NEOPLASMA肿瘤学
NEOPLASMA(英文缩写 NEOPLASMA),ISSN 0028-2685,eISSN 1338-4317,中文译名:肿瘤学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.409 | Q3 |
| 2022 | 3.000 | Q3 |
| 2023 | 2.000 | Q3 |
| 2024 | 2.200 | Q3 |
| 2025 | 2.500 | Q3 |
NEOPLASMA 最新收录文献
-
1. Transcriptomic analysis of vitamin D3 (cholecalciferol)-mediated attenuation of cisplatin sensitivity in gastric cancer cells in vitro.
PMID:日期:2026-09-07Cisplatin remains a cornerstone of chemotherapy for gastric cancer, but acquired resistance frequently limits its therapeutic efficacy. Vitamin D3/cholecalciferol (VD3) is widely used as a nutritional supplement; however, its influence on cisplatin responsiveness in gastric cancer cells remains unclear. In this study, gastric cancer cell lines were treated with cisplatin in the presence or absence of VD3, and cell viability, apoptosis, reactive oxygen species (ROS) accumulation, DNA damage-associated signaling, and transcriptomic changes were evaluated. VD3 significantly attenuated cisplatin-induced cytotoxicity in AGS, HGC-27, and MKN-45 cells. Co-treatment with VD3 reduced cisplatin-induced apoptosis, ROS accumulation, PARP cleavage, and γH2AX activation. Transcriptomic analysis showed that VD3 markedly reduced the number of cisplatin-responsive differentially expressed genes and altered gene programs associated with extracellular matrix organization, steroid metabolism, DNA damage response, and ABC transporter-related pathways. These findings suggest that VD3 exposure can attenuate cisplatin-induced cellular responses in gastric cancer cells and modulate transcriptional programs associated with cisplatin treatment. Given that the study was performed under in vitro conditions, further investigations are required to determine the underlying mechanisms and the potential clinical relevance of these observations.
-
2. Afatinib combined with oral metronomic vinorelbine as second-line treatment for advanced lung squamous cell carcinoma: a retrospective cohort study.
PMID:日期:2026-08-18The aim of this study was to evaluate the efficacy and safety of afatinib combined with oral metronomic vinorelbine as a second-line treatment for patients with advanced lung squamous cell carcinoma (LSCC). A retrospective analysis was conducted on 38 patients with advanced LSCC who had failed first-line platinum-based doublet chemotherapy combined with immunotherapy between January 2022 and June 2024. All patients received afatinib (30 mg or 40 mg orally once daily) combined with oral metronomic vinorelbine (20 mg or 30 mg orally three times weekly on Monday, Wednesday, and Friday) until disease progression or unacceptable toxicity. The primary endpoints were objective response rate (ORR) and progression-free survival (PFS). Secondary endpoints included overall survival (OS), disease control rate (DCR), and treatment-related adverse events (TRAEs). Based on the data, the ORR was 26.3%, and the DCR was 68.4%. The median PFS was 5.0 months (95% CI: 4.7-5.4), and the median OS was 9.0 months (95% CI: 8.6-10.0). Grade ≥3 TRAEs occurred in 23.7% (9/38) of patients, including diarrhea (5.3%), rash (5.3%), neutropenia (5.3%), stomatitis (2.6%), and fatigue (2.6%). No grade 4-5 TRAEs or treatment-related deaths occurred. To conclude, the combination of afatinib and oral metronomic vinorelbine demonstrates promising antitumor activity and a manageable safety profile as a second-line treatment for advanced LSCC. This combo could represent an option as second-line after failure of chemo+IO.
-
3. RNA-binding protein hnRNPD promotes the proliferation of Wilms' tumor cells through activating the p38 MAPK signaling pathway.
PMID:日期:2026-08-11Wilms' tumor (WT) represents a kidney carcinoma predominantly affecting children aged five years and younger. Heterogeneous nuclear ribonucleoprotein D (hnRNPD), an RNA-binding protein, has been implicated in oncogenic processes across various tumor types, whereas its expression pattern and biological function in WT remain largely unknown. hnRNPD expression within WT tissues was evaluated using publicly available databases, and co-expressed genes were identified through bioinformatic analysis. In vitro, hnRNPD expression in WT cell lines 17.94 and HFWT was modulated via gene silencing or overexpression. We subsequently carried out functional assays to assess cell proliferation and apoptosis. Molecular experiments were conducted to determine p38 mitogen-activated protein kinase (p38 MAPK) pathway activation status within cells with altered hnRNPD expression. Furthermore, SB203580 was utilized to pharmacologically inhibit this pathway to investigate the mechanism of hnRNPD in regulating WT cell proliferation. Data showed that hnRNPD was upregulated in WT tissues and cells. Silencing hnRNPD significantly inhibited WT cell proliferation and promoted apoptosis. Conversely, overexpression of hnRNPD produced the opposing effects. MAPK14, the gene encoding the p38α isoform of p38 MAPK, was identified as a core gene within the hnRNPD co-expression network. Furthermore, the phosphorylation level of p38 MAPK in WT cells was markedly elevated compared to that in normal cells. However, inhibition of the p38 MAPK pathway using SB203580 suppressed WT cell proliferation. Notably, SB203580 effectively counteracted the pro-proliferative effect of hnRNPD overexpression on malignant WT cell growth. In conclusion, hnRNPD is highly expressed in WT and plays a significant role in promoting the malignant proliferation of WT cells. The underlying molecular mechanism involves the regulation of p38 MAPK signaling pathway activation.
-
4. CRISPR/Cas9-edited organoids as a platform for tailored research of colorectal cancer.
4. CRISPR/Cas9编辑的类器官作为癌症量身定制研究的平台PMID:日期:2026-08-04Colorectal cancer is one of the most commonly diagnosed cancers worldwide. Mortality rates and limited therapeutic options justify the development of reliable preclinical research models, as their translational value remains limited. Simple in vitro models do not recapitulate tumor heterogeneity, while in vivo research faces ethical concerns and interspecies differences. Patient-derived organoids offer a physiologically more relevant platform that retains the genetic, epigenetic, and phenotypic characteristics of the original tumor. Tumor-derived organoids enable precise investigation of novel treatments, functional genomics, and modeling of cancer development. Integration with CRISPR/Cas9 gene editing further enables accurate manipulation of specific genes to study carcinogenesis and therapeutic resistance. This review highlights recent advances in the use of organoids for colorectal cancer research and explores the potential of gene-edited organoids to discover the genetic and molecular mechanisms underlying colorectal cancer development, progression, and treatment resistance.
-
5. Neuroimmune treatment of advanced solid tumors: 3-year survival after angiotensin 1-7, pineal indoles, and cannabinoids.
PMID:日期:2026-08-04In a recent study, the exogenous administration of angiotensin 1-7 (Ang 1,7) together with melatonin, 5-methoxytryptamine, and cannabidiol increased 1-year survival in advanced cancer patients, underlining the utility of neuromodulation in oncology. We now report a single-arm interventional study to evaluate the effectiveness of introducing Ang 1-7 in the neuroimmune regime, including pineal indoles and cannabinoids. Two cohorts of patients with advanced solid tumors refractory to standard oncologic treatments and with an estimated life expectancy of less than six months were studied. The full neuroimmune regimen cohort consisted of 100 consecutive patients treated over the last three years with Ang 1-7, pineal indoles, and cannabinoids, while the comparator cohort included 212 consecutive patients treated between 2015 and 2019 with pineal indoles and cannabinoids alone. Gastroprotected capsules of Ang 1-7 coupled with cyclodextrin were administered at 0.5 mg p.o. twice/day. Melatonin (100 mg) and 5-methoxytryptamine (20 mg) were given p.o. at bedtime and in the early afternoon, respectively. Cannabidiol or cannabigerol (in the case of glioblastoma) was given at 20 mg p.o. twice/day. Clinical response, disease control, and overall survival, along with the lymphocyte-to-monocyte ratio, were evaluated. In the full regimen cohort, disease control was achieved in 67 of 100 patients, with objective tumor regression observed in 23%. In the comparator cohort, disease control was obtained in 111 of 212 patients, with objective regression in 8%. Three-year overall survival was significantly higher in the full regimen cohort (37%) compared with the comparator cohort (19%). Both treatments were associated with a significant increase in the lymphocyte-to-monocyte ratio, suggesting an improvement in systemic immune status. The addition of Ang 1-7 to a neuroimmune regimen combining pineal indoles and cannabinoids was associated with improved disease control and long-term survival in patients with end-stage solid tumors lacking effective therapeutic options.
-
6. A splice odyssey: periostin's journey through the sea of crabs.
PMID:日期:2026-08-01Periostin is an extracellular matrix protein involved in processes ranging from early embryonic development to life-threatening cancer progression. Instead of acting as a single entity, it exists in numerous alternatively spliced isoforms, primarily differing in their C-terminal region, which drives diversification and context-dependence in its biological functions. Despite growing interest, inconsistencies in nomenclature and fragmented data still complicate the interpretation of isoform-specific roles. Therefore, the aim of this review is to provide a structured overview of periostin isoforms, focusing on their roles in development and carcinogenesis, while addressing challenges in their nomenclature. During embryogenesis, expression of periostin is dynamically regulated across developmental stages and tissues. Distinct isoforms exhibit specific patterns, both spatially and temporally, that reflect specialized functions during organogenesis (particularly in the cardiac, neural, and skeletal systems), and as experimental evidence points out, certain exons play critical roles in morphogenesis. Regulatory mechanisms influencing these patterns persist beyond development and are often changed in pathological conditions. In oncological diseases, expression of periostin isoforms varies widely between tumor types and microenvironments. Many isoforms are present in malignant as well as in adjacent non-malignant tissues, with differences in their relative abundance. Functionally, exon 17-containing variants tend to influence tumor cell-intrinsic properties, while variants with exon 21 are more closely linked to stromal interactions and modulation of the tumor microenvironment. Interesting is also the fact that periostin can exert both tumor-promoting and tumor-limiting effects, depending on the isoform and biological context. Taken together, periostin isoforms represent a complex regulatory system whose better understanding and standardized classification may enhance their potential in diagnostics and therapy.
-
7. Real-world clinical outcomes of newly diagnosed AML unfit for intensive chemotherapy treated with venetoclax and azacitidine: does it depend on the number of days of venetoclax administration?
PMID:日期:2026-08-01Until 2020, patients with acute myeloid leukemia (AML) who were not suitable for intensive treatment were mostly limited to symptomatic and palliative care, or to low-intensity regimens including low-dose cytosine-arabinoside (ARA-C) and azacitidine (AZA) monotherapy, which didn't bring much benefit. The situation changed with the arrival of venetoclax, a Bcl-2 inhibitor that causes leukemic cells to rapidly undergo apoptosis. The aim of our retrospective study was to summarize the treatment outcomes of all newly diagnosed patients with AML, unsuitable for intensive chemotherapy, treated with a combination of venetoclax and AZA at the Department of Hematology and Transfusion Medicine, University Hospital in Bratislava from January 1, 2021, to December 31, 2025. A total of 108 patients underwent treatment with a median follow-up of 35.9 months; median age was 69.5 years (47-84 years), and median number of cycles was 3 (1-34). Induction mortality rate was 7.4%, and tumor lysis syndrome occurred in 4.5%. The overall response rate, which included the number of complete remissions, complete remissions with incomplete hematopoietic recovery, and morphologically leukemia-free status (CR/CRi/MLFS), was 64%, the median overall survival was 9 months, and disease-free survival was 8 months. As of December 31, 2025, 23 patients are alive, and 85 have died. The main cause of death was the progression of the disease. The main contribution of our study is the finding that shortening the duration of venetoclax treatment maintains efficacy. There was no significant difference in remission rate achieved or in overall survival based on the number of days of venetoclax administration (<14 vs. 14 vs. 21 vs. 28 days). The combination of AZA and venetoclax in AML has proven to be highly effective in inducing complete remission, usually immediately after the first cycle. Unfortunately, remission is not long-lasting, relapses are frequent, and the median overall survival in real-world data is 7.9 to 13.6 months.
-
8. YTHDF2-regulated hsa_circ_0005882 functions as a sponge for miR-654-3p to suppress nasopharyngeal carcinoma proliferation.
PMID:日期:2026-08-01Circular RNAs (circRNAs) are a subclass of non-coding RNAs, playing an important regulatory role in tumor progression. Accumulating evidence has revealed that circRNAs can be regulated by m6A machinery, influencing their expression and biological functions. However, the functions and mechanisms of m6A-mediated circRNAs in nasopharyngeal carcinoma (NPC) remain to be elucidated. In this study, the sequence of hsa_circ_0005882 (circ_0005882) was determined by Sanger sequencing, and its localization in both the cytoplasm and nucleus was confirmed by fluorescence in situ hybridization. Furthermore, m6A RNA immunoprecipitation followed by qPCR (MeRIP-qPCR) and the single-base elongation- and ligation-based qPCR amplification (SELECT) assays revealed that circ_0005882 may harbor m6A modifications. Overexpression of circ_0005882 significantly suppressed NPC cell proliferation. Mechanistically, the m6A reader YTHDF2 binds to circ_0005882 to promote its degradation, thereby reducing circ_0005882 stability. Additionally, circ_0005882 functions as a sponge for miR-654-3p, contributing to the inhibition of NPC proliferation. These findings collectively demonstrate that circ_0005882, which is negatively regulated by YTHDF2, functions as a tumor suppressor by sponging miR-654-3p to inhibit NPC cell proliferation, unveiling a novel regulatory model centered on the YTHDF2/circ_0005882/miR-654-3p axis in NPC pathogenesis.
-
9. Targeting the MDM2/Caspase-3/GSDME axis: apatinib and cinobufagin synergistically induce pyroptosis to suppress gastric cancer progression.
9. 靶向MDM2/Caspase-3/GSDME轴：apatinib和cinobufagin协同诱导焦下垂以抑制癌症进展PMID:日期:2026-08-01Gastric cancer (GC) is a highly heterogeneous and aggressive malignancy with a poor prognosis, especially in advanced stages. Apatinib and cinobufagin (CS-1) have shown promising antitumor potential. However, the therapeutic efficacy and underlying mechanisms of their combined use in GC remain unclear. GC cell lines (AGS and GPM-1) were treated with apatinib, CS-1, or both. Cell viability, proliferation, migration, apoptosis, stemness, and pyroptosis-related protein expression were evaluated using cell counting kit-8 (CCK-8), colony formation, wound healing assays, flow cytometry, tumorsphere assays, and western blotting. The role of mouse double minute 2 homolog (MDM2) in modulating treatment response was investigated via overexpression experiments. Antitumor efficacy in vivo was assessed using a subcutaneous xenograft mouse model, and tumor apoptosis and proliferation were analyzed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunohistochemistry. Combined treatment with apatinib and CS-1 significantly inhibited GC cell viability, proliferation, migration, and stemness, while inducing apoptosis and pyroptosis more effectively than either agent alone. Mechanistically, the combination therapy downregulated MDM2 expression and upregulated cleaved caspase-3 (C-caspase-3) and gasdermin E-N (GSDME-N). Overexpression of MDM2 partially reversed these effects both in vitro and in vivo, leading to reduced apoptosis, pyroptosis, and antitumor efficacy. Apatinib combined with CS-1 synergistically suppresses GC progression by inducing MDM2/C-caspase-3/GSDME-regulated pyroptosis. These findings highlight MDM2 as a critical therapeutic target and provide novel insights into the molecular mechanisms underlying the combined use of targeted agents and natural compounds in GC therapy.
-
10. Postoperative clinical prognosis in 160 cases of glioblastoma and efficacy of vascular targeted therapy for recurrence.
PMID:日期:2026-08-01Glioblastoma (GBM) is the most common primary malignant brain tumor. Concurrent chemoradiotherapy and adjuvant chemotherapy have become the standard treatment modalities after surgery. However, despite such aggressive treatment, the overall survival (OS) rate remains low, and the disease is highly prone to recurrence with an extremely poor prognosis after recurrence. Currently, there is no standard salvage treatment regimen. This study conducted a clinical prognostic analysis of 160 patients with GBM after surgery and evaluated the clinical efficacy of anti-angiogenic drugs (apatinib/bevacizumab) as salvage treatment after recurrence, providing a strong direction for future treatment. Among the 160 patients with GBM included in the study, univariate analysis showed that age, use of apatinib, adjuvant chemotherapy, and radiotherapy were significantly associated with OS, while gender, CD34 expression, Ki-67 expression, bevacizumab, and P53 expression were not significantly associated with OS. Multivariate analysis revealed that adjuvant chemotherapy, age, and radiotherapy were independent prognostic factors for OS in patients with GBM. The median OS of the entire cohort was 20.0 months, with 1-year, 3-year, and 5-year survival rates of 74.6%, 28.7%, and 12.4%, respectively. Analysis of the clinical efficacy of salvage chemotherapy in 65 patients with recurrent GBM showed that the combined anti-angiogenic drug group had a significant survival advantage compared to the chemotherapy-only group (33 months vs. 19 months). Among patients in the combined anti-angiogenic drug group, 36 patients achieved clinical control, with a disease control rate (DCR) of 73.47%, significantly higher than the 43.75% DCR in the control group. The chemotherapy combined with apatinib group had a significant survival advantage in OS (p=0.012) and also benefited in DCR (66.67% vs. 43.75%); however, the chemotherapy combined with the bevacizumab group did not show a survival benefit in OS (p=0.078).