Medical Oncology最新文献

{"title":"Integrative analysis of ubiquitination-related genes identifies HSPA1A as a critical regulator in colorectal cancer progression.","authors":"Xinji Gao, Ting Yan, Xiang Yu, Qiang Li, Lan Zhao, QingShui Wang, Jun Wang","doi":"10.1007/s12032-025-02662-z","DOIUrl":"10.1007/s12032-025-02662-z","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a prevalent and lethal malignancy, with ubiquitination significantly influencing cellular processes involved in cancer progression. However, the contributions of ubiquitination-related genes in CRC remain unclear. This study conducted a detailed analysis of gene expression profiles associated with ubiquitination in CRC, evaluating 1006 genes across 46 pathways. By comparing CRC tissues to adjacent normal tissues, we identified differentially expressed genes and developed a ubiquitination-related pathway gene signature (URPGS) using LASSO regression analysis on genes with prognostic significance. The prognostic capability of the URPGS was validated in independent cohorts, and its associations with clinical characteristics, including post-chemotherapy survival outcomes, were examined. Machine learning techniques identified HSPA1A as a key gene relevant to CRC both in vitro and in vivo. Our analysis revealed 307 differentially expressed ubiquitination-related genes, with 24 significantly associated with patient prognosis. The developed 14-gene URPGS exhibited strong prognostic value, effectively stratifying patients into high-risk and low-risk groups for overall survival. The URPGS correlated with advanced clinical stages, lymph node metastasis, and recurrence, with higher scores linked to poorer post-chemotherapy survival outcomes. Knockdown of HSPA1A significantly inhibited CRC cell proliferation, migration, and invasion in vitro, as well as tumor growth and metastasis in vivo. This research establishes a novel URPGS that effectively predicts prognosis and chemotherapy outcomes in CRC, enhancing our understanding of ubiquitination's role and suggesting personalized treatment strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"123"},"PeriodicalIF":2.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11922989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663966","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":"An investigative study on the impact of DLK1 and NCoR1 knockdown by siRNA transfection on endometrial cancer proliferation: unveiling notch interactions.","authors":"Swathi Chandran Manimegalai, Sathiya Priya Krishnamoorthy, Vignesh Kalimuthu, Ramani Devi Thirunavukarasu, Sureka Chandrabose, Kadalmani Balamuthu","doi":"10.1007/s12032-025-02676-7","DOIUrl":"10.1007/s12032-025-02676-7","url":null,"abstract":"<p><p>Endometrial cancer is the most common gynecological malignancy. Despite advances in treatment, many patients experience disease recurrence or metastasis. This study investigates the impact of siRNA-mediated gene knockdown of NCoR1 and DLK1 genes in the proliferation of endometrial cancer cell lines Ishikawa and AN3CA and normal HEK 293 cells. Cellular growth and survival before and after the treatment of predesigned siRNAs in the endometrial cancer cell lines were evidenced using fluorescent stains. The mRNA expression of BID, BAX, BCL2, Caspases 3, 8, and 9 GPR78, EGFR, VEGF, NCoR1, DLK1 and ARID1A was analyzed in the untreated HEK 293, Ishikawa, and AN3CA cell lines to substantiate the oncogenic property of Ishikawa and AN3CA cell lines. Then, to evidence the successful transfection of NCoR1 and DLK1 gene in endometrial cancer cells, the mRNA and protein expression of targeted genes before and after being transfected were also validated. As a result, the mRNA expression significantly increased in BID, BAX, BCL2, GPR78, EGFR and VEGF. On the other hand, Caspases 3, 8, and 9 were down-regulated in Ishikawa and AN3CA compared to the control cell line (HEK 293). The mRNA and protein expression of NCoR1 and DLK1 in siRNA-mediated transfection supported the reduced proliferation in endometrial cancer cells by interfering with certain pathways like Notch, MAPK, SWI/SNF, and NF-κB, which have crucial roles in the grade of receptor to the histone remodeling. With these findings, the study recommends exploring the possible role and interactions of NCoR1 and DLK1, signaling pathways that favor the progression of endometrial cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"124"},"PeriodicalIF":2.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670271","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":"ADAM9 mediates Cisplatin resistance in gastric cancer cells through DNA damage response pathway.","authors":"Xiao-Yu Zhang, Chan-Yuan Zhao, Jia-Ming Dong, Cun-Pu Du, Chen-Li Zhang, Ai-Jun Yang, Quan Zhou, Wei Liu, Yun Dang, Li-Na Shang, Yong-Ning Zhou, Yu-Ping Wang, Chen-Yu Wang, Min Wang, Min Li","doi":"10.1007/s12032-025-02645-0","DOIUrl":"10.1007/s12032-025-02645-0","url":null,"abstract":"<p><p>Gastric cancer is one of the most common malignant tumors in the world. The occurrence of chemotherapy resistance seriously affects the survival and prognosis of middle and advanced patients. Enhancing DNA repair ability is one of the important mechanisms of chemotherapy resistance. ADAM9, a member of the disintegrin and metalloproteinase family, is involved in many biological processes, such as tumor cells proliferation, apoptosis, invasion and migration, vascular invasion, and drug resistance. In this study, we found that the high expression of ADAM9 in gastric cancer tissues was associated with a variety of clinicopathological factors and poor prognosis in patients. Gastric cancer cells with high ADAM9 expression reduced sensitivity to Cisplatin, decreased DNA damage, increased expression of ATM and CHK2, the key proteins in DNA damage repair pathway, and improved cancer cells survival rate. Further studies showed that the expression of ADAM9 was selectively interfered with gastric cancer cells, the expression levels of ATM and CHK2 were decreased, while the expression of damage protein γ-H2AX was significantly increased, the degree of DNA damage was increased, and the sensitivity of gastric cancer cells to Cisplatin was significantly enhanced. It is suggested that ADAM9 is involved in Cisplatin resistance in gastric cancer cells, and its mechanism is related to the activation of ATM-CHK2 pathway in DNA damage repair. These data demonstrate that ADAM9 plays a pro-cancer role and mediates Cisplatin resistance in gastric cancer, which may be a new target to overcome chemotherapy resistance.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"122"},"PeriodicalIF":2.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663961","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":"Pan-cancer analysis unveils the role and mechanisms of neddylation modifications in tumorigenesis.","authors":"Qianhua Hu, Xiang Li, Ping Wang, Ying Xie","doi":"10.1007/s12032-025-02658-9","DOIUrl":"10.1007/s12032-025-02658-9","url":null,"abstract":"<p><p>This study explores the roles of ubiquitin-like modification genes in pan-cancer, focusing on their regulatory mechanisms, prognostic implications, and drug sensitivity. Data on five key neddylation pathway genes (RBX1, NEDD8, NAE1, UBA3, UBE2M) were collected from TCGA and GTEx databases, covering mRNA expression, DNA methylation, SNVs, and CNVs. Gene expression differences between normal and cancer tissues, along with associations with genetic alterations, methylation, and cancer-related pathways, were analyzed. Drug sensitivity correlations were assessed using GDSC and CTRP databases. Neddylation pathway genes exhibit hypomethylation and overexpression across various cancers, correlating with poor prognosis. SNVs are predominantly missense mutations, while CNVs are mostly heterozygous deletions and amplifications. These genes regulate several key cancer-related pathways, such as DNA damage repair, cell cycle modulation, and inhibition of RTK/RAS/MAPK pathways. Ubiquitin-like modification genes are associated with poor prognosis due to their low methylation and high expression in cancers. Their genetic alterations impact cancer pathways, underscoring their potential as therapeutic targets and prognostic biomarkers.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"119"},"PeriodicalIF":2.8,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663986","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":"Addition of thalidomide for prevention of chemotherapy-induced nausea and vomiting in the second cycle after the failure of four-drug regimen in the first cycle.","authors":"Nishil Gowda, Mirunalini Ravichandran, Jeyaselvi Indrajithu, Tamizharasan Paninathan, Biswajit Dubashi, Smita Kayal, Prasanth Ganesan","doi":"10.1007/s12032-025-02655-y","DOIUrl":"10.1007/s12032-025-02655-y","url":null,"abstract":"<p><p>Four-drug antiemetic prophylaxis achieves emesis control in 70-90% of patients receiving highly emetogenic chemotherapy (HEC). However, less than half achieve control of nausea. We added thalidomide to OAOD (ondansetron, aprepitant, dexamethasone, and olanzapine) to try and improve nausea control. Adults (> 18 years) who had failed (\"any nausea\" in 0-120 h after HEC) OAOD prophylaxis in cycle 1, were randomly assigned to thalidomide (T = 50 mg OD for 5 days) + OAOD or placebo (P) + OAOD in cycle 2. The primary endpoint was the proportion of patients achieving \"no nausea\" in 0-120 h from chemotherapy in the second cycle. A sample size of 50 (including dropouts) would be able to detect 30% \"no nausea\" in the T arm (β = 80%, α = 0.05). We enrolled 105 patients in cycle 1 and randomized 49 patients (25 thalidomide/ 24 placebo; median age 45(30-60) years; all anthracycline/ cyclophosphamide for breast cancer). The addition of thalidomide did not improve the proportion with \"no nausea\" in the overall (0-120 h) [T (16%) vs. P (21%); p = 0.72)], acute (0-24 h) (32% vs. 25%, p = 0.58), and delayed (24-72 h) (32% vs. 25%, p = 0.46) periods. Severe nausea (VAS ≥ 7) in the delayed period was reduced (T = 4% vs. P = 30%, p = 0.02). Sedation and dizziness were not increased, but mild constipation was higher with thalidomide [T (84%) vs. P (58%), p = 0.047)]. The addition of thalidomide to standard 4-drug CINV prophylaxis in cycle 2 did not improve nausea control among patients who \"failed\" the 4-drug regimen in cycle 1.Trial Registration: The trial was registered ( www.ctri.nic.in ; CTRI/2021/08/035980).</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"121"},"PeriodicalIF":2.8,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663964","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":"Isoliquiritigenin attenuates tumor progression and PD-L1 expression by inhibiting the phosphorylation of STAT3 in melanoma.","authors":"Haiyan Zeng, Aoxiang Guo, Zhenyang Liu, Shijian Xiang, Fanghao Zheng","doi":"10.1007/s12032-025-02666-9","DOIUrl":"10.1007/s12032-025-02666-9","url":null,"abstract":"<p><p>Isoliquiritigenin (ISL) has been reported with antitumor activities. While, the underlying molecular mechanisms remain largely unknown. The transcription factor of programmed cell death ligand 1 (PD-L1), STAT3, plays an important role in tumor metastasis. In this study, we first verified that ISL suppressed the growth and metastasis ability of melanoma cells both in vitro and in vivo. Then, we found that ISL could repress the expression of PD-L1 and STAT3 phosphorylation. TIMER algorithm analysis showed that the levels of immune infiltration were positively correlated with the expression of STAT3. Furthermore, the STAT3 phosphorylation inhibitor Stattic could enhance the effect of ISL in suppressing cell proliferation, promoting apoptosis, and restraining the ability of migration and invasion of melanoma cells. This study revealed that ISL inhibited melanoma metastasis and repressed PD-L1 expression by repressing the phosphorylation of STAT3, which help us to understand the mechanism of ISL in melanoma therapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"118"},"PeriodicalIF":2.8,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663968","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":"NEK2 promotes the progression of osteosarcoma through the AKT/p-AKT pathway and interacts with FoxM1.","authors":"Xin Tan, Xiaojing Liang, Yi Feng, Ming Xie, Kun Zhong, Wenwu Luo, Yurao Wang, Yu Yin, Yongping Cai","doi":"10.1007/s12032-025-02657-w","DOIUrl":"10.1007/s12032-025-02657-w","url":null,"abstract":"<p><p>Osteosarcoma is a highly invasive and metastatic primary malignant bone tumor, and resistance to chemotherapy remains a major therapeutic challenge. Our previous studies showed that increased Forkhead box protein M1 (FoxM1) expression promotes osteosarcoma progression. While NIMA-related kinase 2 (NEK2) has emerged as a potential oncogenic factor, its functional role and molecular mechanisms in osteosarcoma remain poorly understood. Pearson's correlation analysis was performed to assess the relationship between FoxM1 and NEK2 expression using the GSE33382 dataset from GEO. Coimmunoprecipitation (Co-IP) was employed to investigate FoxM1-NEK2 interactions. NEK2 expression was modulated in the HOS and U2OS osteosarcoma cell lines through pharmacological inhibition (MBM-55), siRNA-mediated knockdown, and plasmid-mediated overexpression. Cellular proliferation was evaluated via CCK-8 and colony formation assays. Transwell migration/invasion assays and flow cytometry were performed to assess the metastatic potential and apoptosis, respectively. The protein levels of FoxM1, NEK2, and AKT/p-AKT were analyzed by Western blotting. Western blot analyses of FoxM1-overexpressing cell lines and RCM-1-treated cells revealed a positive correlation between NEK2 and FoxM1 levels. Co-IP confirmed their interaction. NEK2 knockdown significantly suppressed proliferation, migration, and invasion; enhanced cisplatin sensitivity (reduced the IC₅₀); and promoted apoptosis. Conversely, NEK2 overexpression exacerbated malignant phenotypes and decreased chemosensitivity. Mechanistically, NEK2 activation was shown to drive osteosarcoma progression via AKT/p-AKT pathway activation. This study revealed that NEK2 promotes osteosarcoma proliferation, invasion, migration, and chemoresistance while inhibiting apoptosis, likely through AKT/p-AKT signaling. These effects may be regulated by FoxM1.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"120"},"PeriodicalIF":2.8,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663971","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":"Tumor microenvironment: recent advances in understanding and its role in modulating cancer therapies.","authors":"Disha D Shah, Mehul R Chorawala, Neha R Raghani, Rajanikant Patel, Mohammad Fareed, Vivekanand A Kashid, Bhupendra G Prajapati","doi":"10.1007/s12032-025-02641-4","DOIUrl":"10.1007/s12032-025-02641-4","url":null,"abstract":"<p><p>Tumor microenvironment (TME) denotes the non-cancerous cells and components presented in the tumor, including molecules produced and released by them. Interactions between cancer cells, immune cells, stromal cells, and the extracellular matrix within the TME create a dynamic ecosystem that can either promote or hinder tumor growth and spread. The TME plays a pivotal role in either promoting or inhibiting tumor growth and dissemination, making it a critical factor to consider in the development of effective cancer therapies. Understanding the intricate interplay within the TME is crucial for devising effective cancer therapies. Combination therapies involving inhibitors of immune checkpoint blockade (ICB), and/or chemotherapy now offer new approaches for cancer therapy. However, it remains uncertain how to best utilize these strategies in the context of the complex tumor microenvironment. Oncogene-driven changes in tumor cell metabolism can impact the TME to limit immune responses and present barriers to cancer therapy. Cellular and acellular components in tumor microenvironment can reprogram tumor initiation, growth, invasion, metastasis, and response to therapies. Components in the TME can reprogram tumor behavior and influence responses to treatments, facilitating immune evasion, nutrient deprivation, and therapeutic resistance. Moreover, the TME can influence angiogenesis, promoting the formation of blood vessels that sustain tumor growth. Notably, the TME facilitates immune evasion, establishes a nutrient-deprived milieu, and induces therapeutic resistance, hindering treatment efficacy. A paradigm shift from a cancer-centric model to a TME-centric one has revolutionized cancer research and treatment. However, effectively targeting specific cells or pathways within the TME remains a challenge, as the complexity of the TME poses hurdles in designing precise and effective therapies. This review highlights challenges in targeting the tumor microenvironment to achieve therapeutic efficacy; explore new approaches and technologies to better decipher the tumor microenvironment; and discuss strategies to intervene in the tumor microenvironment and maximize therapeutic benefits.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"117"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657689","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":"Nanotechnology in Imatinib delivery: advancing cancer treatment through innovative nanoparticles.","authors":"Azam Ghadami, Sonia Fathi-Karkan, Bazla Siddiqui, Sonia Ashfaq Gondal, Abbas Rahdar, Negar Abbaszadeh Garousi, Zelal Kharaba, Suresh Ghotekar","doi":"10.1007/s12032-025-02660-1","DOIUrl":"10.1007/s12032-025-02660-1","url":null,"abstract":"<p><p>Nanotechnology-based drug delivery systems have improved target medicines' therapeutic efficacy and specificity in cancer therapy. Imatinib, one of the tyrosine kinase inhibitors widely used for treating chronic myeloid leukemia and gastrointestinal stromal tumors (GIST), faces many drawbacks, such as poor solubility, reduced bioavailability, and the development of resistance. The paper critically reviews advances in nanotechnology-based approaches toward the delivery of Imatinib, relating to polymeric, lipid-based, carbon-based, and stimuli-responsive nanoparticles. These methods enhance solubility, stability, and targeted distribution and are often used to facilitate the co-delivery of other anticancer drugs with considerable problems in cancer treatment. Although much potential for these technologies exists, scalability, safety, and regulatory approval, among other features, need resolution before real cost can meet clinical efficacy. Further directions would go toward bio-inspired system development, enhancing regulatory frameworks, and cost-effective manufacturing processes that bring nanotechnology into the realm of standard treatment for cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"116"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657676","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":"EM-12, a natural sesquiterpene lactone extracted from Elephantopus mollis, promotes cancer cell apoptosis by activating ER stress.","authors":"Xiang Huang, Junzhen Zhou, Zhenhua Li, Meijun Ye, Changyan Hou, Qing Zhang, Yuanhong Chen, Qiang Li, Fengying Li, Xiaofeng Zhu, Jianwei Jiang","doi":"10.1007/s12032-025-02654-z","DOIUrl":"10.1007/s12032-025-02654-z","url":null,"abstract":"<p><p>The Elephantopus mollis H.B.K. contains various sesquiterpene lactones that have shown anti-proliferative and proapoptotic effects in various cancers, although the underlying mechanisms are partially understood. Inducing of excessive ER stress is a potential cancer therapeutic strategy. However, ER stress activator remain limited in current clinical applications. In this study, we identified that EM-12, an uncovered sesquiterpene lactone isolated from Elephantopus mollis H.B.K., as a BiP ATPase activity inhibitor through BiP ATPase activity assay in vitro. This molecule also exhibits significantly greater cytotoxicity in numerous ovarian cancer cell lines, including paclitaxel-resistance ovarian cancer cell line, compared to transformed ovarian epithelial cell lines. In addition, EM-12 exerts broad-spectrum cytotoxicity against various human cancer cell lines, including liver, nasopharyngeal, and breast cancer cell lines. Mechanically, EM-12 promotes ER stress and ER-stress-related apoptosis to against cancer cells through inhibiting BiP ATPase activity.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"115"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657597","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}