Asia-Pacific journal of clinical oncology最新文献

{"title":"Program in Detail","authors":"","doi":"10.1111/ajco.14119","DOIUrl":"10.1111/ajco.14119","url":null,"abstract":"","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 S3","pages":"24-39"},"PeriodicalIF":1.4,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"International Speakers","authors":"","doi":"10.1111/ajco.14114","DOIUrl":"10.1111/ajco.14114","url":null,"abstract":"","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 S3","pages":"9-10"},"PeriodicalIF":1.4,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poster Abstracts","authors":"","doi":"10.1111/ajco.14117","DOIUrl":"10.1111/ajco.14117","url":null,"abstract":"","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 S3","pages":"115-271"},"PeriodicalIF":1.4,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expert consensus on the optimal management of BRAFV600E-mutant metastatic colorectal cancer in the Asia-Pacific region","authors":"Oliver Piercey,&nbsp;Lorraine Chantrill,&nbsp;Hung-Chih Hsu,&nbsp;Brigette Ma,&nbsp;Timothy Price,&nbsp;Iain Beehuat Tan,&nbsp;Hao-Wei Teng,&nbsp;Jeanne Tie,&nbsp;Jayesh Desai","doi":"10.1111/ajco.14132","DOIUrl":"10.1111/ajco.14132","url":null,"abstract":"<p>The burden of colorectal cancer (CRC) is high in the Asia-Pacific region, and several countries in this region have among the highest and/or fastest growing rates of CRC in the world. A significant proportion of patients will present with or develop metastatic CRC (mCRC), and <i>BRAF^V600E</i>-mutant mCRC represents a particularly aggressive phenotype that is less responsive to standard chemotherapies. In light of recent therapeutic advances, an Asia-Pacific expert consensus panel was convened to develop evidence-based recommendations for the diagnosis, treatment, and management of patients with <i>BRAF^V600E</i>-mutant mCRC. The expert panel comprised nine medical oncologists from Australia, Hong Kong, Singapore, and Taiwan (the authors), who met to review current literature and develop eight consensus statements that describe the optimal management of <i>BRAF^V600E</i>-mutant mCRC in the Asia-Pacific region. As agreed by the expert panel, the consensus statements recommend molecular testing at diagnosis to guide individualized treatment decisions, propose optimal treatment pathways according to microsatellite stability status, advocate for more frequent monitoring of <i>BRAF^V600E</i>-mutant mCRC, and discuss local treatment strategies for oligometastatic disease. Together, these expert consensus statements are intended to optimize treatment and improve outcomes for patients with <i>BRAF^V600E</i>-mutant mCRC in the Asia-Pacific region.</p>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"21 1","pages":"31-45"},"PeriodicalIF":1.4,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Procollagen C-protease enhancer protein promotes glioma growth by activating ERK signaling","authors":"Zhenchao Ma,&nbsp;Daxing Huang,&nbsp;Lixin Ru,&nbsp;Ming Chen","doi":"10.1111/ajco.14127","DOIUrl":"10.1111/ajco.14127","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Procollagen C-proteinase enhancer (PCOLCE) promotes tumor progression in multiple cancers. However, the specific role of PCOLCE in gliomas remains enigmatic. In this study, we focused on analyzing PCOLCE expression and its correlation with clinicopathological parameters in glioma specimens; moreover, we explored the effects of PCOLCE in glioma proliferation in vitro and in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A tissue microarray containing 159 human glioma specimens was pressed to explore the correlation between PCOLCE expression and the survival of glioma patients. Cell Counting Kit-8 (CCK8), colony formation, and immunoblot assays were used to detect the role of PCOLCE on cell proliferation in glioma. Furthermore, the in vivo role of PCOLCE was investigated using a subcutaneous glioma xenograft model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The expression of PCOLCE was higher in grade III and IV gliomas than in grade I and II gliomas. High PCOLCE expression was related to a remarkably worse prognosis in glioma patients. Additionally, PCOLCE downregulation impeded glioma cell proliferation. Furthermore, PCOLCE knockdown markedly abrogated p-ERK expression in glioma cells, whereas, it negligibly influenced p38 and JNK signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These results indicate that PCOLCE is a feasible prognostic biomarker for glioma, and PCOLCE-induced activation of ERK signaling may be a pro-growth mechanism in glioma cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"21 1","pages":"48-57"},"PeriodicalIF":1.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The prognostic and immune significance of Rab11A in pan-cancer and its function and mechanism underlying estrogen receptor targeting in breast cancer","authors":"Yilun Li,&nbsp;Baifang Ding,&nbsp;Mengyu Wei,&nbsp;Xiaolu Yang,&nbsp;Ruihuan Fu,&nbsp;Yinfeng Liu,&nbsp;Lin Zhu,&nbsp;Yan Ding,&nbsp;Wenjin Zhang,&nbsp;Geng Zhang,&nbsp;Shuo Zhang,&nbsp;Yuhui Bu,&nbsp;Jianchao He,&nbsp;Jianye Deng,&nbsp;Xiaohuan Bao,&nbsp;Jun Hao,&nbsp;Li Ma","doi":"10.1111/ajco.14130","DOIUrl":"10.1111/ajco.14130","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Rab11A is an important molecule for recycling endosomes and is closely related to the proliferation, invasion, and metastasis of tumors. This study investigated the prognostic and immune significance of Rab11A and validated its potential function and mechanism in breast cancer (BRCA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>RNA sequencing data for 33 tumors were downloaded from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression databases. Correlation analysis was used to evaluate the relationship between Rab11A expression and immune characteristics. Potential pathways were identified using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analysis. Immunohistochemical analysis, colony formation assay, bromodeoxyuridine incorporation assay, immunofluorescence, and Western blot were used to explore potential function and mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Analysis of the TCGA database showed significant upregulation of Rab11A expression in a variety of cancers. Rab11A was up-regulated in 82.4% of BRCA. High Rab11A expression is associated with poor survival in cancer patients and is a predictor of poor prognosis. CIBERSORT analysis showed that Rab11A was negatively associated with almost all immune cycle activity scores pan-cancer. The results of the TCGA-BRCA cohort were further confirmed by using pathological samples from clinical BRCA patients. The results showed that Rab11A expression was correlated with estrogen receptor (ER) and progesterone receptor expression in BRCA (<i>p</i> &lt; 0.05). Knockdown and overexpression of Rab11A affected the proliferation of BRCA cells. Further mechanistic studies revealed that down-regulation of ER alpha (ERα) and up-regulation of ER beta (ERβ) mediated Rab11A-induced inhibition of BRCA cell proliferation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Rab11A expression in pan-cancer is associated with poor prognosis and immune profile. In particular, in BRCA, Rab11A expression regulates cell proliferation by targeting ERα and ERβ. High Rab11A expression is tightly associated with immune characteristics, tumor microenvironment, and genetic mutations. These results provide a reference for exploring the role of Rab11A in pan-cancer and provide a new perspective for revealing potential therapeutic targets in BRCA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"21 1","pages":"12-30"},"PeriodicalIF":1.4,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author List","authors":"","doi":"10.1111/ajco.14129","DOIUrl":"https://doi.org/10.1111/ajco.14129","url":null,"abstract":"","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 S2","pages":"65-68"},"PeriodicalIF":1.4,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142435103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical breast examination: A screening tool for lower- and middle-income countries","authors":"Divya Khanna,&nbsp;Priyanka Sharma,&nbsp;Atul Budukh,&nbsp;Ajay Kumar Khanna","doi":"10.1111/ajco.14126","DOIUrl":"10.1111/ajco.14126","url":null,"abstract":"<p>Breast cancer (BC) remains a global health challenge, devastatingly impacting women's lives. Low-and-middle-income countries (LMIC), such as India, experience a concerning upward trend in BC incidence, necessitating the implementation of cost-effective screening methods. While mammography, ultrasonography, and magnetic resonance imaging are preferred screening modalities in resource-rich settings, limited resources in LMICs make clinical breast examination (CBE) the method of choice. This review explores the merits of CBE, its coverage, barriers, and facilitators in the Indian context for developing strategies in resource-constrained settings. CBE has shown significant down-staging and cost-effectiveness. Performed by trained health workers in minutes, CBE offers an opportunity for education about BC. Various individual and health system barriers, such as stigma, financial constraints, and the absence of opportunistic screening hinder CBE coverage. Promising facilitators include awareness programs, capacity building, and integrating CBE through universal health care. No healthcare provider must miss any screening opportunity through CBE.</p>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 6","pages":"690-699"},"PeriodicalIF":1.4,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/ajco.14126","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xanthine negatively regulates c-MYC through the PI3K/AKT signaling pathway and inhibits the proliferation, invasion, and migration of breast cancer cells","authors":"Aijia Zhang,&nbsp;Limei Ai","doi":"10.1111/ajco.14125","DOIUrl":"10.1111/ajco.14125","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background aim</h3>\u0000 \u0000 <p>Breast cancer is a prevalent and aggressive malignancy associated with elevated mortality rates worldwide. Dysregulation of the c-MYC oncogene and aberrant activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway are common features in breast cancer progression, rendering them attractive therapeutic targets. Here, we assessed the effects of the plant derivative, xanthine, on breast cancer cells and explored the molecular mechanisms underlying its activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Breast cancer cell lines were treated with xanthine, followed by assessment of c-MYC expression levels. Cell proliferation, invasion, and migration were analyzed to assess the effects of xanthine treatment on breast cancer cell behavior.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Xanthine treatment induced a decrease in c-MYC expression, resulting in significant inhibition of breast cancer cell proliferation, invasion, and migration. Mechanistic investigations revealed that these effects were mediated by suppression of the PI3K/AKT signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Xanthine shows great potential for breast cancer treatment by targeting c-MYC via the PI3K/AKT signaling pathway. Our findings indicate that development of xanthine as a novel treatment option for breast cancer, which acts by influencing key oncogenic pathways involved in tumor progression, may be warranted.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"21 1","pages":"3-11"},"PeriodicalIF":1.4,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E74-like factor 4 promotes the proliferation, invasion, and migration of colorectal cancer cells via long non-coding RNA integrin subunit beta 8 antisense RNA 1-mediated histone H3 lysine 27 trimethylation modification","authors":"Qi Wang,&nbsp;Shaofeng Liu","doi":"10.1111/ajco.14112","DOIUrl":"10.1111/ajco.14112","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Colorectal cancer (CRC) is a common malignancy in the gastrointestinal tract. The main objective of this study is to explore the potential mechanisms of E74-like factor 4 (ELF4) in CRC progression, providing a novel therapeutic target for CRC treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>CRC cells and normal control cells were cultured. Levels of ELF4/long non-coding RNA integrin subunit beta 8 antisense RNA 1 (LncRNA ITGB8-AS1)/claudin-23 (CLDN23) were detected by real-time quantitative polymerase chain reaction or Western blot assay. ELF4 siRNA, ITGB8-AS1 pcDNA3.1, or CLDN23 siRNA were transfected into cells. Cell proliferation, migration, and invasion were evaluated. The enrichment of ELF4 on the ITGB8-AS1 promoter was detected. Dual-luciferase assay was employed to assess the binding between ELF4 and the ITGB8-AS1 promoter. RNA pull-down and RNA immunoprecipitation assays were conducted to investigate the binding between ITGB8-AS1 and enhancer of zeste homolog 2 (EZH2). The binding of EZH2 and histone H3 lysine 27 trimethylation (H3K27me3) to the CLDN23 promoter was detected.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ELF4 and ITGB8-AS1 were upregulated in CRC cells, while CLDN23 was downregulated. Knockdown of ELF4 inhibited cell proliferation, invasion, and migration. Mechanistically, ELF4 transcriptionally activated ITGB8-AS1 and promoted the binding between ITGB8-AS1 and EZH2. EZH2 catalyzed H3K27me3 modification on the CLDN23 promoter, leading to decreased CLDN23 expression. Overexpression of ITGB8-AS1 or downregulation of CLDN23 could reduce the inhibitory effects of silencing ELF4 on CRC cell proliferation, migration, and invasion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ELF4 accelerates CRC progression through the ITGB8-AS1/CLDN23 axis, providing new therapeutic targets for CRC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":"20 6","pages":"761-770"},"PeriodicalIF":1.4,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340208","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}