Molecular Oncology最新文献

{"title":"Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence.","authors":"Zuzana Liblova, Dominika Maurencova, Barbora Salovska, Marek Kratky, Tomas Mracek, Zuzana Korandova, Alena Pecinova, Pavla Vasicova, David Rysanek, Ladislav Andera, Ivo Fabrik, Rudolf Kupcik, Pavel Kashmel, Pinky Sultana, Vojtech Tambor, Jiri Bartek, Josef Novak, Marie Vajrychova, Zdenek Hodny","doi":"10.1002/1878-0261.70039","DOIUrl":"10.1002/1878-0261.70039","url":null,"abstract":"<p><p>Cellular senescence has recently been recognized as a significant contributor to the poor prognosis of glioblastoma, one of the most aggressive brain tumors. Consequently, effectively eliminating senescent glioblastoma cells could benefit patients. Human ADP/ATP translocases (ANTs) play a role in oxidative phosphorylation in both normal and tumor cells. Previous research has shown that the sensitivity of senescent cells to mitochondria-targeted senolytics depends on the level of ANT2. Here, we systematically mapped the transcript and protein levels of ANT isoforms in various types of senescence and glioblastoma tumorigenesis. We employed bioinformatics analysis, targeted mass spectrometry, RT-PCR, immunoblotting, and assessment of cellular energy state to elucidate how individual ANT isoforms are expressed during the development of senescence in noncancerous and glioblastoma cells. We observed a consistent elevation of ANT1 protein levels across all tested senescence types, while ANT2 and ANT3 exhibited variable changes. Alterations in ANT protein isoform levels correlated with shifts in the cellular oxygen consumption rate. Our findings suggest that ANT isoforms are mutually interchangeable for oxidative phosphorylation and manipulating individual ANT isoforms could have potential for senolytic therapy.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2619-2647"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic profiling of cancer-fibroblast interactions reveals drug combinations in ovarian cancer.","authors":"Greta Gudoityte, Osheen Sharma, Laura Leuenberger, Emelie Wallin, Josefin Fernebro, Päivi Östling, Rebecka Bergström, Johan Lindberg, Ulrika Joneborg, Olli Kallioniemi, Brinton Seashore-Ludlow","doi":"10.1002/1878-0261.70051","DOIUrl":"10.1002/1878-0261.70051","url":null,"abstract":"<p><p>Ovarian cancer (OC) is a leading cause of death of gynecological cancers in women. Poor patient response to treatment highlights the need to better understand how the tumor microenvironment affects OC progression. Growing evidence indicates the crucial role of non-cancerous components, such as cancer-associated fibroblasts, in establishing a complex network of cellular and molecular interactions, influencing cancer progression and response to treatment. Therefore, in this study, we sought to characterize the impact of fibroblasts on OC cell behavior and drug response. Using both direct and indirect cell co-culture systems, we observed distinct changes in cancer cell proliferation, morphology, and secretome in the presence of fibroblasts. Furthermore, an imaging-based high-throughput drug screen of 528 oncology compounds revealed multiple drugs that showed altered efficacy in the co-culture conditions, demonstrating the role of fibroblasts in driving cancer cell resistance to treatment. Most importantly, our data identified the two drug combinations of Birinapant or Vorinostat with Carboplatin as promising treatments, exploiting the altered cancer cell phenotype in co-cultures. These findings were supported by the increased sensitivity of ex vivo cultures to these combinations.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2574-2593"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting carbonic anhydrase IX/XII prevents the anti-ferroptotic effect of stromal lactic acid in prostate carcinoma.","authors":"Elisa Pardella, Giuseppina Comito, Luigi Ippolito, Erica Pranzini, Marta Iozzo, Giulia Gangarossa, Francesca Virgilio, Silvia Bua, Alessio Nocentini, Giada Sandrini, Nicla Lorito, Marina Bacci, Gabriella Nesi, Pietro Spatafora, Sergio Serni, Claudiu T Supuran, Andrea Morandi, Paola Chiarugi, Elisa Giannoni","doi":"10.1002/1878-0261.70083","DOIUrl":"10.1002/1878-0261.70083","url":null,"abstract":"<p><p>Ferroptosis is a form of regulated cell death dependent on iron-driven phospholipid peroxidation and is controlled by both cell autonomous and non-cell autonomous mechanisms. In prostate cancer (PCa), tumor cells engage in a metabolic crosstalk with cancer-associated fibroblasts (CAFs), resulting in increased utilization of CAF-secreted lactic acid, that ultimately supports cancer aggressiveness. In this context, the effect of the prostate tumor microenvironment in modulating ferroptosis sensitivity has not yet been extensively investigated. Here, we demonstrate that CAF-secreted lactic acid protects PCa cells from ferroptosis induction and supports the upregulation of the antioxidant enzyme glutathione peroxidase 4 (GPX4). Interestingly, targeting carbonic anhydrase IX/XII (CA IX/XII), the main regulators of microenvironmental acidosis, in tumor and stromal compartments hinders lactic acid shuttle within the tumor-stroma interplay and thus, prevents ferroptosis resistance induced by lactic acid. Analyses of tissue samples from PCa patients also revealed that GPX4, CA IX, and CA XII expression levels increase during PCa progression. Overall, these findings support a role for stromal lactic acid in mediating ferroptosis resistance in PCa, identifying CA IX/XII as potential therapeutic targets regulating ferroptosis sensitivity.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2515-2536"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144506843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A DIA-MS-based proteomics approach to find potential serum prognostic biomarkers in glioblastoma patients.","authors":"Anne Clavreul, François Guillonneau, Odile Blanchet, Hamza Lasla, Audrey Rousseau, Catherine Guette, Alice Boissard, Cécile Henry, Morgan Dhondt, Pascal Jézéquel, Philippe Menei, Jean-Michel Lemée","doi":"10.1002/1878-0261.70068","DOIUrl":"10.1002/1878-0261.70068","url":null,"abstract":"<p><p>No blood-based protein biomarkers are currently available for routine clinical use to determine the prognosis of patients with glioblastoma (GB). We performed data-independent acquisition mass spectrometry (DIA-MS)-based proteomics on 96 presurgical serum samples from patients with GB and 30 serum samples from healthy controls to identify such markers. Among the 622 serum proteins differentially expressed between the GB and control groups, 191 had a |log₂(fold change)| ≥ 0.58 and an area under the curve ≥ 0.75. An analysis of their prognostic value revealed that high levels of IL1R2 and low levels of CRTAC1 and HRG were associated with poor survival. Multivariate Cox regression analysis identified IL1R2 as an independent prognostic factor for PFS and CRTAC1 as an independent prognostic factor for OS. The concentration of CRTAC1 in serum samples from an independent cohort of short- and long-term survivors of GB (STS and LTS, respectively) by ELISA was shown to be lower in the STS than in the LTS group. CRTAC1, HRG, and IL1R2 could potentially be used to better inform prognosis and predict treatment response in GB patients.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2686-2699"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Raphin-1 mediates the survival and sensitivity to radiation of pediatric-type diffuse high-grade glioma via phosphorylated eukaryotic initiation factor 2α-dependent and -independent processes.","authors":"Karin Eytan, Moshe Leitner, Amos Toren, Shoshana Paglin, Michal Yalon","doi":"10.1002/1878-0261.70081","DOIUrl":"10.1002/1878-0261.70081","url":null,"abstract":"<p><p>The primary treatment for fatal pediatric-type diffuse high-grade glioma (PED-DHGG) which harbor the H3K27M or H3G34R/V mutation is radiation, but it provides only short-term relief. Inhibitors of phosphorylated eIF2α (PeIF2α) phosphatase-namely raphin-1 and salubrinal-decrease survival of PED-DHGG cell lines and sensitize them to radiation. However, although both drugs increase PeIF2α, they have different effects on common targets and different targets altogether. Here, we aimed to identify PeIF2α-phosphatase-dependent and PeIF2α-phosphatase-independent molecular targets. Raphin-1 but not salubrinal, decreased the level of BiP and CReP and increased that of DR5, in an ISRIB-independent manner. Raphin-1 induced similar changes in MEF^S51A cells and in irradiated PED-DHGG, suggesting a PeIF2α-independent contribution to raphin-1's radiosensitizing effect. Importantly, while the expression of [S51D] eIF2α decreased the survival of PED-DHGG and both raphin-1 and salubrinal decreased the survival of MEF^WT cells, only raphin-1 decreased the survival of mutant MEF^S51A cells. Our results suggest that the sensitivity of PED-DHGG to raphin-1 is mediated by both PeIF2α-dependent and PeIF2α-independent processes. Elucidating these processes could reveal targets for the development of drugs to overcome radiotherapy resistance of PED-DHGG.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2648-2669"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoglin mediates the tumor- and metastasis-promoting traits of stromal myofibroblasts in human breast carcinomas.","authors":"Shoki Okubo, Yoshihiro Mezawa, Zixu Wang, Ahmet Acar, Yasuhiko Ito, Atsushi Takano, Yohei Miyagi, Tomoyuki Yokose, Toshinari Yamashita, Yataro Daigo, Takuya Shirakihara, Akira Orimo","doi":"10.1002/1878-0261.70074","DOIUrl":"10.1002/1878-0261.70074","url":null,"abstract":"<p><p>Carcinoma-associated fibroblasts (CAFs), which are abundant in the tumor microenvironment, influence cancer hallmarks. We previously described transforming growth factor-β (TGF-β)-Smad2/3 signaling as being activated in myofibroblastic CAFs (myCAFs) in an autocrine fashion by increasing TGF-β production. However, factors regulating such autocrine TGF-β signaling remain poorly understood. Herein, we show that the abundance of endoglin (ENG), a TGF-β superfamily coreceptor expressed on human breast myCAFs, is significantly associated with poorer outcomes of breast cancer patients. Inhibition of ENG expression on myCAFs not only suppressed the TGF-β-Smad2/3 pathway and TGF-β1 expression but also attenuated the ability of myCAF to promote primary tumor growth and metastasis. Mechanistically, ENG facilitates TGF-β-Smad2/3 signaling in myCAFs, presumably through association with a TGF-β ligand-receptor complex, leading to self-stimulating TGF-β1 production. Stromal TGF-β1, in turn, induces partial epithelial-mesenchymal transition in cancer cells in a paracrine manner, resulting in suppression of primary tumor growth and promotion of invasion and metastasis. ENG-primed TGF-β autocrine signaling also produces other factors that could mediate primary tumor growth promotion by myCAFs. Collectively, these findings suggest that ENG-primed TGF-β autocrine and paracrine signaling mediates tumor- and metastasis-promoting abilities of myCAFs.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2557-2573"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells.","authors":"Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan-Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk","doi":"10.1002/1878-0261.70021","DOIUrl":"10.1002/1878-0261.70021","url":null,"abstract":"<p><p>Transforming growth factor-β (TGF-β) signaling and cellular senescence are key hallmarks of hepatocellular carcinoma (HCC) pathogenesis. Despite provoking senescence-associated growth arrest in epithelial HCC cells, elevated TGF-β activity paradoxically correlates with increased aggressiveness and poor prognosis in advanced tumors. Whether the transition between these dichotomous functions involves modulation of the senescence phenotype during disease progression remains elusive. Exploiting the epithelial HCC cell line Huh7 as a robust model, we demonstrate that chronic exposure to TGF-β prompts escape from Smad3-mediated senescence, leading to the development of TGF-β resistance. This altered state is characterized by an optimal proliferation rate and the acquisition of molecular and functional traits of less-differentiated mesenchymal cells, coinciding with differential growth capacity in 2D and 3D culture conditions, epithelial-to-mesenchymal transition (EMT), and increased invasiveness in vitro, and metastasis in vivo. Mechanistically, resistant cells exhibit defective activation and nuclear trafficking of Smad molecules, particularly Smad3, as ectopic activation of the TGF-β/Smad3 axis is able to reinstate TGF-β sensitivity. An integrated transcriptomic landscape reveals both shared and distinct gene signatures associated with senescent and TGF-β resistant states. Importantly, genetic ablation and molecular studies identify microtubule affinity regulating kinase 1 (MARK1) and glutamate metabotropic receptor 8 (GRM8) as critical modulators of the resistance phenomenon, potentially by impairing spatiotemporal signaling dynamics of Smad activity. Our findings unveil a novel phenomenon wherein epithelial HCC cells may exploit senescence plasticity as a mechanism to oppose TGF-β anti-tumor responses and progress towards more aggressive HCC phenotypes.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2594-2618"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pericytes change function depending on glioblastoma vicinity: emphasis on immune regulation.","authors":"Carolina Buizza, Robert Carlsson, Coralie Gamper, Gayatri Chitale, Johan Bengzon, Gesine Paul","doi":"10.1002/1878-0261.70095","DOIUrl":"10.1002/1878-0261.70095","url":null,"abstract":"<p><p>Glioblastoma (GBM), the most aggressive brain tumor in adults, is characterized by its infiltrative growth along the perivascular space. Mural cells (MCs), encompassing pericytes and smooth muscle cells, are multifunctional perivascular cells implicated in GBM progression. MCs not only facilitate vascular co-option but have also been suggested to contribute to the immunosuppressive tumor microenvironment, promoting tumor growth and migration. However, whether MC interactions with immune cells differ based on their proximity to the tumor remains unclear. Using single-cell RNA sequencing, we analyzed MC transcriptome profiles across distinct regions relative to the tumor mass in mouse and human GBM samples. Tumor-residing MCs exhibited profound phenotypic changes, showing upregulated gene expression and enhanced signaling activity toward immune cells, with region-specific ligand-receptor interactions. Conversely, border-residing MCs, despite their abundance, showed reduced activation and lacked distinct transcriptional profiles. These findings reveal spatially defined transcriptional heterogeneity in MCs within the GBM microenvironment, underscoring their dynamic role in the GBM microenvironment. This study provides novel insights into MC responses in GBM, identifying potential avenues for targeting MC-immune-cell interactions in therapeutic interventions.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2491-2514"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitor of DNA binding-1 is a key regulator of cancer cell vasculogenic mimicry.","authors":"Emma J Thompson, Emma L Dorward, Kristyn Jurrius, Nathalie Nataren, Markus Tondl, Kay K Myo Min, Michaelia P Cockshell, Anahita Fouladzadeh, John Toubia, Mark DeNichilo, Delphine Merino, Claudine S Bonder","doi":"10.1002/1878-0261.70027","DOIUrl":"10.1002/1878-0261.70027","url":null,"abstract":"<p><p>Solid tumours routinely access the blood supply by promoting endothelium-dependent angiogenesis; but tumour vasculature can also be formed by cancer cells themselves via vasculogenic mimicry (VM). Investigation of the gene expression profile during the early stages of VM formation by MDA-MB-231-LM2 breast cancer cells identified the transcriptional regulator inhibitor of DNA binding 1 (ID1) to be elevated ~ 10-fold within the first 2 hours. This role for ID1 in promoting VM was supported by ID1 genetic knockdown or chemical inhibition interrupting VM formation by MDA-MB-231-LM2 (breast) and BxPC-3 (pancreatic) cancer cells. More specifically, reducing ID1 lowered cancer cell expression of endothelial cell genes (e.g. CDH5, TIE2) and production of pro-angiogenic proteins (e.g. VEGF, CD31, MMP9 and IL-8). In silico analysis of MDA-MB-231 cells engrafted into mice identified elevated ID1 expression in cancer cells that had metastasised to the lungs or liver, and an enrichment of pro-angiogenic genes. Additionally, Id1 knockdown in 4T1.13 murine breast cancer cells demonstrated reduced tumour growth and metastasis in vivo. Taken together, this study further implicates ID1 in a vascular program within cancer cells that supports disease progression.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"2537-2556"},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing the salivary RNA landscape to identify potential diagnostic, prognostic, and follow-up biomarkers for breast cancer.","authors":"Nicholas Rajan, Irina Primac, Emre Etlioglu, Laurens Debruyne, Ann Janssen, Magy Sallam, Kevin Tabury, Roel Quintens, Wiebren Tjalma, Mohammed Abderrafi Benotmane","doi":"10.1002/1878-0261.70101","DOIUrl":"https://doi.org/10.1002/1878-0261.70101","url":null,"abstract":"<p><p>Breast cancer (BC) diagnostics and prognostics traditionally rely on invasive tissue biopsies, presenting limitations for large-scale screening and continuous patient monitoring. Salivary biomarkers have recently emerged as a compelling noninvasive and accessible alternative, offering significant potential for population-level screening and long-term monitoring of BC. In this study, we conducted a comprehensive salivary transcriptomic profiling of BC patients using high-throughput RNA sequencing. Our analysis captured a wide spectrum of RNA species, including mRNAs, lncRNAs, miRNAs, and snRNAs, highlighting their collective contributions in the molecular landscape of BC patient saliva. We identified robust human gene expression signatures that distinguish BC patients from healthy individuals. Importantly, we discovered RNA profiles that were differentially expressed relative to control samples, enabling the discrimination of noninvasive, invasive, and mixed histological types, as well as hormone receptor-positive molecular subtypes. These salivary markers showed substantial concordance with established tumor gene expression datasets, strengthening their potential relevance in clinical stratification. Furthermore, we identified subsets of salivary genes associated with nodal involvement and others linked to poor survival outcomes, highlighting their potential as prognostic indicators. A prospective follow-up analysis revealed a decline in the expression of several cancer-related salivary transcripts 1-year posttreatment, indicating that salivary RNA might also reflect treatment response over time. This study establishes a proof-of-concept for salivary RNA biomarkers as a versatile, accessible, and robust tool for BC diagnosis, prognosis, and follow-up, paving the way for innovative biomarker-driven strategies in oncology.</p>","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}