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Cancer pathogenesis and therapy

Pub Date : 2025-03-01 Epub Date: 2025-03-13 DOI: 10.1016/S2949-7132(25)00018-7

引用次数: 0

Loss of phosphatase and tensin homolog (PTEN) increases Lysyl oxidase-like 2 (LOXL2) expression enhancing the growth of fallopian tube epithelial cells as three-dimensional spheroids PTEN 缺失会增加 LOXL2 的表达，从而促进输卵管上皮细胞作为三维球体的生长

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-03-26 DOI: 10.1016/j.cpt.2024.03.003

Angela Russo , Junlone Moy , Manead Khin , Timothy R. Dorsey , Alfredo Lopez Carrero , Joanna E. Burdette

Background

High-grade serous ovarian cancer (HGSOC) accounts for 70–80% of all ovarian cancer-related deaths. Multiple studies have suggested that the fallopian tube epithelium (FTE) serves as the cell of origin of HGSOC. Phosphatase and tensin homolog (PTEN) is a tumor suppressor and its loss is sufficient to induce numerous tumorigenic changes in FTE, including increased migration, formation of multicellular tumor spheroids (MTSs), and ovarian colonization. In murine oviductal epithelial (MOE) cells (the equivalent of human FTE) loss of PTEN results in the upregulation of transcripts associated with the extracellular matrix, with a specific focus on the elevation of lysyl oxidase-like 2 (LOXL2). Although LOXL2 is known to drive transformation and invasion in solid tumors and is associated with a poor prognosis in ovarian cancer, its specific role in the tumorigenesis of ovarian cancer originating from FTE remains unclear. Therefore, we aim to investigate whether LOXL2 mediates tumorigenesis from the fallopian tube epithelium.

Methods

In this study, we utilized clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein 9 (CAS9) technology to delete LOXL2 in PTEN-deficient MOE cells to understand its role in mediating the oncogenic effects of PTEN loss. In addition, CRISPR-CAS9 was used to delete LOXL2 in OVCAR8 ovarian cancer cells. We monitored the changes in tumorigenic properties, such as migration, invasion, and growth of three-dimensional (3D) spheroids, to assess whether the loss of LOXL2 resulted in any changes.

Results

We found that a reduction in LOXL2 expression did not significantly change the migration or invasive capabilities of PTEN-depleted MOE or human ovarian cancer cells. However, we found that a reduction in LOXL2 expression resulted in a significant reduction in 3D MTS formation and survival in both lines.

Conclusions

These results reveal for the first time that PTEN loss in FTE cells increases LOXL2 expression through downregulation of Pax2, and LOXL2 deletion blocks 3D spheroid formation.

背景：高级别浆液性卵巢癌（HGSOC）占所有卵巢癌相关死亡的70-80%。多项研究表明，输卵管上皮（FTE）是HGSOC的起源细胞。磷酸酶和紧张素同源物（PTEN）是一种肿瘤抑制因子，它的缺失足以诱导FTE发生许多致瘤性变化，包括迁移增加、多细胞肿瘤球体（mts）的形成和卵巢定植。在小鼠输卵管上皮（MOE）细胞（相当于人类的FTE）中，PTEN的缺失会导致与细胞外基质相关的转录本上调，并特别关注赖氨酸氧化酶样2 （LOXL2）的升高。虽然已知LOXL2在实体瘤中驱动转化和侵袭，并与卵巢癌预后不良相关，但其在FTE卵巢癌发生中的具体作用尚不清楚。因此，我们的目的是研究LOXL2是否介导输卵管上皮的肿瘤发生。方法在本研究中，我们利用聚集规律间隔短回文重复(CRISPR)-CRISPR相关蛋白9 （CAS9）技术在PTEN缺失的MOE细胞中删除LOXL2，以了解其在介导PTEN缺失的致癌作用中的作用。此外，利用CRISPR-CAS9删除OVCAR8卵巢癌细胞中的LOXL2。我们监测了致瘤性的变化，如三维球体的迁移、侵袭和生长，以评估LOXL2的丢失是否会导致任何变化。结果我们发现LOXL2表达的降低并没有显著改变pten缺失的MOE或人卵巢癌细胞的迁移或侵袭能力。然而，我们发现LOXL2表达的减少导致两种细胞系中3D MTS的形成和存活显著减少。结论PTEN缺失在FTE细胞中通过下调Pax2表达增加LOXL2的表达，LOXL2缺失阻断3D球体的形成。

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引用次数: 0

Three-dimensional (3D) augmented reality during Retzius-sparing robot-assisted radical prostatectomy (RS-RARP): First experience 三维（3D）增强现实在Retzius-sparing机器人辅助根治性前列腺切除术（RS-RARP）：第一次体验。

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-06-20 DOI: 10.1016/j.cpt.2024.06.003

Silvia Secco , Alberto Olivero , Stefano Tappero , Paolo Dell’Oglio , Luca Carbonaro , Alessandro Marando , Angelo Vanzulli , Emanuela Bonoldi , Aldo Massimo Bocciardi , Antonio Galfano

引用次数: 0

Biochemical mechanisms and molecular interactions of vitamins in cancer therapy 维生素在癌症治疗中的生化机制和分子相互作用

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-05-16 DOI: 10.1016/j.cpt.2024.05.001

Abdullahi T. Aborode , Isreal A. Onifade , Mercy M. Olorunshola , Gladys O. Adenikinju , Ibude J. Aruorivwooghene , Adeboboye C. Femi , Osasere Jude-Kelly Osayawe , Abraham Osinuga , Ebenezer A. Omojowolo , Adekunle F. Adeoye , Segun Olapade , Ibrahim O. Adelakun , Ogundepo D. Moyinoluwa , Oluwatosin M. Adeyemo , Godfred Y. Scott , Ruth A. Ogbonna , Emmanuel A. Fajemisin , Omama Ehtasham , Soyemi Toluwalashe , Adetolase A. Bakre , Terungwa H. Iorkula

Recently, the potential role of vitamins in cancer therapy has attracted considerable research attention. However, the reported findings are inconsistent, with limited information on the biochemical and molecular interactions of different vitamins in various cancer cells. Importantly, the presence of vitamin receptors in tumor cells suggests that vitamins play a significant role in the molecular and biochemical interactions in cancers. Additionally, studies on the efficacy of vitamin supplementation and dosage levels on tumor progression and mortality risk have yielded inconsistent results. Notably, molecular and biochemical investigations have reported the function of vitamins in the proliferation, growth, and invasiveness of tumor cells, as well as in cell cycle arrest and inflammatory signaling. Additionally, different vitamins may regulate the cancer microenvironment by activating various molecular pathways. Vitamins significantly affect immunological function, antioxidant defense, inflammation, and epigenetic control, and can improve treatment outcomes by affecting cell behavior and combating stress and DNA damage. However, further research is necessary to confirm the efficacy of vitamins, establish ideal dosages, and develop effective cancer prevention and treatment plans. Individualized supplementation plans guided by medical knowledge are crucial to achieving optimal results in clinical and preclinical settings. In this review, we critically evaluated the effects of different vitamins on the risk and development of cancer. Additionally, we examined the potential of vitamin supplements to enhance the efficacy of drug therapy and counteract resistance mechanisms that often arise during cancer treatment.

最近，维生素在癌症治疗中的潜在作用引起了相当大的研究关注。然而，报告的发现是不一致的，关于不同维生素在各种癌细胞中的生化和分子相互作用的信息有限。重要的是，肿瘤细胞中维生素受体的存在表明维生素在癌症的分子和生化相互作用中起着重要作用。此外，关于维生素补充和剂量水平对肿瘤进展和死亡风险的功效的研究得出了不一致的结果。值得注意的是，分子和生化研究已经报道了维生素在肿瘤细胞的增殖、生长和侵袭以及细胞周期阻滞和炎症信号传导中的作用。此外，不同的维生素可能通过激活不同的分子途径来调节癌症微环境。维生素显著影响免疫功能、抗氧化防御、炎症和表观遗传控制，并能通过影响细胞行为、对抗压力和DNA损伤来改善治疗结果。然而，需要进一步的研究来确认维生素的功效，建立理想的剂量，并制定有效的癌症预防和治疗计划。以医学知识为指导的个性化补充计划对于在临床和临床前环境中取得最佳结果至关重要。在这篇综述中，我们批判性地评估了不同维生素对癌症风险和发展的影响。此外，我们还研究了维生素补充剂的潜力，以提高药物治疗的疗效，并抵消癌症治疗过程中经常出现的耐药性机制。

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引用次数: 0

Connecting scientists and oncologists for advances 将科学家和肿瘤学家联系起来，促进进步

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-07-01 DOI: 10.1016/j.cpt.2024.06.006

Yunlong Yang, Changhao Wu, Wei Zhu

引用次数: 0

Characteristics and outcomes of secondary acute lymphoblastic leukemia (sALL) after multiple myeloma (MM): SEER data analysis in a single-center institution 多发性骨髓瘤后继发性急性淋巴细胞白血病的特征和预后：单中心机构的 SEER 数据分析

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-07-02 DOI: 10.1016/j.cpt.2024.06.007

Jing Jia, Jiahui Yin, Chuanying Geng, Aijun Liu

Background

Secondary acute lymphoblastic leukemia (sALL) is rare in patients diagnosed with antecedent multiple myeloma (MM). This study aimed to elucidate the clinical features and outcomes of patients with sALL after MM.

Methods

We conducted this population-based study using the Surveillance, Epidemiology, and End Results (SEER) database and retrospectively reviewed patients with sALL following MM treatment at our institution. Cox regression analysis was performed to investigate the prognostic factors for survival in patients with sALL.

Results

We identified 64,629 cases of MM (including 18 sALL from the SEER Plus 9 database, and three sALL from our institution). Younger patients with MM and those who received chemotherapy were at a higher risk of developing sALL. The novel agent era witnessed an increased incidence of sALL (post-novel agent era vs. pre-novel agent era: 0.31% [10/32,640] vs. 0.25% [8/31,989]) and shorter latency time (post-novel agent era vs. pre-novel agent era [median]: 51.5 vs. 74.5 months, P = 0.516), though the difference was not significant. The median age at sALL onset was 65 (range: 47–78) years. Significant cytopenia and absence of BCR/ABL fusion genes were common features in this patient population. The treatment of sALL is complicated by old age and poor performance status. The median survival of patients with sALL is 18 months, whereas those who received chemotherapy had significantly prolonged survival.

Conclusions

Patients with sALL combined with an antecedent MM, especially those with long-term exposure to immunomodulatory agents such as thalidomide or lenalidomide, should be cautiously evaluated and managed with a comprehensive approach.

背景继发性急性淋巴细胞白血病（sALL）在诊断为多发性骨髓瘤（MM）的患者中很少见。本研究旨在阐明MM后小血管性白血病患者的临床特征和结局。方法我们使用监测、流行病学和最终结果（SEER）数据库进行了这项基于人群的研究，并回顾性分析了我们机构MM后小血管性白血病患者。采用Cox回归分析探讨影响小细胞白血病患者生存的预后因素。结果共发现64,629例MM（其中18例来自SEER Plus 9数据库，3例来自本机构）。年轻的MM患者和接受化疗的患者发生小淋巴细胞白血病的风险更高。新型药物使用后，sALL发生率增加（新型药物使用后vs.前：0.31% [10/32,640]vs. 0.25%[8/31,989]），潜伏期缩短（新型药物使用后vs.前[中位数]:51.5 vs. 74.5个月，P = 0.516），但差异无统计学意义。小发病的中位年龄为65岁（47-78岁）。明显的细胞减少和缺乏BCR/ABL融合基因是该患者群体的共同特征。由于年龄大和运动状态不佳，治疗变得复杂。小细胞白血病患者的中位生存期为18个月，而接受化疗的患者的生存期明显延长。结论small - all合并既往MM的患者，特别是长期暴露于免疫调节剂如沙利度胺或来那度胺的患者，应谨慎评估并采用综合方法进行治疗。

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引用次数: 0

Integrative analysis of cuproptosis-related lncRNAs: Unveiling prognostic significance, immune microenvironment, and copper-induced mechanisms in prostate cancer 杯突相关lncRNA的整合分析：揭示前列腺癌的预后意义、免疫微环境和铜诱导机制

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-03-29 DOI: 10.1016/j.cpt.2024.03.004

Haitao Zhong , Yiming Lai , Wenhao Ouyang , Yunfang Yu , Yongxin Wu , Xinxin He , Lexiang Zeng , Xueen Qiu , Peixian Chen , Lingfeng Li , Jie Zhou , Tianlong Luo , Hai Huang

Background

Long non-coding ribonucleic acids (lncRNAs) regulate messenger RNA (mRNA) expression and influence cancer development and progression. Cuproptosis, a newly discovered form of cell death, plays an important role in cancer. Nonetheless, additional research investigating the association between cuproptosis-related lncRNAs and prostate cancer (PCa) prognosis is required.

Methods

Sequencing data and copy number variant data were obtained from 492 patients with PCa from The Cancer Genome Atlas (TCGA) Program. Prognostic models of PCa based on cuproptosis-related lncRNAs were constructed using a multi-level attention graph neural network (MLA-GNN) deep learning algorithm. Immune escape scoring was performed using Tumor Immune Dysfunction and Exclusion. Cellular experiments were conducted to explore the correlation between key lncRNAs and cuproptosis.

Results

Data from 492 patients with PCa were randomized into two groups at a 1:1 ratio. Prognostic modeling was successfully established using MLA-GNN. Survival analysis suggested that patients could be divided into high- and low-risk groups according to model scores and that there was a significant difference in disease-free survival (DFS) (P < 0.01). The area under the receiver operating characteristic (ROC) curve (AUC) indicated a strong predictive performance for the model, with AUCs of 0.913, 0.847, and 0.863 for the training group and 0.815, 0.907, and 0.866 for the test group at 12, 36, and 60 months, respectively. The immune escape score and immune microenvironment analysis suggested that the high-risk group corresponded to a stronger immune escape and a poorer immune microenvironment (P < 0.05). Cellular experiments revealed that the expression of all six key lncRNAs was upregulated in the presence of copper ion carriers (P < 0.05).

Conclusions

This study identified cuproptosis-related lncRNAs that were strongly associated with PCa prognosis. Key lncRNAs could affect copper metabolism and may serve as new therapeutic targets.

长链非编码核糖核酸（lncRNAs）调节信使RNA （mRNA）的表达并影响癌症的发生和进展。cuprotosis是一种新发现的细胞死亡形式，在癌症中起着重要作用。尽管如此，需要进一步的研究来调查前列腺癌相关lncrna与前列腺癌（PCa）预后之间的关系。方法从癌症基因组图谱（TCGA）项目中获取492例PCa患者的测序数据和拷贝数变异数据。采用多层次注意图神经网络（MLA-GNN）深度学习算法，构建了基于cuprotosis相关lncrna的PCa预后模型。采用肿瘤免疫功能障碍和排斥评分法进行免疫逃逸评分。通过细胞实验探索关键lncrna与铜突起的相关性。结果492例PCa患者的数据按1:1的比例随机分为两组。利用MLA-GNN成功建立了预后模型。生存分析提示，根据模型评分可将患者分为高危组和低危组，无病生存期（DFS）差异有统计学意义(P <；0.01)。受试者工作特征曲线下面积（AUC）显示该模型具有较强的预测性能，在12个月、36个月和60个月时，训练组的AUC分别为0.913、0.847和0.863，试验组的AUC分别为0.815、0.907和0.866。免疫逃逸评分和免疫微环境分析提示高危组免疫逃逸较强，免疫微环境较差(P <；0.05)。细胞实验显示，在铜离子载体存在的情况下，所有六个关键lncrna的表达都上调(P <；0.05)。结论本研究发现与前列腺增生相关的lncrna与前列腺癌预后密切相关。关键lncrna影响铜代谢，可能成为新的治疗靶点。

{"title":"Integrative analysis of cuproptosis-related lncRNAs: Unveiling prognostic significance, immune microenvironment, and copper-induced mechanisms in prostate cancer","authors":"Haitao Zhong , Yiming Lai , Wenhao Ouyang , Yunfang Yu , Yongxin Wu , Xinxin He , Lexiang Zeng , Xueen Qiu , Peixian Chen , Lingfeng Li , Jie Zhou , Tianlong Luo , Hai Huang","doi":"10.1016/j.cpt.2024.03.004","DOIUrl":"10.1016/j.cpt.2024.03.004","url":null,"abstract":"<div><h3>Background</h3><div>Long non-coding ribonucleic acids (lncRNAs) regulate messenger RNA (mRNA) expression and influence cancer development and progression. Cuproptosis, a newly discovered form of cell death, plays an important role in cancer. Nonetheless, additional research investigating the association between cuproptosis-related lncRNAs and prostate cancer (PCa) prognosis is required.</div></div><div><h3>Methods</h3><div>Sequencing data and copy number variant data were obtained from 492 patients with PCa from The Cancer Genome Atlas (TCGA) Program. Prognostic models of PCa based on cuproptosis-related lncRNAs were constructed using a multi-level attention graph neural network (MLA-GNN) deep learning algorithm. Immune escape scoring was performed using Tumor Immune Dysfunction and Exclusion. Cellular experiments were conducted to explore the correlation between key lncRNAs and cuproptosis.</div></div><div><h3>Results</h3><div>Data from 492 patients with PCa were randomized into two groups at a 1:1 ratio. Prognostic modeling was successfully established using MLA-GNN. Survival analysis suggested that patients could be divided into high- and low-risk groups according to model scores and that there was a significant difference in disease-free survival (DFS) (<em>P</em> < 0.01). The area under the receiver operating characteristic (ROC) curve (AUC) indicated a strong predictive performance for the model, with AUCs of 0.913, 0.847, and 0.863 for the training group and 0.815, 0.907, and 0.866 for the test group at 12, 36, and 60 months, respectively. The immune escape score and immune microenvironment analysis suggested that the high-risk group corresponded to a stronger immune escape and a poorer immune microenvironment (<em>P</em> < 0.05). Cellular experiments revealed that the expression of all six key lncRNAs was upregulated in the presence of copper ion carriers (<em>P</em> < 0.05).</div></div><div><h3>Conclusions</h3><div>This study identified cuproptosis-related lncRNAs that were strongly associated with PCa prognosis. Key lncRNAs could affect copper metabolism and may serve as new therapeutic targets.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 1","pages":"Pages 48-59"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140401211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fecal methylated syndecan-2 (SDC2) testing for early screening of colorectal cancerous and precancerous lesions: A real-world retrospective study in China 粪便甲基化SDC2检测用于早期筛查结直肠癌和癌前病变：中国的一项真实世界回顾性研究

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-02-24 DOI: 10.1016/j.cpt.2024.02.002

Boyu Qin , Haitao Niu , Lupeng Qiu , Hongfeng Zhou , Peng Lyu

Background

Colorectal cancer (CRC) is a major public health concern and the second leading cause of cancer-related deaths worldwide. However, challenges remain in deploying effective screening strategies for early-stage CRC. This study aimed to evaluate the effectiveness of a fecal-based syndecan-2 (SDC2) methylation test for the detection of colorectal lesions and CRC.

Methods

We retrospectively collected data on participants who underwent fecal SDC2 methylation testing from January 1, 2019, to May 30, 2023. Patients with positive results were recommended to undergo colonoscopy. Performance indicators associated with certain clinical characteristics, including positive rate (PR), positive predictive value (PPV), and colonoscopy compliance rate (CCR), were subjected to statistical analysis.

Results

We analyzed data from 113,209 participants, of whom 11,841 (10.4% PR) had positive fecal SDC2 methylation test results. A total of 4315 participants with positive results adhered to the colonoscopy recommendations, and the CCR was 36.4%. Finally, 3169 colorectal lesions were detected, including 1134 polyps, 875 non-advanced adenomas (NAAs), 770 advanced adenomas (AAs), and 390 CRCs, with PPV values of 26.3% (1134/4315), 20.3% (875/4315), 17.8% (770/4315), and 9.0% (390/4315), respectively. Notably, the PPV for CRC increased significantly with age (χ² = 164.40, P < 0.0001). In addition, as the cycle threshold (CT) values increased, the PPVs of AAs and CRCs generally decreased, whereas those of NAAs and polyps significantly increased. Moreover, the clinical patient group had the highest incidence of late-stage CRC (stage II and higher), whereas asymptomatic populations from the staff physical examination group and rural town-based screening programs had the highest number of stage 0 and I CRCs detected (P = 0.0107).

Conclusions

This study indicates that fecal SDC2 methylation testing combined with colonoscopy may be an effective screening method for colorectal lesions and CRC.

结直肠癌（CRC）是一个主要的公共卫生问题，也是全球癌症相关死亡的第二大原因。然而，在部署有效的早期结直肠癌筛查策略方面仍然存在挑战。本研究旨在评估基于粪便的syndecan-2 （SDC2）甲基化检测在检测结直肠癌和结直肠癌中的有效性。方法回顾性收集2019年1月1日至2023年5月30日接受粪便SDC2甲基化检测的参与者的数据。阳性结果的患者建议接受结肠镜检查。与某些临床特征相关的性能指标，包括阳性率（PR）、阳性预测值（PPV）、结肠镜检查依从率（CCR）进行统计分析。结果我们分析了来自113,209名参与者的数据，其中11,841名（10.4% PR）的粪便SDC2甲基化检测结果呈阳性。共有4315名参与者符合结肠镜检查建议的阳性结果，CCR为36.4%。共检出结直肠病变3169个，其中息肉1134个，非晚期腺瘤（NAAs） 875个，晚期腺瘤（AAs） 770个，crc 390个，PPV值分别为26.3%(1134/4315),20.3%(875/4315),17.8%(770/4315),9.0%（390/4315）。值得注意的是，结直肠癌的PPV随着年龄的增长而显著增加(χ2 = 164.40, P <；0.0001)。此外，随着周期阈值（CT）的升高，AAs和CRCs的ppv普遍降低，而NAAs和息肉的ppv显著升高。此外，临床患者组晚期CRC （II期及以上）的发病率最高，而工作人员体检组和农村城镇筛查项目的无症状人群检测到的0期和I期CRC数量最高（P = 0.0107）。结论粪便SDC2甲基化检测联合结肠镜检查可能是筛查结直肠病变和结直肠癌的有效方法。

{"title":"Fecal methylated syndecan-2 (SDC2) testing for early screening of colorectal cancerous and precancerous lesions: A real-world retrospective study in China","authors":"Boyu Qin , Haitao Niu , Lupeng Qiu , Hongfeng Zhou , Peng Lyu","doi":"10.1016/j.cpt.2024.02.002","DOIUrl":"10.1016/j.cpt.2024.02.002","url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is a major public health concern and the second leading cause of cancer-related deaths worldwide. However, challenges remain in deploying effective screening strategies for early-stage CRC. This study aimed to evaluate the effectiveness of a fecal-based syndecan-2 (<em>SDC2</em>) methylation test for the detection of colorectal lesions and CRC.</div></div><div><h3>Methods</h3><div>We retrospectively collected data on participants who underwent fecal <em>SDC2</em> methylation testing from January 1, 2019, to May 30, 2023. Patients with positive results were recommended to undergo colonoscopy. Performance indicators associated with certain clinical characteristics, including positive rate (PR), positive predictive value (PPV), and colonoscopy compliance rate (CCR), were subjected to statistical analysis.</div></div><div><h3>Results</h3><div>We analyzed data from 113,209 participants, of whom 11,841 (10.4% PR) had positive fecal <em>SDC2</em> methylation test results. A total of 4315 participants with positive results adhered to the colonoscopy recommendations, and the CCR was 36.4%. Finally, 3169 colorectal lesions were detected, including 1134 polyps, 875 non-advanced adenomas (NAAs), 770 advanced adenomas (AAs), and 390 CRCs, with PPV values of 26.3% (1134/4315), 20.3% (875/4315), 17.8% (770/4315), and 9.0% (390/4315), respectively. Notably, the PPV for CRC increased significantly with age (<em>χ</em><sup>2</sup> = 164.40, <em>P</em> < 0.0001). In addition, as the cycle threshold (CT) values increased, the PPVs of AAs and CRCs generally decreased, whereas those of NAAs and polyps significantly increased. Moreover, the clinical patient group had the highest incidence of late-stage CRC (stage II and higher), whereas asymptomatic populations from the staff physical examination group and rural town-based screening programs had the highest number of stage 0 and I CRCs detected (<em>P</em> = 0.0107).</div></div><div><h3>Conclusions</h3><div>This study indicates that fecal <em>SDC2</em> methylation testing combined with colonoscopy may be an effective screening method for colorectal lesions and CRC.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 1","pages":"Pages 60-67"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140467413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cover 封面

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2025-01-04 DOI: 10.1016/S2949-7132(24)00090-9

引用次数: 0

Despicable role of epithelial–mesenchymal transition in breast cancer metastasis: Exhibiting de novo restorative regimens 上皮-间质转化在乳腺癌转移中的卑劣作用：展示全新的修复方案

Cancer pathogenesis and therapy

Pub Date : 2025-01-01 Epub Date: 2024-01-12 DOI: 10.1016/j.cpt.2024.01.001

Paras Famta , Saurabh Shah , Biswajit Dey , Kondasingh Charan Kumar , Deepkumar Bagasariya , Ganesh Vambhurkar , Giriraj Pandey , Anamika Sharma , Dadi A. Srinivasarao , Rahul Kumar , Santosh Kumar Guru , Rajeev Singh Raghuvanshi , Saurabh Srivastava

Breast cancer (BC) is the most prevalent cancer in women globally. Anti-cancer advancements have enabled the killing of BC cells through various therapies; however, cancer relapse is still a major limitation and decreases patient survival and quality of life. Epithelial-to-mesenchymal transition (EMT) is responsible for tumor relapse in several cancers. This highly regulated event causes phenotypic, genetic, and epigenetic changes in the tumor microenvironment (TME). This review summarizes the recent advancements regarding EMT using de-differentiation and partial EMT theories. We extensively review the mechanistic pathways, TME components, and various anti-cancer adjuvant and neo-adjuvant therapies responsible for triggering EMT in BC tumors. Information regarding essential clinical studies and trials is also discussed. Furthermore, we also highlight the recent strategies targeting various EMT pathways. This review provides a holistic picture of BC biology, molecular pathways, and recent advances in therapeutic strategies.

乳腺癌（BC）是全球女性中最常见的癌症。抗癌的进步使得通过各种疗法杀死BC细胞成为可能；然而，癌症复发仍然是一个主要的限制，降低患者的生存和生活质量。上皮-间质转化（EMT）是几种癌症复发的原因。这种高度调控的事件导致肿瘤微环境（TME）的表型、遗传和表观遗传变化。本文综述了用去分化和部分EMT理论研究EMT的最新进展。我们广泛地回顾了在BC肿瘤中触发EMT的机制途径、TME成分以及各种抗癌辅助和新辅助疗法。关于基本临床研究和试验的信息也进行了讨论。此外，我们还强调了针对各种EMT途径的最新策略。本文综述了BC的生物学、分子途径和治疗策略的最新进展。

{"title":"Despicable role of epithelial–mesenchymal transition in breast cancer metastasis: Exhibiting de novo restorative regimens","authors":"Paras Famta , Saurabh Shah , Biswajit Dey , Kondasingh Charan Kumar , Deepkumar Bagasariya , Ganesh Vambhurkar , Giriraj Pandey , Anamika Sharma , Dadi A. Srinivasarao , Rahul Kumar , Santosh Kumar Guru , Rajeev Singh Raghuvanshi , Saurabh Srivastava","doi":"10.1016/j.cpt.2024.01.001","DOIUrl":"10.1016/j.cpt.2024.01.001","url":null,"abstract":"<div><div>Breast cancer (BC) is the most prevalent cancer in women globally. Anti-cancer advancements have enabled the killing of BC cells through various therapies; however, cancer relapse is still a major limitation and decreases patient survival and quality of life. Epithelial-to-mesenchymal transition (EMT) is responsible for tumor relapse in several cancers. This highly regulated event causes phenotypic, genetic, and epigenetic changes in the tumor microenvironment (TME). This review summarizes the recent advancements regarding EMT using de-differentiation and partial EMT theories. We extensively review the mechanistic pathways, TME components, and various anti-cancer adjuvant and neo-adjuvant therapies responsible for triggering EMT in BC tumors. Information regarding essential clinical studies and trials is also discussed. Furthermore, we also highlight the recent strategies targeting various EMT pathways. This review provides a holistic picture of BC biology, molecular pathways, and recent advances in therapeutic strategies.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 1","pages":"Pages 30-47"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139633753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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