Molecular and clinical oncology最新文献

{"title":"Usefulness of pharmacy outpatient clinic follow-up for maintaining relative dose intensity in patients on adjuvant CAPOX chemotherapy for gastric cancer.","authors":"Masashi Nakamura, Takashi Yokokawa, Kazuyoshi Kawakami, Yuka Kimura, Hisanori Shimizu, Kazuo Kobayashi, Takeshi Aoyama, Wataru Suzuki, Masahiro Hatori, Kenichi Suzuki, Daisuke Takahari, Mariko Ogura, Keisho Chin, Takeru Wakatsuki, Kensei Yamaguchi, Masakazu Yamaguchi","doi":"10.3892/mco.2026.2943","DOIUrl":"10.3892/mco.2026.2943","url":null,"abstract":"<p><p>Capecitabine plus oxaliplatin (CAPOX) is a frequently used treatment regimen for colorectal and gastric cancer as postoperative adjuvant chemotherapy. Nausea, vomiting and diarrhea are reported to be the main causes of decreased adherence to CAPOX therapy. The Cancer Institute Hospital, Japanese Foundation for Cancer Research, provides a pharmaceutical outpatient clinic for patients undergoing outpatient chemotherapy. In the present study, dose intensity and severity of side effects of CAPOX therapy as adjuvant chemotherapy after surgery for gastric cancer were evaluated before and after outpatient pharmacy clinic follow-up. This was a retrospective, observational study. Data from consecutive patients who received CAPOX therapy as adjuvant therapy after surgery for gastric cancer from November 2015 to April 2021 were obtained. Two patients were excluded, and 59 patients were included in the analysis. In total, there were 243 prescription recommendations at the pharmacy outpatient clinic. The most common prescription recommendation was prescription of supportive care medications (53.9%, 131 instances), followed by postponement of treatment (10.3%, 25 instances) and dose reduction of each drug (8.2%, 20 instances). The mean relative dose intensity (RDI) was 67.8±20.2% [95% confidence interval (CI), 62.5-73.1%] for capecitabine and 62.2±20.7% (95% CI, 56.9-67.6%) for oxaliplatin. The mean RDI was 72.5±18.8% (95% CI, 61.2-83.7%) before capecitabine dose reduction and 90.4±14.8% (95% CI, 81.4-99.3%) after dose reduction. The pharmacy outpatient clinic maintained RDI and contributed to the continuation of treatment by suggesting supportive care medications and recommending reduction of the dosage of anticancer drugs to the physicians.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"34"},"PeriodicalIF":1.9,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13040532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics analysis reveals psoralen to suppresses renal cell carcinoma through the PI3K/AKT pathway.","authors":"Di Chen, Tingting Chen, Yuru Yang, Andong Wang","doi":"10.3892/mco.2026.2942","DOIUrl":"10.3892/mco.2026.2942","url":null,"abstract":"<p><p>Psoralen (PSO) is the active component of <i>Trigonostemon xyphophyllorides</i> (TX) and exhibits therapeutic potential against renal cell carcinoma (RCC). Despite this, there is a lack of research investigating the therapeutic efficacy of PSO specifically on RCC. In the present study, an integrated multi-omics strategy was employed to systematically evaluate the anti-RCC effects of PSO. PSO was subjected to network pharmacology analysis, identifying 78 RCC-related target genes. Pathway enrichment analysis suggested the involvement of the PI3K/AKT signaling pathway as a key regulatory mechanism. Molecular docking analysis and molecular dynamics simulations indicated a strong binding affinity and enhanced structural stability of the bound complexes between PIK3CA (PDB ID: 9B4T) and PSO. <i>In vitro</i> experiments demonstrated a potent antiproliferative effect of PSO on multiple RCC cell lines, with the strongest inhibition observed in ACHN cells (IC₅₀ = 1.74±0.90 µM), By contrast, minimal cytotoxicity was observed towards the non-cancerous renal epithelial cell line HK-2 at concentrations ≤8 µM. Furthermore, PSO treatment resulted in the significant downregulation of the PI3K-AKT signaling pathway-related genes, which was supported by results from transcriptomic analysis identifying 593 differentially expressed genes. The present findings offer quantitative and mechanistic evidence supporting the clinical utilization of TX in the treatment of RCC, thereby advancing its further research and development.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"33"},"PeriodicalIF":1.9,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13040130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A cascade via CD276/PI3K/SIRT1/E-Cad in overcoming contact inhibition of proliferation in hepatocellular carcinoma cells.","authors":"Xiaobo Yu, Rong Su, Guoqiang Cao, Haiyang Xie, Lin Zhou, Shusen Zheng","doi":"10.3892/mco.2026.2941","DOIUrl":"10.3892/mco.2026.2941","url":null,"abstract":"<p><p>Contact inhibition of proliferation (CIP) halts normal cell proliferation upon confluence, a mechanism often lost in cancer cells, leading to disorganized proliferation. CD276, frequently overexpressed in cancers, promotes proliferation by activating the PI3K/AKT pathway; however, its role in CIP is unexplored. Human HCC cell lines and an immortalized human hepatocyte cell line were cultured under sparse or confluent conditions. Small interfering RNA was transfected to knockdown CD276 expression and plasmid DNA was transfected to overexpress CD276. The cell cycle was analyzed by flow cytometry. Western blotting was used to detect the expression of CD276, E-Cad, SIRT1 and cell cycle proteins. Analysis revealed higher CD276 levels in HCC lines than in HepLi5, with increased CD276 correlating with reduced CIP severity and lower E-Cad expression. Overexpression of CD276 alleviated G0/G1 phase arrest induced by high-density contact, while CD276 knockdown enhanced it. CD276 emerged as a critical regulator of E-Cad in confluent HCC cells through modulating SIRT1 protein via the PI3K/AKT pathway. The findings of the present study highlighted CD276's pivotal role in regulating the cell cycle under confluent culture conditions, revealing a novel regulatory cascade involving CD276/PI3K/SIRT1/E-Cad that may influence tumor progression. This insight into CD276's undisclosed function provides potential treatment strategies for HCC intervention.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"32"},"PeriodicalIF":1.9,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13040135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long non-coding RNAs affect the metastasis of hepatocellular carcinoma cells by regulating the epithelial-to-mesenchymal transition.","authors":"Qiaomei Deng, Jilu Zhou, Yanxi Zhou, Xiaoxia Lao, Qingwei Ma, Tian Gan, Liping Ma","doi":"10.3892/mco.2026.2940","DOIUrl":"10.3892/mco.2026.2940","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, and, in terms of its global incidence and mortality rates across all types of cancer, HCC is ranked sixth and third, respectively. Therefore, HCC is a notable global health burden. Dysregulation of long non-coding RNAs (lncRNAs) has a key role in human tumorigenesis. However, the lncRNAs involved in the epithelial-to-mesenchymal transition (EMT) that affects the migration and recurrence of HCC are yet to be fully elucidated. In the present study, the EMT was induced in Huh7 cells using transforming growth factor-β (TGF-β) and it was revealed that this process may promote HCC metastasis. RNA sequencing was then used to screen the lncRNAs and mRNAs that were differentially expressed (DE) during the TGF-β-induced EMT process. Subsequently, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were carried out on the identified DE lncRNAs and mRNAs. By constructing a co-expression network of DE lncRNAs and mRNAs, key lncRNAs possibly involved in the TGF-β-induced EMT that may promote the metastasis of HCC were predicted. Therefore, although preliminary, the present study suggested a list of potential candidates for further investigation of the molecular mechanism of the TGF-β-induced EMT in HCC. Further research may reveal key information on tumorigenesis and potential therapeutic targets in HCC in the future.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"31"},"PeriodicalIF":1.9,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13041190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated TNF-α level is correlated with NF-κB/p65 activation in patients with sporadic colorectal cancer.","authors":"Uriel Francisco Santana-Bejarano, David Fernandez-Sanchez, Lucina Bobadilla-Morales, Alejandro Brukman-Jimenez, Jesús Alonso Valenzuela-Pérez, Jorge Román Corona-Rivera, Alfredo Corona-Rivera","doi":"10.3892/mco.2026.2939","DOIUrl":"10.3892/mco.2026.2939","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a major global health issue, and inflammation plays a crucial role in its development. Nuclear factor-κB (NF-κB) activation, typically mediated by tumor necrosis factor-α (TNF-α), is involved in the inflammatory response leading to cancer. The present study aimed to investigate the TNF-α/NF-κB signaling in sporadic CRC. NF-κB activation was evaluated by measuring the phosphorylation of the p65 subunit at specific residues (pS536 and pS529) through phospho-flow cytometry. TNF-α protein levels were measured using flow cytometry/ELISA and <i>TNF-α</i>, <i>NFKB1</i>, and <i>RELA</i> gene expression was assessed using reverse transcription-quantitative PCR. The results were then correlated with the Tumor-Node-Metastasis (TNM) classification. The findings of the present study revealed that NF-κB activation was higher in tumoral tissue than in normal adjacent mucosa. TNF-α gene expression and protein levels were also elevated in patients with CRC, particularly in advanced stages. The present study demonstrated a positive correlation between TNF-α and NF-κB/p65. The analysis of TNM groups suggested that the correlation between TNF-α and p65 (pS536) plays an essential role in CRC tumorigenesis. By contrast, TNF-α and p65 (pS529) signaling was revealed to be relevant for CRC progression. Evaluating <i>RELA</i> and <i>NFKB1</i> gene expression revealed molecular feedback during the inflammation response. The findings of the present study highlighted the TNF-α/NF-κB signaling pathway role in CRC development and may serve as a potential diagnostic and prognostic marker for the disease. Further research could provide valuable insights into the clinical implications of targeting this pathway in CRC diagnosis and treatment.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"30"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13041193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of MGST3 promotes colorectal cancer progression.","authors":"Yuchun Wu, Changjiang Fan, Jiaqi Zhou, Fengshan Huang, Yang Zhang, Yuqi He, Jianxun Wang","doi":"10.3892/mco.2026.2938","DOIUrl":"10.3892/mco.2026.2938","url":null,"abstract":"<p><p>Colorectal cancer (CRC), the third most common malignancy worldwide, presents significant treatment challenges due to an incomplete understanding of its molecular progression. Therefore, identifying the specific developmental mechanisms of CRC holds potential to improve diagnosis, treatment and prognosis. In the present study, RNA-sequencing analysis of samples from patients with an early-stage tumor, advanced carcinoma or adenoma was conducted with the aim of uncovering differentially expressed genes. At the same time, gene knockdown and tumor-related phenotype verification were conducted using a normal colon epithelial cell line. Subsequently, a group of genes related to the target gene was analyzed using The Cancer Genome Atlas (TCGA) database and the differences in colon tumor mutation burden, immune infiltration, epithelial-mesenchymal transition (EMT) and ferroptosis were observed between samples with high and low expression of the gene group. Microsomal glutathione S-transferase 3 (MGST3) was identified as a crucial tumor-suppressive gene in colon cancer pathogenesis. Functional studies demonstrated that MGST3 knockdown in normal human colonic epithelial cells activated glutathione metabolic pathways and induced tumorigenic transformation, characterized by accelerated proliferation and suppression of EMT. TCGA database analysis revealed distinct phenotypes associated with low MGST3 expression, including elevated tumor mutational burden, attenuated EMT processes, diminished immune cell infiltration and enhanced ferroptosis. These findings establish MGST3 as a potential novel regulator of colon carcinogenesis, with its downregulation creating a tumor microenvironment conducive to ferroptosis while simultaneously suppressing EMT and immune responses. The present study not only elucidates previously unrecognized mechanisms driving colon cancer progression but also identifies MGST3-related pathways as promising therapeutic targets for intervention.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 5","pages":"29"},"PeriodicalIF":1.9,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>PSMD6</i> as a biomarker for hepatocellular carcinoma: A comprehensive bioinformatics analysis and <i>in vitro</i> validation.","authors":"Jian Liu, Ting Wang, Zhenhua Zhu","doi":"10.3892/mco.2026.2937","DOIUrl":"10.3892/mco.2026.2937","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a lethal malignancy with limited diagnostic biomarkers. The present study aims to comprehensively investigate the expression, clinical prognostic significance, and potential mechanisms of PSMD6 in HCC through comprehensive bioinformatics analyses and <i>in vitro</i> experimental validation. <i>PSMD6</i> expression in HCC was analyzed using data from the UALCAN, SANGERBOX and TIMER databases. The association between PSMD6 expression and clinicopathological features, patient prognosis, and immune cell filtration was evaluated. Functional enrichment analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) were performed to identify PSMD6-related signaling pathways, and a protein-protein interaction (PPI) network was constructed using the BioGRID and STRING databases. Key findings from bioinformatics analyses were validated <i>in vitro</i> using reverse transcription-quantitative (RT-qPCR) and western blotting in HCC cell lines. <i>PSMD6</i> expression was significantly upregulated in HCC compared with adjacent normal tissues (P<0.001), which has been consistently validated by various databases and confirmed by <i>in vitro</i> experiments using RT-qPCR and western blotting. High PSMD6 expression was significantly associated with advanced tumor grade and patient age and served as an independent predictor of poor overall survival (P<0.001). In addition, <i>PSMD6</i> demonstrated high diagnostic accuracy for HCC (area under the curve=0.877). Moreover, <i>PSMD6</i> expression showed a positive correlation with the infiltration levels of CD4⁺ T cells and B cells in HCC (P<0.05), independent of tumor purity (P>0.05). Functional enrichment analysis indicated that PSMD6 was involved in critical oncogenic pathways, including the cell cycle. PPI network analysis revealed that <i>PSMD6</i> interact with several key proteins, such as <i>PSMC3, PSMD7</i> and <i>UCHL5</i> to achieve a regulatory function in HCC. In conclusion, <i>PSMD6</i> is significantly overexpressed in HCC and is strongly associated with tumor progression and poor prognosis. It represents a promising diagnostic biomarker and a potential therapeutic target for HCC.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 4","pages":"28"},"PeriodicalIF":1.9,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12976850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unmasking intratumoral heterogeneity: Postoperative revelation of subclonal divergence in <i>de novo</i> metastatic HR-positive/HER2-negative breast cancer: A case report.","authors":"Zeliha Birsin, Emir Çerme, Ceyda Sönmez Wetherilt, Zeynep Hande Turna","doi":"10.3892/mco.2026.2936","DOIUrl":"10.3892/mco.2026.2936","url":null,"abstract":"<p><p>Intratumoral heterogeneity poses a significant challenge in the management of metastatic hormone receptor-positive (HR⁺), human epidermal growth factor receptor 2 (HER2)-negative (HER2^-) breast cancer (BC), as it may contribute to treatment resistance and disease progression. Two cases of <i>de novo</i> metastatic HR⁺/HER2^- BC with bone-only metastases were reported. Both patients responded well to first-line systemic therapy with CDK4/6 inhibitors and endocrine agents. Locoregional surgery was subsequently performed and revealed HER2-positive subclones in the primary tumors that were not detected in the initial core biopsies. In one patient, HER2-targeted therapy was initiated with sustained clinical benefit. In the second patient, CDK4/6 inhibitor therapy was initially continued, but the disease later progressed. Post-treatment pathology can uncover distinct subclones, reflecting the dynamic nature of tumor biology. These cases highlight the potential value of surgical reassessment in selected patients with metastatic BC to guide individualized treatment strategies.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 4","pages":"27"},"PeriodicalIF":1.9,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research advances in early screening for colorectal cancer (Review).","authors":"Jiaojiao Jiang","doi":"10.3892/mco.2026.2935","DOIUrl":"10.3892/mco.2026.2935","url":null,"abstract":"<p><p>Early detection and intervention for colorectal cancer (CRC) play crucial roles in reducing the disease burden. However, existing screening methods remain limited in terms of sensitivity, specificity, and compliance. The present review systematically examines and compares cutting-edge research in the field of early screening for CRC performed in recent years, evaluates mainstream screening technologies from multiple dimensions, and provides a theoretical reference basis for the construction of efficient, accurate and sustainable early CRC screening strategies.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 4","pages":"26"},"PeriodicalIF":1.9,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in semaphorin 3B research in tumors (Review).","authors":"Xue Zhang, Ruizeng Feng, Huanfen Zhao, Jie Wei, Xing Xu","doi":"10.3892/mco.2026.2934","DOIUrl":"10.3892/mco.2026.2934","url":null,"abstract":"<p><p>Advancing precision oncology has driven breakthroughs in understanding oncogenes, tumor suppressors, signaling pathway regulation, apoptosis, and cell cycle control. Molecularly targeted therapies, now integral to malignant tumor treatment, exploit these insights. Functioning as a tumor suppressor, semaphorin 3B (SEMA3B) is frequently inactivated across malignancies via promoter hypermethylation, loss of heterozygosity, and proteolytic cleavage. Its structure-function relies on receptor complex formation, enabling activation of multiple pathways that induce tumor cell apoptosis, arrest the cell cycle, and competitively inhibit vascular endothelial growth factor-binding to neuropilin 1. This blockade of the PI3K/Akt pathway suppresses tumor angiogenesis, metastasis, and proliferation. Therefore, comprehensively elucidating SEMA3B and its interactors is crucial for identifying novel biomarkers for early cancer detection and molecular therapeutic targets. Future research should focus on translating these findings into clinical applications, including the development of SEMA3B-based epigenetic therapies and combination strategies with anti-angiogenic agents. Key challenges remain in fully delineating the context-dependent dual roles of SEMA3B, understanding its complex interactions within the tumor microenvironment, and overcoming its inactivation mechanisms for effective therapeutic restoration.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 4","pages":"25"},"PeriodicalIF":1.9,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}