Neoplasma最新文献

{"title":"Research progress on the role of DDR1 in cancer and targeted therapy strategy.","authors":"Xiaoying Guan, Yajie Zhang, Xiaoli Guan, Hong Yan","doi":"10.4149/neo_2026_251010N426","DOIUrl":"10.4149/neo_2026_251010N426","url":null,"abstract":"<p><p>Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by various types of collagen. Abnormal activation of DDR1 is closely related to the occurrence and development of solid tumors and plays an important role in the regulation of cell adhesion, survival, proliferation, migration, and invasion. Thus, DDR1 is a promising therapeutic target in the field of oncology. This review introduces the structural characteristics of DDR1, focusing on its role in tumor progression and related signaling pathways. It also explores the relationship between DDR1 and tumor chemotherapy resistance, and elaborates on the current research status and development prospects for inhibitors and antibodies targeting DDR1. Thus, the DDR1 inhibition strategy may serve as a new alternative for treating cancer patients.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"75-87"},"PeriodicalIF":2.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146220517","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":"DNA methylation-predicted GDF-15 and mortality in cancer survivors: a cohort study.","authors":"Jingying Nong, Kejian Shi, Yi Zhang","doi":"10.4149/neo_2025_250629N284","DOIUrl":"10.4149/neo_2025_250629N284","url":null,"abstract":"<p><p>Developing non-invasive prognostic biomarkers remains critical to improving personalized cancer care. Growth differentiation factor-15 (GDF-15), a TGF-β family cytokine, plays a key role in tumorigenesis and immune evasion. Circulating GDF-15 serves as a biomarker for cancer prognosis, and DNA methylation (DNAm)-predicted GDF-15 has been linked to mortality risk in the general population. However, the association between DNAm-predicted GDF-15 and mortality risk in cancer survivors remains unexplored. We analyzed the association between DNAm-predicted GDF-15 and all-cause, long-term all-cause, and cancer mortality risks using a cohort of 343 cancer survivors from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 with a median follow-up of 138 months. Multivariable Cox regression reporting hazard ratios (HRs) and 95% confidence intervals (CIs) demonstrated that each 1-standard deviation (SD) increment in DNAm-predicted GDF-15 was associated with a 60% higher all-cause mortality risk adjusted with model 1 of age and sex, and a 54% greater all-cause mortality risk in model 2 adjusted additionally for ethnicity, education, smoking, and coronary heart disease. Participants in the high GDF-15 tertile showed a 201% and 166% higher mortality risk in model 1 and model 2, respectively (both p for trend <0.0001) compared to the low tertile. Its association with long-term mortality risk remains unchanged. Stratified analyses indicated consistent relationships across multiple subgroups. Kaplan-Meier and competing risk analyses revealed a graded increase in cancer mortality risk across ascending GDF-15 tertiles; Cox models confirmed a significant positive association per 1-SD increment in the unadjusted model and model 1, which remained consistent in direction and magnitude in model 2, with a marginally significant (p=0.052). The current study provided evidence that DNAm-predicted GDF-15, an alternative and precise estimate of GDF-15 based on DNA methylation, is positively associated with all-cause and long-term all-cause mortality risks and showed a trend of positive association with cancer mortality among cancer survivors. Future larger longitudinal studies with serial DNAm-predicted GDF-15 assessments are needed to verify potential causal links.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"59-67"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019129","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":"Prognostic value and clinical significance of tumoral PD-L1 and stromal α-SMA expression in diffuse pleural mesothelioma.","authors":"Yeqi Sun, Lan Li, Lei Cai, Jihua Yang, Jun Qian, Fajiu Wang, Lifeng Wang","doi":"10.4149/neo_2026_251018N437","DOIUrl":"10.4149/neo_2026_251018N437","url":null,"abstract":"<p><p>Diffuse pleural mesothelioma (PM) is a rare malignant neoplasm with an extremely poor prognosis. Prognostic assessment remains challenging, highlighting the urgent need for reliable biomarkers to guide precise and effective therapy. Programmed death ligand 1 (PD-L1) has been suggested as a predictive biomarker for PM, but existing data are limited and controversial. Although advances have been made in understanding cancer-associated fibroblasts (CAFs) within the PM tumor microenvironment, their clinical and prognostic significance remains poorly elucidated. A retrospective analysis of 51 pathologically diagnosed PM was performed. We evaluated clinicopathological factors (including tumoral PD-L1, stromal α-SMA, and Ki-67 percentage by immunohistochemistry) and analyzed their correlation with overall survival (OS) using Kaplan-Meier and multivariate Cox regression. A total of 12 potential prognostic factors were evaluated in the univariate analysis, and 6 factors were found to be significantly associated with a poor prognosis in PM patients. Multivariate analysis identified histological classification, TNM stage, and PD-L1 expression as independent prognostic factors in PM patients. Stromal α-SMA positivity, a marker of poor prognosis, was significantly correlated with male, non-epithelioid subtype, and a high Ki-67 index. Moreover, α-SMA positivity tended to show an increased likelihood of PD-L1 expression (p=0.065). The expression of tumor PD-L1 could serve as an adverse prognostic factor for PM patients. Its potential association with tumor stromal α-SMA expression warrants further investigation, particularly in the context of unmet needs in tumor immunotherapy.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"68-73"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018640","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":"Efficacy and safety of adebrelimab plus bevacizumab in combination with hepatic artery infusion chemotherapy for advanced stage hepatocellular carcinoma: a retrospective cohort study.","authors":"Chen Li, Letao Lin, Shuanggang Chen, Gulijiayina Nuerhashi, Hongtong Tan, Chunyong Wen, Yujia Wang, Guanglei Zheng, Ruizhi Tang, Jiayu Pan, Lujun Shen, Weijun Fan","doi":"10.4149/neo_2025_200508N198","DOIUrl":"10.4149/neo_2025_200508N198","url":null,"abstract":"<p><p>Hepatic arterial infusion chemotherapy using a combination of oxaliplatin, fluorouracil, and leucovorin (HAIC-FOLFOX) has shown promise for patients with advanced-stage hepatocellular carcinoma (HCC). In this study, we aim to evaluate the efficacy and safety of combining adebrelimab (anti-PD-L1 antibody) and bevacizumab with HAIC-FOLFOX for HCC patients in BCLC stage C. This retrospective study included 32 untreated advanced-stage HCC patients receiving HAIC-FOLFOX combined with adebrelimab and bevacizumab as first-line therapy. The primary endpoint is overall response rate (ORR) based on the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1. From January 14th, 2024, to December 5th, 2024, a total of 32 patients received the triplet combination of HAIC-FOLFOX, adebrelimab, and bevacizumab. Median follow-up time was 6.1 months. According to RECIST v1.1 criteria, the confirmed ORR was 71.8% (95% CI: 55.4-88.3%), with a disease control rate (DCR) of 93.7% (95% CI: 84.9-99.9%). Only one case (3.1%) had a grade 3 treatment-related adverse event (rash), which could be alleviated after symptomatic management. The combination of adebrelimab, bevacizumab, and HAIC-FOLFOX demonstrated encouraging results and manageable safety concerns for patients with HCC at BCLC stage C.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"52-58"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145605350","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":"Bystin-like protein forms a functional complex with DDX49 to enhance thyroid cancer progression.","authors":"Yue Wang, Xiaoxiao Xing, Dongpo Zhang, Tao Sun, Yuren Zhang, Jun Li, Daixiang Liao, Junyi Li","doi":"10.4149/neo_2025_250729N326","DOIUrl":"10.4149/neo_2025_250729N326","url":null,"abstract":"<p><p>The incidence of thyroid cancer is rising worldwide, underscoring the urgent need for novel molecular targets in the management of aggressive disease. This study identifies bystin-like protein (BYSL) as a previously unrecognized oncogenic driver in thyroid carcinoma. Comprehensive analyses of clinical specimens, established cell lines, and patient-derived tumor-like clusters revealed that BYSL is significantly upregulated in thyroid malignancies and is strongly correlated with adverse patient outcomes. Functional assays demonstrated that BYSL promotes tumor cell proliferation, migration, and invasion while suppressing apoptosis. Mechanistically, BYSL interacts directly with DEAD-box helicase 49 (DDX49) to form a functional protein complex that impairs the biogenesis of the tumor suppressor miR-145-5p by inhibiting its DICER-mediated processing. Dual knockdown of BYSL and DDX49 synergistically suppressed tumor growth and induced apoptosis in patient-derived tumor-like cell clusters, with these effects reversed by inhibition of miR-145-5p. Collectively, these findings demonstrate the BYSL-DDX49 complex as a pivotal modulator of thyroid cancer progression and underscore its promise as a therapeutic intervention for restoring tumor-suppressive pathways.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"37-51"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775162","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":"SLC44A1 promotes AML progression and chemoresistance by regulating the Notch signaling pathway.","authors":"Shuyun Cao, Chengyun Pan, Xiuying Hu, Tianzhen Hu, Yanju Li, Qin Fang, Jishi Wang","doi":"10.4149/neo_2025_250518N209","DOIUrl":"10.4149/neo_2025_250518N209","url":null,"abstract":"<p><p>Despite advances in treatment, acute myeloid leukemia (AML) remains a formidable therapeutic challenge, highlighting the urgent need for novel biomarkers and therapeutic targets. The choline transporter SLC44A1 has been implicated in cancer progression; however, its role in AML remains largely unexplored. Here, we investigated the clinical relevance and molecular mechanisms of SLC44A1 in AML. Analysis of The Cancer Genome Atlas (TCGA) datasets revealed significant upregulation of SLC44A1 in AML patients, correlating with poor patient prognosis. Functional studies demonstrated that SLC44A1 knockdown markedly inhibited AML cell proliferation and enhanced chemosensitivity to cytarabine and venetoclax. RNA sequencing and pathway analysis identified the NOTCH signaling pathway as a key downstream target of SLC44A1, which was further validated by western blot. Collectively, our findings establish SLC44A1 as a crucial regulator of AML progression and chemoresistance, highlighting its dual potential as a prognostic biomarker and a therapeutic target.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"26-36"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018794","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":"Immune checkpoint remodeling across disease progression in multiple myeloma.","authors":"Zuzana Valuskova, Dana Cholujova, Gabor Beke, Milan Hucko, Lubos Klucar, Gabriela Grofova, Lubos Drgona, Jana Jakubíková","doi":"10.4149/neo_2025_251026N448","DOIUrl":"10.4149/neo_2025_251026N448","url":null,"abstract":"<p><p>Immune checkpoint dynamics within the bone marrow (BM) critically shape disease evolution and therapeutic responses in multiple myeloma (MM). To delineate immune remodeling in the BM during plasma cell malignancy evolution, we profiled inhibitory (PD-1, CTLA-4, LAG-3, TIM-3, TIGIT, BTLA, and 2B4) and co-stimulatory (ICOS, CD27, DNAM-1, 4-1BB, and OX40) checkpoints across adaptive and select innate compartments in healthy donors (HD, n=25), monoclonal gammopathy of undetermined significance (MGUS, n=17), newly diagnosed MM (NDMM, n=57), and relapsed/relapsed-refractory MM (MM, n=72; on-treatment n=27, off-treatment n=12). Progressive disease featured loss of mature, memory, and activated/proliferating B cell subsets and an NDMM-specific expansion of plasmablasts/plasma cells. B cell maturation was accompanied by broad remodeling of inhibitory receptors (notably reduced PD-1, TIM-3, TIGIT, and 2B4 on mature B cells; decreased CTLA-4 on activated B cells and plasmablasts/plasma cells; and reduced TIM-3, LAG-3, and 2B4 on plasmablasts/plasma cells) alongside selective co-stimulatory changes (OX40 decreased on mature B cells; CD27 loss on activated and plasmablast/plasma compartments; divergent 4-1BB regulation). T cell compartments showed early CD4+ expansion with CD8+ cytotoxic reduction and checkpoint shifts: broad PD-1 downregulation with subset-restricted increases in LAG-3, TIM-3, TIGIT, and BTLA; variable upregulation of CD27, DNAM-1, and ICOS; and consistent 4-1BB loss. NKT and γδ T cell frequencies were stable, but their checkpoints were reconfigured: NKT cells exhibited decreased PD-1 and 4-1BB and increased TIGIT, LAG-3, and DNAM-1, whereas γδ T cells showed reduced CTLA-4, BTLA, and the co-stimulatory receptor OX40. Innate NK cells demonstrated reduced frequency and phenotypic shifts, including decreased TIM-3 and PD-1, loss of 4-1BB and OX40, stage-specific increases in TIGIT and 2B4, and elevated DNAM-1. Checkpoint alterations, such as low TIGIT or CTLA-4 and elevated OX40 expression, were correlated with superior progression-free survival. MM progression entails extensive, stage- and subset-specific remodeling of inhibitory and activating immune checkpoints in the BM, with implications for immunotherapeutic targeting.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"10-25"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775171","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":"Stem cells-derived suicide gene exosomes: a promising platform for innovative cancer therapy.","authors":"Dajana Vanova, Michal Andrezal, Ursula Altanerova, Miroslava Matuskova, Cestmir Altaner","doi":"10.4149/neo_2025_251119N487","DOIUrl":"10.4149/neo_2025_251119N487","url":null,"abstract":"<p><p>Innovative cancer treatments are needed for metastatic tumors that currently do not have adequate therapies. This review highlights recent progress in suicide gene therapy using small extracellular vesicles, particularly exosomes, as a novel form of intracellular anticancer therapy. Suicide gene exosomes are produced by tumor-targeting human mesenchymal stem cells (MSC) that have been genetically modified to express the yeast cytosine deaminase::uracil phosphoribosyl transferase fused gene (yCD::UPRT) along with the prodrug 5-fluorocytosine (5-FC). The yCD::UPRT-MSC-secretome containing tumor-targeted exosomes converts 5-FC into the cytotoxic compound 5-fluorouracil (5-FU) and its metabolites within the tumor environment. The second popular system we are investigating involves the suicide gene exosomes derived from thymidine kinase of Herpes Simplex Virus in conjunction with a prodrug ganciclovir. Extracellular vesicles secreted by tumor-associated cells contribute to tumor growth and metastasis. When these cells are transduced with yCD::UPRT suicide gene, they can act as a source of therapeutic exosomes capable of intracellularly converting nontoxic prodrug 5-FC to a cytotoxic 5-FU. Combined action of suicide gene exosomes from MSCs and cancer-associated fibroblasts is a promising platform for aggressive tumor treatment. Furthermore, suicide gene exosomes can be enhanced with additional anticancer drugs and customized for targeted delivery. In this review, we trace the history of these findings, present therapeutic outcomes from in vitro and in vivo studies, and explore the future potential of therapeutically beneficial exosomes for cancer treatment.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"1-9"},"PeriodicalIF":2.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775201","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":"Peroxisome proliferator-activated receptors as novel targets of small cell lung cancer circulating tumor cells.","authors":"Gerhard Hamilton, Marie-Therese Eggerstorfer, Lukas Weigl, Maximilian Johannes Hochmair, Sandra Stickler","doi":"10.4149/neo_2025_250917N396","DOIUrl":"10.4149/neo_2025_250917N396","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) has a dismal prognosis with a low 2-year survival rate. Chemotherapy for recurrent SCLC fails invariably, and novel tumor targets are needed. Here, the effects of agents targeting the peroxisome proliferator-activated receptors (PPARs) in SCLC are investigated. Initial screening of 96 PPAR-directed agents was performed in two SCLC CTC-derived lines (BHGc10, BHGc16). Compounds showing high cytotoxicity were subsequently tested in two pleural effusion-derived lines (S457, S1392) and the SCLC line NCI-H69. Several PPARs emerged as actionable targets: eight PPARγ ligands and nine ligands for PPARα, PPARα/δ, or PPARβ/δ. For the six most effective compounds, treatment-induced protein changes were further profiled in BHGc16 using protein arrays. Cytotoxicity varied by compound, while the PPARγ agonist pioglitazone and the PPARα agonist fenofibrate were preferentially active in CTC lines, DG172 hydrochloride was selective for pleural effusion-derived lines, while rosiglitazone maleate, cloxiquine, and agrimol B showed no selectivity. Mechanistically, in the CTC-derived cell line BHGc16, these six PPAR-directed agents increased pro-apoptotic proteins (Bax, Bad, caspase-3/9), decreased anti-apoptotic and invasion proteins (Bcl-2, Bcl-XL, c-FLIP-L, ICAM-1, CXCR4), and suppressed Akt/mTOR, MEK/ERK, p38 MAPK, and JAK2/STAT3 signaling. These findings support PPARs as clinically relevant targets in SCLC, with PPAR-directed agents showing cytotoxic effects comparable to those reported in other malignancies. Such agents may aid SCLC treatment and help delineate biological differences between CTCs and resident tumor cells.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"383-393"},"PeriodicalIF":2.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145605318","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":"LINC00324 suppresses abnormal proliferation and promotes apoptosis of leukemia cells through the miR-10b-5p/PTEN pathway.","authors":"Yiyu Li, Bo Wang, Faquan Lin, Yangyang Zhang, Yue Lan, Yi Liu, Wei Bao, Binbin Xie, Qingniao Zhou, Jicheng Zhou, Qiyan Zeng","doi":"10.4149/neo_2025_250619N270","DOIUrl":"https://doi.org/10.4149/neo_2025_250619N270","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are known to participate in leukemia development, but the molecular mechanisms of many remain unclear. The expression of LINC00324 was examined in peripheral blood samples from leukemia patients and in leukemia cell lines by RT-qPCR. Functional studies were performed to evaluate how LINC00324 overexpression or knockdown affected cell proliferation and apoptosis. Flow cytometry was used to detect apoptosis. Western blotting was applied to measure Ki-67, BAX, Bcl-2, and PTEN protein levels. Dual-luciferase reporter assays were used to confirm the interaction among LINC00324, miR-10b-5p, and PTEN. LINC00324 expression was markedly reduced in leukemia samples and cell lines. Upregulation of LINC00324 inhibited the proliferation of Jurkat and HL-60 cells and increased apoptosis, while its silencing produced the opposite trend. Western blotting showed that LINC00324 overexpression decreased Ki-67 and Bcl-2 but increased BAX expression. Rescue experiments demonstrated that miR-10b-5p mimics reversed, whereas inhibitors restored, the effects of LINC00324. Bioinformatics prediction and luciferase validation identified PTEN as a direct target of miR-10b-5p, and LINC00324 enhanced PTEN expression by sponging miR-10b-5p. LINC00324 regulates the proliferation and apoptosis of leukemia cells through the miR-10b-5p/PTEN axis. These findings add to the understanding of lncRNA-mediated regulatory mechanisms in leukemia.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":"72 6","pages":"405-414"},"PeriodicalIF":2.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019174","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}