Medical Oncology最新文献

{"title":"Young-onset metastatic colorectal cancer: an opportunity and a vision for progress in cancer.","authors":"Prasad D Cooray, Nicole Jane Cooper","doi":"10.1007/s12032-025-02640-5","DOIUrl":"10.1007/s12032-025-02640-5","url":null,"abstract":"<p><p>Metastatic young-onset colorectal cancer (yo-CRC) is a distinct and aggressive disease subtype that is becoming increasingly prevalent worldwide with Australia leading the world in this trend. This article provides an evidence-based perspective, through the prism of authors' personal experience, to craft an effective pathway not only to deliver improved outcomes for the patients but also to reduce disparities and foster collaboration amongst the cancer-treating community and indeed patients. It highlights an opportunity to re-define, re-design, and create a model that is rewarding to patients and cancer-treating community. Although our focus is on the high unmet needs group of yo-CRC, this model has the potential to expand to other cancer types and care models. We analyse the unique epidemiological trends, challenges, and burdens, emphasising the need for tailored treatment approaches for younger patients with colorectal cancer especially in the metastatic setting. We identify current gaps in clinical practice and research. To improve real-world outcomes, we propose a conceptual framework to enhance clinician-patient communication and treatment planning. Central to our approach is the integration of a Registry of Incidence, Intervention, and Outcomes (RIIO), which enables real-time data collection and analysis, improving treatment personalisation and efficacy. This registry could revolutionise patient care and drive research innovation through enhanced data sharing and collaboration. We advocate for a patient-centric integrated care model that utilises all available therapies to maximise survival and quality of life. Our perspective underscores the urgent need for a paradigm shift in how yo-CRC is viewed, researched and managed, proposing a pathway to significantly enhanced outcomes. Whilst it is feasible to expand the concepts discussed here for all colorectal cancer and indeed all cancer types, we believe this approach is most relevant and acutely needed in yo-CRC setting for reasons detailed in the manuscript.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"95"},"PeriodicalIF":2.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selinexor in the treatment of liposarcoma: from preclinical evidence to clinical practice.","authors":"Piotr Remiszewski, Wiktor Gaik, Aleksandra Skora, Julia Wąż, Kinga Filipek, Agata Pisklak, Monika Dudzisz-Śledź, Piotr Rutkowski, Anna Czarnecka","doi":"10.1007/s12032-025-02651-2","DOIUrl":"10.1007/s12032-025-02651-2","url":null,"abstract":"<p><p>Selinexor is a new compound studied for the treatment of liposarcoma, particularly dedifferentiated liposarcoma (DDLPS), where treatment options remain limited. As a first-in-class oral exportin-1 (XPO1) inhibitor, selinexor has shown anti-tumour activity in preclinical models, particularly in MDM2- and CDK4-amplified DDLPS, where it induces apoptosis, inhibits tumour growth and promotes nuclear retention of p53. Preclinical studies have also suggested potential synergy with doxorubicin and eribulin, although these findings have yet to be validated in randomised clinical trials. The phase II/III SEAL trial (NCT02606461) evaluated selinexor versus placebo in patients with advanced, previously treated DDLPS. While the study demonstrated a statistically significant, albeit modest, improvement in median progression-free survival (PFS) from 2.1 to 2.8 months, no overall survival benefit was observed. In addition, selinexor was associated with significant toxicity, including fatigue, nausea and weight loss. Similarly, a phase Ib/II study (NCT03042819) evaluating selinexor in combination with doxorubicin reported a 21% response rate and a median PFS of 5.5 months, although this regimen was also associated with high rates of neutropenia and fatigue. Despite these results, selinexor is not currently approved for the treatment of liposarcoma and its clinical utility remains under investigation. Ongoing studies, such as the SeliSarc trial (NCT04595994) evaluating selinexor in combination with gemcitabine and the NRSTS2021 trial (NCT06239272) evaluating selinexor in paediatric soft tissue sarcoma, aim to further define its role. The results of these studies will be critical in determining whether selinexor can be incorporated into standard sarcoma treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"94"},"PeriodicalIF":2.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582322","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":"Prodelphinidin from purple sweet potato induces apoptosis in human triple-negative breast cancer cells via ROS-mediated ER stress activation.","authors":"Jiluan Zhang, Zihan Chen, Shibo Wang, Lingxue Kong, Jinjuan Liu","doi":"10.1007/s12032-025-02642-3","DOIUrl":"10.1007/s12032-025-02642-3","url":null,"abstract":"<p><p>Triple negative breast cancer (TNBC), a highly aggressive and heterogeneous subtype of breast cancer, lacks an effective targeted therapy. Conventional medication has limited efficacy in treating TNBC, which highlights the potential of developing therapeutic agents from natural bioactive compounds. This study aimed to investigate the cytotoxicity of prodelphinidin (PD), an anthocyanin found in purple sweet potato, in human MDA-MB-231 and MDA-MB-436 cells. The results showed that PD selectively inhibited human breast cancer, particularly TNBC. Furthermore, PD demonstrated significant dose- and time-dependent inhibition of MDA-MB-231 and MDA-MB-436 cell activity. Flow cytometry and western blot analysis revealed that PD induced cell apoptosis by down-regulating Bcl-2, activating caspase-3/9, and cleaving PARP. Additionally, PD treatment upregulated the expression of p-elF2α, GRP78, and CHOP, indicating the involvement of endoplasmic reticulum stress (ERS). PD treatment also increased the production of reactive oxygen species (ROS) and decreased superoxide dismutase (SOD) activity in TNBC cells. The cytotoxicity of PD reduced significantly by pre-treatment with caspase inhibitors (Ac-DEVD-CHO and Z-LEHD-FMK). In conclusion, PD effectively inhibited the proliferation and induced apoptosis in TNBC cells through the activation of ROS and endoplasmic reticulum stress.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"92"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567517","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":"Macrophage-derived lncRNAs in cancer: regulators of tumor progression and therapeutic targets.","authors":"Muath Suliman, Raed Obaid Saleh, Muktesh Chandra, Khetam Habeeb Rasool, Majid Jabir, Sabrean F Jawad, Thikra F Hasan, Mithilesh Singh, Manmeet Singh, Abhayveer Singh","doi":"10.1007/s12032-025-02643-2","DOIUrl":"10.1007/s12032-025-02643-2","url":null,"abstract":"<p><p>Macrophages are key tumor microenvironment (TME) regulators, exhibiting remarkable plasticity that enables them to either suppress or promote cancer progression. Emerging evidence highlights the critical role of macrophage-derived long non-coding RNAs (lncRNAs) in shaping tumor immunity, influencing macrophage polarization, immune evasion, angiogenesis, metastasis, and therapy resistance. This review comprehensively elucidates the functional roles of M1- and M2-associated lncRNAs, detailing their molecular mechanisms and impact on cancer pathogenesis. In summary, elucidating the roles of lncRNAs derived from macrophages in cancer progression offers new avenues for therapeutic strategies, significantly improving patient outcomes in the fight against the disease. Further research into the functional significance of these lncRNAs and the development of targeted therapies is essential to harness their potential fully in clinical applications. We further explore their potential as biomarkers for cancer prognosis and therapeutic targets for modulating macrophage activity to enhance anti-cancer immunity. Targeting macrophage-derived lncRNAs represents a promising avenue for precision oncology, offering novel strategies to reshape the TME and improve cancer treatment outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"91"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567516","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":"Nanomaterials in gastric cancer: pioneering precision medicine for diagnosis, therapy, and prevention.","authors":"Tiantian Liu, Yanmei Gu, Yang Zhao, Yumin Li","doi":"10.1007/s12032-025-02650-3","DOIUrl":"10.1007/s12032-025-02650-3","url":null,"abstract":"<p><p>Gastric cancer (GC) continues to be a major health issue globally due to its high rates of both occurrence and mortality. Despite advancements in treatment, the outlook for those affected remains poor, highlighting the critical need for new diagnostic and treatment methods. Nanotechnology, especially nanoparticles, is emerging as a crucial innovation in cancer care by improving imaging, targeting drug delivery, and enhancing early detection. These nanoparticles are also enhancing the effectiveness of treatments like phototherapy, chemotherapy, and immunotherapy. Notably, they show potential in addressing infections like Helicobacter pylori (H. pylori), which is known to increase the risk of developing GC. This review underscores the pivotal role of nanotechnology in enhancing the integrated management of GC, offering a basis for future advancements in the field.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"93"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573439","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":"Bone marrow mesenchymal stem cells enrich breast cancer stem cell population via targeting metabolic pathways.","authors":"Zahra Ghanbari Movahed, Kamran Mansouri, Ali Hamrahi Mohsen, Maryam M Matin","doi":"10.1007/s12032-025-02632-5","DOIUrl":"10.1007/s12032-025-02632-5","url":null,"abstract":"<p><p>The role of cancer cell metabolic reprogramming in the formation and maintenance of cancer stem cells (CSCs) has been well established. This reprogramming involves alterations in the metabolic pathways of cancer cells, leading to the acquisition of stem cell-like properties such as self-renewal and differentiation. This study aimed to investigate the potential effects of bone marrow mesenchymal stem cells (BM-MSCs) on the enrichment of breast CSCs. Exosomes (Exo) and conditioned media (CM) were isolated from BM-MSCs for use in this experimental study. The impact of BM-MSCs-Exo and BM-MSCs-CM on the expression of stemness genes NANOG and OCT-4, as well as CD24 and CD44 markers, was assessed in MCF-7 and MDA-MB-231 cell cultures to identify CSCs. Furthermore, the effects of BM-MSCs-Exo and BM-MSCs-CM on cancer cell metabolism were evaluated by examining changes in glycolysis, the pentose phosphate pathway (PPP), and amino acid profiles. Additionally, the influence of BM-MSCs-Exo and BM-MSCs-CM on tumor growth in vivo was also investigated. The analysis of stemness marker expression in cells treated with BM-MSCs-Exo and BM-MSCs-CM revealed an increase in stemness characteristics compared to the control group. Furthermore, the examination of changes in cell metabolism following these treatments showed alterations in glycolysis, PPP, and amino acid metabolism pathways. Additionally, it was demonstrated that BM-MSCs-Exo and BM-MSCs-CM can promote tumor growth in mice following transplantation of 4T1 cells. These findings suggest that BM-MSCs-Exo and BM-MSCs-CM can enrich the population of CSCs in MCF-7 and MDA-MB-231 cells by targeting metabolic pathways, however, further studies are required to elicit the exact mechanisms of these phenomena.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"90"},"PeriodicalIF":2.8,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567515","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":"Effects of royal jelly on ovary cancer cells proliferation and apoptosis.","authors":"Ender Deniz Asmaz, Sabire Güler, Berrin Zık","doi":"10.1007/s12032-025-02638-z","DOIUrl":"10.1007/s12032-025-02638-z","url":null,"abstract":"<p><p>The aim of the present study is to investigate the proliferative or apoptotic effects of different doses and durations of Royal jelly (RJ) on serous type epithelial ovarian cancer, which is the most common epithelial ovarian cancer. For this purpose, cells of the Skov-3 human ovarian adenocarcinoma cell line were grown in McCoy medium and seeded in 6-well plates. RJ was prepared as a stock solution (1000 mg RJ/10 ml dH₂O) and 1, 5, 10, 20, and 50 mg/ml RJ doses from the prepared stock solution were added to the medium for 24, 48, and 72 h incubated. After the treatment of RJ, the cell viability test (Tripan Blue), Ki-67 to determine the proliferative effect, cleaved-Caspase-3 and cleaved PARP expressions to determine its apoptotic effect were examined by immunocytochemical and immunofluorescence methods. In addition, findings were supported by the TUNEL method. As a result of the experiments, it was determined that 1 mg/ml and 24 h treatment of RJ did not affect cell proliferation and apoptosis, but generally, 50 mg/ml of RJ for 72 h inhibited proliferation in cancer cells and induced apoptosis. The use of royal jelly both monotherapeutically and in combination as an alternative treatment for ovarian cancer may provide the basis for new experimental protocols.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"89"},"PeriodicalIF":2.8,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Botanical sources, biopharmaceutical profile, anticancer effects with mechanistic insight, toxicological and clinical evidence of prunetin: a literature review.","authors":"Sumaya Akter Bithi, Md Sakib Al Hasan, Md Shimul Bhuia, Emon Mia, Noshin Tasnim Yana, Ali Mohamod Wasaf Hasan, Mohammed Burhan Uddin, Md Abu Sayeed, Yasin Emon, Rubel Hasan, Raihan Chowdhury, Muhammad Torequl Islam","doi":"10.1007/s12032-025-02646-z","DOIUrl":"10.1007/s12032-025-02646-z","url":null,"abstract":"<p><p>Prunetin (PRU), a naturally occurring flavonoid, has gained recognition for its wide-ranging therapeutic benefits, though its anticancer properties have yet to be extensively reviewed. This study explores the potential of PRU in targeting critical molecular pathways involved in tumor progression, including oxidative stress, apoptosis, cell cycle regulation, and metastasis. Data were compiled from reputable sources, including PubMed, Springer Link, Scopus, Wiley Online, Web of Science, ScienceDirect, and Google Scholar. The findings emphasize PRU's ability to mitigate oxidative stress, promote apoptosis, and regulate the cell cycle in cancer cells. Its anti-inflammatory and anti-angiogenic properties further enhance its effectiveness against cancer. Mechanistic studies reveal that PRU suppresses oncogenic pathways such as PI3K/Akt/mTOR (Phosphoinositide 3-kinase/Protein kinase B/Mammalian target of rapamycin) while activating tumor-suppressor mechanisms. Experimental models show that PRU effectively inhibits cancer cell proliferation and metastasis. Additionally, PRU exhibits favorable pharmacokinetics, demonstrating high intestinal absorption (95.5%), good Caco-2 permeability, and metabolism via CYP1A2, CYP2C19, CYP2C9, and CYP3A4, though it has poor blood-brain barrier (BBB) permeability and limited aqueous solubility, posing challenges for systemic bioavailability. Beyond its anticancer properties, PRU displays broad pharmacological relevance, including anti-inflammatory, cardioprotective, neuroprotective, anti-obesity, and osteoprotective effects, mediated through pathways, such as NF-κB, MAPK, and AMPK. Toxicological studies indicate a favorable safety profile, with low cytotoxicity in normal cells and no significant toxicity at high doses in preclinical models. While clinical evidence on PRU remains limited, studies on structurally related isoflavones suggest promising therapeutic potential, necessitating further clinical trials to establish its efficacy and safety in humans.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"87"},"PeriodicalIF":2.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542589","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":"Deciphering FOXM1 regulation: implications for stemness and metabolic adaptations in glioblastoma.","authors":"Kumari Swati, Saniya Arfin, Kirti Agrawal, Saurabh Kumar Jha, Ramya Lakshmi Rajendran, Anand Prakash, Dhruv Kumar, Prakash Gangadaran, Byeong-Cheol Ahn","doi":"10.1007/s12032-025-02639-y","DOIUrl":"10.1007/s12032-025-02639-y","url":null,"abstract":"<p><p>The Forkhead box M1 (FOXM1) gene-mediated Wnt signaling pathway plays a significant role in the development and growth of glioblastoma multiforme (GBM), an exceptionally aggressive form of brain cancer. Our research explores the crucial involvement of the FOXM1 gene, a key transcription factor within the Wnt signaling pathway using bioinformatics techniques in both GBM and glioma stem cells (GSCs). Elevated FOXM1 gene expression is strongly associated with poor patient survival in GBM. Furthermore, FOXM1 gene expression is correlated with stemness-related factors, such as SOX2 and SOX9, which act as key drivers in the progression of cancer stem cells. Moreover, we specifically look into the direct associations of the FOXM1 gene with angiogenetic-related factors, metabolic genes, metastatic genes, pluripotency-related factors, immune cell infiltration, transcriptional networks, and functional category enrichment analysis, shedding light on the intricate molecular mechanisms involved in GBM initiation and progression. Additionally, our research identifies FOXM1-targeting miRNAs, revealing their potential as therapeutic candidates with implications for patient survival rates and DNA methylation patterns of the FOXM1 gene, uncovering insights into its epigenetic regulation. This knowledge contributes to a comprehensive understanding of the molecular landscape and potential avenues for developing more effective therapeutic approaches against GBM and GSCs.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"88"},"PeriodicalIF":2.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542593","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":"The reciprocal effects of autophagy and the Warburg effect in pancreatic ductal adenocarcinoma: an in vitro study.","authors":"Bita Azizzadeh, Maryam Majidinia, Ali Gheysarzadeh","doi":"10.1007/s12032-025-02631-6","DOIUrl":"10.1007/s12032-025-02631-6","url":null,"abstract":"<p><p>Autophagy and the Warburg effect are two common pathways in pancreatic ductal adenocarcinoma (PDAC). To date, the reciprocal effects of these pathways have not yet been elucidated. Therefore, this study was designed to investigate the relationship between these factors in vitro and may provide therapeutic targets in the future. The Mia-Paca-2 and AsPc-1 cell lines were cultured under normal conditions. To achieve autophagy, starvation was induced by Hank's balanced salt solution (HBSS), whereas autophagy was inhibited by 3-methyladenine (3-MA). The Warburg effect is mimicked by lactic acid, and the Warburg effect is inhibited by oxamate, the main inhibitor of lactate dehydrogenase. Cell viability was checked through the MTT assay method. Autophagy was checked via evaluation of Beclin-1 via western blotting. The amount of lactic acid was also measured with a lactate dehydrogenase (LDH) assay kit. The cells were incubated with different concentrations of 3-MA, lactic acid and oxamate. The viability of AsPc-1 cells decreased, and the IC₅₀ values were 1195 µM, 23.06 mM and 8.617 mM for 3-MA, lactic acid and oxamate, respectively. Similarly, the IC₅₀ values of Mia-Paca-2 were 873.9 µM, 35.9 mM and 26.74 mM for 3-MA, lactic acid and oxamate, respectively. Our data revealed that starvation increased the expression of the autophagy-related protein Beclin-1 (P value < 0.05); however, 3-MA significantly reduced its expression (P value < 0.05). In addition, lactic acid alone did not affect the expression level of Beclin-1 (P value > 0.05), but oxamate treatment increased its expression (P value < 0.05). We also showed that starvation reduced lactic acid levels, but an autophagy inhibitor, 3MA, significantly increased lactic acid production (P value < 0.05). Our findings showed that lactic acid alone has no significant effect on autophagy and that oxamate induces autophagy, possibly because of caloric restriction. On the other hand, autophagy inhibits lactic acid production, whereas the inhibition of autophagy leads to increased lactic acid production.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"86"},"PeriodicalIF":2.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531242","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}