Daniela Gonsalves, Raquel Ciérvide, Felipe Couñago
Chen et al explored clinicopathological features and prognostic factors, revealing advanced tumor stage, lung metastases, HER-2 overexpression, and triple-negative status as key contributors. Recent research connects astrocytes' role in brain metastasis with signaling pathways and the impact of Trastuzumab on HER-2 tumor survival. Factors such as positive HER2 status, lack of estrogen receptor expression, and liver metastasis are identified as additional risk factors. The routine use of magnetic resonance imaging, insights into gene mutations associated with metastasis, and the role of radiotherapy, including prophylaxis possibilities, is controversial in clinical practice. Understanding these risk factors in a multidisciplinary collaboration is precise for local treatments and targeted therapies, particularly for HER2+ tumors, impacting directly on longer survival.
{"title":"Bridging the gap: Predicting brain metastasis in breast cancer.","authors":"Daniela Gonsalves, Raquel Ciérvide, Felipe Couñago","doi":"10.5306/wjco.v15.i2.356","DOIUrl":"10.5306/wjco.v15.i2.356","url":null,"abstract":"<p><p>Chen <i>et al</i> explored clinicopathological features and prognostic factors, revealing advanced tumor stage, lung metastases, HER-2 overexpression, and triple-negative status as key contributors. Recent research connects astrocytes' role in brain metastasis with signaling pathways and the impact of Trastuzumab on HER-2 tumor survival. Factors such as positive HER2 status, lack of estrogen receptor expression, and liver metastasis are identified as additional risk factors. The routine use of magnetic resonance imaging, insights into gene mutations associated with metastasis, and the role of radiotherapy, including prophylaxis possibilities, is controversial in clinical practice. Understanding these risk factors in a multidisciplinary collaboration is precise for local treatments and targeted therapies, particularly for HER2+ tumors, impacting directly on longer survival.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"356-359"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060670","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}
Background: Breast cancer is a multifaceted and formidable disease with profound public health implications. Cell demise mechanisms play a pivotal role in breast cancer pathogenesis, with ATP-triggered cell death attracting mounting interest for its unique specificity and potential therapeutic pertinence.
Aim: To investigate the impact of ATP-induced cell death (AICD) on breast cancer, enhancing our understanding of its mechanism.
Methods: The foundational genes orchestrating AICD mechanisms were extracted from the literature, underpinning the establishment of a prognostic model. Simultaneously, a microRNA (miRNA) prognostic model was constructed that mirrored the gene-based prognostic model. Distinctions between high- and low-risk cohorts within mRNA and miRNA characteristic models were scrutinized, with the aim of delineating common influence mechanisms, substantiated through enrichment analysis and immune infiltration assessment.
Results: The mRNA prognostic model in this study encompassed four specific mRNAs: P2X purinoceptor 4, pannexin 1, caspase 7, and cyclin 2. The miRNA prognostic model integrated four pivotal miRNAs: hsa-miR-615-3p, hsa-miR-519b-3p, hsa-miR-342-3p, and hsa-miR-324-3p. B cells, CD4+ T cells, CD8+ T cells, endothelial cells, and macrophages exhibited inverse correlations with risk scores across all breast cancer subtypes. Furthermore, Kyoto Encyclopedia of Genes and Genomes analysis revealed that genes differentially expressed in response to mRNA risk scores significantly enriched 25 signaling pathways, while miRNA risk scores significantly enriched 29 signaling pathways, with 16 pathways being jointly enriched.
Conclusion: Of paramount significance, distinct mRNA and miRNA signature models were devised tailored to AICD, both potentially autonomous prognostic factors. This study's elucidation of the molecular underpinnings of AICD in breast cancer enhances the arsenal of potential therapeutic tools, offering an unparalleled window for innovative interventions. Essentially, this paper reveals the hitherto enigmatic link between AICD and breast cancer, potentially leading to revolutionary progress in personalized oncology.
{"title":"Elucidating the molecular basis of ATP-induced cell death in breast cancer: Construction of a robust prognostic model.","authors":"Hao-Ling Zhang, Sandai Doblin, Zhong-Wen Zhang, Zhi-Jing Song, Babu Dinesh, Yasser Tabana, Dahham Sabbar Saad, Mowaffaq Adam Ahmed Adam, Yong Wang, Wei Wang, Hao-Long Zhang, Sen Wu, Rui Zhao, Barakat Khaled","doi":"10.5306/wjco.v15.i2.208","DOIUrl":"10.5306/wjco.v15.i2.208","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is a multifaceted and formidable disease with profound public health implications. Cell demise mechanisms play a pivotal role in breast cancer pathogenesis, with ATP-triggered cell death attracting mounting interest for its unique specificity and potential therapeutic pertinence.</p><p><strong>Aim: </strong>To investigate the impact of ATP-induced cell death (AICD) on breast cancer, enhancing our understanding of its mechanism.</p><p><strong>Methods: </strong>The foundational genes orchestrating AICD mechanisms were extracted from the literature, underpinning the establishment of a prognostic model. Simultaneously, a microRNA (miRNA) prognostic model was constructed that mirrored the gene-based prognostic model. Distinctions between high- and low-risk cohorts within mRNA and miRNA characteristic models were scrutinized, with the aim of delineating common influence mechanisms, substantiated through enrichment analysis and immune infiltration assessment.</p><p><strong>Results: </strong>The mRNA prognostic model in this study encompassed four specific mRNAs: P2X purinoceptor 4, pannexin 1, caspase 7, and cyclin 2. The miRNA prognostic model integrated four pivotal miRNAs: hsa-miR-615-3p, hsa-miR-519b-3p, hsa-miR-342-3p, and hsa-miR-324-3p. B cells, CD4+ T cells, CD8+ T cells, endothelial cells, and macrophages exhibited inverse correlations with risk scores across all breast cancer subtypes. Furthermore, Kyoto Encyclopedia of Genes and Genomes analysis revealed that genes differentially expressed in response to mRNA risk scores significantly enriched 25 signaling pathways, while miRNA risk scores significantly enriched 29 signaling pathways, with 16 pathways being jointly enriched.</p><p><strong>Conclusion: </strong>Of paramount significance, distinct mRNA and miRNA signature models were devised tailored to AICD, both potentially autonomous prognostic factors. This study's elucidation of the molecular underpinnings of AICD in breast cancer enhances the arsenal of potential therapeutic tools, offering an unparalleled window for innovative interventions. Essentially, this paper reveals the hitherto enigmatic link between AICD and breast cancer, potentially leading to revolutionary progress in personalized oncology.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"208-242"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060672","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}
Angeles C Tecalco-Cruz, Karen H Medina-Abreu, Enrique Oropeza-Martínez, Jesus Zepeda-Cervantes, Aleida Vázquez-Macías, Marina Macías-Silva
Interferon-gamma (IFN-γ) plays a dual role in cancer; it is both a pro- and an antitumorigenic cytokine, depending on the type of cancer. The deregulation of the IFN-γ canonic pathway is associated with several disorders, including vulnerability to viral infections, inflammation, and cancer progression. In particular, the interplay between lung adenocarcinoma (LUAD) and viral infections appears to exist in association with the deregulation of IFN-γ signaling. In this mini-review, we investigated the status of the IFN-γ signaling pathway and the expression level of its components in LUAD. Interestingly, a reduction in IFNGR1 expression seems to be associated with LUAD progression, affecting defenses against viruses such as severe acute respiratory syndrome coronavirus 2. In addition, alterations in the expression of IFNGR1 may inhibit the antiproliferative action of IFN-γ signaling in LUAD.
{"title":"Deregulation of interferon-gamma receptor 1 expression and its implications for lung adenocarcinoma progression.","authors":"Angeles C Tecalco-Cruz, Karen H Medina-Abreu, Enrique Oropeza-Martínez, Jesus Zepeda-Cervantes, Aleida Vázquez-Macías, Marina Macías-Silva","doi":"10.5306/wjco.v15.i2.195","DOIUrl":"10.5306/wjco.v15.i2.195","url":null,"abstract":"<p><p>Interferon-gamma (IFN-γ) plays a dual role in cancer; it is both a pro- and an antitumorigenic cytokine, depending on the type of cancer. The deregulation of the IFN-γ canonic pathway is associated with several disorders, including vulnerability to viral infections, inflammation, and cancer progression. In particular, the interplay between lung adenocarcinoma (LUAD) and viral infections appears to exist in association with the deregulation of IFN-γ signaling. In this mini-review, we investigated the status of the IFN-γ signaling pathway and the expression level of its components in LUAD. Interestingly, a reduction in <i>IFNGR1</i> expression seems to be associated with LUAD progression, affecting defenses against viruses such as severe acute respiratory syndrome coronavirus 2. In addition, alterations in the expression of <i>IFNGR1</i> may inhibit the antiproliferative action of IFN-γ signaling in LUAD.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"195-207"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060671","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}
Zhuo et al looked into the part of transmembrane 9 superfamily member 1 (TM9SF1) in bladder cancer (BC), and evaluated if it can be used as a therapeutic target. They created a permanent BC cell line and tested the effects of TM9SF1 overexpression and suppression on BC cell growth, movement, invasion, and cell cycle advancement. Their results show that TM9SF1 can boost the growth, movement, and invasion of BC cells and their access into the G2/M stage of the cell cycle. This research gives a novel direction and concept for targeted therapy of BC.
{"title":"TM9SF1 is implicated in promoting the proliferation and invasion of bladder cancer cells.","authors":"Shu-Qing Zhou, Lian-Xiang Luo","doi":"10.5306/wjco.v15.i2.175","DOIUrl":"10.5306/wjco.v15.i2.175","url":null,"abstract":"<p><p>Zhuo <i>et al</i> looked into the part of transmembrane 9 superfamily member 1 (TM9SF1) in bladder cancer (BC), and evaluated if it can be used as a therapeutic target. They created a permanent BC cell line and tested the effects of TM9SF1 overexpression and suppression on BC cell growth, movement, invasion, and cell cycle advancement. Their results show that TM9SF1 can boost the growth, movement, and invasion of BC cells and their access into the G2/M stage of the cell cycle. This research gives a novel direction and concept for targeted therapy of BC.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"175-177"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060676","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}
Background: X-ray gastric cancer (GC) screening has been shown to decrease mortality. Population-based X-ray GC screening has been performed in Hiroshima Prefecture, Japan, since 1983 but time trends and the efficacy of the method over 39 years have not been assessed.
Aim: To evaluate time trends and efficacy of population-based X-ray GC screening and identify challenges and suggested solutions for the future.
Methods: This was a population-based retrospective study. The data were derived from aggregated data of the Hiroshima Regional Health Medical Promotion Organization, including the number and rate of participants and those requiring esophagogastroduodenoscopies (EGDs), the number and rate of participants diagnosed as having GC, and the positive predictive value of the abnormal findings detected by X-ray and confirmed by EGDs. The number and rate of esophageal cancers were also collected. Further, the cost of detecting one GC was evaluated.
Results: The number of participants has decreased during the last four decades, from 39925 in 1983 to 12923 in 2021. The rate of those requiring EGDs decreased significantly in recent years (P < 0.001). The number of participants diagnosed as having GC has also declined, from 76 to 10 cases. However, the rate of cases diagnosed as GC among the participants remained around 0.1%. The positive predictive value increased significantly in recent years except during 1983-1991. The number and rate of accidentally detected esophageal cancers have risen recently, from 0% in 2008 to 0.02% in 2021, one-fifth of the diagnosis rate of GC. One GC diagnosis costs approximately 4200000 Japanese Yen (30000 United States Dollars) for the X-ray screenings and EGDs.
Conclusion: X-ray GC screening in Hiroshima has been efficient, but one challenge is the cost. Esophageal cancers may also need to be considered because they have gradually increased in recent years.
{"title":"Population-based X-ray gastric cancer screening in Hiroshima prefecture, Japan.","authors":"Nhu Thi Hanh Vu, Yuji Urabe, Duc Trong Quach, Shiro Oka, Toru Hiyama","doi":"10.5306/wjco.v15.i2.271","DOIUrl":"10.5306/wjco.v15.i2.271","url":null,"abstract":"<p><strong>Background: </strong>X-ray gastric cancer (GC) screening has been shown to decrease mortality. Population-based X-ray GC screening has been performed in Hiroshima Prefecture, Japan, since 1983 but time trends and the efficacy of the method over 39 years have not been assessed.</p><p><strong>Aim: </strong>To evaluate time trends and efficacy of population-based X-ray GC screening and identify challenges and suggested solutions for the future.</p><p><strong>Methods: </strong>This was a population-based retrospective study. The data were derived from aggregated data of the Hiroshima Regional Health Medical Promotion Organization, including the number and rate of participants and those requiring esophagogastroduodenoscopies (EGDs), the number and rate of participants diagnosed as having GC, and the positive predictive value of the abnormal findings detected by X-ray and confirmed by EGDs. The number and rate of esophageal cancers were also collected. Further, the cost of detecting one GC was evaluated.</p><p><strong>Results: </strong>The number of participants has decreased during the last four decades, from 39925 in 1983 to 12923 in 2021. The rate of those requiring EGDs decreased significantly in recent years (<i>P</i> < 0.001). The number of participants diagnosed as having GC has also declined, from 76 to 10 cases. However, the rate of cases diagnosed as GC among the participants remained around 0.1%. The positive predictive value increased significantly in recent years except during 1983-1991. The number and rate of accidentally detected esophageal cancers have risen recently, from 0% in 2008 to 0.02% in 2021, one-fifth of the diagnosis rate of GC. One GC diagnosis costs approximately 4200000 Japanese Yen (30000 United States Dollars) for the X-ray screenings and EGDs.</p><p><strong>Conclusion: </strong>X-ray GC screening in Hiroshima has been efficient, but one challenge is the cost. Esophageal cancers may also need to be considered because they have gradually increased in recent years.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"271-281"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060674","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}
Nhu Thi Hanh Vu, Huy Minh Le, Diem Thi-Ngoc Vo, Hoang Anh Vu, Nhan Quang Le, Dung Dang Quy Ho, Duc Trong Quach
Background: Sessile serrated lesions (SSLs) are considered precancerous colorectal lesions that should be detected and removed to prevent colorectal cancer. Previous studies in Vietnam mainly investigated the adenoma pathway, with limited data on the serrated pathway.
Aim: To evaluate the prevalence, risk factors, and BRAF mutations of SSLs in the Vietnamese population.
Methods: This is a cross-sectional study conducted on patients with lower gastrointestinal symptoms who underwent colonoscopy at a tertiary hospital in Vietnam. SSLs were diagnosed on histopathology according to the 2019 World Health Organization classification. BRAF mutation analysis was performed using the Sanger DNA sequencing method. The multivariate logistic regression model was used to determine SSL-associated factors.
Results: There were 2489 patients, with a mean age of 52.1 ± 13.1 and a female-to-male ratio of 1:1.1. The prevalence of SSLs was 4.2% [95% confidence interval (CI): 3.5-5.1]. In the multivariate analysis, factors significantly associated with SSLs were age ≥ 40 [odds ratio (OR): 3.303; 95%CI: 1.607-6.790], male sex (OR: 2.032; 95%CI: 1.204-3.429), diabetes mellitus (OR: 2.721; 95%CI: 1.551-4.772), and hypertension (OR: 1.650, 95%CI: 1.045-2.605). The rate of BRAF mutations in SSLs was 35.5%.
Conclusion: The prevalence of SSLs was 4.2%. BRAF mutations were present in one-third of SSLs. Significant risk factors for SSLs included age ≥ 40, male sex, diabetes mellitus, and hypertension.
{"title":"Prevalence, risk factors, and BRAF mutation of colorectal sessile serrated lesions among Vietnamese patients.","authors":"Nhu Thi Hanh Vu, Huy Minh Le, Diem Thi-Ngoc Vo, Hoang Anh Vu, Nhan Quang Le, Dung Dang Quy Ho, Duc Trong Quach","doi":"10.5306/wjco.v15.i2.290","DOIUrl":"10.5306/wjco.v15.i2.290","url":null,"abstract":"<p><strong>Background: </strong>Sessile serrated lesions (SSLs) are considered precancerous colorectal lesions that should be detected and removed to prevent colorectal cancer. Previous studies in Vietnam mainly investigated the adenoma pathway, with limited data on the serrated pathway.</p><p><strong>Aim: </strong>To evaluate the prevalence, risk factors, and BRAF mutations of SSLs in the Vietnamese population.</p><p><strong>Methods: </strong>This is a cross-sectional study conducted on patients with lower gastrointestinal symptoms who underwent colonoscopy at a tertiary hospital in Vietnam. SSLs were diagnosed on histopathology according to the 2019 World Health Organization classification. BRAF mutation analysis was performed using the Sanger DNA sequencing method. The multivariate logistic regression model was used to determine SSL-associated factors.</p><p><strong>Results: </strong>There were 2489 patients, with a mean age of 52.1 ± 13.1 and a female-to-male ratio of 1:1.1. The prevalence of SSLs was 4.2% [95% confidence interval (CI): 3.5-5.1]. In the multivariate analysis, factors significantly associated with SSLs were age ≥ 40 [odds ratio (OR): 3.303; 95%CI: 1.607-6.790], male sex (OR: 2.032; 95%CI: 1.204-3.429), diabetes mellitus (OR: 2.721; 95%CI: 1.551-4.772), and hypertension (OR: 1.650, 95%CI: 1.045-2.605). The rate of BRAF mutations in SSLs was 35.5%.</p><p><strong>Conclusion: </strong>The prevalence of SSLs was 4.2%. BRAF mutations were present in one-third of SSLs. Significant risk factors for SSLs included age ≥ 40, male sex, diabetes mellitus, and hypertension.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"290-301"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060675","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}
Long Wei, Shi-Shuo Wang, Zhi-Guang Huang, Rong-Quan He, Jia-Yuan Luo, Bin Li, Ji-Wen Cheng, Kun-Jun Wu, Yu-Hong Zhou, Shi Liu, Sheng-Hua Li, Gang Chen
Background: Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To improve the survival rate and prognosis of BC patients, it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention. Transmembrane 9 superfamily member 1 (TM9SF1), also known as MP70 and HMP70, is a member of a family of nine transmembrane superfamily proteins, which was first identified in 1997. TM9SF1 can be expressed in BC, but its biological function and mechanism in BC are not clear.
Aim: To investigate the biological function and mechanism of TM9SF1 in BC.
Methods: Cells at 60%-80% confluence were transfected with lentiviral vectors for 48-72 h to achieve stable TM9SF1 overexpression or silencing in three BC cell lines (5637, T24, and UM-UC-3). The effect of TM9SF1 on the biological behavior of BC cells was then investigated through CCK8, wound-healing assay, transwell assay, and flow cytometry.
Results: Overexpression of TM9SF1 increased the in vitro proliferation, migration, and invasion of BC cells by promoting the entry of BC cells into the G2/M phase. Silencing of TM9SF1 inhibited in vitro proliferation, migration, and invasion of BC cells and blocked BC cells in the G1 phase.
Conclusion: TM9SF1 may be an oncogene in BC.
背景:膀胱癌(BC)是最常见的泌尿系统肿瘤:膀胱癌(BC)是最常见的泌尿系统肿瘤。它具有复发率高、导师异质性和耐化疗等特点。此外,几十年来,膀胱癌患者的长期生存率一直未变,严重影响了患者的生存质量。为了改善 BC 患者的生存率和预后,有必要探索 BC 发生和发展的分子机制,并确定治疗和干预的靶点。跨膜 9 超家族成员 1(TM9SF1)又称 MP70 和 HMP70,是九种跨膜超家族蛋白家族中的一员,于 1997 年首次被发现。目的:研究 TM9SF1 在 BC 中的生物学功能和机制:方法:用慢病毒载体转染汇合度为60%-80%的细胞48-72 h,使TM9SF1在三种BC细胞系(5637、T24和UM-UC-3)中稳定过表达或沉默。然后通过CCK8、伤口愈合试验、Transwell试验和流式细胞术研究了TM9SF1对BC细胞生物学行为的影响:结果:通过促进 BC 细胞进入 G2/M 期,过表达 TM9SF1 增加了 BC 细胞的体外增殖、迁移和侵袭。沉默TM9SF1可抑制BC细胞的体外增殖、迁移和侵袭,并阻止BC细胞进入G1期:结论:TM9SF1可能是BC的致癌基因。
{"title":"TM9SF1 promotes bladder cancer cell growth and infiltration.","authors":"Long Wei, Shi-Shuo Wang, Zhi-Guang Huang, Rong-Quan He, Jia-Yuan Luo, Bin Li, Ji-Wen Cheng, Kun-Jun Wu, Yu-Hong Zhou, Shi Liu, Sheng-Hua Li, Gang Chen","doi":"10.5306/wjco.v15.i2.302","DOIUrl":"10.5306/wjco.v15.i2.302","url":null,"abstract":"<p><strong>Background: </strong>Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To improve the survival rate and prognosis of BC patients, it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention. Transmembrane 9 superfamily member 1 (TM9SF1), also known as MP70 and HMP70, is a member of a family of nine transmembrane superfamily proteins, which was first identified in 1997. <i>TM9SF1</i> can be expressed in BC, but its biological function and mechanism in BC are not clear.</p><p><strong>Aim: </strong>To investigate the biological function and mechanism of <i>TM9SF1</i> in BC.</p><p><strong>Methods: </strong>Cells at 60%-80% confluence were transfected with lentiviral vectors for 48-72 h to achieve stable <i>TM9SF1</i> overexpression or silencing in three BC cell lines (5637, T24, and UM-UC-3). The effect of <i>TM9SF1</i> on the biological behavior of BC cells was then investigated through CCK8, wound-healing assay, transwell assay, and flow cytometry.</p><p><strong>Results: </strong>Overexpression of <i>TM9SF1</i> increased the <i>in vitro</i> proliferation, migration, and invasion of BC cells by promoting the entry of BC cells into the G2/M phase. Silencing of <i>TM9SF1</i> inhibited <i>in vitro</i> proliferation, migration, and invasion of BC cells and blocked BC cells in the G1 phase.</p><p><strong>Conclusion: </strong><i>TM9SF1</i> may be an oncogene in BC.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"302-316"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060677","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}
Prostate cancer poses a significant health challenge globally, demanding proactive prevention strategies. This editorial explores the emerging role of vitamin D in prostate cancer prevention. While traditionally associated with bone health, vitamin D is increasingly recognized for its broader impact on immune function, cellular signaling, and cancer prevention. Epidemiological studies suggest an intriguing link between vitamin D deficiency and elevated prostate cancer risk, particularly in regions with limited sunlight exposure. Mechanistically, vitamin D regulates cellular processes, inhibiting unchecked cancer cell growth and bolstering immune surveillance. Personalized prevention strategies, considering individual factors, are deemed essential for harnessing the full potential of vitamin D. To unlock this potential, the future calls for robust research, public awareness campaigns, dietary improvements, and vigilant medical guidance. Collaborative efforts are poised to pave the way toward a future where vitamin D stands as a sentinel in prostate cancer prevention, ushering in hope and improved health for men worldwide.
前列腺癌对全球健康构成重大挑战,需要采取积极的预防策略。这篇社论探讨了维生素 D 在前列腺癌预防中的新作用。虽然维生素 D 传统上与骨骼健康有关,但人们越来越认识到它对免疫功能、细胞信号传导和癌症预防的广泛影响。流行病学研究表明,维生素 D 缺乏与前列腺癌风险升高之间存在着有趣的联系,尤其是在日光照射有限的地区。从机理上讲,维生素 D 可调节细胞过程,抑制癌细胞肆意生长,并加强免疫监测。考虑到个体因素的个性化预防策略被认为是充分发挥维生素 D 潜力的关键所在。要释放这一潜能,未来需要大力开展研究、提高公众意识活动、改善膳食和警惕性医疗指导。各方的共同努力将为未来铺平道路,让维生素 D 成为预防前列腺癌的哨兵,为全世界的男性带来希望和健康。
{"title":"Unlocking the potential-vitamin D in prostate cancer prevention.","authors":"Ayun Cassell, Solomane Konneh","doi":"10.5306/wjco.v15.i2.169","DOIUrl":"10.5306/wjco.v15.i2.169","url":null,"abstract":"<p><p>Prostate cancer poses a significant health challenge globally, demanding proactive prevention strategies. This editorial explores the emerging role of vitamin D in prostate cancer prevention. While traditionally associated with bone health, vitamin D is increasingly recognized for its broader impact on immune function, cellular signaling, and cancer prevention. Epidemiological studies suggest an intriguing link between vitamin D deficiency and elevated prostate cancer risk, particularly in regions with limited sunlight exposure. Mechanistically, vitamin D regulates cellular processes, inhibiting unchecked cancer cell growth and bolstering immune surveillance. Personalized prevention strategies, considering individual factors, are deemed essential for harnessing the full potential of vitamin D. To unlock this potential, the future calls for robust research, public awareness campaigns, dietary improvements, and vigilant medical guidance. Collaborative efforts are poised to pave the way toward a future where vitamin D stands as a sentinel in prostate cancer prevention, ushering in hope and improved health for men worldwide.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"169-174"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060678","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}
Ali Ahmed Mohamed, Rakan Alshaibi, Steven Faragalla, Youssef Mohamed, Brandon Lucke-Wold
Gliomas are primary brain tumors derived from glial cells of the central nervous system, afflicting both adults and children with distinct characteristics and therapeutic challenges. Recent developments have ushered in novel clinical and molecular prognostic factors, reshaping treatment paradigms based on classification and grading, determined by histological attributes and cellular lineage. This review article delves into the diverse treatment modalities tailored to the specific grades and molecular classifications of gliomas that are currently being discussed and used clinically in the year 2023. For adults, the therapeutic triad typically consists of surgical resection, chemotherapy, and radiotherapy. In contrast, pediatric gliomas, due to their diversity, require a more tailored approach. Although complete tumor excision can be curative based on the location and grade of the glioma, certain non-resectable cases demand a chemotherapy approach usually involving, vincristine and carboplatin. Additionally, if surgery or chemotherapy strategies are unsuccessful, Vinblastine can be used. Despite recent advancements in treatment methodologies, there remains a need of exploration in the literature, particularly concerning the efficacy of treatment regimens for isocitrate dehydrogenase type mutant astrocytomas and fine-tuned therapeutic approaches tailored for pediatric cohorts. This review article explores into the therapeutic modalities employed for both adult and pediatric gliomas in the context of their molecular classification.
{"title":"Updates on management of gliomas in the molecular age.","authors":"Ali Ahmed Mohamed, Rakan Alshaibi, Steven Faragalla, Youssef Mohamed, Brandon Lucke-Wold","doi":"10.5306/wjco.v15.i2.178","DOIUrl":"10.5306/wjco.v15.i2.178","url":null,"abstract":"<p><p>Gliomas are primary brain tumors derived from glial cells of the central nervous system, afflicting both adults and children with distinct characteristics and therapeutic challenges. Recent developments have ushered in novel clinical and molecular prognostic factors, reshaping treatment paradigms based on classification and grading, determined by histological attributes and cellular lineage. This review article delves into the diverse treatment modalities tailored to the specific grades and molecular classifications of gliomas that are currently being discussed and used clinically in the year 2023. For adults, the therapeutic triad typically consists of surgical resection, chemotherapy, and radiotherapy. In contrast, pediatric gliomas, due to their diversity, require a more tailored approach. Although complete tumor excision can be curative based on the location and grade of the glioma, certain non-resectable cases demand a chemotherapy approach usually involving, vincristine and carboplatin. Additionally, if surgery or chemotherapy strategies are unsuccessful, Vinblastine can be used. Despite recent advancements in treatment methodologies, there remains a need of exploration in the literature, particularly concerning the efficacy of treatment regimens for isocitrate dehydrogenase type mutant astrocytomas and fine-tuned therapeutic approaches tailored for pediatric cohorts. This review article explores into the therapeutic modalities employed for both adult and pediatric gliomas in the context of their molecular classification.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"178-194"},"PeriodicalIF":2.6,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060607","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}
Background: Calcifying fibrous tumors (CFTs) are rare mesenchymal lesions that can occur in various sites throughout the body, including the tubular gastrointestinal (GI) tract.
Aim: To analyze the clinical findings of 36 patients with GI tract CFTs to provide guidance for diagnosis and treatment.
Methods: This retrospective study included 36 patients diagnosed with CFTs of the GI tract. We collected demographic and clinical information and conducted regular follow-ups to assess for local recurrence.
Results: The stomach was the most commonly involved site, accounting for 72.2% of the 36 CFTs. Endoscopic mucosal resection (n = 1, 2.8%), endoscopic submucosal dissection (n = 14, 38.9%), endoscopic full-thickness resection (n = 16, 44.4%), and submucosal tunneling endoscopic resection (n = 5, 13.9%) were used to resect calcifying fibrous tumors. Overall, 34 (94.4%) CFTs underwent complete endoscopic resections with a mean procedure time of 39.8 ± 29.8 min. The average maximum diameter of the tumors was 10.6 ± 4.3 cm. No complications, such as bleeding or perforation, occurred during an average hospital stay of 2.9 ± 1.2 d. In addition, two patients developed new growth of CFTs near the primary tumor sites, and none of the patients developed distant metastases during the follow-up period.
Conclusion: GI tract CFTs are rare and typically benign tumors that can be effectively managed with endoscopic procedures.
{"title":"Endoscopic resection for calcifying fibrous tumors of the gastrointestinal tract.","authors":"Zi-Han Geng, Yan Zhu, Pei-Yao Fu, Yi-Fan Qu, Shi-Yao Chen, Yun-Shi Zhong, Yi-Qun Zhang, Wei-Feng Chen, Wen-Zheng Qin, Jian-Wei Hu, Ming-Yan Cai, Li-Qing Yao, Quan-Lin Li, Ping-Hong Zhou","doi":"10.5306/wjco.v15.i2.282","DOIUrl":"10.5306/wjco.v15.i2.282","url":null,"abstract":"<p><strong>Background: </strong>Calcifying fibrous tumors (CFTs) are rare mesenchymal lesions that can occur in various sites throughout the body, including the tubular gastrointestinal (GI) tract.</p><p><strong>Aim: </strong>To analyze the clinical findings of 36 patients with GI tract CFTs to provide guidance for diagnosis and treatment.</p><p><strong>Methods: </strong>This retrospective study included 36 patients diagnosed with CFTs of the GI tract. We collected demographic and clinical information and conducted regular follow-ups to assess for local recurrence.</p><p><strong>Results: </strong>The stomach was the most commonly involved site, accounting for 72.2% of the 36 CFTs. Endoscopic mucosal resection (<i>n</i> = 1, 2.8%), endoscopic submucosal dissection (<i>n</i> = 14, 38.9%), endoscopic full-thickness resection (<i>n</i> = 16, 44.4%), and submucosal tunneling endoscopic resection (<i>n</i> = 5, 13.9%) were used to resect calcifying fibrous tumors. Overall, 34 (94.4%) CFTs underwent complete endoscopic resections with a mean procedure time of 39.8 ± 29.8 min. The average maximum diameter of the tumors was 10.6 ± 4.3 cm. No complications, such as bleeding or perforation, occurred during an average hospital stay of 2.9 ± 1.2 d. In addition, two patients developed new growth of CFTs near the primary tumor sites, and none of the patients developed distant metastases during the follow-up period.</p><p><strong>Conclusion: </strong>GI tract CFTs are rare and typically benign tumors that can be effectively managed with endoscopic procedures.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"15 2","pages":"282-289"},"PeriodicalIF":2.8,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10915946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060673","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}