Journal of Cancer Prevention最新文献

{"title":"Efficacy of Bacillus Calmette-Guérin in Cancer Prevention and Its Putative Mechanisms","authors":"Sakshi Gupta, Saurabh Yadav, Pawan Kumar","doi":"10.15430/JCP.23.036","DOIUrl":"https://doi.org/10.15430/JCP.23.036","url":null,"abstract":"Bacillus Calmette-Guérin (BCG) is an attenuated strain of Mycobacterium bovis. Although it was developed as a prophylactic vaccine against tuberculosis (TB), researchers have also evaluated it for preventing cancer development or progression. These studies were inspired by the available data regarding the protective effects of microbial infection against cancers and an inverse relationship between TB and cancer mortality. Initial studies demonstrated the efficacy of BCG in preventing leukemia, melanoma and a few other cancers. However, mixed results were observed in later studies. Importantly, these studies have led to the successful use of BCG in the tertiary prevention of non-muscle invasive bladder cancer, wherein BCG therapy has been found to be more effective than chemotherapy. Moreover, in a recently published 60-year follow-up study, childhood BCG vaccination has been found to significantly prevent lung cancer development. In the present manuscript, we reviewed the studies evaluating the efficacy of BCG in cancer prevention and discussed its putative mechanisms. Also, we sought to explain the mixed results of BCG efficacy in preventing different cancers.","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"55 6","pages":"6 - 15"},"PeriodicalIF":2.5,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140367847","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}

{"title":"Potent Suppression of Prostate Cancer Cell Growth and Eradication of Cancer Stem Cells by CD44-targeted Nanoliposome-quercetin Nanoparticles.","authors":"Kader Turkekul, Suat Erdogan","doi":"10.15430/JCP.2023.28.4.160","DOIUrl":"10.15430/JCP.2023.28.4.160","url":null,"abstract":"<p><p>The bioavailability of quercetin, a natural compound, is hindered by low solubility, limited absorption, and restricted systemic availability. Therefore, encapsulating it in biocompatible nanoparticles presents a promising solution. This study aimed to target prostate cancer stem cells (CSCs) overexpressing CD44+ receptors as well as cancer cells, employing quercetin-loaded hyaluronic acid-modified nanoliposomes (LP-Quer-HA). Synthesized via a green ethanol injection method, these nanoliposomes had an average diameter of 134 nm and an impressive loading efficiency of 96.9%. Human prostate cancer cells were treated with either 10 μM of free quercetin or the same concentration delivered by LP-Quer-HA for 72 hours. Free quercetin reduced androgen-resistant PC3 cell viability by 16%, while LP-Quer-HA significantly increased cell death to 60%. It induced apoptosis, upregulating cytochrome <i>c</i>, Bax, caspases 3 and 8, and downregulating survivin and Bcl-2 expression. Compared to free quercetin, LP-Quer-HA upregulated E-cadherin expression while inhibiting cell migration and reducing the expression of fibronectin, N-cadherin, and MMP9. Treatment of PC3 cell tumor spheroids with LP-Quer-HA decreased the number of CD44 cells and expression of CD44, Oct3/4 and Wnt. Moreover, LP-Quer-HA inhibited p-ERK expression while increasing p38/MAPK and NF-κB protein expression. In androgen-sensitive LNCaP cells, LP-Quer-HA efficacy was notable, reducing cell viability from 10% to 52% compared to free quercetin. Utilizing HA-modified nanoliposomes as a quercetin delivery system enhanced its potency at lower concentrations, reducing the CD44+ cell population and effectively impeding prostate cancer cell proliferation and migration. These findings underscore the potential of quercetin-loaded cationic nanoliposomes as a robust therapeutic approach.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"160-174"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417115","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}

{"title":"Erratum: The Protective Effect of <i>Roseburia faecis</i> Against Repeated Water Avoidance Stress-induced Irritable Bowel Syndrome in a Wister Rat Model.","authors":"Soo In Choi, Nayoung Kim, Ryoung Hee Nam, Jae Young Jang, Eun Hye Kim, SungChan Ha, Kisung Kang, Wonseok Lee, HyeLim Choi, Yeon-Ran Kim, Yeong-Jae Seok, Cheol Min Shin, Dong Ho Lee","doi":"10.15430/JCP.2023.28.4.219","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.4.219","url":null,"abstract":"<p><p>[This corrects the article on p. 93 in vol. 28, PMID: 37830115.].</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"219"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417112","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}

{"title":"Effects of Black Raspberry Supplementation on Methylation Pathways in <i>Vav-cre</i><i>Asxl1</i>^<i>fl/fl</i><i>Tet2</i>^<i>fl/fl</i> Double Knockout Mice with Early-stage Myelodysplastic Syndrome.","authors":"Athena Dong, Yi-Wen Huang, Ben Niu, Ruiling Liu, Weijie Wu, Haiyan Gao, Jianhua Yu, Li-Shu Wang","doi":"10.15430/JCP.2023.28.4.212","DOIUrl":"10.15430/JCP.2023.28.4.212","url":null,"abstract":"<p><p>Myelodysplastic syndromes (MDS) are a subset of myeloid malignancies defined by clonality of immature hematopoietic stem cells that leads to faulty blood cell development. These syndromes can lead to an increased risk of infection and may transform into acute myeloid leukemia, making it critical to determine effective treatments for the condition. While hypomethylating agents such as azacitidine and decitabine, as well as stem cell transplants, have been delineated as favored treatments for MDS, not all patients are physiologically receptive to these treatments. However, black raspberries (BRBs) have been shown to exert hypomethylating effects in various malignancies, with minimal adverse effects and thus a broader range of potential candidacies. This study aimed to investigate the potential of BRBs to exert such effects on MDS using <i>Addition of Sex Combs Like</i>/<i>Tet Methylcytosine Dioxygenase 2</i> (<i>Asxl1</i>/<i>Tet2</i>) double knockout mice (<i>Vav-cre</i> <i>Asxl1</i>^<i>fl/fl</i> <i>Tet2</i>^<i>fl/fl</i>), which typically manifest symptoms around 25 weeks of age, mirroring genetic mutations found in humans with MDS. Following a 12-week dietary supplementation of <i>Vav-cre</i> <i>Asxl1</i>^<i>fl/fl</i> <i>Tet2</i>^<i>fl/fl</i> mice with 5% BRBs, we observed both hyper- and hypomethylation at multiple transcription start sites and intragenic locations linked to critical pathways, including hematopoiesis. This methylation profile may have implications for delaying the onset of MDS, prompting a need for in-depth investigation. Our results emphasize the importance of exploring whether an extended BRB intervention can effectively alter MDS risk and elucidate the relationship between BRB-induced methylation changes, thus further unlocking the potential benefits of BRBs for MDS patients.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"212-218"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417111","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}

{"title":"Induction of Hepatocellular Carcinoma Cell Cycle Arrest and Apoptosis by <i>Dendropanax morbifera</i> Leveille Leaf Extract via the PI3K/AKT/mTOR Pathway.","authors":"Gi Dae Kim","doi":"10.15430/JCP.2023.28.4.185","DOIUrl":"10.15430/JCP.2023.28.4.185","url":null,"abstract":"<p><p>Liver cancer is prevalent worldwide and associated with a high mortality rate. Therefore, developing novel drugs derived from natural products to reduce the side effects of chemotherapy is urgently needed. In this study, the inhibitory effect of <i>Dendropanax morbifera</i> Leveille extract (DME) on growth of hepatocellular carcinoma (HCC) cells and its underlying mechanisms were investigated. DME suppressed the growth, migration, and invasion of SK-Hep1 human HCC cells. It also reduced the expression of the G0/G1 phase regulator proteins cyclin-dependent kinase (CDK) 4, cyclin D, CDK2, and cyclin E, thereby inducing G0/G1 arrest. Moreover, DME treatment reduced the expression of antiapoptotic proteins, including caspase-9, caspase-3, PARP, and Bcl-2 and increased the expression of the proapoptotic protein, Bax. DME also increased reactive oxygen species production and reduced the cellular uptake of rhodamine 123. DME treatment increased the levels of p-p38 and p-FOXO3a in a dose-dependent manner and decreased those of p-PI3K, p-AKT, p-mTOR, and p-p70 in SK-Hep1 cells. In addition, combined treatment with DME and LY294002, an AKT inhibitor, significantly reduced p-AKT levels. In summary, these results show that the PI3K/AKT/mTOR signaling pathway is involved in DME-mediated inhibition of proliferation, migration, and invasiveness, and induction of apoptosis of HCC cells.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"185-193"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417113","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}

{"title":"Antiproliferative Activity of Gibbosic Acid H through Induction of G₀/G₁ Cell Cycle Arrest and Apoptosis in Human Lung Cancer Cells.","authors":"Jaeho Han, Donghwa Kim, Hyen Joo Park, Hee-Juhn Park, Sang Kook Lee","doi":"10.15430/JCP.2023.28.4.201","DOIUrl":"10.15430/JCP.2023.28.4.201","url":null,"abstract":"<p><p>Lung cancer is one of the most common causative cancers worldwide. Particularly, non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases. NSCLC is a serious form of lung cancer that requires prompt diagnosis, and the 5-year survival rate for patients with this disease is only 24%. Gibbosic acid H (GaH), a natural lanostanoid obtained from the <i>Ganoderma</i> species (Ganodermataceae), has antiproliferative activities against colon and lung cancer cells. The aim of the present study was to evaluate the antiproliferative activity of GaH in NSCLC cells and to elucidate the underlying molecular mechanisms. GaH was found to induce G₀/G₁ cell cycle arrest and autophagy by activating adenosine monophosphate-activated protein kinase in A549 and H1299 cells. The induction of this cell cycle arrest was associated with the downregulation of cyclin E1 and CDK2. Additionally, the induction of autophagy by GaH was correlated with the upregulation of LC3B, beclin-1, and p53 expression. GaH also induced apoptosis by upregulating cleaved caspase-3 and Bax in the lung cancer cells. These findings suggest that GaH has a potential in the growth inhibition of human lung cancer cells.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"201-211"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417107","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}

{"title":"Prognostic Significance of Tumor Mutation Burden among Patients with Non-small Cell Lung Cancer Who Received Platinum-based Adjuvant Chemotherapy: An Exploratory Study.","authors":"Wei-Xi Shen, Guang-Hua Li, Yu-Jia Li, Peng-Fei Zhang, Jia-Xing Yu, Di Shang, Qiu-Shi Wang","doi":"10.15430/JCP.2023.28.4.175","DOIUrl":"10.15430/JCP.2023.28.4.175","url":null,"abstract":"<p><p>This study aimed to investigate the prognostic significance of tumor mutation burden (TMB) among patients with non-small cell lung cancer (NSCLC) who received platinum-based adjuvant chemotherapy. Tumor tissue specimens after surgical resection were collected for DNA extraction. Somatic mutation detection and TMB analysis were conducted using next-generation sequencing (NGS). Recurrence status of the patients was assessed in the hospital during the adjuvant chemotherapy period, and long-term survival data of patients were obtained by telephone follow-up. Univariate analysis between TMB status and prognosis was carried out by survival analysis. A retrospective review of 78 patients with non-squamous NSCLC who received platinum-based adjuvant chemotherapy showed a median disease-free survival of 3.6 years and median overall survival (OS) of 5.3 years. NGS analysis exhibited that the most common mutated somatic genes among the 78 patients were tumor suppressor protein p53 (TP53), epidermal growth factor receptor, low-density lipoprotein receptor related protein 1B, DNA methyltransferase 3 alpha and FAT atypical cadherin 3, and their prevalence was 56.4%, 48.7%, 37.2%, 30.7%, and 25.6%, respectively. TMB status was divided into TMB-L (≤ 4.5/Mb) and TMB-H (> 4.5/Mb) based on the median TMB threshold. Relevance of TMB to prognosis suggested that the median OS of patients with TMB-L was significantly longer than that of patients with TMB-H (NR vs. 4.6, <i>P</i> = 0.014). Higher TMB status conferred a worse implication on OS among patients with non-squamous NSCLC who received platinum-based adjuvant chemotherapy.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"175-184"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417127","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}

{"title":"Cadmium-induced Carcinogenesis in Respiratory Organs and the Prostate: Insights from Three Perspectives on Toxicogenomic Approach.","authors":"Jun Lee, Dong Yeop Shin, Yujin Jang, Jun Pyo Han, Eun-Min Cho, Young Rok Seo","doi":"10.15430/JCP.2023.28.4.150","DOIUrl":"10.15430/JCP.2023.28.4.150","url":null,"abstract":"<p><p>Cadmium (Cd) exposure primarily occurs through inhalation, either by smoking or occupational exposure to contaminated air. Upon inhalation, Cd ultimately reaches the prostate through the bloodstream. In this review, we investigate the carcinogenic potential of Cd in both respiratory organs and the prostate. Specifically, this review examines cellular metabolism, comprehensive toxicity, and carcinogenic mechanisms by exploring gene ontology, biological networks, and adverse outcome pathways. In the respiratory organs, Cd induces lung cancer by altering the expression of <i>IL1B</i> and <i>FGF2</i>, causing DNA damage, reducing cell junction integrity, and promoting apoptosis. In the prostate, Cd induces prostate cancer by modifying the expression of <i>EDN1</i> and <i>HMOX1</i>, leading to abnormal protein activities and maturation, suppressing tumor suppressors, and inducing apoptosis. Collectively, this review provides a comprehensive understanding of the carcinogenic mechanisms of Cd in two different organs by adopting toxicogenomic approaches. These insights can serve as a foundation for further research on cadmium-induced cancer, contributing to the establishment of future cancer prevention strategies.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"150-159"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417108","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}

{"title":"Diagnostic Validity of a Serological Test with the Current Infection Marker in Thai Adults before and after <i>Helicobacter pylori</i> Eradication Therapy.","authors":"Setthachai Piwchan, Kittipoom Tossapornpong, Suppana Chuensakul, Ekawee Sripariwuth","doi":"10.15430/JCP.2023.28.4.194","DOIUrl":"10.15430/JCP.2023.28.4.194","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> infection poses significant health risks, such as gastric adenocarcinoma, necessitating accurate diagnosis and effective treatment in primary care. This study evaluated the diagnostic efficacy of the serological current infection marker (CIM) test in identifying current <i>H. pylori</i> infection. The CIM test samples from 159 participants undergoing gastroscopy were collected, and <i>H. pylori</i>-positive outpatients received triple therapy based on histology or rapid urease test results. Following treatment, 45 patients underwent a ¹³C-urea breath test and the CIM test for eradication assessment. For pre-eradication, the CIM test demonstrated 89.6% sensitivity, 95.7% specificity, 93.8% positive predictive value, 92.6% negative predictive value, and 93.1% accuracy. Following post-eradication, the CIM test exhibited sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 71.4%, 92.1%, 62.5%, 94.6%, and 88.9%, respectively, using the ¹³C-urea breath test as the reference standard. The CIM test showcased commendable diagnostic performance, emphasizing its efficacy in both pre- and post-eradication scenarios. Notably, the accuracy, non-invasiveness, user-friendliness, and cost-effectiveness of the CIM test advocate for its recommendation as a preferred diagnostic tool in primary care settings for <i>H. pylori</i> infection detection.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"194-200"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417110","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}

{"title":"Nrf2, A Target for Precision Oncology in Cancer Prognosis and Treatment.","authors":"Hoang Kieu Chi Ngo, Hoang Le, Young-Joon Surh","doi":"10.15430/JCP.2023.28.4.131","DOIUrl":"10.15430/JCP.2023.28.4.131","url":null,"abstract":"<p><p>Activating nuclear factor-erythroid 2-related factor (Nrf2), a master regulator of redox homeostasis, has been shown to suppress initiation of carcinogenesis in normal cells. However, this transcription factor has recently been reported to promote proliferation of some transformed or cancerous cells. In tumor cells, Nrf2 is prone to mutations that result in stabilization and concurrent accumulation of its protein product. A hyperactivated mutant form of Nrf2 could support the cancer cells for enhanced proliferation, invasiveness, and resistance to chemotherapeutic agents and radiotherapy, which are associated with a poor clinical outcome. Hence understanding mutations in Nrf2 would have a significant impact on the prognosis and treatment of cancer in the era of precision medicine. This perspective would provide an insight into the genetic alterations in Nrf2 and suggest the application of small molecules, RNAi, and genome editing technologies, particularly CRISR-Cas9, in therapeutic intervention of cancer in the context of the involvement of Nrf2 mutations.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 4","pages":"131-142"},"PeriodicalIF":2.5,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417114","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}