Journal of cancer science and clinical therapeutics最新文献

{"title":"Insect Venoms and their Bioactive Components: A Novel Therapeutic Approach in Chronic Diseases and Cancer","authors":"Deepshikha Moran, U. Dutta, Ajaikumar B Kunnumakkara, Enush Daimari, B. Deka","doi":"10.26502/jcsct.5079176","DOIUrl":"https://doi.org/10.26502/jcsct.5079176","url":null,"abstract":"To counteract the growing burden of chronic diseases, discovery of highly selective target specific drugs is of utmost importance in present scenario. Various advanced therapeutic procedures and modern drugs have been developed and approved in last three decades for treating these disorders. The very first limitation of these therapies is their side effects, which are severe and long term. Also, these treatments are a costly affair and of limited therapeutic advantages. To overcome it, exploration and mining of natural products is much necessary. Phytotherapy is already well-established in the field of drug discovery. Focus should also be provided on zoo-therapy, as it is loaded with paramount of possibilities regarding disease treatment. Insect venoms are cocktail of bioactive components with different physiological actions that have undergone evolutionary refinement through a long time-scale. This evolutionary selection over time makes them more suitable candidate for target specific drug discovery. In this review we are trying to throw some light on some significant insect venom components with their mechanism of patho-physiological actions, relevance in the field of advanced drug discovery targeting chronic diseases including cancer.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348335","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":"Obtaining a Recombinant Protein Based on the E7 Antigen of Human Papillomavirus Type 18","authors":"Rodriguez Rodriguez N,, Alfonso Chaviano AB,, Granadillo Rodríguez M,, Batte Figueredo A,, Torrens I","doi":"10.26502/jcsct.5079172","DOIUrl":"https://doi.org/10.26502/jcsct.5079172","url":null,"abstract":"Background: Cervical cancer is the fourth most common cancer in women worldwide and was the leading cause of death among approximately 300 000 cases in 2018. The main risk factor for developing this disease is the persistent infection of high-risk types of Human Papillomavirus (HPV); specifically, HPV-18 is recognized as one of the major contributors for adenocarcinoma and squamous cancer. There are three prophylactic vaccines to prevent infection by HPV, but these vaccines are not effective in infected people. On the other hand, despite the success of various types of therapeutic vaccine candidates in clinical trials, none of them is commercially available to treat women with HPV-related malignancies. As the methods used for obtaining those therapeutic candidates are awfully expensive, they could be inaccessible for developing countries. In this scenario, E7 antigen of HPV is considered an ideal target for developing therapeutic vaccines. In accordance with this, the aim of this work is to obtain a recombinant fusion protein with high levels of purity through a profitable process, which could be used as therapeutic alternative for treating tumors expressing the E7 antigen of HPV-18. Results: We have obtained the novel recombinant protein CIGB550-E718 that comprises the fusion between an E7 mutein of HPV-18 and the cell-penetrating peptide with immunostimulatory properties CIGB550. The expression of the fusion protein evaluated using two strains of E. coli and 16 culture media with different composition enabled us to choose the best setting in which the interest protein accounted for approximately 16% of the total cellular protein. The best results were obtained using BL21(DE3) cells as host system grown in a culture medium containing M9 salt, casein hydrolysate and glycerol as a carbon source. The recombinant protein was purified by a single affinity chromatographic step up to 90% purity. Yields of 32 mg of the CIGB550-E718 per liter of culture were achieved from 2.5 L scale. Conclusions: These results are a promising and cost-effective approach for the future production and scale-up of the protein CIGB550-E718, which could be a therapeutic alternative for treating women with lesions associated to HPV-18 infection.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348783","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":"Systemic Delivery of a Dual PI3K/mTOR Inhibitor More Effective than Topical Delivery in Preventing Anal Carcinogenesis in an HPV Transgenic Mouse Model.","authors":"Laura C Gunder,&nbsp;Tyra H Moyer,&nbsp;Marissa R Ziolkowski,&nbsp;Margaret K Keating,&nbsp;Glen E Leverson,&nbsp;Wei Zhang,&nbsp;Evie H Carchman","doi":"10.26502/jcsct.5079153","DOIUrl":"https://doi.org/10.26502/jcsct.5079153","url":null,"abstract":"<p><strong>Introduction: </strong>Anal dysplasia is a growing health concern that over time can result in squamous cell carcinoma (SqCC) of the anus. In this study, we compare a topical versus systemic (oral) administration of LY3023414, a dual PI3K/mTOR inhibitor, to prevent anal carcinogenesis in a Human Papillomavirus (HPV) mouse model of anal cancer.</p><p><strong>Materials and methods: </strong><i>K14E6/E7</i> transgenic mice were used to model HPV-induced anal carcinogenesis. Mice with varying starting anal histologies (normal histology, low-grade, and high-grade anal dysplasia) were treated topically at the anus or systemically via oral gavage with LY3023414 with or without topical carcinogen for 20 weeks. Mice were monitored for overt anal tumor development and anal tissue was assessed for histology and markers of PI3K and mTOR activity (pAKT and pS6, respectively).</p><p><strong>Results: </strong>LY3023414 treatment, regardless of the mode of delivery, significantly decreased overt tumor development in mice starting with normal histology and low-grade anal dysplasia. Systemic LY3023414 treatment was more effective in delaying tumor onset than topical treatment. Mice treated with systemic LY3023414 had significantly reduced rates of anal SqCC when starting with normal and low-grade anal dysplasia compared to topical treatment. Topical treatment was only effective in reducing SqCC in the setting of low-grade dysplasia. LY3023414 inhibition of pAKT and pS6 expression varied with starting histology. Neither treatment mode was effective in the setting of high-grade anal dysplasia.</p><p><strong>Conclusion: </strong>Systemic LY3023414 treatment was more effective than topical application in delaying the progression of normal anal histology and low-grade dysplasia to anal cancer in HPV-associated mice.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"6 2","pages":"157-173"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9851170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10057096","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":"The Mechanism of Hepatitis B Virus X Gene in Promoting Hepatocellular Carcinoma","authors":"Xinyu Zhou, Donghong Liu, Zishuai Li, Jun Zhao, Shiliang Cai, Guangwen Cao","doi":"10.26502/jcsct.5079158","DOIUrl":"https://doi.org/10.26502/jcsct.5079158","url":null,"abstract":"The Mechanism of Hepatitis B Virus X Gene in Promoting Abstract Primary liver cancer (PLC) was the third leading cause of cancer death worldwide and hepatocellular carcinoma (HCC) accounts for 75-85% of PLC cases. Chronic hepatitis B virus (HBV) infection is the major cause of HCC globally. HBV carcinogenesis depends on three factors: viral replication, integration and evolution, and HBV X gene (HBx) plays a major role in these processes. HBx determines HBV replication and is also the main viral gene for integration and evolution. Recently, numerous new carcinogenic mechanisms of HBx, including epigenetic modification, stem-like signal pathway, metabolic regulation, immune suppression, and drug resistance, have being continuously explored. This article reviews the mechanism of HBx and its mutation in the occurrence and development of HCC, in order to provide a reference for a comprehensive understanding of HBV-HCC.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348320","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":"Revisiting the Role of Immunotherapy for Colorectal Cancer Treatment in Patients with Constitutional Mismatch Repair Deficiency","authors":"E. L. Eikenboom, E. Michiels, D. Grünhagen, M. de Vries, A. Wagner, M. Spaander","doi":"10.26502/jcsct.5079181","DOIUrl":"https://doi.org/10.26502/jcsct.5079181","url":null,"abstract":"","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348364","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":"Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma.","authors":"Manuela Malsy,&nbsp;Veronika Hofer,&nbsp;Stephan Schmidbauer,&nbsp;Bernhard Graf,&nbsp;Anika Bundscherer","doi":"10.26502/jcsct.5079183","DOIUrl":"https://doi.org/10.26502/jcsct.5079183","url":null,"abstract":"<p><strong>Introduction: </strong>Pancreatic ductal adenocarcinoma is one of the most aggressive malignancies in humans. The main reason for its unfavourable prognosis is the combination of rapid tumour growth, early-onset metastasis and currently still inadequate diagnostic and therapeutic options. Thus, only very few patients are eligible for radical resection of the primary tumour as the only curative treatment option available so far. In the perioperative period, tumour progression and metastasis are facilitated by the activation of key signalling pathways and the altered regulation of transcription factors. Various tumour entities have shown increased expression of the integrin-3 receptor subunit, which correlates with more rapid tumour progression and metastasis through advanced migration, invasion and proliferation. The influence of perioperative medication and postoperative pain management remains unclear. To investigate the effects of ketamine, s-ketamine and MK 801 on integrin beta-3-mediated cell migration in pancreatic cancer cells <i>in vitro</i>.</p><p><strong>Methods: </strong>The effects of ketamine, s-ketamine and MK 801 on integrin beta-3 expression were investigated with immunoblot. Cell migratory potentials were analysed using a Cell Migration Assay Kit with a Boyden chamber, in which cells migrate through a semipermeable membrane under different stimuli.</p><p><strong>Results: </strong>Stimulation with ketamine and MK 801 significantly promoted migration in pancreatic cancer cells, increasing the expression of integrin beta-3.</p><p><strong>Conclusion: </strong>Novel therapeutic approaches target the effective modulation of specific signalling and transcription pathways. The prerequisite for such 'target therapies' is comprehensive knowledge about the respective carcinogenesis. Further studies are required to identify the underlying disease mechanisms of pancreatic carcinoma.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"6 4","pages":"446-451"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9910313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10707593","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":"<i>MET</i>-FISH Evaluation Algorithm: Proposal of a Simplified Method.","authors":"Roberta Castiglione,&nbsp;Christina Alidousty,&nbsp;Barbara Holz,&nbsp;Nicolai Duerbaum,&nbsp;Maike Wittersheim,&nbsp;Elke Binot,&nbsp;Sabine Merkelbach-Bruse,&nbsp;Nicolaus Friedrichs,&nbsp;Matthias S Dettmer,&nbsp;Alexander Bosse,&nbsp;Reinhard Buettner,&nbsp;Anne Maria Schultheis","doi":"10.26502/jcsct.5079180","DOIUrl":"https://doi.org/10.26502/jcsct.5079180","url":null,"abstract":"<p><p>MET amplifications (METamp) occur in 5% of NSCLC and represent in most case mechanisms of resistance to ALK and/or EGFR-targeted therapies. METamp detection can be performed using different techniques, although Fluorescence In-Situ Hybridization (FISH) remains the gold-standard, especially in the context of subclonality. To date current evaluation algorithms of MET amplifications are time consuming. Aim of the study was to identify a faster, equally reliable diagnostic algorithm for the detection of METamp, which is currently classified in negativity and low/intermediate/high-level amplification. N=497 NSCLC cases with available MET-FISH data had been selected. The results based on the first evaluated 20 cells had been re-calculated and compared with the definitive results based on 60 cells. For n=464 (93.4%) identical results had been obtained when counting 20 cells instead of 60 cells. Thirty-three cases (5.6%) showed a discrepancy, leading to an incorrect upgrade to a higher diagnostic category (n=25) and to an incorrect downgrade (n=8). We propose a simplified, yet equally reliable MET FISH-algorithm: after accurate screening of the whole tumor slide, twenty tumor cells have to be evaluated and results calculated: If the result is negative, or if all criteria of high-level METamp are fulfilled, the case can be signed out as such. All other cases should be considered as equivocal and additional 40 cells have to be counted. Given that, reliable results can be obtained by counting 20 cells only and an \"equivocal\" category for cases that need further investigation have been clearly defined.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"6 4","pages":"411-427"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9878991/pdf/nihms-1861566.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10592870","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":"Immunohistochemical Analysis of Prostein in Needle Core Biopsies of Acinar and Intraductal Prostatic Adenocarcinoma in Western Kenya Population","authors":"Tyrus Omondi Swaya, D. Opondo, David O. Atandi, Benard Guyah, Ng’wena Gideon Magak","doi":"10.26502/jcsct.5079164","DOIUrl":"https://doi.org/10.26502/jcsct.5079164","url":null,"abstract":"Background: Prostein is a newly reported prostate cancer biomarker. Nonetheless, no reports on African population are available. The current study aimed to determine the prostein expression in archived prostatic core biopsies in Western Kenya. Methods: This was a retrospective study conducted on malignant and benign prostatic tissue core biopsies of 106 patients from Jaramogi Oginga Odinga Teaching and Referral Hospital and division of urology at Synergy Clinics, Kisumu between January 2018 to May 2021. Manual Immunohistochemical technique was performed on each of the 106 samples and on the following non-prostatic male control biopsies; Testis, Penis, Liver and Esophagus. Cellular location of prostein staining was evaluated microscopically and classified as cytoplasmic or nucleocytoplasmic. Intensity of prostein expression was assessed and graded according the immunohistochemistry composite score. Results: The mean (SE) age was 72.00 ± 0.93 years. 97.2% of malignant and all the benign prostate tissue stained positive for prostein whereas the four non-prostatic male tissues were negative. Staining intensities were weak (24.5%), Moderate (17.0%), strong (55.7%) and non-stained (2.8%). The staining was highly immunolocalized within the cytoplasm (95.1% cases) as compared to nucleocytoplasmic (2.0% cases). The mean immunoreactivity composite score was 1.91 ± 0.96 (0.0-3.14). Strongly stained sections of both acinar and intraductal adenocarcinoma had a staining pattern clustered within the cytoplasm in a perinuclear location whereas the weakly stained sections had less coarse brown cytoplasmic granular appearing. Conclusion: Prostein is expressed in both acinar and intraductal adenocarcinoma and can be routinely used in differential diagnosis of prostate cancer even in remote settings.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69347874","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":"Clinical Characteristics and Prognostic Values of PIK3CA Mutation in Colorectal Cancer Patients","authors":"Jinming Han, Jianxiang Shi, Miao Jiang, Ruowen Zhang, Shuiling Jin, Yongliang Jia, H. Zong","doi":"10.26502/jcsct.5079149","DOIUrl":"https://doi.org/10.26502/jcsct.5079149","url":null,"abstract":"Clinical Characteristics and Prognostic Values of PIK3CA Mutation in Colorectal Patients. Clinical Therapeutics (2022): Abstract Objective: This study aimed to investigate the role of PIK3CA mutation in the prognosis of Colorectal Cancer (CRC). Methods: The clinical data of 386 CRC patients who underwent next-generation sequencing (NGS) test in the First Affiliated Hospital of Zhengzhou University from January 2017 to December 2020 were retrospectively reviewed. The associations between PIK3CA mutation and clinicopathologic characteristics of CRC patients were analyzed by chi-square test and Fisher’s exact test. Kaplan-Meier curves and Cox models were conducted to assess possible prognostic values of PIK3CA mutation. Results: PIK3CA mutation was found in 88 (22.8%) of the 386 CRC patients. The percentage of MSI-H in PIK3CA mutated patients were higher than that in PIK3CA wild-type patients (P < 0.0001). The Median Overall Survival (mOS) of patients with PIK3CA mutation was significantly higher than that of wild-type patients (P = 0.0112). The progression free survival (PFS) of the mutated patients was also significantly prolonged compared with that of the wild type (P = 0.0132). Results of multivariate analysis showed that PIK3CA wild-type was independent risk factor for the survival of CRC patients. Conclusion: PIK3CA mutation had an important impact on the clinic pathologic features and the prognosis for CRC patients. The survival of PIK3CA mutated patients was significantly prolonged, which needs further studies of large sample size, and long follow-up period to provide robust evidence.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348268","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":"Hair Growth and Restoration by Transcriptional Control of Tissue Regeneration in Cancer Recovery Process by Huaier","authors":"Manami Tanaka, Tomoo Tanaka, Xiaolong Zhu, Fei Teng, Hong Lin, Zhu-Quan Luo, Ying Pan, S. Sadahiro, Toshiyuki Suzuki, Y. Maeda, Ding Wei, Zheng Lu","doi":"10.26502/jcsct.5079167","DOIUrl":"https://doi.org/10.26502/jcsct.5079167","url":null,"abstract":"Manami Tanaka (  tubu0125@gmail.com ) Bradeion Institute of Medical Sciences, Co., Ltd. Tomoo Tanaka Bradeion Institute of Medical Sciences, Co., Ltd. Xiaolong Zhu Beijing Genomics Institute Teng Fei Hong Lin BGI-Shenzhen Zhu Luo BGI-Japan Ying Pan BGI-Shenzhen Sotaro Sadahiro Tokai University School of Medicine Toshiyuki Suzuki Oiso Hospital attached to Tokai University School of Medicine Yuji Maeda Kanagawa National Hospital Ding Wei Japan Kampo NewMedicine, Co., Ltd. Zhengxin Lu QiDong Gaitianli Medicines Co. Ltd.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348719","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}