pathogenesis of hemangioblastoma, such as TSC, SDH and PTEN. RESULTS: Based on the above findings, the diagnosis of hemangioblastoma was made. The differential diagnosis included hemangioma, lymphangioma, neuroendocrine tumor, metastatic renal cell carcinoma, perivascular epithelioid cell tumor, gastrointestinal stromal tumor, and well-differentiated liposarcoma. CONCLUSION: This case underscored the importance of considering hemangioblastoma in the differential diagnosis of rectal submucosal lesions. It highlighted the need for a thorough diagnostic approach that integrates colonoscopic evaluation with histopathological examination, particularly in patients presenting with altered stool consistency or melena. Furthermore, the NGS results implicated that TSC, SDH and PTEN may contribute to hemangioblastoma development. These alterations could constitute a novel diagnostic signature, a premise that warrants definitive investigation through larger, multi-institutional studies.
Patient-reported outcomes following various incision techniques in breast reconstruction: an observational cohort study in China.
Wang L, Song Y, Huang W … +3 more , Guo S, Wu X, Zheng H
J Cancer Res Clin Oncol · 2025 Nov · PMID 41240120 · Full text
BACKGROUND: To evaluate patient satisfaction with different incision types in breast reconstruction surgery in China and to explore the factors related to these outcomes. METHODS: This single-center, retrospective cohort...
BACKGROUND: To evaluate patient satisfaction with different incision types in breast reconstruction surgery in China and to explore the factors related to these outcomes. METHODS: This single-center, retrospective cohort study included patients who underwent breast reconstruction at Hubei Cancer Hospital from September 2022 to September 2024. The patients were divided into four groups based on the incision type: (1) lateral axillary incision, (2) radial incision, (3) inferolateral inframammary fold incision, and (4) endoscopic-assisted surgery. Patient-reported outcomes (PROs) were collected ≥ 3 months after surgery using the Breast Cancer Core Scale (BREAST-Q) V2.0, the EuroQol five-dimension five-level health questionnaire (EQ-5D-5L), and the Decision Regret Scale (DRS). It should be noted that the type of incision was non-randomly allocated, although multivariate regression was performed to adjust for potential confounding factors. RESULTS: A total of 209 patients were included in this study. 34 (16.3%), 67 (32.1%), 64 (30.6%), and 44 (21.1%) patients underwent lateral axillary incision, radial incision, inferolateral inframammary fold incision, and endoscopic-assisted surgery, respectively. The endoscopic-assisted surgery group had the highest satisfaction (59.00 [IQR 57.75, 65.00]), and the radial incision group had the lowest satisfaction (53.00 [IQR 47.00-60.50]) (P = 0.007). Multivariable linear regression showed that a reduction in bra size was negatively independently associated with breast satisfaction (β = - 18.662, 95%CI: -26.789, -10.535, P < 0.001), while an inferolateral inframammary fold incision was positively independently associated with breast satisfaction (β = 6.430, 95%CI: 0.199, 12.662, P = 0.043). Skin-sparing mastectomy (SSM) (β = 7.468, 95%CI: 0.557-14.308, P = 0.034) and prepectoral implant plane (β = 6.756, 95%CI: 0.278-13.234, P = 0.041) were both positively independently associated with the DRS scores. CONCLUSION: Despite the study's limitations, our findings indicate that traditional techniques such as radial incision and inferolateral inframammary fold incision are still prevalent in China. Endoscopic-assisted surgery is associated with superior patient-reported satisfaction, highlighting its potential value for wider dissemination in clinical practice. Factors influencing patient satisfaction include reduced bra cup size, surgical approach, and implant plane.
Retraction Note: Signaling network involved in the GPC3-induced inhibition of breast cancer progression: role of canonical Wnt pathway.
Fernández D, Guereño M, Huvelle MAL … +2 more , Cercato M, Peters MG
J Cancer Res Clin Oncol · 2025 Nov · PMID 41222774 · Full text
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A clinical report and analysis of metachronous multiple primary cancers occurred in four sites.
Sun R, Xie H, He S … +1 more , Li Q
J Cancer Res Clin Oncol · 2025 Nov · PMID 41217553 · Full text
PURPOSE: This case report describes a rare occurrence of quadruple primary malignancies-specifically, bilateral primary breast cancer, ovarian cancer, and pleomorphic malignant fibrous histiocytoma/undifferentiated high-...
PURPOSE: This case report describes a rare occurrence of quadruple primary malignancies-specifically, bilateral primary breast cancer, ovarian cancer, and pleomorphic malignant fibrous histiocytoma/undifferentiated high-grade pleomorphic sarcoma-and explores its potential association with hereditary tumor syndromes. METHODS: We conducted a detailed clinical and histopathological analysis of the case. Repeated imaging and pathological examinations were performed to confirm the diagnosis of each primary malignancy. RESULTS: The patient was diagnosed with four distinct primary tumors, and pathological evaluation confirmed each malignancy. CONCLUSION: This case emphasizes the importance of comprehensive pathological and genetic evaluation in patients with multiple primary malignancies. It highlights the growing incidence of such tumors among long-term cancer survivors and provides valuable insights for diagnosis and management in the context of hereditary cancer syndromes.
DCN, NPM3 and SULF1 are hub genes related to vasculogenic mimicry in lung adenocarcinoma.
Sun C, Ye M, Cao W … +6 more , Zeng J, Liang Z, Li Y, Wei S, Zhao Z, Zhao Z
J Cancer Res Clin Oncol · 2025 Nov · PMID 41205056 · Full text
AIM: Vasculogenic mimicry (VM), a process in which cancer cells form endothelial cell-independent vascular networks, is a hallmark of tumor aggressiveness in lung adenocarcinoma (LUAD) and supports tumor growth and metas...
AIM: Vasculogenic mimicry (VM), a process in which cancer cells form endothelial cell-independent vascular networks, is a hallmark of tumor aggressiveness in lung adenocarcinoma (LUAD) and supports tumor growth and metastasis. This study aims to identify and validate key genes associated with VM formation in LUAD, and to elucidate their functional roles and clinical significance. METHODS: Transcriptomic data from LUAD samples were analyzed using differential expression analysis (DEA) and weighted gene co-expression network analysis (WGCNA) to identify VM-associated genes. Machine learning algorithms were applied to refine the selection and identify hub genes. Functional enrichment and immune infiltration analyses were performed. The role of SULF1 in VM was further validated through in vitro and in vivo experiments. RESULTS: We identified 10,810 differentially expressed genes. WGCNA revealed 101 VM-associated genes, predominantly within the "yellow" and "brown" modules. Machine learning pinpointed three key regulators: downregulated decorin (DCN) and upregulated nucleoplasmin 3 (NPM3) and sulfatase 1 (SULF1). Functional enrichment analysis highlighted their involvement in extracellular matrix (ECM) organization and ribosomal pathways. Immune infiltration analysis indicated a positive correlation between DCN and immune cell presence, whereas NPM3 and SULF1 showed negative correlations. Critically, SULF1 overexpression promoted VM formation in vitro by enhancing cell migration and invasion, mediated through the vascular endothelial growth factor (VEGF)/transforming growth factor beta (TGF-β)/Vimentin signaling axis, and accelerated tumor growth in vivo. CONCLUSION: We identified DCN, NPM3, and SULF1 as key biomarkers of VM in LUAD. SULF1, in particular, plays a central role in driving VM formation and tumor progression. These findings offer novel mechanistic insights and highlight potential therapeutic targets for LUAD treatment.
Fertility-sparing treatment for overweight patients with early-stage endometrial cancer or atypical endometrial hyperplasia under weight loss intervention.
Fu M, Cao D, Liu Q … +6 more , Feng Y, Yu M, Yang J, Zhou H, Cheng N, Wu X
J Cancer Res Clin Oncol · 2025 Nov · PMID 41203996 · Full text
OBJECTIVE: To evaluate various body fat indicators under weight management on the time to complete response (CR) in overweight patients undergoing fertility-sparing treatment for endometrial cancer (EC) or atypical hyper...
OBJECTIVE: To evaluate various body fat indicators under weight management on the time to complete response (CR) in overweight patients undergoing fertility-sparing treatment for endometrial cancer (EC) or atypical hyperplasia (AEH). METHODS: Clinical data and weight indicators of obese patients (percent body fat ≥ 30%) with AEH or early-stage EC who received fertility-sparing treatment from 2018 to 2023 were retrospectively collected from the Peking Union Medical College Hospital. Cox proportional hazards regression analysis was used for univariate and multivariate analyses. RESULTS: Fifty-three patients with AEH (45.28%) or EC (54.72%) were finally included. Percent body fat > 8% (p = 0.018) was identified as an independent predictor of time to CR. Patients with body fat mass loss > 15%, and percent body fat loss > 8% had a lower recurrence rate (p = 0.043 and p = 0.007, respectively). Patients with visceral fat area loss > 18%, body fat mass loss > 15%, and percent body fat loss > 8% had a slightly higher pregnancy rate. CONCLUSION: When overweight patients with AEH or EC receive fertility-sparing treatment, multiple body fat indicators, especially the loss of percent body fat, are more meaningful for evaluating the time to CR, recurrence rate, and pregnancy rate than weight loss. Registration: ChiCTR2200067099
Prognostic impact of extranodal extension in oral cavity cancers: a retrospective analysis and implications for treatment intensification.
Thakur P, I V, Dwivedi A … +6 more , Dora TK, Singla A, Sancheti S, Goel A, Gulia A, Kaur A
J Cancer Res Clin Oncol · 2025 Nov · PMID 41186730 · Full text
PURPOSE: Extranodal extension (ENE) and positive surgical margins are recognized high-risk factors in head and neck cancers. Despite their prognostic significance, ENE was incorporated into the AJCC 8th edition staging o...
PURPOSE: Extranodal extension (ENE) and positive surgical margins are recognized high-risk factors in head and neck cancers. Despite their prognostic significance, ENE was incorporated into the AJCC 8th edition staging only recently. This study evaluates survival outcomes in patients with oral cavity squamous cell carcinoma (OCSCC) based on ENE status and its association with radiological ENE and other intermediate-risk features, including lymphovascular invasion (LVI), perineural invasion (PNI), T stage, and depth of infiltration (DoI). METHODS: We retrospectively analyzed 198 patients with OCSCC treated between 2015 and 2022 with surgery followed by adjuvant radiotherapy (60 Gy in 30 fractions), with or without concurrent chemotherapy. Chemotherapy was administered in cases with ENE or margin positivity. Patients were followed at 3-month intervals with clinical evaluations and imaging as indicated. Kaplan-Meier analysis was used to estimate overall survival (OS) and disease-free survival (DFS). Differences between groups were assessed using the log-rank test, and univariate and multivariate Cox regression analyses identified prognostic factors. RESULTS: The mean age was 55 ± 12 years, with 86.4% male patients. The buccal mucosa (61.6%) was the most common subsite. After a median follow-up of 36 months, the 3-year OS and DFS rates were 56.0% and 53.1%, respectively. Patients with pathological ENE had significantly worse outcomes: 3-year DFS was 34.7% vs. 68.6% (HR: 0.303; p < 0.001), and OS was 35.3% vs. 74.0% (HR: 0.270; p < 0.001). Radiological node positivity, LVI, and PNI were also independently associated with poorer survival. CONCLUSION: ENE significantly worsens OS and DFS in OCSCC patients, even with standard adjuvant chemoradiotherapy. These findings support the need for treatment intensification strategies, such as radiation dose escalation and/or additional systemic therapy, in this high-risk group.
Correspondence on "Deficient DNA mismatch repair and Nectin-4 expression in upper tract urothelial carcinoma (UTUC)".
Peker P
J Cancer Res Clin Oncol · 2025 Nov · PMID 41186726 · Full text
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Mapping the frontiers: a bibliometric perspective on t cell-based immunotherapy in pancreatic cancer since the twenty-first century.
Tang Z, Wang C, Ma Z … +3 more , Shang P, Yuan Q, Yue J
J Cancer Res Clin Oncol · 2025 Nov · PMID 41186710 · Full text
PURPOSE: T-cell immunotherapy is reshaping cancer care and offers a targeted strategy for pancreatic carcinoma (PC), yet a comprehensive map of its research trajectory is lacking. We aimed to chart the evolution of the f...
PURPOSE: T-cell immunotherapy is reshaping cancer care and offers a targeted strategy for pancreatic carcinoma (PC), yet a comprehensive map of its research trajectory is lacking. We aimed to chart the evolution of the field, identify leading contributors, and clarify the thematic shifts that are shaping clinical translation. METHODS: We systematically analyzed articles and reviews indexed in the Science Citation Index Expanded of the Web of Science Core Collection from January 2000 to December 2024. Bibliographic metadata were aggregated for descriptive trend analyses and science-mapping of co-authorship, co-citation, and keyword co-occurrence networks. Temporal trend profiling was used to highlight emerging topics. RESULTS: Global output on T-cell immunotherapy for PC has expanded markedly over the past two decades but remains unevenly distributed across regions. The United States leads in academic influence and translational impact, with China closely following in publication volume and contributions from high-impact institutions. Research has converged at the interface of immunotherapy, tumor-microenvironment modulation, and cellular engineering. Dominant themes include engineered T-cell approaches, immune-checkpoint modulation, and strategies leveraging tumor-infiltrating lymphocytes. Emerging fronts encompass AI-enabled target/drug discovery, biomarker-guided patient stratification, and individualized treatment designs. Persisting barriers include limited efficacy in the desmoplastic and immunosuppressive PC microenvironment, primary and acquired immune resistance, safety concerns, and regulatory and trial-design complexities. CONCLUSIONS: T-cell immunotherapy for PC is a rapidly advancing, interdisciplinary domain led by the United States with rising contributions from China. Accelerating clinical translation will require: integrated T-cell engineering with microenvironment remodeling; rational combinations with checkpoint and stroma-targeted agents; robust predictive biomarkers with standardized endpoints; safety-engineering and risk-mitigation frameworks; and coordinated, multicenter collaboration. This bibliometric synthesis delineates the field's structure and priorities to improve outcomes for patients with PC.
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