Oncology reports最新文献_第2页

[Corrigendum] Umbilical cord‑derived mesenchymal stem cells promote proliferation and migration in MCF‑7 and MDA‑MB‑231 breast cancer cells through activation of the ERK pathway. [勘误]脐带来源的间充质干细胞通过激活ERK通路促进MCF - 7和MDA - MB - 231乳腺癌细胞的增殖和迁移。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-06-20 DOI: 10.3892/or.2025.8933

Tao Li, Chunfu Zhang, Yanling Ding, Wei Zhai, Kui Liu, Fan Bu, Tao Tu, Lingxian Sun, Wei Zhu, Fangfang Zhou, Wenkai Qi, Jiabo Hu, Huabiao Chen, Xiaochun Sun

{"title":"[Corrigendum] Umbilical cord‑derived mesenchymal stem cells promote proliferation and migration in MCF‑7 and MDA‑MB‑231 breast cancer cells through activation of the ERK pathway.","authors":"Tao Li, Chunfu Zhang, Yanling Ding, Wei Zhai, Kui Liu, Fan Bu, Tao Tu, Lingxian Sun, Wei Zhu, Fangfang Zhou, Wenkai Qi, Jiabo Hu, Huabiao Chen, Xiaochun Sun","doi":"10.3892/or.2025.8933","DOIUrl":"10.3892/or.2025.8933","url":null,"abstract":"Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that a pair of data panels appeared to contain overlapping data in each of Fig. 3A and C on p. 1473, showing the results of Transwell migration and scratch‑wound assay experiments respectively, where the data panels were intended to have shown the results from differently performed experiments; moreover, control GAPDH western blotting data featured in Fig. 4B and 5A appeared to be matching, albeit the bands had been inserted into these figure parts in reversed orientations. The authors were able to re‑examine their original data, and realized that errors had occurred in the assembly of these figures through mislabelling of certain of their data files. Owing to the time that had passed since this paper was published, the authors offered to repeat the affected experiments, and the revised versions of Figs. 3, 4 and 5, showing new data for Figs. 3A, 3C, 4B and 5A, are shown on the next two pages. Given that the new experiments yielded data that were not significantly different from those obtained previously, the authors wish to emphasize that the re‑presentation of these figures with the new data does not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this corrigendum, and all the authors agree with the publication of this corrigendum; moreover, they apologize to the readership for any inconvenience caused. [Oncology Reports 34: 1469‑1477, 2015; DOI: 10.3892/or.2015.4109].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CYP8B1 is a prognostic biomarker with important functional implications in hepatocellular carcinoma. CYP8B1是一种预后生物标志物，在肝细胞癌中具有重要的功能意义。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-06-27 DOI: 10.3892/or.2025.8937

Feng Li, Qing Dong, Zhe Kai, Qi Pan, Chunsheng Liu

{"title":"CYP8B1 is a prognostic biomarker with important functional implications in hepatocellular carcinoma.","authors":"Feng Li, Qing Dong, Zhe Kai, Qi Pan, Chunsheng Liu","doi":"10.3892/or.2025.8937","DOIUrl":"10.3892/or.2025.8937","url":null,"abstract":"Cytochrome P450 8B1 (CYP8B1) is a critical enzyme in bile acid metabolism. Using multiple databases, including Gene Expression Omnibus, UALCAN (The University of Alabama at Birmingham Cancer data analysis Portal, GEPIA (Gene Expression Profiling Interactive Analysis), TCGA (The Cancer Genome Atlas) and GTEx (Genotype‑Tissue Expression), the present study analyzed CYP8B1 expression and its prognostic value in hepatocellular carcinoma (HCC). The results showed that CYP8B1 expression was significantly lower in HCC compared with normal tissues, and reduced CYP8B1 expression was associated with poor prognosis in patients with HCC. CYP8B1 was overexpressed in HCC cell lines (Huh7 and Hep3b cells); cell proliferation was assessed using Cell Counting Kit‑8 and EdU assays, while apoptosis was evaluated using the TUNEL assay. CYP8B1 overexpression inhibited proliferation and promoted apoptosis in HCC cells. Additionally, analyses via UALCAN and the Metascape platform showed that CYP8B1 expression was negatively associated with YWHAZ (Tyrosine 3/tryptophan 5 monooxygenase activation protein ζ), the regulation of PLK (Polo‑like kinase) activity during G2/M transition, and the intrinsic apoptosis pathway. Immunoblotting revealed that CYP8B1 overexpression decreased YWHAZ levels. Consistently, the expression of cyclin‑dependent kinase 1) and CCNB1 (Cyclin B1), key markers of G2/M transition, was also diminished following CYP8B1 overexpression. Furthermore, the pro‑apoptotic protein Bax was upregulated, while the anti‑apoptotic protein Bcl‑2 was downregulated. In conclusion, CYP8B1 holds promise as a potential prognostic target for HCC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Angiotensin‑converting enzyme 2 expression in human tumors: Implications for prognosis and therapy (Review). 血管紧张素转换酶2在人类肿瘤中的表达：对预后和治疗的影响（综述）

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-06-27 DOI: 10.3892/or.2025.8934

Theodoros Rizopoulos, Martha Assimakopoulou

引用次数: 0

Evaluation of HMGB1 as possible marker via breast organoid cultures research. 通过乳腺类器官培养研究评价HMGB1作为标记物的可能性。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-04 DOI: 10.3892/or.2025.8939

Vincenza Ciaramella, Barbara Carrese, Luigi Coppola, Giovanni Smaldone, Massimiliano D'Aiuto, Gennaro Mossetti, Andrea Soricelli, Marco Salvatore

{"title":"Evaluation of HMGB1 as possible marker via breast organoid cultures research.","authors":"Vincenza Ciaramella, Barbara Carrese, Luigi Coppola, Giovanni Smaldone, Massimiliano D'Aiuto, Gennaro Mossetti, Andrea Soricelli, Marco Salvatore","doi":"10.3892/or.2025.8939","DOIUrl":"10.3892/or.2025.8939","url":null,"abstract":"High mobility group box 1 (HMGB1) is a non‑histone protein widely expressed in the nucleus of mammalian cells, and it can be released by both immune and tumor cells. In the extracellular context HMGB1 can act as a proinflammatory mediator and boosting cancer progression. High HMGB1 mRNA expression levels are usually observed in various malignant diseases, including breast cancer (BC). Several studies have demonstrated the potential clinical value of HMGB1 in BC diagnosis and therapy. The present data, using in vitro protocols and molecular technologies, demonstrated the presence of HMGB1 in organoids derived from patients with BC with significantly elevated expression correlating with poorer prognosis. By blocking the activity of HMGB1 protein, cell cycle arrest and induction of apoptosis was observed in ex vivo 3D organoids, suggesting a potential antitumor effect. The localization by immunofluorescence, of HMGB1, β‑catenin and NF‑kB in organoids and the subsequent inhibition of the entire molecular pathway by switching off HMGB1 signaling suggests that there is a crosstalk between these molecules demonstrating their involvement in inflammation and inflammation‑associated diseases such as cancer. The current results aim to investigate the role of HMGB1 in BC progression and find innovative applications based on HMGB1 as a therapeutic target and early disease biomarker.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12242370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EIF3B‑METTL3 complex promotes cell proliferation, invasion and EGFR/AKT signaling in cervical cancer. EIF3B - METTL3复合物促进宫颈癌细胞增殖、侵袭和EGFR/AKT信号传导。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-06-27 DOI: 10.3892/or.2025.8936

Chao Zhang, Xiang Fan, Jia Yang, Pengfeng Zhu

{"title":"EIF3B‑METTL3 complex promotes cell proliferation, invasion and EGFR/AKT signaling in cervical cancer.","authors":"Chao Zhang, Xiang Fan, Jia Yang, Pengfeng Zhu","doi":"10.3892/or.2025.8936","DOIUrl":"10.3892/or.2025.8936","url":null,"abstract":"Eukaryotic translation initiation factor 3B (EIF3B), a translation initiation factor, has been identified to directly interact with methyltransferase‑like (METTL) family members to regulate translation and oncogenic transformation in various types of cancers. However, the interaction mechanism of EIF3B with METTL3 has not yet been reported in cervical cancer (CC). The present study further investigated the interaction between EIF3B and METTL3, as well as their regulatory effect on the malignant behaviors of CC cells. EIF3B overexpression plasmid (oeEIF3B) or small interfering RNA (siRNA; siEIF3B) and negative controls (oeNC and siNC) were transfected into HeLa and SiHa cells. In addition, METTL3 siRNA (siMETTL3) and siNC were transfected along with oeEIF3B or oeNC into HeLa and SiHa cells. Co‑immunoprecipitation was performed to determine the interaction between EIF3B and METTL3. EIF3B expression was found to be elevated in CC cell lines (C‑33A, HeLa, SiHa and CaSki) compared with the control cell line. oeEIF3B accelerated the proliferation and invasion and attenuated the apoptosis of both HeLa and SiHa cells, while siEIF3B exerted an opposite effect. In addition, oeEIF3B activated the EGFR/AKT signaling pathway, whereas siEIF3B suppressed it. Of note, EIF3B and METTL3 formed a complex, according to co‑immunoprecipitation assay; moreover, EIF3B and METTL3 could not regulate the expression of each other. Regardless of the presence or absence of oeEIF3B, siMETTL3 suppressed cell proliferation and invasion, and inhibited EGFR/AKT signaling, while promoting the apoptosis of HeLa and SiHa cells. More importantly, oeEIF3B lost its effect on these cellular functions following the addition of siMETTL3, suggesting that the EIF3B‑METTL3 complex, but not EIF3B alone, plays a cancer‑promoting role in CC. On the whole, the present study demonstrates that the EIF3B‑METTL3 complex induces cell proliferation and invasion, and activates EGFR/AKT signaling in CC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Retracted] Silencing of GP73 inhibits invasion and metastasis via suppression of epithelial‑mesenchymal transition in hepatocellular carcinoma. [撤回]沉默GP73通过抑制肝细胞癌上皮-间质转化抑制侵袭和转移。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/or.2025.8943

Ying Yang, Qiang Liu, Hua Zhang, Huarong Zhao, Ruin Mao, Zhipeng Li, Sha Ya, Chunli Jia, Yongxing Bao

{"title":"[Retracted] Silencing of GP73 inhibits invasion and metastasis via suppression of epithelial‑mesenchymal transition in hepatocellular carcinoma.","authors":"Ying Yang, Qiang Liu, Hua Zhang, Huarong Zhao, Ruin Mao, Zhipeng Li, Sha Ya, Chunli Jia, Yongxing Bao","doi":"10.3892/or.2025.8943","DOIUrl":"10.3892/or.2025.8943","url":null,"abstract":"Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that Fig. 3A (showing the results of scratch‑wound assay experiments) and Fig. 4C (showing the results of cell morphological experiments) both contained internally a pair of data panels containing duplicated data. Moreover, four of the six data panels shown in Fig. 3B (showing the results of Transwell migration assay experiments), contained either matching or overlapping data panels. In addition, the western blot data in Fig. 4A selected to show the Vimentin protein bands for the MHCC97H cell line and the Snail protein bands for the Bel‑7404 cell line were seemingly identical. Finally, it was noted that certain of the western blot data in Fig. 4A of the above paper were also apparently included in Figs. 2A and 3A of another paper published by the same group in the journal Carcinogenesis. Owing to the number of identified instances of data duplication in this paper, the Editor of Oncology Reports has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 37: 1182‑1188, 2017; DOI: 10.3892/or.2017.5351].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Corrigendum] Overexpression of IL‑9 induced by STAT3 phosphorylation is mediated by miR‑155 and miR‑21 in chronic lymphocytic leukemia. [勘误]在慢性淋巴细胞白血病中，STAT3磷酸化诱导的IL - 9过表达是由miR - 155和miR - 21介导的。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-04 DOI: 10.3892/or.2025.8940

Na Chen, Lili Feng, Huiting Qu, Kang Lu, Peipei Li, Xiao Lv, Xin Wang

{"title":"[Corrigendum] Overexpression of IL‑9 induced by STAT3 phosphorylation is mediated by miR‑155 and miR‑21 in chronic lymphocytic leukemia.","authors":"Na Chen, Lili Feng, Huiting Qu, Kang Lu, Peipei Li, Xiao Lv, Xin Wang","doi":"10.3892/or.2025.8940","DOIUrl":"10.3892/or.2025.8940","url":null,"abstract":"Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 1A on p. 3067, the western blots shown for the STAT3 data in the upper right‑hand gels (for the N3, N4, and C5‑C8 experiments) were strikingly similar to the GAPDH data shown in the lower right‑hand gels (for the C14‑C16 and N6‑N8 experiments). Furthermore, in Fig. 2A on p. 3068, the phosphorylated (p‑)STAT western blots had apparently already appeared in a paper published by the same research group in the journal International Journal of Clinical and Experimental Pathology. After inspecting their original data, the authors realized that the data of interest in Figs. 1 and 2 had inadvertently been chosen incorrectly. The revised and corrected versions of Figs. 1 and 2, now showing replacement data for the upper and lower right‑hand gels in Fig. 1A and the upper three left‑hand panels in Fig. 2A, are shown on the next two pages. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors apologize to the Editor of Oncology Reports and to the readership for any inconvenience caused. [Oncology Reports 39: 3064‑3072, 2018; DOI: 10.3892/or.2018.6367].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12242365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Harnessing CRISPR/Cas9 to overcome targeted therapy resistance in non‑small cell lung cancer: Advances and challenges (Review). 利用CRISPR/Cas9克服非小细胞肺癌的靶向治疗耐药：进展和挑战（综述）

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/or.2025.8944

Jianting Du, Xian Gong, Renjie Huang, Bin Zheng, Chun Chen, Zhang Yang

{"title":"Harnessing CRISPR/Cas9 to overcome targeted therapy resistance in non‑small cell lung cancer: Advances and challenges (Review).","authors":"Jianting Du, Xian Gong, Renjie Huang, Bin Zheng, Chun Chen, Zhang Yang","doi":"10.3892/or.2025.8944","DOIUrl":"10.3892/or.2025.8944","url":null,"abstract":"Targeted therapy has markedly improved outcomes for patients with non‑small cell lung cancer (NSCLC). However, the emergence of drug resistance remains a major clinical challenge, limiting long‑term treatment efficacy. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9, a revolutionary gene‑editing technology, offers precise and efficient genetic modifications, providing new insights into the mechanisms of drug resistance in NSCLC. The present review explored the application of CRISPR/Cas9 in overcoming resistance associated with key oncogenic drivers, including EGFR, KRAS, ALK, ROS1, MET and BRAF. It summarized recent advances in CRISPR‑based strategies to reverse resistance, enhance targeted therapy effectiveness and develop potential therapeutic interventions. Additionally, it discussed current limitations, including off‑target effects, delivery challenges and ethical concerns, while highlighting future directions for clinical translation. Using CRISPR/Cas9 technology may pave the way for novel, personalized treatment approaches in NSCLC, ultimately improving patient outcome.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12288633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Widespread activation and critical role of EMT and stemness in the neuroendocrine differentiation of prostate cancer (Review). EMT和stemness在前列腺癌神经内分泌分化中的广泛激活和关键作用（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/or.2025.8942

Yun-Fan Li, Shuai Su, Yu Luo, Chengcheng Wei, Jingke He, Liang-Dong Song, Kun Han, Jue Wang, Xiangzhi Gan, De-Lin Wang

{"title":"Widespread activation and critical role of EMT and stemness in the neuroendocrine differentiation of prostate cancer (Review).","authors":"Yun-Fan Li, Shuai Su, Yu Luo, Chengcheng Wei, Jingke He, Liang-Dong Song, Kun Han, Jue Wang, Xiangzhi Gan, De-Lin Wang","doi":"10.3892/or.2025.8942","DOIUrl":"10.3892/or.2025.8942","url":null,"abstract":"Neuroendocrine (NE) prostate cancer (NEPC) is an aggressive and lethal subtype of prostate cancer. It is typically characterized by the expression of NE markers and the loss of androgen receptor expression. De novo NEPC is rare, accounting for <2% of all prostate cancer cases at diagnosis. More commonly, NEPC arises from prostate adenocarcinoma following androgen deprivation therapy, with 20‑25% of metastatic castration‑resistant prostate cancers undergoing NE differentiation due to lineage plasticity. During this transition, pathways associated with epithelial‑mesenchymal transition (EMT) and stemness are broadly activated, which is considered to be a key driver of NEPC's high metastatic potential, resistance to chemotherapy and radiotherapy and poor prognosis. EMT facilitates metastasis by enhancing cellular motility and invasiveness, while stemness properties contribute to post‑metastatic colonization, immune evasion, therapy resistance and cellular dormancy. As manifestations of cellular plasticity, these processes share overlapping molecular mechanisms. Targeting key regulators within these pathways may offer promising therapeutic strategies for NEPC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Advances in lymphoma biomarkers research based on proteomics technology (Review). 基于蛋白质组学技术的淋巴瘤生物标志物研究进展（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-09-01 Epub Date: 2025-07-04 DOI: 10.3892/or.2025.8941

Qibei Liu, Jianmin Ling, Zhao Li, Lintao Bi

{"title":"Advances in lymphoma biomarkers research based on proteomics technology (Review).","authors":"Qibei Liu, Jianmin Ling, Zhao Li, Lintao Bi","doi":"10.3892/or.2025.8941","DOIUrl":"10.3892/or.2025.8941","url":null,"abstract":"Lymphoma is a common malignancy characterized by diverse pathological types and marked heterogeneity. Distinct subtypes of lymphomas are markedly different in their clinical manifestations, treatment approaches and prognostic outcomes. With the rapid development of molecular biology techniques, antitumor research has stepped into an era of precision medicine. Biomarkers, with high sensitivity and specificity, are expected to function in early diagnosis, targeted treatment and prognostic estimation for cancer and enhance the survival rate and life quality of patients. In this regard, proteomics technology, with the capability to systematically identify and quantify the dynamic protein alterations in tissues or cells, thereby facilitating the discovery of novel tumor potential candidates, has attracted significant scientific attention. The present article aimed to review most up‑to‑date research progress of lymphoma‑related biomarkers discovered based on proteomics technology, focusing on the potential application of these markers in the diagnosis, therapy and prognosis of each lymphoma subtype, and discuss the role proteomics may serve in future development of lymphoma research and clinical practice.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12242372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0