Medical Oncology最新文献

{"title":"The role of the tumour microenvironment in lung cancer and its therapeutic implications.","authors":"Devindi Thathsara Edirisinghe, Jasleen Kaur, Yue Qi Lee, Huey Xin Lim, Sharis Wan Ting Lo, Sri Vishupriyaa, Ee Wern Tan, Rebecca Shin Yee Wong, Bey Hing Goh","doi":"10.1007/s12032-025-02765-7","DOIUrl":"10.1007/s12032-025-02765-7","url":null,"abstract":"<p><p>Lung cancer is the leading cause of cancer-related deaths globally, with tumour growth, invasion, and treatment response heavily influenced by the tumour microenvironment (TME). The TME promotes tumour progression by creating an immunosuppressive environment that hampers the body's antitumour immune response, primarily through the Nuclear Factor Kappa B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) pathways. These pathways contribute to chronic inflammation, immune evasion, and angiogenesis. Targeting the TME and its signalling pathways has shown potential to enhance treatment efficacy. STAT3, a key transcription factor in lung cancer, drives tumour growth and immune suppression via the mTOR and JAK pathways. Inhibiting these pathways can block STAT3 and slow cancer progression. Promising results have been observed with mTOR inhibitors like CC-115 and Vistusertib, especially when combined with immune checkpoint inhibitors, and with JAK inhibitors such as Ruxolitinib, AZD4205, and Filgotinib. These strategies represent a promising direction for lung cancer therapy. This review explores the intricate relationship between the TME and lung cancer, focussing on novel therapeutic approaches that target immune cells, signalling molecules, and fibroblasts within the TME to improve patient outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"219"},"PeriodicalIF":2.8,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128136","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":"In vitro and in vivo anticancer activity of nickel (II) tetraazamacrocyclic diperchlorate complex, [(Ni-Me₈[14]diene)(ClO₄)₂] against ehrlich ascites carcinoma (EAC) and MCF7 cells.","authors":"Arifur Rahman, Tasfik Ul Haque Pronoy, Kazi Soha, Abdul Auwal, M Matakabbir Hossain, K M Rashel, Md Royhan Gofur, M Habibur Rahman, Saswata Rabi, Tapashi Ghosh Roy, Nitai Roy, Jahan Ara Khanam, Md Abdur Rakib, Farhadul Islam","doi":"10.1007/s12032-025-02762-w","DOIUrl":"10.1007/s12032-025-02762-w","url":null,"abstract":"<p><p>Cancer remains a global health burden, with a pressing need for more effective treatments. This study uses a novel compound, Nickel (II) diperchlorate complex of the ligand (L): 3,10-C-meso-3,5,7,7,10,12,14,14-octamethyl-1,4,8,11-tetraazacyclotetradeca-4,11-diene, Me₈[14]diene, designated as [Ni(II)L](ClO₄)₂, to explore its potential as an anticancer agent. Its efficacy was evaluated against Ehrlich Ascites Carcinoma (EAC)-bearing Swiss albino mice by monitoring tumor cell growth inhibition, survival time, tumor mass reduction, and hematological profiles. Additionally, cytotoxicity was investigated in vitro using MCF7 breast cancer cells. The apoptotic potential was evaluated through Hoechst staining, with changes in apoptosis-related gene expression (p53, BCL2, BAX, PARP1, CASP3, CASP8, and CASP9) using RT-qPCR. The test compound's toxicity was evaluated by monitoring hematological, biochemical, and histological changes. The compound exhibited dose-dependent growth inhibition of EAC cells with 88.45% inhibition at a dose of 200 µg/kg (p < 0.01), extended lifespan by 52.63%, reduced tumor weight by 47.83%, and restored hematological parameters in EAC-bearing mice. Cytotoxicity assays yielded LC₅₀ and IC₅₀ values of 23.73 µg/mL and 71.52 µg/mL, respectively. Apoptosis induction was evidenced by cell membrane blebbing, apoptotic body formation, chromosomal condensation, and nuclear fragmentation in MCF7 cells. Significant upregulation of pro-apoptotic genes such as p53, BAX, PARP1, CASP3, CASP8, and CASP9, alongside downregulation of anti-apoptotic gene BCL2, implied activation of the apoptotic pathway in cancer cells, followed by compound treatment. Moreover, no long-term negative impacts on tissue levels or hematological or biochemical markers were noted in the mice. Altogether, [Ni(II)L](ClO₄)₂ demonstrates promising anticancer activity and could serve as a potential chemotherapeutic agent, pending further studies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"218"},"PeriodicalIF":2.8,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128087","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":"Dual roles of long non-coding RNAs in thyroid cancer: regulation of programmed cell death pathways.","authors":"Mohamed J Saadh, Ashok Kumar Bishoyi, M M Rekha, Ashish Verma, Anima Nanda, Rajashree Panigrahi, Rajni Verma, Baneen C Gabble","doi":"10.1007/s12032-025-02750-0","DOIUrl":"10.1007/s12032-025-02750-0","url":null,"abstract":"<p><p>Thyroid cancer (TC) represents the most common endocrine malignancy; however, the intricacies of its carcinogenesis pose significant challenges to therapeutic interventions. A comprehensive understanding of the molecular mechanisms that drive TC progression is crucial for the development of effective treatment strategies, especially considering the increasingly recognized role of non-coding RNAs (ncRNAs) in oncogenesis. Notwithstanding recent advancements, the regulatory functions of long non-coding RNAs (lncRNAs) and their interactions with microRNAs (miRNAs) in the context of TC are not yet fully elucidated. This review aims to address this knowledge deficiency by investigating the dual roles of lncRNAs in the pathogenesis of TC, specifically their regulation of programmed cell death (PCD) pathways. Current literature indicates that disrupted competitive endogenous RNA (ceRNA) networks are involved in drug resistance, epithelial-mesenchymal transition (EMT), as well as tumor proliferation, angiogenesis, invasion, and metastasis in TC. The basis of cancer therapy-induced tumor cell elimination is programmed cell death (PCD), which includes well-studied processes such as apoptosis, autophagy, and ferroptosis as well as novel pathways, such as cuproptosis, immunogenic cell death (ICD), and PANoptosis. Recent research has shown the critical function of long non-coding RNAs (lncRNAs) in modifying these several PCD pathways, impacting TC growth and therapy response. This review synthesizes evidence on how lncRNAs regulate PCD to influence TC progression and therapeutic outcomes. Additionally, we examine the clinical relevance of lncRNAs in TC, highlighting their potential as biomarkers for diagnosis and prognosis, therapeutic targets, and contributors to drug resistance, while emphasizing recent advancements in this field.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"217"},"PeriodicalIF":2.8,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128057","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":"Exosomes in bridging macrophage-fibroblast polarity and cancer stemness.","authors":"Keywan Mortezaee","doi":"10.1007/s12032-025-02774-6","DOIUrl":"10.1007/s12032-025-02774-6","url":null,"abstract":"<p><p>Exosome roles in cellular cross-talking within tumor microenvironment (TME) is a critical event in tumorigenesis. Type 2 macrophages (M2), cancer-associated fibroblasts (CAFs) and cancer stem cells (CSCs) are the three most important cells in cancer progression and metastasis, and targeting their connectome route can be an effective anti-cancer strategy. Exosomes mediate bidirectional cross-talking between the three cell types in which exosomes secreted from CSCs promote polarization of M2 macrophages and CAFs, and that M2- and CAF-derived exosomes promote cancer stemness through activation of epithelial-mesenchymal transition (EMT)-related signaling including transforming growth factor (TGF)-β, WNT/β-catenin and epidermal growth factor (EGF). CSC-derived exosomal TGF-β is a key driver of CAF and M2 macrophage polarization, with the latter mediated through activation of signal transducer and activator of transcription 3 (STAT3). β-catenin activity also seems to take important role in exosomal cross-talk between CAFs and stemness state of cancer. Incubation of exosomes with inhibitors of signaling inter-connecting CSCs, M2 and CAFs is a key anti-cancer strategy and a promising supplementary to the routine immunotherapeutic approaches in cancer therapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"216"},"PeriodicalIF":2.8,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110949","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":"Application of mass cytometry in the immune microenvironment of breast cancer.","authors":"Yuefeng Shang, Yuheng Pang, Tong Liu, Wenjing Wang","doi":"10.1007/s12032-025-02770-w","DOIUrl":"10.1007/s12032-025-02770-w","url":null,"abstract":"<p><p>The rapid development of immunotherapy has shown preliminary clinical efficacy and significant anti-tumor effects in some cancer patients. Although immunotherapy has been approved for breast cancer, some breast cancer patients still do not benefit from it due to issues such as immunotherapy insensitivity and resistance. Mass cytometry, as a mature single-cell proteomic analysis method, with its high-throughput capabilities, has been widely used in the analysis of tumor immune microenvironments and immune cell subpopulations. Using mass cytometry to analyze the immune microenvironment of breast cancer and explore new immunotherapy targets can help improve the current status of breast cancer immunotherapy and develop personalized treatment plans for more patients. This review surveys the recent advancements in analyzing the single-cell components of breast cancer using mass cytometry technology and reviews the immune microenvironment of breast cancer as well as potential targets for immunotherapy. These results provide new insights for the subsequent research of the immune microenvironment of breast cancer and targeted immunotherapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"215"},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094176","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":"Molecular mechanisms and clinical value of the correlation between depression and cancer.","authors":"Yuxiao Chen, Yafei Lu, Siyi Chen, Pengyi Liu, Junzhe He, Lingxi Jiang, Jun Zhang","doi":"10.1007/s12032-025-02763-9","DOIUrl":"10.1007/s12032-025-02763-9","url":null,"abstract":"<p><p>According to the World Health Organization, cancer remains the primary cause of death of millions of individuals annually and the foremost cause of mortality worldwide. Cancer imposes substantial economic and mental challenges on patients and their families and strains healthcare systems. Depression, one of the most prevalent mental health conditions, affects approximately 3.8% of the global population and is a significant global health challenge. Research indicates increasing incidence rates of depression among patients with cancer. Depression also appears to influence cancer development and progression, worsening patient prognosis and quality of life, thereby creating additional challenges for clinical treatment. Correlation of depression and cancer is a complicated yet promising field with fast-paced progression and vital clinical values. Therefore, we discussed in this review the associations between depression and cancer and their potential mechanisms by analyzing the specific role of depression in the development and progression of tumors from the perspective of suppressing tumor immunity, inhibiting tumor cell apoptosis, inducing DNA damage, promoting tumor cell mesenchymal transition, enhancing tumor cell stemness, and promoting tumor angiogenesis. This review also discusses how tumors influence the development of depression via inflammatory factors and the significance of identifying and treating depression to enhance the quality of life and prognosis of patients with cancer. Promising biomarkers and effective treatments are also highlighted. Despite available data, limited research exists on how treating depression affects cancer prognosis, and whether timely treatment can reduce cancer risk remains unclear, which necessitates further investigation. This review summarizes the molecular mechanisms involved in the relationship between cancer and depression to help identify new biomarkers and provide precise medical care for patients with depression. We hope this review will lay the foundation for future research, advancing new biomarkers and therapies for early diagnosis of cancer and depression comorbidity.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"214"},"PeriodicalIF":2.8,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086490","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":"Epigenetic reprogramming and antitumor immune responses in gliomas: a systematic review.","authors":"Fathima Raahima Riyas Mohamed, Ahmed Yaqinuddin","doi":"10.1007/s12032-025-02760-y","DOIUrl":"10.1007/s12032-025-02760-y","url":null,"abstract":"<p><p>Gliomas, particularly glioblastoma, are among the most aggressive and treatment-resistant brain tumors. Their immunosuppressive tumor microenvironment (TME) and intrinsic molecular heterogeneity hinder effective therapeutic responses. Epigenetic dysregulation in gliomas significantly impacts tumor progression and immune evasion, presenting an opportunity for therapeutic intervention. This systematic review evaluates the role of epigenetic reprogramming in modulating antitumor immune responses in gliomas and explores its potential to enhance treatment outcomes. A comprehensive literature search across major databases, adhering to PRISMA guidelines, identified preclinical and clinical studies examining the effects of epigenetic therapies on glioma-associated immune modulation. Inclusion criteria focused on studies involving DNA methylation inhibitors, histone deacetylase inhibitors, chromatin remodelers, and non-coding RNA-based therapies. Key outcomes included immune activation, tumor progression, survival, and TME modulation. Among 22 included studies, epigenetic therapies demonstrated substantial efficacy in reprogramming the glioma immune landscape. DNA methylation inhibitors such as decitabine enhanced antigen presentation and immune recognition, while histone deacetylase inhibitors improved T-cell-mediated cytotoxicity. Non-coding RNA-targeted interventions disrupted immune suppression and facilitated immune cell infiltration. These strategies showed synergistic potential with immune checkpoint inhibitors, leading to tumor growth inhibition and improved survival in preclinical models. Epigenetic therapies hold promise in overcoming glioma-induced immune resistance by modulating immune escape mechanisms and reprogramming the TME. Their integration with existing treatment modalities, including immunotherapy, represents a transformative avenue for glioma management. Further clinical validation is warranted to optimize their therapeutic potential and safety.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"213"},"PeriodicalIF":2.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086479","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":"Genetically engineered K562 cells augment NK cell cytotoxicity against acute myeloid leukemia and reduce dependency on IL-15.","authors":"Saman Sohrabi Akhkand, Masoud Soleimani, Mina Soufi Zomorrod, Jafar Kiani","doi":"10.1007/s12032-025-02769-3","DOIUrl":"10.1007/s12032-025-02769-3","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is an aggressive malignancy with limited treatment options. Enhancing natural killer (NK) cell functionality through artificial antigen-presenting cells (aAPCs) represents a promising immunotherapeutic strategy. This study evaluates the potential of genetically modified K562 cells, expressing CD137L and CD86, to enhance NK cell-mediated cytotoxicity against AML cell lines (HL-60, KG-1, and THP-1). Lentiviral transduction was used to generate aAPCs, confirmed by PCR, RT-PCR, and flow cytometry. Cord NK cells and the NK-92 cell line were co-cultured with aAPCs, and their cytotoxicity against cell lines was assessed using 7-AAD staining. The ability of transduced K562 cells to substitute for interleukin-15 (IL-15) was also evaluated. These cells significantly enhanced NK cell-mediated cytotoxicity, with greater effects observed at higher effector-to-target (E:T) ratios. The aAPCs partially replaced IL-15 in activating cord blood NK cells but were ineffective for NK-92 cells. The aAPCs effectively enhance NK cell cytotoxicity and may reduce cytokine dependence in therapeutic applications. These findings highlight the potential of aAPCs to improve NK cell-based immunotherapies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"211"},"PeriodicalIF":2.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079004","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":"Natural sesquiterpene lactones in prostate cancer therapy: mechanisms and sources.","authors":"Keshav Kaushal, Devesh U Kapoor, Sanjesh Kumar, Anakha Sony, Aswin Viswanath, M V N L Chaitanya, Mansi Singh, Sachin Kumar Singh, Avijit Mazumder","doi":"10.1007/s12032-025-02740-2","DOIUrl":"10.1007/s12032-025-02740-2","url":null,"abstract":"<p><p>Prostate cancer is a condition characterized by the uncontrolled proliferation of abnormal cells inside the prostate gland, part of the male reproductive system. Prostate cancer is the most common cancer among men and the second largest cause of cancer-related mortality in the United States. A novel approach to treating advanced Prostate cancer has emerged, attributable to the enhanced effectiveness of new pharmacological agents sourced from natural origins and this has led to increased rates of global existence and progression-free survival. Sesquiterpene lactones and their derivatives are now used worldwide to create and manufacture innovative cancer therapeutics. A thorough search was performed according to PRISMA guidelines in SciMed, PubMed, and Google Scholar, focusing on publications published from 1999 to 2024. The safety, efficacy, and bioactivity of sesquiterpene lactones must be evaluated via clinical trials, in vitro studies, and in vivo research and data was rigorously gathered and validated to verify its accuracy and usefulness. Prostate cancer may be treated far more effectively using naturally occurring sesquiterpene lactone molecules. The most prominent sesquiterpene lactones identified were artemisinin, alantolactone, costunolide, helenalin, cynaropicrin, parthenolide, and inuviscolide, which are originated from botanical sources like Ferula penninervis, Tanacetum argenteum, Artemisia kopetdaghensis, Cichorium intybus, Carpesium divaricatum, and Leptocarpha rivularis. Numerous studies indicated that sesquiterpene lactones may treat cancer by modifying many cellular signaling pathways, including PI3K/AKT, MAPK, JNK, NF-κB, TNF-α, and STAT3. Sesquiterpene lactones were shown to be significant in suppressing the proliferation of prostate cancer cell lines (DU-145, PC-3, LNCaP, MR49F, and BPH-1) in both laboratory and clinical settings.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"212"},"PeriodicalIF":2.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079009","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":"Integrated management of metastatic spinal tumors: current status and future directions.","authors":"Min J Kim, Neelan J Marianayagam, Ankush Chandra, Carlotta Ranalli, Ethan Schonfeld, Juan P Avila-Madrigal, Ann Marie E Flusche, Katherine Schoeffler, Safwan Alomari, Namratha B Rao, Kelly Yoo, Fred C Lam, David J Park, Andrew A Fanous, Steven D Chang, Michael Lim, Anand Veeravagu","doi":"10.1007/s12032-025-02764-8","DOIUrl":"10.1007/s12032-025-02764-8","url":null,"abstract":"<p><p>With improved cancer survivorship, the incidence of metastatic bone disease has risen, and metastatic spinal tumors (MSTs) have emerged as a common yet significant clinical challenge. These tumors may compromise the integrity of vertebral bodies leading to pathological fractures and neurological compromise from nerve root or spinal cord compression dramatically affecting the patient's quality of life. Despite the associated morbidity and mortality, optimal treatment strategies remain elusive. Here, in our review, we provide a comprehensive analysis of the contemporary MST treatment strategies, encompassing surgical interventions, advanced radiotherapy modalities, and evolving systemic therapies including chemotherapeutic and immunotherapeutic approaches. We critically evaluate each modality's development trajectory, clinical efficacy, therapeutic advantages, and inherent limitations. Our analysis reveals a definitive shift toward precision-guided radiotherapy and minimally invasive surgical techniques that balance therapeutic efficacy with reduced morbidity. These findings underscore the necessity for multidisciplinary management and highlight promising avenues for therapeutic innovation. As treatment paradigms evolve, integration of these advanced modalities offers new hope for this vulnerable patient population facing a challenging oncological complication.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"210"},"PeriodicalIF":2.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004360","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}