Cancer treatment and research communications最新文献_第4页

Understanding Patient and Oncologist Preferences in the Management of Metastatic Renal Cell Carcinoma 了解患者和肿瘤学家在转移性肾细胞癌治疗中的偏好。

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2025.101067

Omid Yazdanpanah , Aditya Mahadevan , David J. Benjamin , Elham Vosoughi , Ali Raad , Madina Popal , Piyanuch Kongtim , Nataliya Mar , Arash Rezazadeh Kalebasty

Introduction

Treatment of metastatic renal cell carcinoma (mRCC) has expanded with development of combination therapies containing tyrosine kinase inhibitors (TKIs) with immune checkpoint inhibitors (ICI) agents or dual ICI agents. However, patient preferences may not necessarily be incorporated into management decisions. We aimed to understand patient preferences in the management of mRCC and compare it with oncologists’ perspectives.

Methods

A single-arm, prospective study surveyed patients with mRCC utilizing a questionnaire containing descriptions of 5 treatment options in simple language. Patients rated their preference for each option on a scale from 1 (least preferred) to 10 (most preferred). The same questionnaire plus basic de-identified patients' characteristics were provided to 2 academic oncologists and 1 community oncologist.

Results

A total of 54 patients were surveyed. The most preferred patient treatment option was TKI with mean score of 7.9 while the least popular was early phase clinical trials (CTs) with a mean score of 5.9 (p < 0.01). Patient’s employment status, speaking language, and denovo metastatic disease were the variables found to be associated with likelihood of picking a particular treatment option. Among oncologists, the most selected treatment options were enrollment in early and late phase CTs with mean scores of 7.61 and 7.52 respectively and single-agent TKI was least preferred with a mean score of 5.69 (p < 0.01). Age and performance status influenced oncologist therapy choices based on the multivariable analysis.

Conclusions

This study unveils differences between patients and oncologists’ treatment preferences for mRCC and underscores the importance of individualized discussion with each patient to evaluate his or her therapeutic objectives.

随着酪氨酸激酶抑制剂（TKIs）与免疫检查点抑制剂（ICI）药物或双重ICI药物的联合治疗的发展，转移性肾细胞癌（mRCC）的治疗已经扩大。然而，患者的偏好可能不一定会纳入管理决策。我们旨在了解患者对mRCC管理的偏好，并将其与肿瘤学家的观点进行比较。方法：一项单臂前瞻性研究对mRCC患者进行了问卷调查，问卷用简单的语言描述了5种治疗方案。患者对每种选择的偏好从1（最不喜欢）到10（最喜欢）进行评分。2名学术肿瘤学家和1名社区肿瘤学家提供了相同的问卷和基本的未识别患者特征。结果：共调查54例患者。患者最喜欢的治疗方案是TKI，平均评分为7.9分，而最不受欢迎的是早期临床试验（CTs），平均评分为5.9分（p < 0.01）。患者的就业状况、说话语言和复发转移性疾病是与选择特定治疗方案的可能性相关的变量。在肿瘤学家中，最受欢迎的治疗方案是早期和晚期ct的纳入，平均评分分别为7.61和7.52，最不受欢迎的是单药TKI，平均评分为5.69 （p < 0.01）。基于多变量分析，年龄和体能状况影响肿瘤医生的治疗选择。结论：本研究揭示了患者和肿瘤学家对mRCC治疗偏好的差异，并强调了与每位患者进行个性化讨论以评估其治疗目标的重要性。

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引用次数: 0

Treatments and survival outcomes of patients with synchronous and metachronous metastatic bladder cancer: A population-based nationwide cohort study 同步和异时转移性膀胱癌患者的治疗和生存结果：一项基于人群的全国队列研究

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101099

Anke Richters , Mira D. Franken , Richard P. Meijer , Antoine G. van der Heijden , ProBCI Study Group, Franchette W.P.J. van den Berkmortel , Katja K.H. Aben

Objective

To describe and compare clinicopathological characteristics, treatment patterns and overall survival outcomes of contemporary patients diagnosed with synchronous (smBC) or metachronous metastatic bladder cancer (mmBC) in the Netherlands.

Methods

All patients newly diagnosed with bladder cancer in the Netherlands in 2020–2023 were identified through the Netherlands Cancer Registry. The smBC group consisted of patients with mBC at initial diagnosis in 2020 – 2023. The mmBC group included all patients who developed metastatic disease <3 years after being diagnosed with muscle-invasive bladder cancer (MIBC) between January 2020 – June 2022 and was stratified into early (≤6 months) and late mmBC (>6 months). Vital status was available until January 2025.

Results

The cohort included 2375 patients (1584 smBC, 371 early mmBC and 420 late mmBC). Lung and liver metastases were equally common across subcohorts; visceral disease was more common among mmBC patients. Less than half of patients received systemic therapy in all subcohorts (carboplatin most common for smBC and late mmBC patients; immunotherapy for early mmBC patients). Median OS regardless of treatment was 4.6, 3.9 and 7.4 months for smBC, early mmBC and late mmBC patients, respectively. Among those who received systemic treatment, median OS was 11.8, 8.5 and 12.6 months. Median OS differences were smaller when further restricting to systemic treatment-naïve patients.

Conclusions

Patient populations with smBC and early and late mmBC showed moderate differences in patient or disease characteristics that may be of clinical relevance. Many patients were unable to receive systemic treatment, with only small differences between groups, resulting from prior treatment, emphasizing the unmet need among both smBC and mmBC patients. Patients with mBC have a poor prognosis, irrespective of time to metastasis with limited OS differences.

目的描述和比较荷兰同步（smBC）或异时性转移性膀胱癌（mmBC）患者的临床病理特征、治疗模式和总体生存结果。方法2020-2023年荷兰所有新诊断为膀胱癌的患者均通过荷兰癌症登记处确定。smBC组由2020 - 2023年首次诊断为mBC的患者组成。mmBC组包括所有在2020年1月至2022年6月期间被诊断为肌肉浸润性膀胱癌（MIBC）后3年内发生转移性疾病的患者，并分为早期（≤6个月）和晚期mmBC（≤6个月）。关键状态一直保留到2025年1月。结果该队列包括2375例患者（smBC 1584例，早期mmBC 371例，晚期mmBC 420例）。肺和肝转移在亚队列中同样常见；内脏疾病在mmBC患者中更为常见。在所有亚组中，不到一半的患者接受了全身治疗（卡铂最常见于smBC和晚期mmBC患者；免疫治疗用于早期mmBC患者）。smBC、早期mmBC和晚期mmBC患者不考虑治疗的中位OS分别为4.6、3.9和7.4个月。在接受全身治疗的患者中，中位OS分别为11.8、8.5和12.6个月。当进一步局限于全身性treatment-naïve患者时，中位OS差异较小。结论smBC患者群体与早期和晚期mmBC患者群体在患者或疾病特征上存在中度差异，可能具有临床相关性。许多患者无法接受全身治疗，组间差异很小，这是由于既往治疗所致，强调了smBC和mmBC患者的需求未得到满足。与转移时间无关，mBC患者预后较差，OS差异有限。

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引用次数: 0

Synergistic regulation of tumor angiogenesis via flavonoid modulation of lncRNAs: Mechanistic insights and therapeutic potential 通过类黄酮调节lncRNAs对肿瘤血管生成的协同调节：机制见解和治疗潜力

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101114

Akanksha Gupta , G.S.N. Koteswara Rao , Hardeep Singh Tuli , Ginpreet Kaur , Pallavi Mishra , Shafiul Haque

Angiogenesis is a hallmark process of tumor growth, metastatic progression, and therapeutic resistance. The role of long noncoding RNAs (lncRNAs) in the regulation of angiogenesis has emerged as a critical factor influencing cancer progression. Flavonoids are natural polyphenolic compounds known for antioxidant and anti-inflammatory activities and have been recognized for their potential to regulate epigenetic and transcriptional networks involved in angiogenesis. This review seems to incorporate recent experimental evidence supporting that flavonoids such as quercetin, luteolin, curcumin, and resveratrol modulate angiogenesis-related lncRNAs (MALAT1, HOTAIR, PVT1, MEG3), leading to the inhibition of VEGF/HIF-1α, PI3K/Akt/mTOR, and NF-κB signaling pathways, which reduces endothelial proliferation and neovascularization. The recent advances in flavonoid bioavailability through nanoformulation, like liposomes, PLGA nanoparticles, and phytosomes, result in increased tumor specificity and more precise delivery. The quantitative evidence from numerous in vitro and in vivo studies has consistently demonstrated that flavonoid lncRNA modulation leads to a significant reduction in micro vessel density, expression of VEGF, and tumor burden. Improved bioavailability with more advanced nanoformulation and enhancement in preclinical validation of flavonoid lncRNA therapeutics, despite the remaining challenges like limited clinical data and off-target effects, offer low-toxicity targeted means of reprogramming tumor angiogenesis and overcoming resistance to the current therapies.

血管生成是肿瘤生长、转移进展和治疗抵抗的一个标志性过程。长链非编码rna （lncRNAs）在血管生成调控中的作用已成为影响癌症进展的关键因素。黄酮类化合物是一种天然多酚类化合物，具有抗氧化和抗炎活性，并因其调节血管生成的表观遗传和转录网络的潜力而得到认可。这篇综述似乎结合了最近的实验证据，支持类黄酮如槲皮素、木草素、姜黄素和白藜芦醇调节血管生成相关的lncRNAs (MALAT1、HOTAIR、PVT1、MEG3)，从而抑制VEGF/HIF-1α、PI3K/Akt/mTOR和NF-κB信号通路，从而减少内皮细胞增殖和新生血管形成。近年来，通过脂质体、PLGA纳米颗粒和磷脂质体等纳米制剂，类黄酮生物利用度的研究取得了新的进展，从而增加了肿瘤特异性和更精确的给药。大量体外和体内研究的定量证据一致表明，黄酮类lncRNA调节导致微血管密度、VEGF表达和肿瘤负荷显著降低。尽管存在临床数据有限和脱靶效应等挑战，但通过更先进的纳米配方和增强黄酮类lncRNA治疗方法的临床前验证，提高了生物利用度，为肿瘤血管生成重编程和克服对当前治疗方法的耐药性提供了低毒性的靶向手段。

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引用次数: 0

Dual-jet transition cold atmospheric plasma suppresses colon cancer stem cells via matrix metalloproteinase regulation 双射流过渡冷大气等离子体通过基质金属蛋白酶调控抑制结肠癌干细胞。

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101096

Abolfazl Soulat , Taghi Mohsenpour , Leila Roshangar

Colon cancer stem cells (CCSCs) are critical drivers of tumor progression, metastasis, and therapeutic resistance, largely mediated by matrix metalloproteinases (MMPs). This study investigates the therapeutic potential of a novel dual-jet transition cold atmospheric plasma (DJTCAP) system to modulateMMP expression and reduce CCSC viability. HT29-derived CCSCs were cultured in 3D Matrigel and exposed to three sequential plasma jets generated by a custom DJTCAP device, applied either via direct irradiation or plasma-activated medium for 120- or 240-seconds using helium or argon.MMP-1, -2, -3, -7, -9, and -14 expression was measured by RT-PCR, and cell viability was assessed using the MTT assay. DJTCAP treatment significantly downregulated allMMPs (p < 0.0001), with the most pronounced effects and cytotoxicity observed following 240-second helium exposure, which consistently outperformed argon. Plasma diagnostics confirmed efficient energy utilization (<1 W) and high generation of reactive oxygen and nitrogen species (RONS), suggesting a RONS-mediated mechanism of action. These results demonstrate that DJTCAP selectively suppressesMMP expression and reduces CCSC viability, highlighting its potential as a safe, energy-efficient, and targeted therapy for metastatic and treatment-resistant colorectal cancer.

结肠癌干细胞（CCSCs）是肿瘤进展、转移和治疗耐药性的关键驱动因素，主要由基质金属蛋白酶（MMPs）介导。本研究探讨了一种新型双射流过渡冷大气等离子体（DJTCAP）系统调节atemmp表达和降低CCSC活力的治疗潜力。ht29衍生的CCSCs在3D Matrigel中培养，并暴露于由定制的DJTCAP装置产生的三个连续等离子体射流中，通过直接照射或等离子体激活介质使用氦气或氩气进行120或240秒。RT-PCR检测MMP-1、-2、-3、-7、-9和-14的表达，MTT法检测细胞活力。DJTCAP处理显著下调了所有mmps (p < 0.0001)，在240秒的氦暴露后观察到最明显的效果和细胞毒性，一直优于氩气。等离子体诊断证实能源利用效率高(

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引用次数: 0

Coconut milk exosomal formulation of curcumin analog targets head and neck cancer progression through alterations in the HABP1 signaling mechanism 姜黄素类似物的椰奶外泌体配方通过改变HABP1信号机制靶向头颈癌的进展

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101102

Kaumudi Pande , Bettadaiah B K , Anbarasu Kannan

Background

Head and neck cancer (HNC) is a malignancy characterized by uncontrolled cell growth with increasing incidence rates and heterogeneity. Hyaluronan binding protein 1 (HABP1) is a glycoprotein that acts as a cell surface marker, influencing the immune tumor environment, and is overexpressed in various epithelial tumors. The role of HABP1 in HNC remains to be investigated. Exosome therapy has emerged as a promising treatment that delivers anticancer compounds directly to tumor sites. Coconut milk is considered a valuable therapeutic agent against cancer. Curcumin Analog Isoleucine (CAI) exhibits better solubility, improved antioxidant properties, and greater antimutagenic effects than curcumin. In the study, we emphasized on exosomal delivery of CAI to affect HABP1 signaling for effective cancer therapy.

Methods

The study focused on the isolation and characterization of tender coconut milk-derived exosomes. Exosomal formulation was developed by loading tender coconut milk-derived exosomes with CAI (TC EXO+CAI) through the sonication method. Bioaccessibility assessment was executed for the TC EXO+CAI along with the MTT assay, morphology, nucleus shape, colony formation, AO-EtBr assays, western blot, and gene expression analysis.

Results

The bioaccessibility of TC EXO+CAI was greater than that of CAI or curcumin. TC EXO+CAI was cytotoxic to HNC cells at a lower IC50 value, indicating effective CAI delivery by exosomes. It causes cell shrinkage, nuclear condensation, fewer colonies, and an increased number of apoptotic HNC cells. It reduced the expression levels of HABP1 and associated molecules in HNC cells. The uptake of TC EXO+CAI by HNC cells increases the expression of p53 and caspases, which effectively activates the apoptosis mechanism.

Conclusion

TC EXO+CAI exhibits target-specific delivery, which affects tumor cell physiology by reducing HABP1 levels and prompting apoptosis in HNC cells.

背景头颈癌（HNC）是一种恶性肿瘤，其特点是细胞生长不受控制，发病率和异质性不断增加。透明质酸结合蛋白1 （HABP1）是一种糖蛋白，作为细胞表面标志物，影响免疫肿瘤环境，在各种上皮肿瘤中过表达。HABP1在HNC中的作用仍有待研究。外泌体疗法已成为一种有前途的治疗方法，可将抗癌化合物直接输送到肿瘤部位。椰奶被认为是一种有价值的抗癌治疗剂。姜黄素异亮氨酸（CAI）具有较姜黄素更好的溶解度、抗氧化性能和抗诱变效果。在这项研究中，我们强调CAI的外泌体递送影响HABP1信号以有效治疗癌症。方法对嫩椰奶源性外泌体进行分离鉴定。外泌体配方是通过超声法将幼嫩的椰奶衍生外泌体装载CAI （TC EXO+CAI）而开发的。对TC EXO+CAI进行生物可及性评估，同时进行MTT检测、形态学、细胞核形状、菌落形成、AO-EtBr检测、western blot和基因表达分析。结果TC EXO+CAI的生物可及性高于CAI和姜黄素。TC EXO+CAI在较低的IC50值下对HNC细胞具有细胞毒性，表明外泌体可以有效地递送CAI。它引起细胞收缩，核凝聚，菌落减少，HNC细胞凋亡数量增加。它降低了HNC细胞中HABP1及相关分子的表达水平。HNC细胞摄取TC EXO+CAI可增加p53和caspases的表达，有效激活凋亡机制。结论tc EXO+CAI具有靶向性，通过降低HABP1水平，促进HNC细胞凋亡影响肿瘤细胞生理。

{"title":"Coconut milk exosomal formulation of curcumin analog targets head and neck cancer progression through alterations in the HABP1 signaling mechanism","authors":"Kaumudi Pande , Bettadaiah B K , Anbarasu Kannan","doi":"10.1016/j.ctarc.2026.101102","DOIUrl":"10.1016/j.ctarc.2026.101102","url":null,"abstract":"<div><h3>Background</h3><div>Head and neck cancer (HNC) is a malignancy characterized by uncontrolled cell growth with increasing incidence rates and heterogeneity. Hyaluronan binding protein 1 (HABP1) is a glycoprotein that acts as a cell surface marker, influencing the immune tumor environment, and is overexpressed in various epithelial tumors. The role of HABP1 in HNC remains to be investigated. Exosome therapy has emerged as a promising treatment that delivers anticancer compounds directly to tumor sites. Coconut milk is considered a valuable therapeutic agent against cancer. Curcumin Analog Isoleucine (CAI) exhibits better solubility, improved antioxidant properties, and greater antimutagenic effects than curcumin. In the study, we emphasized on exosomal delivery of CAI to affect HABP1 signaling for effective cancer therapy.</div></div><div><h3>Methods</h3><div>The study focused on the isolation and characterization of tender coconut milk-derived exosomes. Exosomal formulation was developed by loading tender coconut milk-derived exosomes with CAI (TC EXO+CAI) through the sonication method. Bioaccessibility assessment was executed for the TC EXO+CAI along with the MTT assay, morphology, nucleus shape, colony formation, AO-EtBr assays, western blot, and gene expression analysis.</div></div><div><h3>Results</h3><div>The bioaccessibility of TC EXO+CAI was greater than that of CAI or curcumin. TC EXO+CAI was cytotoxic to HNC cells at a lower IC50 value, indicating effective CAI delivery by exosomes. It causes cell shrinkage, nuclear condensation, fewer colonies, and an increased number of apoptotic HNC cells. It reduced the expression levels of HABP1 and associated molecules in HNC cells. The uptake of TC EXO+CAI by HNC cells increases the expression of p53 and caspases, which effectively activates the apoptosis mechanism.</div></div><div><h3>Conclusion</h3><div>TC EXO+CAI exhibits target-specific delivery, which affects tumor cell physiology by reducing HABP1 levels and prompting apoptosis in HNC cells.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"46 ","pages":"Article 101102"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146023105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pro-apoptotic effects of metformin and cisplatin in non-small cell Lung Cancer: Modulation of apoptosis-related genes and LncRNAs 二甲双胍和顺铂在非小细胞肺癌中的促凋亡作用：凋亡相关基因和lncrna的调节。

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2025.101069

Nazanin Sadeghi , Fatemeh Soleimanifar , Elmira Attar , Hamed Haddad Kashani , Romina Ghayoumi , Seyed-Alireza Etesami

Background

Lung cancer is a leading cause of cancer-related mortality. While cisplatin is a cornerstone of chemotherapy, metformin (Glucophage) has shown anti-cancer potential. This study investigated the effects of cisplatin and metformin (Glucophage) on non-small cell lung cancer (NSCLC) cells, focusing on their combined impact on apoptosis-related genes and lncRNAs.

Methods

The A549 (NSCLC) and MRC5 (normal fibroblast) cell lines were treated with cisplatin, metformin (Glucophage), or a combination thereof. Cell viability was assessed by MTT assay, and apoptosis was quantified by flow cytometry. Expression of Bax, Bcl-2, Caspase 3, PVT1, and MEG3 was analyzed by qRT-PCR.

Results

Both cisplatin and metformin (Glucophage) individually reduced A549 cell viability in a dose-dependent manner. Combination Index (CI) analysis revealed an additive interaction (CI = 0.935) between the two agents. This combination was associated with an upregulation of pro-apoptotic Bax and lncRNA MEG3, and a downregulation of anti-apoptotic Bcl-2 and oncogenic lncRNA PVT1.

Conclusion

The combination of cisplatin and metformin (Glucophage) exerts an additive cytotoxic effect and induces apoptosis in NSCLC cells in vitro. This effect is associated with a favorable modulation of key apoptosis-regulating genes and lncRNAs. These findings provide a strong rationale for further mechanistic and preclinical investigation of this combination therapy for lung cancer.

背景：肺癌是癌症相关死亡的主要原因。顺铂是化疗的基础，二甲双胍（Glucophage）已显示出抗癌潜力。本研究探讨顺铂和二甲双胍（Glucophage）对非小细胞肺癌（NSCLC）细胞的影响，重点关注它们对凋亡相关基因和lncrna的联合影响。方法：A549 （NSCLC）和MRC5（正常成纤维细胞）细胞系用顺铂、二甲双胍（Glucophage）或其联合治疗。MTT法检测细胞活力，流式细胞术检测细胞凋亡。采用qRT-PCR分析Bax、Bcl-2、Caspase 3、PVT1、MEG3的表达。结果：顺铂和二甲双胍（Glucophage）分别以剂量依赖的方式降低A549细胞活力。联合指数（CI）分析显示两剂之间存在加性相互作用（CI = 0.935）。这种组合与促凋亡的Bax和lncRNA MEG3的上调以及抗凋亡的Bcl-2和致癌的lncRNA PVT1的下调有关。结论：顺铂联合二甲双胍（Glucophage）对体外非小细胞肺癌细胞具有加性细胞毒作用，可诱导细胞凋亡。这种作用与关键凋亡调节基因和lncrna的有利调节有关。这些发现为进一步研究这种联合治疗肺癌的机制和临床前研究提供了强有力的依据。

{"title":"Pro-apoptotic effects of metformin and cisplatin in non-small cell Lung Cancer: Modulation of apoptosis-related genes and LncRNAs","authors":"Nazanin Sadeghi , Fatemeh Soleimanifar , Elmira Attar , Hamed Haddad Kashani , Romina Ghayoumi , Seyed-Alireza Etesami","doi":"10.1016/j.ctarc.2025.101069","DOIUrl":"10.1016/j.ctarc.2025.101069","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer is a leading cause of cancer-related mortality. While cisplatin is a cornerstone of chemotherapy, metformin (Glucophage) has shown anti-cancer potential. This study investigated the effects of cisplatin and metformin (Glucophage) on non-small cell lung cancer (NSCLC) cells, focusing on their combined impact on apoptosis-related genes and lncRNAs.</div></div><div><h3>Methods</h3><div>The A549 (NSCLC) and MRC5 (normal fibroblast) cell lines were treated with cisplatin, metformin (Glucophage), or a combination thereof. Cell viability was assessed by MTT assay, and apoptosis was quantified by flow cytometry. Expression of <em>Bax, Bcl-2, Caspase 3, PVT1</em>, and <em>MEG3</em> was analyzed by qRT-PCR.</div></div><div><h3>Results</h3><div>Both cisplatin and metformin (Glucophage) individually reduced A549 cell viability in a dose-dependent manner. Combination Index (CI) analysis revealed an additive interaction (CI = 0.935) between the two agents. This combination was associated with an upregulation of pro-apoptotic <em>Bax</em> and lncRNA <em>MEG3</em>, and a downregulation of anti-apoptotic <em>Bcl-2</em> and oncogenic lncRNA <em>PVT1</em>.</div></div><div><h3>Conclusion</h3><div>The combination of cisplatin and metformin (Glucophage) exerts an additive cytotoxic effect and induces apoptosis in NSCLC cells <em>in vitro</em>. This effect is associated with a favorable modulation of key apoptosis-regulating genes and lncRNAs. These findings provide a strong rationale for further mechanistic and preclinical investigation of this combination therapy for lung cancer.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"46 ","pages":"Article 101069"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145909962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-Coding RNAs in breast cancer bone metastasis: Regulators and novel therapeutic targets 乳腺癌骨转移中的非编码rna：调节因子和新的治疗靶点

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101100

Yuanqing Yang, Xiaobing Li, Yongqiang Yin

Bone metastasis is one of the most common complications in patients with advanced breast cancer, severely impairing quality of life and significantly increasing the risk of mortality. This process is driven by complex interactions between tumor cells and the bone microenvironment, where non-coding RNAs (ncRNAs) act as key regulatory molecules playing a central role. This article systematically reviews the expression changes, molecular mechanisms, and biological functions of microRNAs, long non-coding RNAs, and circular RNAs in breast cancer bone metastasis. Studies have demonstrated that these ncRNAs precisely regulate tumor cell colonization and proliferation in bone, osteoclast-mediated bone resorption, and osteoblast-mediated bone formation through multiple mechanisms — including competitive endogenous RNA networks, signaling pathway modulation, exosome-mediated intercellular communication, and even the encoding of functional short peptides — thereby disrupting bone homeostasis. Simultaneously, ncRNAs can also regulate the occurrence of bone metastasis by modulating the immune microenvironment in breast cancer. Furthermore, ncRNAs exhibit significant clinical translational potential in the early diagnosis, prognostic evaluation, and targeted therapy of breast cancer bone metastasis. By synthesizing the ncRNA regulatory networks, this review aims to provide a theoretical basis and research directions for further exploring the molecular mechanisms of breast cancer bone metastasis and developing novel therapeutic strategies.

骨转移是晚期乳腺癌患者最常见的并发症之一，严重影响生活质量，显著增加死亡风险。这一过程是由肿瘤细胞和骨微环境之间复杂的相互作用驱动的，其中非编码rna （ncRNAs）作为关键的调控分子发挥着核心作用。本文系统综述了microrna、长链非编码rna和环状rna在乳腺癌骨转移中的表达变化、分子机制和生物学功能。研究表明，这些ncRNAs通过多种机制——包括竞争性内源性RNA网络、信号通路调节、外泌体介导的细胞间通讯，甚至编码功能性短肽——精确调节肿瘤细胞在骨中的定植和增殖、破骨细胞介导的骨吸收和成骨细胞介导的骨形成，从而破坏骨稳态。同时，ncRNAs还可以通过调节乳腺癌的免疫微环境来调节骨转移的发生。此外，ncrna在乳腺癌骨转移的早期诊断、预后评估和靶向治疗中显示出显著的临床转化潜力。本文旨在通过对ncRNA调控网络的综合研究，为进一步探索乳腺癌骨转移的分子机制和开发新的治疗策略提供理论依据和研究方向。

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引用次数: 0

Yield of repeat gastric biopsies and Helicobacter pylori serological assessment in Lynch syndrome Lynch综合征重复胃活检产率及幽门螺杆菌血清学评估。

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2025.101081

Jessica Vadaketh , Jake Konigsberg , Omar Elghawy , Kevin Dinh , Linda Zhu , Julia Youngman , Michaela Dungan , Marya Pulaski , Jessica M. Long , Kole H. Buckley , Bryson W. Katona

Background

Upper gastrointestinal surveillance in Lynch syndrome (LS) remains an ongoing debate; some guidelines recommend upper endoscopy with non-targeted biopsies of the gastric antrum/body to detect Helicobacter pylori (HP) and/or gastric intestinal metaplasia (GIM). However, whether non-targeted gastric biopsies should be repeated on successive upper endoscopies remains uncertain. Therefore, we aimed to determine the yield of repeat non-targeted gastric antrum/body biopsies and assess the HP seropositivity of a LS cohort.

Methods

Clinical and pathology data were collected retrospectively from LS carriers who underwent upper endoscopy with non-targeted gastric biopsies. Plasma samples from a LS biobank were tested for HP IgG positivity.

Results

Amongst 683 LS carriers, there were 291 (43 %) with 1+, 145 (21 %) with 2+, and 45 (7 %) with 3+ upper endoscopies with non-targeted gastric antrum and body biopsies performed. The overall prevalence of GIM on those endoscopies was 8 % and the rate of HP was 3 %. Of individuals without GIM detected on the initial upper endoscopy, 4 % had GIM identified on their second, and 2 % had GIM identified on a third or greater upper endoscopy after having two prior upper endoscopies without GIM identified. There was no additional HP identified on subsequent endoscopies. Plasma HP IgG positivity amongst 257 LS carriers was 14 %.

Conclusions

Amongst a LS cohort undergoing serial upper endoscopies, repeat gastric antrum/body biopsies yielded new cases of GIM, providing support for consideration of non-targeted gastric biopsies on all upper endoscopies performed in LS. Additionally, although endoscopic HP detection rates are low, HP exposure in LS is more common.

背景：Lynch综合征（LS）的上胃肠道监测仍然是一个持续的争论；一些指南建议采用胃窦/胃体非靶向活检的上内镜检查来检测幽门螺杆菌（HP）和/或胃肠道化生（GIM）。然而，非靶向胃活检是否应该在连续的上胃镜检查中重复仍然不确定。因此，我们的目的是确定重复非靶向胃窦/身体活检的产量，并评估LS队列的HP血清阳性。方法：回顾性收集LS患者的临床和病理资料，这些患者接受了上胃镜检查和非靶向胃活检。对LS生物库的血浆样本进行HP IgG阳性检测。结果：683例LS携带者中，1+ 291例（43%），2+ 145例（21%），3+上胃镜检查45例（7%），非靶向胃窦和身体活检。在这些内窥镜检查中，GIM的总体患病率为8%，HP的患病率为3%。在首次上肢内窥镜检查未发现GIM的个体中，4%的人在第二次内窥镜检查中发现了GIM， 2%的人在两次未发现GIM的上肢内窥镜检查后在第三次或更多次内窥镜检查中发现了GIM。在随后的内窥镜检查中没有发现额外的HP。257例LS携带者血浆HP IgG阳性率为14%。结论：在接受一系列上胃镜检查的LS队列中，重复胃窦/体活检产生了新的GIM病例，这为考虑在LS患者进行的所有上胃镜检查中进行非靶向胃活检提供了支持。此外，尽管内窥镜HP检出率很低，但LS中HP暴露更为常见。

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引用次数: 0

OTUB1/SLC7A11 axis promoted AKT signaling activation to mediate ovarian cancer progression OTUB1/SLC7A11轴促进AKT信号激活介导卵巢癌进展

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101116

Yujin Zhang, Jing Wang, Sensen Sun, Wenyu Cao, Jinghui Ren, Wen Yang

Purpose

OTUB1 functions as a deubiquitinating enzyme (DUB) and has been reported to be associated with tumor progression. This study aimed to investigate the role of OTUB1 signaling in ovarian cancer progression.

Materials and Methods

Twenty-five patients diagnosed with ovarian cancer were enrolled and divided into groups based on tumor stage (high/low) and the presence or absence of lymphatic metastasis to analyze OTUB1 expression via Immunohistochemical (IHC) staining. Data from 578 ovarian cancer patients sourced from The Cancer Genome Atlas (TCGA) were downloaded for survival analysis. Cell proliferation and migration were evaluated using CCK8 and Transwell assays. Western blotting and immunostaining were performed to assess the activation of the OTUB1/SLC7A11/AKT signaling pathway.

Results

Our study found that OTUB1 expression was upregulated in ovarian cancer tissues and that higher expression was associated with poor prognosis, and more intriguingly, high-stage and lymph node metastasis ovarian cancer samples exhibited significantly elevated expression of OTUB1.Through in vitro experimental validation, OTUB1 overexpression in ovarian cancer cells promoted the increased cell proliferation, migration, and colony formation. Moreover, OTUB1 led to the upregulation of SOX2 expression, which was implicated with cancer cell stemness. Mechanistically, we further identified that OTUB1 could upregulate SLC7A11 expression, which subsequently activated the PI3K/AKT signaling pathway to promote ovarian cancer progression.

Conclusions

This study highlights the pro-tumor role of OTUB1/SLC7A11 in ovarian cancer through the activation of the PI3K/AKT signaling pathway, offering new insights into potential targeted therapies for ovarian cancer.

目的otub1是一种去泛素化酶（DUB），据报道与肿瘤进展有关。本研究旨在探讨OTUB1信号在卵巢癌进展中的作用。材料与方法入选25例确诊为卵巢癌的患者，根据肿瘤分期（高/低）和有无淋巴转移进行分组，通过免疫组化（IHC）染色分析OTUB1的表达。从癌症基因组图谱（TCGA）下载578例卵巢癌患者的数据进行生存分析。采用CCK8和Transwell检测细胞增殖和迁移。Western blotting和免疫染色检测OTUB1/SLC7A11/AKT信号通路的激活情况。结果我们的研究发现OTUB1在卵巢癌组织中表达上调，且高表达与预后不良相关，更有趣的是，高分期和淋巴结转移的卵巢癌样本中OTUB1的表达显著升高。通过体外实验验证，OTUB1在卵巢癌细胞中的过表达促进了细胞增殖、迁移和集落形成的增加。此外，OTUB1导致SOX2表达上调，这与癌细胞的干细胞性有关。在机制上，我们进一步发现OTUB1可以上调SLC7A11的表达，从而激活PI3K/AKT信号通路，促进卵巢癌的进展。结论本研究突出了OTUB1/SLC7A11通过激活PI3K/AKT信号通路在卵巢癌中的促瘤作用，为卵巢癌潜在的靶向治疗提供了新的思路。

{"title":"OTUB1/SLC7A11 axis promoted AKT signaling activation to mediate ovarian cancer progression","authors":"Yujin Zhang, Jing Wang, Sensen Sun, Wenyu Cao, Jinghui Ren, Wen Yang","doi":"10.1016/j.ctarc.2026.101116","DOIUrl":"10.1016/j.ctarc.2026.101116","url":null,"abstract":"<div><h3>Purpose</h3><div>OTUB1 functions as a deubiquitinating enzyme (DUB) and has been reported to be associated with tumor progression. This study aimed to investigate the role of OTUB1 signaling in ovarian cancer progression.</div></div><div><h3>Materials and Methods</h3><div>Twenty-five patients diagnosed with ovarian cancer were enrolled and divided into groups based on tumor stage (high/low) and the presence or absence of lymphatic metastasis to analyze OTUB1 expression via Immunohistochemical (IHC) staining. Data from 578 ovarian cancer patients sourced from The Cancer Genome Atlas (TCGA) were downloaded for survival analysis. Cell proliferation and migration were evaluated using CCK8 and Transwell assays. Western blotting and immunostaining were performed to assess the activation of the OTUB1/SLC7A11/AKT signaling pathway.</div></div><div><h3>Results</h3><div>Our study found that OTUB1 expression was upregulated in ovarian cancer tissues and that higher expression was associated with poor prognosis, and more intriguingly, high-stage and lymph node metastasis ovarian cancer samples exhibited significantly elevated expression of OTUB1.Through in vitro experimental validation, OTUB1 overexpression in ovarian cancer cells promoted the increased cell proliferation, migration, and colony formation. Moreover, OTUB1 led to the upregulation of SOX2 expression, which was implicated with cancer cell stemness. Mechanistically, we further identified that OTUB1 could upregulate SLC7A11 expression, which subsequently activated the PI3K/AKT signaling pathway to promote ovarian cancer progression.</div></div><div><h3>Conclusions</h3><div>This study highlights the pro-tumor role of OTUB1/SLC7A11 in ovarian cancer through the activation of the PI3K/AKT signaling pathway, offering new insights into potential targeted therapies for ovarian cancer.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"46 ","pages":"Article 101116"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptomic landscape of coexisting ovarian clear cell carcinoma and endometriosis: Insights into malignant transformation 卵巢透明细胞癌和子宫内膜异位症共存的转录组学景观：对恶性转化的见解。

IF 2.4 Q3 Medicine

Cancer treatment and research communications

Pub Date : 2026-01-01 DOI: 10.1016/j.ctarc.2026.101098

Mami Shibata , Yuji Kamei , Keisuke Kawamoto , Reiji Muto , Yutaka Ueda , Makoto Hamasaki , Koichi Ohshima , Fusanori Yotsumoto

This study investigateted the malignant transformation of endometriosis (EMS) into ovarian clear cell carcinoma (OCCC) using spatial transcriptomics and single-cell RNA sequencing (scRNA-seq) integration. Tissues with coexisting EMS and OCCC regions were analyzed to elucidate their molecular connections. Spatial transcriptomic profiling revealed shared molecular features between OCCC and EMS, including overexpression of genes related to tissue development and apoptosis. Integration with scRNA-seq data revealed that severe uterine EMS exhibited greater transcriptomic similarities to OCCC than to non-EAOC ovarian cancer subtypes, such as high-grade serous ovarian cancer (HGSOC). Further analysis classified the OCCC-specific genes into EMS epithelial cell-specific and tumor microenvironment (TME)-related categories, highlighting their roles in pathways associated with tumor progression, invasion, and metabolic reprogramming. These findings support the transcriptomic progression pathway from EMS to OCCC, and advance our understanding of the etiology of OCCC, suggesting strategies for targeted therapy and improved diagnostics.

本研究利用空间转录组学和单细胞RNA测序（scRNA-seq）整合研究子宫内膜异位症（EMS）向卵巢透明细胞癌（OCCC）的恶性转化。我们分析了EMS和OCCC区域共存的组织，以阐明它们之间的分子联系。空间转录组学分析揭示了OCCC和EMS之间的共同分子特征，包括组织发育和凋亡相关基因的过表达。结合scRNA-seq数据显示，重度子宫EMS与OCCC的转录组相似性大于非eaoc卵巢癌亚型，如高级别浆液性卵巢癌（HGSOC）。进一步的分析将occc特异性基因分为EMS上皮细胞特异性和肿瘤微环境（TME）相关类别，强调了它们在肿瘤进展、侵袭和代谢重编程相关途径中的作用。这些发现支持了从EMS到OCCC的转录组进展途径，并促进了我们对OCCC病因的理解，提出了靶向治疗和改进诊断的策略。

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引用次数: 0