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Hypofunction of macrophage chemotaxis contributes to defective efficacy of herceptin in HER2-positive breast cancer patients. 巨噬细胞趋化功能低下导致赫赛汀对HER2阳性乳腺癌患者的疗效缺陷
IF 2.1 Q3 ONCOLOGY Pub Date : 2024-02-07 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2309715
Yu Song, Qiao-Chen Geng, Wen-Jing An, Fu-Cheng Zhang, Ran Jiang, Rui-Sheng Zhao, Zhi-Jian Deng, Heng Li

Breast cancer was considered as a kind of prone breast tumors with the complicated pathological mechanisms and diverse clinical classifications. In the clinical treatments of HER2-positive tumor patients, HER2 monoclonal antibodies, such as Herceptin, have shown well-defined therapeutic effects. Nevertheless, due to the heterogeneity of breast cancers, drug resistance inevitably appeared during the application of Herceptin. In order to fully understand the immune tolerance status of the tumor microenvironment in the population of sensitive and insensitive patients, this study carried out a series of studies through Luminex cytokines assay, clinicopathological analysis, immunofluorescence, and PCR. The results confirmed that in clinical samples sensitive to Herceptin, there were a large number of macrophages, and the protein expression levels and in situ expression of macrophage-related chemokines and inflammatory mediators are significantly higher than drug-resistant tumor samples. Further studies found that T cell function has a low correlation with tumor growth, and there are obvious obstacles in the process of peripheral blood immune cells entering the tumor microenvironment. In summary, this study provided clues for understanding the clinical drug resistance of HER2 monoclonal antibody and the clinical rational use of drugs and combination drugs.

乳腺癌被认为是一种病理机制复杂、临床分型多样的易发乳腺肿瘤。在对HER2阳性肿瘤患者的临床治疗中,以赫赛汀为代表的HER2单克隆抗体显示出了良好的治疗效果。然而,由于乳腺癌的异质性,赫赛汀在应用过程中不可避免地出现了耐药性。为了全面了解敏感和不敏感患者人群肿瘤微环境的免疫耐受状态,本研究通过 Luminex 细胞因子检测、临床病理分析、免疫荧光和 PCR 等方法进行了一系列研究。结果证实,对赫赛汀敏感的临床样本中存在大量巨噬细胞,巨噬细胞相关趋化因子和炎症介质的蛋白表达水平和原位表达明显高于耐药肿瘤样本。进一步研究发现,T 细胞功能与肿瘤生长相关性较低,外周血免疫细胞进入肿瘤微环境过程中存在明显障碍。总之,这项研究为了解HER2单克隆抗体的临床耐药性以及临床合理用药和联合用药提供了线索。
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引用次数: 0
Mangifera indica L. kernel ethanol extract inhibits cell viability and proliferation with induction of cell cycle arrest and apoptosis in lung cancer cells. 芒果核乙醇提取物可抑制肺癌细胞的活力和增殖,并诱导细胞周期停滞和凋亡。
IF 2.1 Q3 ONCOLOGY Pub Date : 2024-01-04 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2023.2299046
Hussah Abdullah Alshwyeh, Warqaa Muhammed Shariff Al-Sheikh, Abdullah Rasedee, Sulaiman Mohammed Alnasser, Mothanna Sadiq Al-Qubaisi, Wisam Nabeel Ibrahim

In this study, we investigated the effects of an ethanolic extract of Mangifera indica L. kernel on the viability and proliferation of human lung cancer cells. We utilized MTT and BrdU cell proliferation assays, morphological assessments, cell cycle analyses, and apoptosis assays to investigate the extract's effects on lung cancer (A549 and NCI-H292) and normal lung (MRC-5) cells. The extract demonstrated a toxicity toward cancer cells compared to normal cells with dose-dependent anti-proliferative effect on lung cancer cells. The extract also caused differential effects on the cell cycle, inducing G0/G1 arrest and increasing the Sub-G1 population in both lung cancer and normal lung cells. Notably, the extract induced loss of membrane integrity, shrinkage, membrane blebbing, and apoptosis in lung cancer cells, while normal cells exhibited only early apoptosis. Furthermore, the extract exhibited higher toxicity towards NCI-H292 cells, followed by A549 and normal MRC-5 cells in decreasing order of potency. Our results suggest that the ethanolic extract of M. indica L. kernel has significant potential as a novel therapeutic agent for treating lung cancer cells, given its ability to induce apoptosis in cancer cell lines while causing minimal harm to normal cells.

在这项研究中,我们研究了芒果核乙醇提取物对人类肺癌细胞活力和增殖的影响。我们利用 MTT 和 BrdU 细胞增殖试验、形态学评估、细胞周期分析和细胞凋亡试验,研究了萃取物对肺癌细胞(A549 和 NCI-H292)和正常肺细胞(MRC-5)的影响。与正常细胞相比,萃取物对癌细胞具有毒性,对肺癌细胞具有剂量依赖性的抗增殖作用。该提取物还对细胞周期产生了不同的影响,在肺癌细胞和正常肺细胞中都能诱导 G0/G1 停滞,并增加 Sub-G1 群体。值得注意的是,该提取物能诱导肺癌细胞膜完整性丧失、萎缩、膜出血和凋亡,而正常细胞仅表现出早期凋亡。此外,该提取物对 NCI-H292 细胞的毒性较高,其次是 A549 和正常的 MRC-5 细胞,毒性依次递减。我们的研究结果表明,M. indica L. 果仁乙醇提取物具有诱导癌细胞凋亡的能力,同时对正常细胞的伤害极小,因此具有作为治疗肺癌细胞的新型治疗剂的巨大潜力。
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引用次数: 0
The developmental gene Chordin is amplified and expressed in human cancers. 发育基因 Chordin 在人类癌症中被扩增和表达。
IF 2.1 Q3 ONCOLOGY Pub Date : 2023-05-29 eCollection Date: 2023-01-01 DOI: 10.1080/23723556.2023.2218147
Eric Sosa, Edward M De Robertis

Chordin (CHRD) is a secreted protein important in early development, yet a role for CHRD in human disease has not been identified. In this study we investigated CHRD in cancer and normal adult tissues using the wealth of genome-wide data available in public databases. We found that Chordin is amplified in the DNA of specific cancers such as lung squamous cell and others, although copy number variation did not strictly correlate with higher mRNA expression. In some cancers, such as renal and stomach carcinomas, increased CHRD expression significantly correlated with poor survival. In normal adult human tissues, CHRD mRNA was highest in hepatocytes. Crossveinless-2/BMPER, a component of the Chordin morphogenetic pathway expressed at the opposite side in embryos, was expressed in liver stellate cells. This raises the intriguing possibility that a BMP gradient might be established in the extracellular matrix of the space of Disse that surrounds portal sinusoid capillaries.

Chordin(CHRD)是一种对早期发育很重要的分泌蛋白,但它在人类疾病中的作用尚未确定。在这项研究中,我们利用公共数据库中丰富的全基因组数据,研究了癌症和正常成人组织中的 CHRD。我们发现,Chordin 在肺鳞癌等特定癌症的 DNA 中被扩增,尽管拷贝数变异与较高的 mRNA 表达并无严格关联。在某些癌症(如肾癌和胃癌)中,CHRD表达的增加与生存率低有显著相关性。在正常成人人体组织中,CHRD mRNA 在肝细胞中含量最高。Crossveinless-2/BMPER是Chordin形态发生途径的一个组成部分,在胚胎中表达在另一侧,但在肝星状细胞中也有表达。这就提出了一个耐人寻味的可能性,即在环绕门窦毛细血管的Disse空间的细胞外基质中可能建立了BMP梯度。
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引用次数: 0
Silencing Glypican-1 enhances the antitumor effects of Pictilisib via downregulating PI3K/Akt/ERK signaling in chemo-resistant esophageal adenocarcinoma. 沉默Glypican-1可通过下调PI3K/Akt/ERK信号通路增强Pictilisib在化疗耐药食管腺癌中的抗肿瘤作用。
IF 2.1 Q3 ONCOLOGY Pub Date : 2023-01-01 DOI: 10.1080/23723556.2023.2238873
Akshay Pratap, Andrea Qualman, Hedlund Garrett, Lindsey Westbrook, Erlinda The, Sanchayita Mitra, Mila Cordero, Kenneth Meza Monge, Juan-Pablo Idrovo, Argudit Chauhan, Linling Cheng, Mitchell Jay Cohen, Benedetto Mungo, Sachin Wani, Robert Alexander Meguid, Martin D McCarter, Xianzhong Meng

Poorly differentiated esophageal adenocarcinoma (PDEAC) has a dismal prognosis. Glypican-1(GPC-1) is known to be upregulated in several cancer types in contrast to healthy tissues, rendering it as a biomarker. Nevertheless, the potential therapeutic targeting of GPC-1 has not been explored in PDEAC. There is accumulating evidence that GPC-1, via upregulation of PI3K/Akt/ERK signaling, plays a crucial role in the progression and chemoresistance in cancer. Pictilisib, a class I pan PI3K inhibitor, has shown promising antitumor results in clinical trials, however, has not gained widespread success due to acquired drug resistance. This study investigated the role of GPC-1 in chemo-resistant PDEAC and appraises the impact of targeted silencing of GPC-1 on the antitumor effects of Pictilisib in PDEAC cell lines. Immunohistochemistry assays in PDEAC tissue specimens demonstrated a pronounced intensity of staining with GPC-1. Upregulation of GPC-1 was found to be correlated with advanced stage and poor prognosis. In-vitro studies examined the influence of GPC-1 knockdown and Pictilisib, both as individual agents and in combination, on cytotoxicity, cell cycle distribution, apoptosis, and gene expression profiles. Silencing GPC-1 alone showed significantly reduced cell viability, migration, colony formation, epithelial-mesenchymal transition, and stemness in PDEAC cells. Significantly, knockdown of GPC-1 combined with low-dose Pictilisib led to enhancement of cytotoxicity, cell cycle arrest, and apoptosis in ESO-26 and OE-33 cells. In the xenograft mouse model, the combination of Pictilisib and GPC-1 knockdown exhibited synergy. These findings suggest that GPC-1 represents a promising target to augment chemosensitivity in esophageal adenocarcinoma.

低分化食管腺癌(PDEAC)预后差。已知与健康组织相比,Glypican-1(GPC-1)在几种癌症类型中上调,使其成为一种生物标志物。然而,GPC-1在PDEAC中的潜在治疗靶点尚未被探索。越来越多的证据表明,GPC-1通过上调PI3K/Akt/ERK信号,在癌症的进展和化疗耐药中起着至关重要的作用。Pictilisib是一类泛PI3K抑制剂,在临床试验中显示出良好的抗肿瘤效果,但由于获得性耐药,尚未获得广泛成功。本研究探讨了GPC-1在耐药PDEAC中的作用,并评价了靶向沉默GPC-1对Pictilisib在PDEAC细胞系中抗肿瘤作用的影响。PDEAC组织标本的免疫组化分析显示GPC-1染色强度明显。GPC-1表达上调与晚期及不良预后相关。体外研究检测了GPC-1敲低和Pictilisib对细胞毒性、细胞周期分布、细胞凋亡和基因表达谱的影响,无论是单独使用还是联合使用。单独沉默GPC-1可显著降低PDEAC细胞的细胞活力、迁移、集落形成、上皮-间质转化和干性。值得注意的是,GPC-1的下调与低剂量Pictilisib联合可增强ESO-26和OE-33细胞的细胞毒性、细胞周期阻滞和凋亡。在异种移植小鼠模型中,Pictilisib和GPC-1敲低的组合表现出协同作用。这些发现表明GPC-1是一个有希望的靶点,可以增强食管腺癌的化疗敏感性。
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引用次数: 1
Metagenomic insights into the plasma virome of Brazilian patients with prostate cancer. 巴西前列腺癌患者血浆病毒的宏基因组研究。
IF 2.1 Q3 ONCOLOGY Pub Date : 2023-01-01 DOI: 10.1080/23723556.2023.2188858
Dalila Luciola Zanette, Karoline Brito Caetano Andrade Coelho, Eneas de Carvalho, Mateus Nobrega Aoki, Jeanine Marie Nardin, Larissa Araújo Lalli, Rafael Dos Santos Bezerra, Marta Giovanetti, Victória Simionatto Zucherato, Gabriel Montenegro de Campos, Jardelina de Souza Todão Bernardino, Vincent Louis Viala, Massimo Ciccozzi, Luiz Carlos Junior Alcantara, Sandra Coccuzzo Sampaio, Maria Carolina Elias, Simone Kashima, Dimas Tadeu Covas, Svetoslav Nanev Slavov

Growing evidence suggests that metavirome changes could be associated increased risk for malignant cell transformation. Considering Viruses have been proposed as factors for prostate cancer induction. The objective of this study was to examine the composition of the plasma metavirome of patients with prostate cancer. Blood samples were obtained from 49 male patients with primary prostate adenocarcinoma. Thirty blood donors were included as a control group. The obtained next-generation sequencing data were analyzed using a bioinformatic pipeline for virus metagenomics. Viral reads with higher abundance were assembled in contigs and analyzed taxonomically. Viral agents of interest were also confirmed by qPCR. Anelloviruses and the Human Pegivirus-1 (HPgV-1) were the most abundant component of plasma metavirome. Clinically important viruses like hepatitis C virus (HCV), cytomegalovirus and human adenovirus type C were also identified. In comparison, the blood donor virome was exclusively composed of torque teno virus types (TTV) types. The performed HPgV-1 and HCV phylogeny revealed that these viruses belong to commonly detected in Brazil genotypes. Our study sheds light on the plasma viral abundance in patients with prostatic cancer. The obtained viral diversity allowed us to separate the patients and controls, probably suggesting that malignant processes may influence virome composition. More complex and multiple approach investigations are necessary to examine the likely causal relationship between metavirome and its nvolvement in prostate cancer.

越来越多的证据表明,转移病毒的改变可能与恶性细胞转化的风险增加有关。考虑到病毒被认为是诱发前列腺癌的因素。本研究的目的是检查前列腺癌患者血浆中转移病毒的组成。本文采集了49例男性原发性前列腺癌患者的血液样本。30名献血者作为对照组。获得的下一代测序数据使用病毒宏基因组学生物信息学管道进行分析。将高丰度的病毒序列组装成contigs并进行分类分析。qPCR也证实了感兴趣的病毒因子。Anelloviruses和Human Pegivirus-1 (HPgV-1)是血浆病毒组中最丰富的成分。临床重要的病毒如丙型肝炎病毒(HCV)、巨细胞病毒和C型人腺病毒也被鉴定出来。相比之下,献血者病毒组完全由扭力病毒型(TTV)型组成。HPgV-1和HCV的系统发育表明,这两种病毒属于巴西常见的基因型。我们的研究揭示了前列腺癌患者的血浆病毒丰度。获得的病毒多样性使我们能够将患者和对照组分开,这可能表明恶性过程可能影响病毒组成。需要更复杂和多途径的研究来检验转移病毒及其参与前列腺癌之间可能的因果关系。
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引用次数: 0
The identification of key genes and pathways in glioblastoma by bioinformatics analysis. 胶质母细胞瘤关键基因及通路的生物信息学分析。
IF 2.1 Q3 ONCOLOGY Pub Date : 2023-01-01 DOI: 10.1080/23723556.2023.2246657
Zahra Farsi, Najaf Allahyari Fard

GBM is the most common and aggressive type of brain tumor. It is classified as a grade IV tumor by the WHO, the highest grade. Prognosis is generally poor, with most patients surviving only about a year. Only 5% of patients survive longer than 5 years. Understanding the molecular mechanisms that drive GBM progression is critical for developing better diagnostic and treatment strategies. Identifying key genes involved in GBM pathogenesis is essential to fully understand the disease and develop targeted therapies. In this study two datasets, GSE108474 and GSE50161, were obtained from the Gene Expression Omnibus (GEO) to compare gene expression between GBM and normal samples. Differentially expressed genes (DEGs) were identified and analyzed. To construct a protein-protein interaction (PPI) network of the commonly up-regulated and down-regulated genes, the STRING 11.5 and Cytoscape 3.9.1 were utilized. Key genes were identified through this network analysis. The GEPIA database was used to confirm the expression levels of these key genes and their association with survival. Functional and pathway enrichment analyses on the DEGs were conducted using the Enrichr server. In total, 698 DEGs were identified, consisting of 377 up-regulated genes and 318 down-regulated genes. Within the PPI network, 11 key up-regulated genes and 13 key down-regulated genes associated with GBM were identified. NOTCH1, TOP2A, CD44, PTPRC, CDK4, HNRNPU, and PDGFRA were found to be important targets for potential drug design against GBM. Additionally, functional enrichment analysis revealed the significant impact of Epstein-Barr virus (EBV), Cell Cycle, and P53 signaling pathways on GBM.

GBM是最常见、最具侵袭性的脑肿瘤。世界卫生组织将其列为IV级肿瘤,这是最高级别的肿瘤。预后通常很差,大多数患者只能存活一年左右。只有5%的患者存活超过5年。了解驱动GBM进展的分子机制对于制定更好的诊断和治疗策略至关重要。确定参与GBM发病机制的关键基因对于充分了解该疾病并开发靶向治疗至关重要。本研究从Gene Expression Omnibus (GEO)中获得GSE108474和GSE50161两个数据集,比较GBM和正常样本的基因表达。鉴定并分析差异表达基因(DEGs)。利用STRING 11.5和Cytoscape 3.9.1构建常见上调和下调基因的蛋白-蛋白相互作用(PPI)网络。通过网络分析确定了关键基因。GEPIA数据库用于确认这些关键基因的表达水平及其与生存的关系。使用enrichment服务器对deg进行功能和途径富集分析。共鉴定出698个基因,其中上调基因377个,下调基因318个。在PPI网络中,鉴定出与GBM相关的11个关键上调基因和13个关键下调基因。NOTCH1、TOP2A、CD44、PTPRC、CDK4、HNRNPU和PDGFRA被发现是潜在的抗GBM药物设计的重要靶点。此外,功能富集分析显示eb病毒(EBV)、细胞周期和P53信号通路对GBM有显著影响。
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引用次数: 0
YES, a novel therapeutic target in hepatocellular carcinoma YES,一种新的肝细胞癌治疗靶点
IF 2.1 Q3 ONCOLOGY Pub Date : 2022-05-01 DOI: 10.1080/23723556.2022.2069993
Marjorie Lapouge, S. Meloche
ABSTRACT Identification of dominant, actionable oncogenic signaling pathways is key to guide the development of new targeted treatments for advanced-stage hepatocellular carcinoma (HCC). We have recently unveiled a novel YES-YAP/TAZ signaling axis involved in liver cancer development. Our study identifies the tyrosine kinase YES as a potential therapeutic target in HCC.
摘要:识别显性、可操作的致癌信号通路是指导晚期肝细胞癌(HCC)新靶向治疗方法开发的关键。我们最近公布了一种新型的YES-YAP/TAZ信号轴,它与癌症的发展有关。我们的研究确定酪氨酸激酶YES是HCC的潜在治疗靶点。
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引用次数: 1
How often is each gene mutated within the cancer patient population? 在癌症患者群体中,每种基因突变的频率是多少?
IF 2.6 Q3 ONCOLOGY Pub Date : 2022-05-01 eCollection Date: 2022-01-01 DOI: 10.1080/23723556.2022.2065176
Gaurav Mendiratta, Michael K Jones, Edward C Stites

Genome sequenced samples from cancer patients helped identify roles of different mutation types and enabled targeted therapy development. However, critical questions like what are the gene mutation rates among the patients? or what genes are most commonly mutated, pan-cancer? have only been recently answered. Here, we highlight this recent advance.

癌症患者的基因组测序样本有助于确定不同突变类型的作用,并促进靶向疗法的开发。然而,诸如患者的基因突变率是多少、哪些基因是泛癌症中最常见的突变基因等关键问题直到最近才有了答案。在此,我们将重点介绍这一最新进展。
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引用次数: 0
MAPK signaling regulates the efficacy of chemoimmunotherapy MAPK信号调节化学免疫治疗的疗效
IF 2.1 Q3 ONCOLOGY Pub Date : 2022-04-27 DOI: 10.1080/23723556.2022.2054652
F. Ghiringhelli
ABSTRACT Resistance to chemoimmunotherapy is a major issue for cancer care. We recently unravelled the role of mitogen-activated protein kinase (MAPK) to limit the antitumor efficacy of such combination. Inhibitor of MAPK pathway using mitogen-activated protein kinase (MEK) inhibitor in combination with chemotherapy triggers mitophagy of cancer cells, which induces the release of mitochondrial DNA that interact with Toll Like receptor 9 (TLR9) to promote the production of the chemokine CXCL10. CXCL10 could then turn cold tumor into hot tumor, thus leading to improve efficacy of chemoimmunotherapy.
化疗免疫治疗的耐药是癌症治疗的一个主要问题。我们最近揭示了丝裂原活化蛋白激酶(MAPK)的作用,以限制这种组合的抗肿瘤疗效。使用丝裂原活化蛋白激酶(MEK)抑制剂联合化疗抑制MAPK通路,触发癌细胞的有丝分裂,诱导线粒体DNA的释放,与Toll样受体9 (TLR9)相互作用,促进趋化因子CXCL10的产生。CXCL10可以将冷肿瘤转化为热肿瘤,从而提高化学免疫治疗的疗效。
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引用次数: 0
CircZNF609 as a prototype to elucidate the biological function of circRNA-mRNA interactions CircZNF609作为原型来阐明circRNA-mRNA相互作用的生物学功能
IF 2.1 Q3 ONCOLOGY Pub Date : 2022-04-11 DOI: 10.1080/23723556.2022.2055939
M. Beltran, F. Rossi, I. Bozzoni
ABSTRACT Circular RNAs (circRNAs) are expressed and are regulated in many biological processes but little is known about their ability to directly control mRNA homeostasis. We show that circRNA zinc finger protein 609 (circZNF609) interacts with several mRNAs increasing the final protein levels, which in the case of the cytoskeleton-associated protein 5 (CKAP5) leads to a stabilized microtubule cytoskeleton and an enhanced tumor cell proliferation.
环状rna (circRNAs)在许多生物过程中表达和调控,但对其直接控制mRNA稳态的能力知之甚少。我们发现circRNA锌指蛋白609 (circZNF609)与几种mrna相互作用,增加最终蛋白水平,在细胞骨架相关蛋白5 (CKAP5)的情况下,导致稳定的微管细胞骨架和增强的肿瘤细胞增殖。
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引用次数: 3
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Molecular and Cellular Oncology
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