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The impact of bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy on serum stromal-derived factor-1α (SDF-1α) and chemokine ligand 5 (CXCL-5) levels in patients with ovarian cancer after tumor cell debulking surgery. 贝伐单抗腹腔灌注联合紫杉醇、铂类化疗对卵巢癌患者肿瘤细胞去膨胀手术后血清基质衍生因子-1α (SDF-1α)和趋化因子配体5 (CXCL-5)水平的影响
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-06 DOI: 10.1097/CAD.0000000000001663
Liangliang Wang, Shanshan Ma, Huiwen Su, Dandan Nie, Lihua Wang
<p><p>The aim of this study is to investigate the impact of bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy on serum stromal-derived factor-1α (SDF-1α) and chemokine ligand 5 (CXCL-5) levels in patients with ovarian cancer after tumor cell debulking surgery. This clinical study was conducted on a cohort of 89 ovarian cancer patients who underwent tumor debulking surgery at our hospital from February 2020 to February 2021. The patients were divided into two groups using a random number table: the control group ( n  = 44) received postoperative treatment with paclitaxel and platinum-based chemotherapy, while the research group ( n  = 45) received additional treatment with intraperitoneal perfusion of bevacizumab in addition to the control group's treatment regimen. The analysis included an assessment of the clinical efficacy of both groups, changes in tumor biomarker levels before and after treatment, serum levels of SDF-1α and CXCL-5, T-lymphocyte subset levels, treatment-related adverse reactions, and a 2-year prognosis and survival assessment. The research group showed better performance compared to the control group in terms of disease remission rate (80.00% vs. 59.09%) and treatment effectiveness rate (95.56% vs. 75.00%) ( P  < 0.05). Before treatment, the levels of tumor biomarkers between the two groups were compared ( P  > 0.05). After treatment, the levels of serum ferritin, carbohydrate antigen 125, carbohydrate antigen 199, and human epididymis protein 4 in both groups significantly decreased compared to before treatment, with the research group having lower levels ( P  < 0.05). Before treatment, serum levels of SDF-1α and CXCL-5 between the two groups were compared ( P  > 0.05). After treatment, however, the levels of SDF-1α and CXCL-5 significantly decreased compared to before treatment, with the research group having lower levels than the control group ( P  < 0.05). Before treatment, there was no difference in T-lymphocyte levels between the two groups ( P  > 0.05). In the control group, there was no significant change in T-lymphocyte levels before and after treatment ( P  > 0.05). In the research group, however, after treatment, each indicator increased compared to before treatment, and posttreatment levels of all indicators were higher than those in the control group ( P  < 0.05). The adverse reactions were compared between the two groups ( P  > 0.05). The research group had a longer average survival time than the control group, with 1-year and 2-year survival rates higher than the control group ( P  < 0.05). There was, however, no significant difference between the two groups in terms of local recurrence and metastasis ( P  > 0.05). In conclusion, bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy shows better clinical efficacy in the treatment of ovarian cancer after tumor cell debulking surgery. It can significantly reduce the levels of ser
本研究旨在探讨贝伐单抗腹腔灌注联合紫杉醇和铂类化疗对卵巢癌患者肿瘤细胞去膨胀手术后血清基质衍生因子-1α (SDF-1α)和趋化因子配体5 (CXCL-5)水平的影响。本临床研究是对2020年2月至2021年2月在我院行肿瘤减体积手术的89例卵巢癌患者进行队列研究。采用随机数字表法将患者分为两组:对照组(n = 44)术后给予紫杉醇和铂类化疗,研究组(n = 45)在对照组治疗方案的基础上给予贝伐单抗腹腔灌注治疗。分析包括评估两组患者的临床疗效、治疗前后肿瘤生物标志物水平的变化、血清SDF-1α和CXCL-5水平、t淋巴细胞亚群水平、治疗相关不良反应以及2年预后和生存评估。研究组在疾病缓解率(80.00% vs. 59.09%)和治疗有效率(95.56% vs. 75.00%)方面均优于对照组(P < 0.05)。治疗后,两组患者血清铁蛋白、碳水化合物抗原125、碳水化合物抗原199、人附睾蛋白4水平均较治疗前显著降低,其中研究组较治疗前降低(P < 0.05)。治疗后,SDF-1α、CXCL-5水平较治疗前显著降低,且研究组低于对照组(P < 0.05)。对照组治疗前后t淋巴细胞水平差异无统计学意义(P < 0.05)。而研究组治疗后各项指标均较治疗前升高,且治疗后各项指标均高于对照组(P < 0.05)。研究组患者平均生存时间长于对照组,1年、2年生存率均高于对照组(P < 0.05)。综上所述,贝伐单抗腹腔灌注联合紫杉醇和铂类化疗治疗卵巢癌肿瘤细胞减体积手术后的临床疗效更好。可显著降低患者血清SDF-1α和CXCL-5水平,提高生存率,安全性好。
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引用次数: 0
Transformation of lung adenocarcinoma to small cell lung cancer following osimertinib treatment: a case report and literature review. 奥西替尼治疗后肺腺癌向小细胞肺癌的转化:1例报告及文献复习。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-08 DOI: 10.1097/CAD.0000000000001686
Linwu Kuang, Peng Wang, Lin Zhou, Yangkai Li

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) effectively treat EGFR-mutant lung adenocarcinoma, demonstrating initial efficacy but eventually leading to acquired resistance. Small cell transformation is a rare resistance mechanism to EGFR-TKIs in lung adenocarcinoma, which can complicate clinical diagnosis and treatment. We present a patient with lung adenocarcinoma who underwent a prior pneumonectomy and adjuvant chemotherapy and was treated with osimertinib after the recurrence of lung cancer. Small cell transformation occurred approximately 20 months after starting osimertinib treatment. After this transformation, the patient underwent lung radiotherapy and cisplatin-etoposide chemotherapy, which stabilized the disease. Following the confirmation of small cell lung cancer (SCLC) via thyroid puncture, treatments with irinotecan, irinotecan plus atezolizumab, thyroid radiotherapy, adrenal radiotherapy, and head radiotherapy were sequentially administered, yet the disease continued to progress. The patient succumbed to the disease in May 2023 because of progression and organ failure, with an overall survival of 52.7 months, including 16 months post small cell transformation. This case highlights the possibility of osimertinib causing lung adenocarcinoma to transform into SCLC and underscores rebiopsies' importance in identifying resistance mechanisms to EGFR-TKIs. Increased levels of neuron-specific enolase and pro-gastrin releasing peptide can signal early transformation into SCLC.

表皮生长因子受体(EGFR)-酪氨酸激酶抑制剂(TKIs)可有效治疗EGFR突变型肺腺癌,显示出初始疗效,但最终导致获得性耐药。小细胞转化是肺腺癌中罕见的EGFR-TKIs耐药机制,使临床诊断和治疗复杂化。我们报告了一位肺腺癌患者,他在肺癌复发后接受了肺切除术和辅助化疗,并接受了奥西替尼治疗。开始奥西替尼治疗约20个月后发生小细胞转化。转化后,患者接受了肺部放疗和顺铂-依托泊苷化疗,病情稳定。在通过甲状腺穿刺确认小细胞肺癌(SCLC)后,依次给予伊立替康、伊立替康联合阿特唑单抗、甲状腺放疗、肾上腺放疗和头部放疗,但疾病继续进展。由于进展和器官衰竭,患者于2023年5月死于该疾病,总生存期为52.7个月,其中包括小细胞转化后的16个月。该病例强调了奥西替尼导致肺腺癌转化为SCLC的可能性,并强调了再活检在确定对EGFR-TKIs的耐药机制方面的重要性。神经元特异性烯醇化酶和前胃泌素释放肽水平升高可提示早期转化为SCLC。
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引用次数: 0
WISP1 inhibition of YAP phosphorylation drives breast cancer growth and chemoresistance via TEAD4 activation. WISP1抑制YAP磷酸化通过TEAD4激活驱动乳腺癌生长和化疗耐药。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-06 DOI: 10.1097/CAD.0000000000001687
Tingting Dong, Li Liu, Yikai You, Jin Liu, Fuchao Wang, Shimeng Li, Zhenghong Yu

Wnt1-inducible signaling pathway protein 1 (WISP1) promotes breast cancer. The Hippo signaling pathway demonstrates a potential connection with WISP1, necessitating an exploration of their interaction. This study hypothesized that WISP1 boosts breast cancer by modulating the Hippo signaling pathway. The Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to analyze WISP1 expression and Hippo signaling in breast cancer patients. WISP1, yes-associated protein (YAP), and domain family member 4 (TEAD4) were overexpressed or silenced in breast cancer cells. Epithelial-mesenchymal transition (EMT), and chemoresistance of breast cancer cells were evaluated. Immunofluorescence, PCR, immunoprecipitation, and western blot were used to detect the expression of WISP1 and key Hippo signaling factors and their interactions. Enrichment analysis indicated activation of WISP1 and Hippo signaling pathway and correlated with a worse prognosis in breast cancer. WISP1 overexpression facilitated EMT and chemotherapy resistance in breast cancer. Importantly, overexpression of WISP1 promoted YAP's nuclear translocation. TEAD4 expression in YAP precipitates from nuclear of WISP1-overexpressing MCF-7 cells increased. The promoting effect of WISP1 on breast cancer was counteracted by silencing YAP or TEAD4. Moreover, in WISP1 small interfering RNA-transfected MCF-7 cells, p-YAP expression increased, while interaction between YAP and TEAD4 decreased. WISP1 silencing led to ubiquitin increase and TEAD reduction in the p-YAP precipitates. In conclusion, WISP1 promotes YAP nuclear translocation and binding with TEAD4 by inhibiting YAP phosphorylation, reducing ubiquitin recruitment, and participating in transcriptional regulation in breast cancer.

wnt1诱导的信号通路蛋白1 (WISP1)促进乳腺癌。Hippo信号通路显示了与WISP1的潜在联系,有必要探索它们之间的相互作用。本研究假设WISP1通过调节Hippo信号通路促进乳腺癌。利用Gene Expression Omnibus (GEO)和The Cancer Genome Atlas (TCGA)数据库分析乳腺癌患者中WISP1的表达和Hippo信号。乳腺癌细胞中WISP1、yes-associated protein (YAP)和结构域家族成员4 (TEAD4)过表达或沉默。对乳腺癌细胞的上皮-间质转化(EMT)和化疗耐药进行了评价。采用免疫荧光、PCR、免疫沉淀和western blot检测WISP1和Hippo关键信号因子的表达及其相互作用。富集分析表明,WISP1和Hippo信号通路的激活与乳腺癌预后不良相关。WISP1过表达促进乳腺癌EMT和化疗耐药。重要的是,WISP1的过表达促进了YAP的核易位。过表达wisp1的MCF-7细胞核YAP沉淀中TEAD4的表达增加。沉默YAP或TEAD4可抵消WISP1对乳腺癌的促进作用。此外,在WISP1小干扰rna转染的MCF-7细胞中,p-YAP表达增加,而YAP与TEAD4的相互作用减弱。WISP1沉默导致p-YAP沉淀中泛素增加和TEAD降低。综上所述,WISP1通过抑制YAP磷酸化、减少泛素募集、参与乳腺癌的转录调控,促进YAP核易位并与TEAD4结合。
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引用次数: 0
High CXCL8 expression predicting poor prognosis in triple-negative breast cancer.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-06 DOI: 10.1097/CAD.0000000000001678
Sumin Tang, Yuqing Zhang, Liying Song, Kaiyuan Hui, Xiaodong Jiang

Triple-negative breast cancer (TNBC) is highly prone to early relapse and metastasis following standard treatment. CXCL8 is a key factor in tumor invasion and metastasis, but its role in TNBC prognosis and clinicopathological correlations remains poorly understood. This study investigated CXCL8 expression and its clinical significance in TNBC to develop a prognostic nomogram for guiding intensive treatment and follow-up strategies. Public datasets from the gene expression omnibus public datasets platform were analyzed to assess CXCL8 expression. Additionally, paraffin-embedded TNBC specimens collected from our hospital were examined using immunohistochemistry to explore the relationship between CXCL8 expression and clinicopathological features. Survival analysis was performed to evaluate whether CXCL8 serves as an unfavorable prognostic biomarker for TNBC patients. Univariate Cox regression analysis was conducted to identify prognostic factors. Based on these findings, a nomogram was developed to predict TNBC progression risk. CXCL8 expression was significantly higher in TNBC tissues than in adjacent normal tissues ( P  < 0.05). Among 122 TNBC patients, 46 were CXCL8-positive and 76 were CXCL8-negative. CXCL8 expression was significantly associated with N stage ( P  < 0.05). Progression-free survival (PFS) was markedly shorter in the CXCL8-positive group compared with the CXCL8-negative group ( P  < 0.001). Univariate Cox regression identified N1-3, M1, and CXCL8 positivity as significant risk factors for disease progression. A nomogram incorporating these variables (N, M, and CXCL8) was constructed to predict PFS. Time-dependent receiver operating characteristic curve analysis at 12-, 36-, and 48-month demonstrated strong predictive performance, with area under the curve values of 0.857, 0.839, and 0.795, respectively. CXCL8 is highly expressed in TNBC and promotes lymphatic metastasis, serving as an unfavorable prognostic factor. The developed nomogram offers a valuable tool for guiding personalized treatment and follow-up strategies in TNBC patients.

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引用次数: 0
Research on the mechanism of eugenol in the treatment of liver cancer based on network pharmacology, molecular docking technology, and in vitro experiments. 基于网络药理学、分子对接技术、体外实验研究丁香酚治疗肝癌的作用机制。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-10 DOI: 10.1097/CAD.0000000000001675
Kaiping Liu, Jiuliang Jiang, Zhenyu Yu, Yunhao Wang, Min Wang, Haitao Zhu

Eugenol, a phenolic natural product with diverse pharmacological activities, remains unexplored in liver cancer. Using network pharmacology, we investigated eugenol's therapeutic mechanisms in liver cancer. We obtained eugenol's molecular structure from PubChem and screened its targets using similarity ensemble approach in Swiss Target Predictiondatabases. Overlapping genes with liver cancer-related genes from GeneCards were identified. Protein-protein interaction networks, Gene Ontology annotations, and Kyoto Encyclopedia of Genes and Genomes pathway analyses were conducted. A target-pathway network revealed eugenol's interaction with 122 liver cancer-related genes. Molecular docking confirmed eugenol's high affinity for mitochondrial nicotinamide adenine dinucleotide, reduced form (NADH) dehydrogenase 1 (MT-ND1), AKT1, NDUFB7, and NADH dehydrogenase (complex I) subunit S3 (NDUFS3). Expression levels of these targets in normal liver and liver cancer tissues were examined using GEPIA2 and HPA databases. The CCK-8 assay and colony formation assay demonstrated that eugenol significantly inhibited the proliferation of hepatocellular carcinoma cells. Western blot analysis confirmed that eugenol upregulated MT-ND1 while downregulating the expression of targets such as AKT1, NDUFB7, and NDUFS3. Furthermore, it was found that eugenol could influence the expression of the AKT1 target through the AKT/p70 S6K pathway. This study provides new insights into the potential mechanisms of eugenol in liver cancer and offers novel perspectives for network-based liver cancer research.

丁香酚是一种具有多种药理活性的酚类天然产物,在肝癌中的作用尚未得到充分的研究。采用网络药理学方法,研究丁香酚对肝癌的治疗作用机制。我们从PubChem中获得了丁香酚的分子结构,并在Swiss Target Predictiondatabases中使用相似集成方法筛选其靶标。发现了与GeneCards中肝癌相关基因重叠的基因。进行了蛋白质-蛋白质相互作用网络、基因本体注释和京都基因与基因组百科全书通路分析。靶通路网络揭示了丁香酚与122个肝癌相关基因的相互作用。分子对接证实丁香酚对线粒体烟酰胺腺嘌呤二核苷酸、还原形式(NADH)脱氢酶1 (MT-ND1)、AKT1、NDUFB7和NADH脱氢酶(复合体I)亚基S3 (NDUFS3)具有高亲和力。使用GEPIA2和HPA数据库检测这些靶点在正常肝脏和肝癌组织中的表达水平。CCK-8实验和集落形成实验表明丁香酚能显著抑制肝癌细胞的增殖。Western blot分析证实,丁香酚上调MT-ND1,下调AKT1、NDUFB7、NDUFS3等靶点的表达。此外,我们发现丁香酚可以通过AKT/p70 S6K通路影响AKT1靶点的表达。本研究为丁香酚在肝癌中的潜在作用机制提供了新的见解,为基于网络的肝癌研究提供了新的视角。
{"title":"Research on the mechanism of eugenol in the treatment of liver cancer based on network pharmacology, molecular docking technology, and in vitro experiments.","authors":"Kaiping Liu, Jiuliang Jiang, Zhenyu Yu, Yunhao Wang, Min Wang, Haitao Zhu","doi":"10.1097/CAD.0000000000001675","DOIUrl":"10.1097/CAD.0000000000001675","url":null,"abstract":"<p><p>Eugenol, a phenolic natural product with diverse pharmacological activities, remains unexplored in liver cancer. Using network pharmacology, we investigated eugenol's therapeutic mechanisms in liver cancer. We obtained eugenol's molecular structure from PubChem and screened its targets using similarity ensemble approach in Swiss Target Predictiondatabases. Overlapping genes with liver cancer-related genes from GeneCards were identified. Protein-protein interaction networks, Gene Ontology annotations, and Kyoto Encyclopedia of Genes and Genomes pathway analyses were conducted. A target-pathway network revealed eugenol's interaction with 122 liver cancer-related genes. Molecular docking confirmed eugenol's high affinity for mitochondrial nicotinamide adenine dinucleotide, reduced form (NADH) dehydrogenase 1 (MT-ND1), AKT1, NDUFB7, and NADH dehydrogenase (complex I) subunit S3 (NDUFS3). Expression levels of these targets in normal liver and liver cancer tissues were examined using GEPIA2 and HPA databases. The CCK-8 assay and colony formation assay demonstrated that eugenol significantly inhibited the proliferation of hepatocellular carcinoma cells. Western blot analysis confirmed that eugenol upregulated MT-ND1 while downregulating the expression of targets such as AKT1, NDUFB7, and NDUFS3. Furthermore, it was found that eugenol could influence the expression of the AKT1 target through the AKT/p70 S6K pathway. This study provides new insights into the potential mechanisms of eugenol in liver cancer and offers novel perspectives for network-based liver cancer research.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"177-189"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943245","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}
引用次数: 0
Paeoniflorin sensitizes imatinib mesylate-resistant chronic myeloid leukemia cells via the inhibition of Cyr61 production. 芍药苷通过抑制Cyr61的产生使耐伊马替尼甲磺酸慢性髓系白血病细胞增敏。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-03-01 Epub Date: 2025-01-07 DOI: 10.1097/CAD.0000000000001681
Yanfang Song, Li Luo, Zhen Lin, Taigang Zhang, Zhaozhong Li, Yinping Cao, Xianjin Zhu

Imatinib mesylate (IM) is a first-line therapy for chronic myeloid leukemia (CML) and exhibits good therapeutic effects, but not in all patients with CML owing to drug resistance. Our previous study showed that Cyr61 plays a key role in IM resistance in CML cells. Paeoniflorin (PF) is a bioactive compound isolated from the traditional Chinese medicine Paeonia lactiflora Pall that displays anticancer activity. Little is, however, known regarding the role of PF in IM-resistant CML cells. This study aimed to evaluate whether PF could decrease Cyr61 production and improve IM-resistant CML cell sensitivity to IM and to investigate the underlying mechanisms. CML cell lines (K562 and KCL22) and IM-resistant cell lines (K562G and KCL22R) were used as CML study models. Cyr61 expression was assessed in both parental and IM-resistant CML cells by western blotting, real-time quantitative PCR , and ELISA. Lentiviral vectors were used to induce the knockdown of Cyr61 expression, followed by a comprehensive evaluation of cell proliferation and apoptosis. The results showed that PF decreased the production of Cyr61 in the presence of IM by inhibiting extracellular regulated protein kinases 1/2 activation. PF significantly decreased the IC50 value of IM and increased IM-induced apoptosis of IM-resistant CML cells. Importantly, PF also improved the sensitivity of CML cells to bosutinib and dasatinib via inhibition of Cyr61 production. In conclusion, we report for the first time that PF may effectively improve the sensitivity of IM-resistant CML cells to IM, bosutinib, and dasatinib, at least in part, by subsequently downregulating Cyr61.

甲磺酸伊马替尼(Imatinib mesylate, IM)是治疗慢性髓系白血病(chronic myeloid leukemia, CML)的一线药物,具有良好的治疗效果,但由于耐药,并非对所有CML患者都有效。我们之前的研究表明Cyr61在CML细胞的IM耐药中起关键作用。芍药苷(Paeoniflorin, PF)是从中药芍药中分离得到的具有抗癌活性的生物活性化合物。然而,关于PF在抗im CML细胞中的作用知之甚少。本研究旨在评估PF是否可以减少Cyr61的产生,提高IM耐药CML细胞对IM的敏感性,并探讨其潜在机制。以CML细胞系K562、KCL22和抗im细胞系K562G、KCL22R为CML研究模型。通过western blotting、实时定量PCR和ELISA检测Cyr61在亲代和抗im CML细胞中的表达。采用慢病毒载体诱导Cyr61表达下调,然后综合评价细胞增殖和凋亡情况。结果表明,PF通过抑制胞外调节蛋白激酶1/2的激活,降低了IM存在下Cyr61的产生。PF显著降低IM的IC50值,增加IM诱导的抗IM CML细胞凋亡。重要的是,PF还通过抑制Cyr61的产生提高了CML细胞对博舒替尼和达沙替尼的敏感性。总之,我们首次报道,PF可能通过随后下调Cyr61,至少在一定程度上有效提高IM耐药CML细胞对IM、博舒替尼和达沙替尼的敏感性。
{"title":"Paeoniflorin sensitizes imatinib mesylate-resistant chronic myeloid leukemia cells via the inhibition of Cyr61 production.","authors":"Yanfang Song, Li Luo, Zhen Lin, Taigang Zhang, Zhaozhong Li, Yinping Cao, Xianjin Zhu","doi":"10.1097/CAD.0000000000001681","DOIUrl":"10.1097/CAD.0000000000001681","url":null,"abstract":"<p><p>Imatinib mesylate (IM) is a first-line therapy for chronic myeloid leukemia (CML) and exhibits good therapeutic effects, but not in all patients with CML owing to drug resistance. Our previous study showed that Cyr61 plays a key role in IM resistance in CML cells. Paeoniflorin (PF) is a bioactive compound isolated from the traditional Chinese medicine Paeonia lactiflora Pall that displays anticancer activity. Little is, however, known regarding the role of PF in IM-resistant CML cells. This study aimed to evaluate whether PF could decrease Cyr61 production and improve IM-resistant CML cell sensitivity to IM and to investigate the underlying mechanisms. CML cell lines (K562 and KCL22) and IM-resistant cell lines (K562G and KCL22R) were used as CML study models. Cyr61 expression was assessed in both parental and IM-resistant CML cells by western blotting, real-time quantitative PCR , and ELISA. Lentiviral vectors were used to induce the knockdown of Cyr61 expression, followed by a comprehensive evaluation of cell proliferation and apoptosis. The results showed that PF decreased the production of Cyr61 in the presence of IM by inhibiting extracellular regulated protein kinases 1/2 activation. PF significantly decreased the IC50 value of IM and increased IM-induced apoptosis of IM-resistant CML cells. Importantly, PF also improved the sensitivity of CML cells to bosutinib and dasatinib via inhibition of Cyr61 production. In conclusion, we report for the first time that PF may effectively improve the sensitivity of IM-resistant CML cells to IM, bosutinib, and dasatinib, at least in part, by subsequently downregulating Cyr61.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"190-198"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943244","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}
引用次数: 0
Occult epidermal growth factor receptor-mutant lung adenocarcinoma complicated by prostatic metastasis: a case report.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-02-28 DOI: 10.1097/CAD.0000000000001710
Fan Yang, Xing Zhao, Hua Xie, Yajie Zhu, Yi Wang, Jin Zhou

Herein, we report a case of occult epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma complicated by prostatic metastasis. A 75-year-old male with >30 years of smoking history presented with lower back pain as the initial symptom. Respiratory symptoms, including cough and sputum production, were absent. PET-computed tomography revealed the presence of bone and prostatic metastases, without any lung abnormalities. Biopsies of the space-occupying bone and metastatic lesions suggested that the metastases originated from primary lung adenocarcinoma. Genetic testing indicated EGFR 21L858R(+). The patient had an abnormal serum carcinoembryonic antigen level but a normal prostate-specific antigen level. Following a multidisciplinary discussion, a diagnosis of occult primary lung adenocarcinoma complicated by bone and prostatic metastases (TxN0M1b, Stage IVB) was considered. Following targeted therapy with oral osimertinib, the patient achieved a partial response, with alleviation of pain symptoms alleviated and normalization of carcinoembryonic antigen levels. In the absence of tissue biopsy, such cases can often be misdiagnosed as prostate cancer complicated by multiple bone metastases. Hence, the present case highlights the importance of comprehensive diagnostic testing, including tissue biopsy, to accurately identify the underlying cause of metastatic disease.

在此,我们报告了一例隐匿性表皮生长因子受体(EGFR)突变肺腺癌并发前列腺转移的病例。一名 75 岁男性患者,吸烟史超过 30 年,最初症状为下背部疼痛。患者无咳嗽、咳痰等呼吸道症状。PET 计算机断层扫描显示存在骨转移和前列腺转移,肺部未见异常。对占据空间的骨骼和转移病灶进行的活检表明,转移灶源自原发性肺腺癌。基因检测显示表皮生长因子受体 21L858R(+)。患者血清癌胚抗原水平异常,但前列腺特异性抗原水平正常。经过多学科讨论,考虑诊断为隐匿性原发性肺腺癌并发骨转移和前列腺转移(TxN0M1b,IVB 期)。在口服奥希替尼进行靶向治疗后,患者获得了部分应答,疼痛症状减轻,癌胚抗原水平恢复正常。在没有组织活检的情况下,此类病例往往会被误诊为并发多发性骨转移的前列腺癌。因此,本病例凸显了包括组织活检在内的全面诊断检测对准确确定转移性疾病的根本原因的重要性。
{"title":"Occult epidermal growth factor receptor-mutant lung adenocarcinoma complicated by prostatic metastasis: a case report.","authors":"Fan Yang, Xing Zhao, Hua Xie, Yajie Zhu, Yi Wang, Jin Zhou","doi":"10.1097/CAD.0000000000001710","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001710","url":null,"abstract":"<p><p>Herein, we report a case of occult epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma complicated by prostatic metastasis. A 75-year-old male with >30 years of smoking history presented with lower back pain as the initial symptom. Respiratory symptoms, including cough and sputum production, were absent. PET-computed tomography revealed the presence of bone and prostatic metastases, without any lung abnormalities. Biopsies of the space-occupying bone and metastatic lesions suggested that the metastases originated from primary lung adenocarcinoma. Genetic testing indicated EGFR 21L858R(+). The patient had an abnormal serum carcinoembryonic antigen level but a normal prostate-specific antigen level. Following a multidisciplinary discussion, a diagnosis of occult primary lung adenocarcinoma complicated by bone and prostatic metastases (TxN0M1b, Stage IVB) was considered. Following targeted therapy with oral osimertinib, the patient achieved a partial response, with alleviation of pain symptoms alleviated and normalization of carcinoembryonic antigen levels. In the absence of tissue biopsy, such cases can often be misdiagnosed as prostate cancer complicated by multiple bone metastases. Hence, the present case highlights the importance of comprehensive diagnostic testing, including tissue biopsy, to accurately identify the underlying cause of metastatic disease.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536553","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}
引用次数: 0
Low-dose anlotinib plus immune checkpoint inhibitors offers better efficacy and safety in advanced non-small cell lung cancer treatment.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-02-25 DOI: 10.1097/CAD.0000000000001701
Tingfei Tan, Siyu Yuan, Weiwei Chu, Jiemei Jiang, Meiling Chen, Quan Xia, Junping Wang

The combination of anlotinib with immune checkpoint inhibitors (ICIs) has become a common treatment modality in clinical practice. However, the optimal dose of anlotinib to use remains unclear. We collected patients with advanced non-small cell lung cancer (NSCLC) who received programmed cell death-1 blockade combined with different dose of anlotinib as second-line or later line therapy. Subsequently, the efficacy and safety of the combination therapy as well as subgroup analyses of different doses of anlotinib were analyzed. Cox regression was performed to analyze significant factors correlated with progression-free survival (PFS) and overall survival (OS). A total of 50 eligible patients with NSCLC who received anlotinib combined with ICIs therapy were included, of which 27 received low-dose anlotinib (8 mg), and 23 were administered high-dose anlotinib (12 mg). The median PFS (mPFS) and the median OS (mOS) for all patients were 8.3 months [95% confidence interval (CI): 6.3-10.3] and 17.6 months (95% CI: 16.5-18.7), respectively. Subgroup analyses showed that patients treated with 8 mg of anlotinib plus ICIs had significantly longer mPFS than those treated with 12 mg of anlotinib plus ICIs (8.7 vs 6.7 months, P  = 0.016). The overall incidence of adverse events was 68.0%, and the most common adverse events of all grades were hypertension. Meanwhile, the incidence of adverse events was higher for 12 mg of anlotinib plus ICIs than that of 8 mg of anlotinib plus ICIs (82.6 vs 55.6%, P  = 0.041). Low-dose anlotinib in combination with ICIs for advanced NSCLC may be an effective and well-tolerated option.

{"title":"Low-dose anlotinib plus immune checkpoint inhibitors offers better efficacy and safety in advanced non-small cell lung cancer treatment.","authors":"Tingfei Tan, Siyu Yuan, Weiwei Chu, Jiemei Jiang, Meiling Chen, Quan Xia, Junping Wang","doi":"10.1097/CAD.0000000000001701","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001701","url":null,"abstract":"<p><p>The combination of anlotinib with immune checkpoint inhibitors (ICIs) has become a common treatment modality in clinical practice. However, the optimal dose of anlotinib to use remains unclear. We collected patients with advanced non-small cell lung cancer (NSCLC) who received programmed cell death-1 blockade combined with different dose of anlotinib as second-line or later line therapy. Subsequently, the efficacy and safety of the combination therapy as well as subgroup analyses of different doses of anlotinib were analyzed. Cox regression was performed to analyze significant factors correlated with progression-free survival (PFS) and overall survival (OS). A total of 50 eligible patients with NSCLC who received anlotinib combined with ICIs therapy were included, of which 27 received low-dose anlotinib (8 mg), and 23 were administered high-dose anlotinib (12 mg). The median PFS (mPFS) and the median OS (mOS) for all patients were 8.3 months [95% confidence interval (CI): 6.3-10.3] and 17.6 months (95% CI: 16.5-18.7), respectively. Subgroup analyses showed that patients treated with 8 mg of anlotinib plus ICIs had significantly longer mPFS than those treated with 12 mg of anlotinib plus ICIs (8.7 vs 6.7 months, P  = 0.016). The overall incidence of adverse events was 68.0%, and the most common adverse events of all grades were hypertension. Meanwhile, the incidence of adverse events was higher for 12 mg of anlotinib plus ICIs than that of 8 mg of anlotinib plus ICIs (82.6 vs 55.6%, P  = 0.041). Low-dose anlotinib in combination with ICIs for advanced NSCLC may be an effective and well-tolerated option.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481994","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}
引用次数: 0
BTK inhibitors enhance NKG2D ligand expression by regulating IL-10/STAT3 pathway in activated non-GCB diffuse large B-cell lymphoma cells.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-02-25 DOI: 10.1097/CAD.0000000000001696
Zhu-Xia Jia, Bi-Tao Xiao, Jin Li, Xiao-Hui Cai, Wei Qin, Min Zhou, Xu-Zhang Lu

The aim of this study is to explore the role of the IL-10/STAT3 pathway in the upregulation of natural killer group 2, member D (NKG2D) ligands (MICA and ULBP2) induced by Bruton's tyrosine kinase (BTK) inhibitors in non-germinal center B-cell-like diffuse large B-cell lymphoma cells. The expression levels of NKG2D ligands and the IL-10/STAT3 pathway in SUDHL4, U2932, and OCI-LY3 cells were analyzed using western blotting. After stimulation of the B-cell receptor signaling pathway with IgM antibodies, the expression levels of NKG2D ligands, as well as IL-10 and phosphorylated STAT3 (p-STAT3) were significantly reduced. In contrast, treatment with ibrutinib produced effects opposite to those induced by IgM antibodies. Additionally, treatment of U2932 and OCI-LY3 cells with the STAT3 inhibitor (STAT3-IN-1) led to an increase in NKG2D ligand expression and a decrease in IL-10 levels. When IL-10 neutralizing antibodies were introduced, p-STAT3 levels decreased, and NKG2D ligand expression increased. Similar outcomes were observed when the BTK inhibitors ACP-196 and BGB-3111 were administered. Our findings suggest that the IL-10/STAT3 pathway plays a key role in the upregulation of NKG2D ligands induced by BTK inhibitors in U2932 and OCI-LY3 cells.

{"title":"BTK inhibitors enhance NKG2D ligand expression by regulating IL-10/STAT3 pathway in activated non-GCB diffuse large B-cell lymphoma cells.","authors":"Zhu-Xia Jia, Bi-Tao Xiao, Jin Li, Xiao-Hui Cai, Wei Qin, Min Zhou, Xu-Zhang Lu","doi":"10.1097/CAD.0000000000001696","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001696","url":null,"abstract":"<p><p>The aim of this study is to explore the role of the IL-10/STAT3 pathway in the upregulation of natural killer group 2, member D (NKG2D) ligands (MICA and ULBP2) induced by Bruton's tyrosine kinase (BTK) inhibitors in non-germinal center B-cell-like diffuse large B-cell lymphoma cells. The expression levels of NKG2D ligands and the IL-10/STAT3 pathway in SUDHL4, U2932, and OCI-LY3 cells were analyzed using western blotting. After stimulation of the B-cell receptor signaling pathway with IgM antibodies, the expression levels of NKG2D ligands, as well as IL-10 and phosphorylated STAT3 (p-STAT3) were significantly reduced. In contrast, treatment with ibrutinib produced effects opposite to those induced by IgM antibodies. Additionally, treatment of U2932 and OCI-LY3 cells with the STAT3 inhibitor (STAT3-IN-1) led to an increase in NKG2D ligand expression and a decrease in IL-10 levels. When IL-10 neutralizing antibodies were introduced, p-STAT3 levels decreased, and NKG2D ligand expression increased. Similar outcomes were observed when the BTK inhibitors ACP-196 and BGB-3111 were administered. Our findings suggest that the IL-10/STAT3 pathway plays a key role in the upregulation of NKG2D ligands induced by BTK inhibitors in U2932 and OCI-LY3 cells.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539947","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}
引用次数: 0
Effect of adjuvant chemotherapy with toad venom injection in the treatment of intermediate and advanced colon cancer and its effect on cellular immunity, PTEN, and PI3k.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-02-18 DOI: 10.1097/CAD.0000000000001706
Haijun Ding, Xuedian Tang, Wenjun Tang

The objective of this study is to explore the effect of adjuvant chemotherapy with toad venom injection in patients with intermediate and advanced colon cancer, in order to provide new reference drugs for clinical treatment. Prospectively, 148 patients with mid-stage to late-stage colon cancer in our hospital from January 2021 to May 2023 were selected for the study and randomly divided into two groups of 74 cases each. The control group was treated with FOLFOX4 chemotherapy, and the observation group was treated with four consecutive chemotherapy cycles based on the control group combined with toad venom injection. The treatment effects, adverse reactions, quality of life improvement rate, prognosis and cellular immune indexes [natural killer (NK) cells, CD4+/CD8+, CD4+, CD3+], phosphatase tensin gene (PTEN), phosphatidylinositol-3-kinase (PI3k), and serine threonine protein kinase (pAKT) protein expression before and after treatment were counted in the two groups. The total effective rate of treatment in the observation group was 58.11% (43/74) after four cycles of chemotherapy, which was higher than that in the control group of 41.89% (31/74) (P < 0.05). After two cycles of chemotherapy and four cycles of chemotherapy, PTEN, CD4+/CD8+, CD4+, CD3+, and NK cells in peripheral blood were higher in the observation group than in the control group, and PI3k and pAKT were lower than in the control group (P < 0.05). There was no statistically significant difference in the rate of adverse reactions in the observation group compared with the control group (P > 0.05); the improvement rate of quality of life in the observation group was better than that in the control group after four chemotherapy cycles of treatment (P < 0.05); the survival rate was 75.00% (54/72) in the observation group compared with 54.29% (38/70) in the control group at 1-year follow-up. Toad venom injection adjuvant chemotherapy is effective in treating patients with intermediate and advanced colon cancer, which can upregulate PTEN level, inhibit PI3k and AKT expression, and improve immune function and quality of life of patients, thus improving prognosis.

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Anti-Cancer Drugs
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