Neoplasma最新文献

{"title":"Survival benefit of early radium-223 dichloride therapy in castration-resistant prostate cancer patients with osteoblastic bone metastases.","authors":"Eva Takacsova, Marek Bartovic, Jan Ivancik, Iveta Waczulikova","doi":"10.4149/neo_2025_250308N112","DOIUrl":"https://doi.org/10.4149/neo_2025_250308N112","url":null,"abstract":"<p><p>The aim of the retrospective cohort study was to evaluate the overall survival of patients with castration-resistant prostate cancer and osteoblastic bone metastases without visceral metastases treated with 223Radium dichloride (223Ra). The cohort included 55 patients aged 48 to 86, with a median age of 71. Overall survival from the first administered cycle (from 7/2015 to 7/2019) was evaluated in 10/2024. The median overall survival was, despite a smaller cohort, 16.27 months (CI: 11.87-20.98 months), comparable to other large real-world studies. Asymptomatic or mildly symptomatic patients with good performance status (ECOG 0-1) at the start of therapy had a significantly higher median survival than more symptomatic patients with ECOG 2 and 3 (22.42 vs. 8.06 and 3.28 months). The number of completed cycles of 223Ra was inversely proportional to the patients' performance status (ECOG) - Kendall's Tau-c = -0.625; p < 0.0001. Previous treatment with chemotherapy (41.2 % of patients) was associated with significantly worse survival on multivariable analysis. A decrease of serum PSA by more than 50% (12.7% of patients) was significantly associated with longer survival (31 months; p = 0.0043). Severe (Grade 3) anemia, leukopenia, and thrombocytopenia occurred in only 9.1%, 3.6%, and 3.6% of patients. Earlier indication of 223Ra dichloride therapy in asymptomatic or mildly symptomatic patients with good performance status (ECOG 0-1) and without prior chemotherapy improved survival in our cohort. The decrease in serum PSA during treatment was a good prognostic factor associated with longer survival.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WTAP is a promising diagnosis and treatment biomarker that inhibits the proliferation and invasion of melanoma cells.","authors":"Huixiu Lu, Yanli Zhang, Jiali Li, Dan Lou, Licui Li, Yunchuan Liang, Jianying Li, Yaling Liu","doi":"10.4149/neo_2025_250110N12","DOIUrl":"https://doi.org/10.4149/neo_2025_250110N12","url":null,"abstract":"<p><p>Wilms' tumour 1-associating protein (WTAP) is ubiquitously expressed in many tissues and plays an important role in physiological processes and tumour development. Here, we investigated the specific biological role and underlying mechanism of WTAP in melanoma. We determined the expression of WTAP and its correlation with clinicopathological features in paraffin-embedded tissues. We investigated the effects of WTAP on melanoma cells via a CCK-8 assay, a colony formation assay, an EdU assay, a transwell assay and subcutaneous xenograft experiments. We then applied RNA sequencing to further screen candidate targets, and NT5E was selected as the downstream gene of WTAP. Finally, a series of rescue assays together with nucleotidase assays and ELISA were adopted to confirm the function of NT5E in melanoma progression. We demonstrated that WTAP expression was downregulated in melanoma, which was associated with a poor prognosis, and that WTAP expression served as an independent predictor of melanoma survival. Functionally, WTAP hindered the proliferation, growth, migration and invasion of melanoma cells. Furthermore, NT5E was identified as the downstream effector of WTAP and was subsequently found to rescue the increased proliferation, migration and invasion of melanoma cells induced by WTAP deficiency. Moreover, knockdown of WTAP increased the expression of NT5E, MMP2 and N-cadherin, and simultaneous transfection with siNT5E reversed the increased expression of MMP2 and N-cadherin. Moreover, increased NT5E expression caused by forced WTAP inhibition in melanoma promoted the hydrolysis of AMP to produce more adenosine and further abrogated the secretion of IFN-γ by PBMCs. We found that WTAP expression is significantly downregulated and restrains the progression of melanoma via the downstream effects of NT5E on immunosuppression and molecular adhesion. This study revealed that WTAP plays a crucial inhibitory role in melanoma oncogenesis and highlighted WTAP as a potential novel diagnosis and therapeutic target for melanoma.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factors influencing survival after allogeneic stem cell transplantation for hematologic malignancies in adult patients: A retrospective cohort study.","authors":"Iveta Oravcova, Zuzana Rusinakova, Silvia Cingelova, Miriam Ladicka, Eva Mikuskova, Andrej Vranovsky, Ludmila Demitrovicova, Barbora Kasperova, Lucia Petrikova, Alica Slobodova, Radka Vasickova, Lubos Drgona","doi":"10.4149/neo_2025_250311N119","DOIUrl":"https://doi.org/10.4149/neo_2025_250311N119","url":null,"abstract":"<p><p>Allogeneic stem cell transplantation (alloSCT) remains the established main treatment option with curative potential for many hematologic malignancies. We conducted a retrospective analysis of 104 adult patients who underwent allogeneic stem cell transplantation between March 2013 and November 2023. Kaplan‒Meier survival analysis, the chi-square test, and Cox regression models were used to identify risk factors and outcomes. The median follow-up of the cohort was 19 (0.3-128.1) months. The median age of the recipients was 49 (19-65) years, and 57 (54.8%) recipients were males. Ninety (86.5%) patients had a matched sibling, and 14 (13.5%) had a haploidentical donor. According to the multivariable analysis, a body mass index (BMI) ≥ 30 kg/m2 (p = 0.02) and status without chronic graft-versus-host disease (cGVHD) (p = 0.04) were significantly associated with worse overall survival. A BMI ≥ 30 kg/m2 was also predictive of worse relapse-free survival (p = 0.01). The cumulative incidence rates of nonrelapse mortality (NRM) and relapse mortality (RM) at 1 year were 8.5% (95% CI; 4.3-16.5%) and 26.7% (95% CI; 19.1-37.4%), respectively. Patients without cGVHD had significantly higher RM than patients with cGVHD (p < 0.001), whereas patients with cGVHD had significantly higher NRM (p = 0.01). Patients with a BMI ≥ 30 kg/m2 had significantly more posttransplant fatal events (p < 0.001). Our analysis revealed that a BMI ≥ 30 kg/m2 and a status without cGVHD were significantly associated with worse OS. NRM was higher in patients with cGVHD, whereas patients without cGVHD died mostly from relapses.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCL18 derived from M2-polarized tumor-associated macrophages promotes endometrial cancer progression by activating the TWIST1/HMGA1 axis.","authors":"Hongxia Li, Jiansheng Li","doi":"10.4149/neo_2025_240820N357","DOIUrl":"10.4149/neo_2025_240820N357","url":null,"abstract":"<p><p>CCL18, originating from M2-polarized tumor-associated macrophages (M2-TAMs) is recognized for its vital role in endometrial cancer (EC) development. Nonetheless, its precise mechanisms remain largely undefined. The primary objective of this research was to elucidate the underlying mechanism of M2-TAM-isolated CCL18 in EC progression. TWIST1 and HMGA1 expressions were assessed in EC tissues and cells by qRT-PCR or western blotting. M2 macrophages were differentiated from human monocyte THP-1 cells, and characterized via flow cytometry and western blotting. CCL18 levels were evaluated using western blotting and ELISA assay. CCK8, Transwell, and wound healing assays were employed to assess EC cell vitality, invasion, and migration, respectively, while western blotting was utilized to measure related protein markers. The binding relationship between TWIST1 and HMGA1 was validated via ChIP and dual-luciferase reporter assays. TWIST1 and HMGA1 were increased in EC tissues and cells. After being treated with M2-TAM-isolated CCL18, EC cell vitality, migration, and invasion were enhanced. Additionally, CCL18 derived from M2-TAM upregulated TWIST1 levels in EC cells. Further mechanistic analyses unveiled that TWIST could positively regulate HMGA1 in EC cells. Notably, HMGA1 knockdown restrained the malignancy of EC cells, which was reversed by TWIST1 overexpression. M2-TAM-isolated CCL18 facilitated EC progression by activating the TWIST1/HMGA1 axis. These observations might offer new directions for developing targeted curative interventions for EC.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 1-2","pages":"106-117"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL4I1 knockdown inhibits the epithelial-mesenchymal transition process in glioma via downregulation of the JAK2/STAT3 signaling pathway.","authors":"Jianwei Zhuo, Tong Wang, Ting Lu, Xiangying Li, Zhengquan Yu, Gang Cui, Haitao Shen","doi":"10.4149/neo_2025_250110N13","DOIUrl":"10.4149/neo_2025_250110N13","url":null,"abstract":"<p><p>Gliomas are primary intracranial tumors that cause considerable morbidity and mortality. The effect of interleukin 4-induced gene-1 (IL4I1) on the progression of various diseases has been demonstrated to be significant. However, the specific molecular mechanisms of how IL4I1 contributes to the progression and the epithelial-mesenchymal transition (EMT) process of glioma remain inadequately elucidated. IL4I1 expression in glioma was assessed using public datasets and immunohistochemistry. In in vitro experiments, IL4I1 expression was quantified through real-time quantitative PCR and western blotting. The effects of IL4I1 knockdown on the malignant phenotypes of glioma cells were investigated through in vitro studies. The evaluation of biomarkers associated with EMT and the Janus-activated kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway was conducted using western blotting and immunofluorescence assays after IL4I1 knockdown. A xenograft tumor model was established to validate the influence of IL4I1 knockdown in glioma progression. The results revealed that high expression of IL4I1 is linked to an unfavorable prognosis in human gliomas. IL4I1 knockdown effectively impeded the malignant phenotypes of glioma cells. IL4I1 knockdown induced EMT reversal, characterized by alterations in the expression levels and localization of EMT-related biomarkers. This reversal is partially mediated through the JAK2/STAT3 signaling pathway. The results of in vivo experiments confirmed that IL4I1 knockdown effectively suppressed glioma growth. Our research demonstrates that IL4I1 knockdown reverses the EMT process via JAK2/STAT3 signaling pathway and suppresses the malignant phenotypes of glioma, thereby highlighting its potential as both a prognostic marker and therapeutic target for glioma.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 1-2","pages":"91-105"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triptonide inhibits the progression of oral squamous cell carcinoma by suppressing the TRIP13/c-Myc axis.","authors":"Hongbo Zhang, Zheng Wei, Shengwei Han, Sufeng Zhao","doi":"10.4149/neo_2025_240918N387","DOIUrl":"10.4149/neo_2025_240918N387","url":null,"abstract":"<p><p>Triptonide, an active ingredient of Tripterygium wilfordii Hook. F., has been found to have anticancer effects on various cancers; however, its effect on oral squamous cell carcinoma (OSCC) has not yet been studied. This study aims to reveal the effect and mechanism of triptonide on OSCC. The inhibitory effect of triptonide on OSCC progression was ascertained by CCK-8 assay, EdU incorporation assay, wound healing assay, Transwell assay, and xenograft tumor model, while western blotting, qRT-PCR, and immunohistochemistry revealed that triptonide could inhibit c-Myc expression in OSCC. RNA-seq was conducted to explore the mechanism by which triptonide inhibited the progression of OSCC, and thyroid hormone receptor interactor 13 (TRIP13) was identified as a key differentially expressed gene. TRIP13-knockdown OSCC cells constructed with siRNA showed weaker progression ability in CCK-8 assay, EdU incorporation assay, wound healing assay, and Transwell assay. Finally, TRIP13-overexpressing OSCC cells constructed through plasmid were used in rescue experiments, which demonstrated that TRIP13 was located upstream of c-Myc and the overexpression of TRIP13 could partially restore the decreased c-Myc expression caused by triptonide treatment. Collectively, this study demonstrated that triptonide might reduce the expression of c-Myc by suppressing TRIP13 expression, thereby inhibiting the progression of OSCC. These findings have revealed a partial mechanism by which triptonide acts on OSCC and suggested its potential application value in OSCC treatment.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"36-47"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLHL7 enhances cell viability and cell cycle progression in glioma via glutamine metabolism by activating the β-catenin signaling pathway.","authors":"Rui Liu, Xiaoju Cheng, Peirui Wang, Xiangping Xia, Gang Li, Fuan Zhang, Chong Han, Shengtao Yao","doi":"10.4149/neo_2025_241227N539","DOIUrl":"10.4149/neo_2025_241227N539","url":null,"abstract":"<p><p>Kelch-like family member 7 (KLHL7) is associated with cancer development and occurrence, but its role and mechanism in the malignant progression of gliomas remain poorly understood. This study aimed to investigate the regulatory effects and mechanisms of KLHL7 on cell cycle and glutamine metabolism in glioma. Glioma cell lines A172 and U87 and a xenograft mouse model were used to analyze the function of KLHL7 in vitro and in vivo, respectively. Gene expression levels and protein amounts were assessed by quantitative reverse-transcription polymerase chain reaction and western blotting, respectively. Cell viability was assessed using the CCK-8 assay, and the cell cycle was analyzed via flow cytometry. The glutamine content was measured using a biochemical assay. The level of KLHL7 was upregulated in patients with glioma. KLHL7 knockdown reduced cell viability, inhibited cell cycle progression, and decreased the glutamine content in A172 cells. KLHL7 silencing inhibited tumor growth in vivo. Furthermore, KLHL7 overexpression enhanced cell viability, cell cycle progression, and glutamine metabolism and activated the β-catenin signaling pathway in U87 cells. These findings indicate that KLHL7 promotes the malignant progression of glioma via the β-catenin signaling pathway and may serve as a biomolecule for the clinical prediction and treatment of the disease.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 1-2","pages":"80-90"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EGFR/STAT3 signaling mediates the upregulation of CD47 in HPV-positive cervical cancer by activating p65 and exosome transporter RAB31.","authors":"Xiaoping Ke, Li Li, Qi Yan, Xianjing Wang, Ping Liu","doi":"10.4149/neo_2025_241017N421","DOIUrl":"10.4149/neo_2025_241017N421","url":null,"abstract":"<p><p>In cervical cancer, the regulatory mechanisms of CD47 and its enrichment in exosomes have not been fully elucidated. In this study, we aim to explore the mechanisms of how EGFR/STAT3 signaling regulates CD47 expression in cervical cancer, and whether p65 or RAB31 is involved in this process. RNA interference was used to knock down the fragment of HPV in cervical cancer cells. EGFR and RAB31 phosphorylation were detected by western blot, and exosomal CD47 was determined by ELISA. EGFR or STAT3 was then knocked down and western blot was used to detect the expression or phosphorylation of EGFR, STAT3, p65, CD47, RAB31, and its related proteins. ChIP-qPCR was used to investigate p65 enrichment in the CD47 promoter region. Our results showed that HPV fragment knockdown reduced the phosphorylation of EGFR and RAB31, and exosomal CD47 expression. Knocking down EGFR inhibited phosphorylation of STAT3 and p65, and expression of RAB31-related proteins. Phosphorylated p65 was bound to the P3 and P7 promoter regions of CD47. EGFR/STAT3 signaling upregulated CD47 expression by phosphorylating p65 and enhanced exosomal CD47 by activated RAB31. Thus, a dual regulatory role of EGFR/STAT3 signaling on CD47 expression and secretion involving transcriptional factor p65 and exosome transporter RAB31 was demonstrated.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 1-2","pages":"59-66"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin for recurrent colorectal polyp or adenoma prevention after polypectomy in patients without diabetes mellitus: a prospective study.","authors":"Wen Wang, Baoxiang Luo, Zhengjun Wang, Ji Zhang, Zhou Ye, Xiaojian He, Dazhou Li, Dongjie Sun","doi":"10.4149/neo_2025_250319N130","DOIUrl":"10.4149/neo_2025_250319N130","url":null,"abstract":"<p><p>To reduce the burden of colorectal cancer (CRC), the chemopreventive effects of 1-year metformin on polyps or adenoma recurrence in patients without diabetes mellitus (DM) who underwent polypectomy were evaluated. Patients without DM aged between 40 and 70 years old, with no polyp or adenoma after polypectomy, were randomly assigned to the control (no intervention), low-dose (500 mg/day), or high-dose (1,000 mg/day) metformin groups in a 1:1:1 ratio. After the 1-year intervention, the numbers of polyps and adenomas were measured and recorded, then resected. Plasma lipid and blood glucose were measured at baseline and 1-year follow-up. Data from the three groups were compared statistically. A total of 272 patients were enrolled in the analysis. In the control group, 48.9% of patients had adenoma recurrence, which was significantly higher than those in the low-dose (30.8%, p=0.012) and the high-dose (29.9%, p=0.009) metformin group. For the number of recurrent adenomas per subject, the difference between the control and the high-dose metformin groups was significant (0.86±1.09 vs. 0.47±0.83, p=0.020). No significant difference among the three groups and between baseline and 1-year follow-up was found in the lipid and glucose parameters. In conclusion, 1-year metformin use reduced the prevalence of recurrent adenoma significantly in patients without DM after polypectomy and may not be related to lipid and glucose metabolism.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 1-2","pages":"144-151"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress on the regulation mechanism of DEPTOR expression and its role in tumorigenesis.","authors":"Jinni Jiang, Chengyu Zhao, Minglei Yang, Guofang Zhao, Jianfeng Shu","doi":"10.4149/neo_2025_241203N504","DOIUrl":"10.4149/neo_2025_241203N504","url":null,"abstract":"<p><p>The mammalian target of rapamycin (mTOR) is a critical sensor and integrator of extracellular stimuli and intracellular signaling pathways, forming structurally and functionally distinct protein complexes (mTORC1, mTORC2, and mTORC3) with various proteins. It serves as a central regulator of vital biological processes like cell proliferation, survival, and autophagy. Numerous studies have linked mTOR pathway activation to tumor progression. DEPTOR, a common negative regulator of mTORC1 and mTORC2, exhibits complex loop regulatory mechanisms beyond simple mTOR pathway modulation. Depending on the cell type or tissue environment, DEPTOR can act as either an oncogene or a tumor suppressor gene. Given its complex role in tumorigenesis, precise regulation of DEPTOR expression across different tumor types is imperative. DEPTOR has emerged as a key focus in research on human malignant tumors. While recent years have seen through investigations into DEPTOR expression regulation in tumors, a systematic literature review is lacking. This review provides a detailed summary of the mechanisms regulating DEPTOR expression, an mTOR inhibitor in tumors, covering DNA induction, transcription, translation, and post-translational modification. Additionally, it explores the potential applications of DEPTOR/mTOR signaling axis-related compounds in tumor therapy.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"1-15"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}