Journal of cancer research updates最新文献

{"title":"Poor Science; Poorly Trained Scientists; Poor Policies: Major Deterrents to the War on Cancer.","authors":"Leslie C Costello","doi":"10.6000/1929-2279.2018.07.03.3","DOIUrl":"10.6000/1929-2279.2018.07.03.3","url":null,"abstract":"<p><p>Although the availability of funding has been described as the major limitation on advances in cancer, the progress in the war on cancer has been deterred mainly by poor science, poorly trained scientists, and poor NIH policies. This is the result of NIH policies of its extreme focus on molecular biology (genomics, molecular genetics, molecular biology) identification of the molecular factors and pathways; which are required for the acceptability of treatment and preventive protocols. As such, this has influenced virtually all agencies that provide grants for medical research to adopt the NIH policies. This has impacted the funding of the research as well as the focus of the training of scientists. Directors of NCI Dr. Varmus (also Nobel Prize awardee) and Dr. Zerhouni had addressed this issue; and they rejected the necessity of molecular biology studies and information. NIH should return to the holistic physiological/pathophysiological approach to studies of cancer issues. This would provide the best approach for winning the war on cancer.</p>","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"7 3","pages":"79-83"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6038816/pdf/nihms-977683.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36307673","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":"Aberrant DNA damage response and DNA repair pathway in high glucose conditions.","authors":"Amy Zhong,&nbsp;Melissa Chang,&nbsp;Theresa Yu,&nbsp;Raymond Gau,&nbsp;Daniel J Riley,&nbsp;Yumay Chen,&nbsp;Phang-Lang Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Higher cancer rates and more aggressive behavior of certain cancers have been reported in populations with diabetes mellitus. This association has been attributed in part to the excessive reactive oxygen species generated in diabetic conditions and to the resulting oxidative DNA damage. It is not known, however, whether oxidative stress is the only contributing factor to genomic instability in patients with diabetes or whether high glucose directly also affects DNA damage and repair pathways.</p><p><strong>Results: </strong>Normal renal epithelial cells and renal cell carcinoma cells are more chemo- and radiation resistant when cultured in high concentrations of glucose. In high glucose conditions, the CHK1-mediated DNA damage response is not activated properly. Cells in high glucose also have slower DNA repair rates and accumulate more mutations than cells grown in normal glucose concentrations. Ultimately, these cells develop a transforming phenotype.</p><p><strong>Conclusions: </strong>In high glucose conditions, defective DNA damage responses most likely contribute to the higher mutation rate in renal epithelial cells, in addition to oxidative DNA damage. The DNA damage and repair are normal enzyme dependent mechanisms requiring euglycemic environments. Aberrant DNA damage response and repair in cells grown in high glucose conditions underscore the importance of maintaining good glycemic control in patients with diabetes mellitus and cancer.</p>","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"7 3","pages":"64-74"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6258084/pdf/nihms973124.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36782420","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":"Isoniazid Induced Toxicities and Idiosyncratic Responses in Male Albino Wistar Rats","authors":"S. Owumi, M. A. Gbadegesin, F. Olotu, O. Odunola","doi":"10.6000/1929-2279.2017.06.02.2","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.02.2","url":null,"abstract":"Isoniazid (INH) is an anti-tuberculosis drug administered over a long period. Upon metabolism in the liver, INH generates nitrogen-centered radicals, reacting with cellular macromolecules, and induces toxic and transformational changes in cells and tissues. Here we examined the side effects of long-term (chronic) administration of isoniazid (2.5 and 5mg/kg) once daily for 30, 60 and 90 days consecutively: on hepatic transaminases, histological changes in hepatocytes and induction of micronuclei in the bone marrow and possible genotoxicity in E. coli PQ37. In addition, blood glucose was monitored during the various treatment period. Biochemical analysis of hepatic transaminases (I³ -glutamyl-, alanine amino-, aspartate aminotransferases and alkaline phosphatase) in INH treated group was significantly (p 0.05) in GST in both treatment groups at day 60. There was also a significant increase ( p <0.05) in the activity of superoxide dismutase activity. Micronucleus analysis further revealed an induction of micronucleated polychromatic erythrocytes (mPCEs), which was significant ( p <0.05) for both treatment doses at days 30, 60 and 90 respectively. In addition, INH genotoxicity assessed by UMU chromotest indicated that the 5mg/kg dosage has an induction ratio above the genotoxicity threshold of 1.5 suggesting genotoxicity in E.coli PQ37. Taken together, INH treatment at both doses (2.5 and 5mg/kg body weight) was hepatotoxic and induced nephrotoxic damages, in addition to mutagenic effect which is more pronounced at 2.5mg/kg dose, thereby suggesting dose-dependent cellular and genetic toxicity.","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 1","pages":"29-37"},"PeriodicalIF":0.0,"publicationDate":"2017-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42158999","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":"Isolation of Chamuangone, a Cytotoxic Compound against Leishmania major and Cancer Cells from Garcinia cowa Leaves and its HPLC Quantitative Determination Method","authors":"A. Sakunpak, K. Matsunami, H. Otsuka, P. Panichayupakaranant","doi":"10.6000/1929-2279.2017.06.02.3","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.02.3","url":null,"abstract":": On the basis of a leishmanicidal assay-guided isolation, chamuangone was purified from Garcinia cowa leaves together with four inactive compounds; 5-hydroxymethylfurfural; D-glyceropentaric acid,2-deoxy-3- C -(methoxycarbonyl)-1,4-lactone,5-ethyl ester; isoorientin-6\"- O -rhamnoside; and dulcinoside. Chamuangone possessed a cytotoxic activity against Leishmania major with an IC 50 value of 10.7 µM, and also exhibited strong inhibitory activity against lung adenocarcinoma (SBC3 and A549) and leukemia (K562, and K562/ADM) cells with IC 50 values of 6.5, 7.5, 3.8, and 2.2 µM, respectively. The HPLC method utilised a TSK-gel ODS-80Tm column with the mixture of acetonitrile and 2% phosphoric acid in water (97:3, v/v) as the mobile phase at a flow rate of 1 mL/min, and UV detection at 245 nm. The parameters of linearity, precision, accuracy, specificity and sensitivity of the method were evaluated. The recoveries of the method were 100.4-101.6% and good linearity (r 2 ³ 0.9999) was obtained. A high degree of specificity, sensitivity and precision were also achieved.","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 1","pages":"38-45"},"PeriodicalIF":0.0,"publicationDate":"2017-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43326194","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":"Analysis of the Efficiency of Photothermal and Photodynamic Cancer Therapy via Nanogolds and Photosensitizers","authors":"Jui-Teng Lin","doi":"10.6000/1929-2279.2017.06.01.2","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.01.2","url":null,"abstract":"Factors influencing the cancer therapy efficiency in both photothermal therapy (PTT) and photodynamic therapy (PDT) using nanogold particles and photosensitizers, respectively, are analyzed. In PTT, heat diffusion kinetics is used to calculate the temperature increase resulted from the nanogold absorption of light energy, whereas photochemical kinetics is used to find the efficacy of PDT, or the generation rate of reactive oxygen species. The critical factors of the PTT/PDT synergistic efficacy include: the concentration of the initiator (nanogold or photosensitizers) in the treated medium, the wavelength and energy of the light applied to the medium. Optimal parameters are calculated for maximum PDT efficacy. In PTT, diode laser (at 810 nm) is used to heat nanogolds (rod-shape or core-shell). In PDT, photosensitizers of riboflavin, 5-ALA, methylene blue and indocyanine green may be used with the associate light at wavelength of (365, 430 nm), (530-670 nm) and (780-850 nm) respectively. Both single light or dual light in infrared or visible wavelength are proposed to activate the photosensitizers or nanogolds. Optimization is required for maximum synergistic efficacy.","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 1","pages":"12-18"},"PeriodicalIF":0.0,"publicationDate":"2017-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47429389","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":"Evaluation of the Type and Frequency of Errors Discovered During Routine Secondary Patient Chart Review","authors":"M. Hardin, A. Harrison, V. Lockamy, Jun Li, C. Peng, P. Potrebko, Yan Yu, L. Doyle, J. Cao","doi":"10.6000/1929-2279.2017.06.01.3","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.01.3","url":null,"abstract":"Purpose : Desire to improve efficiency and throughput inspired a review of the frequency and scope of our physics chart check procedures. Departmental policy mandates review of a patient’s treatment plan prior to port-filming, after first treatment and “weekly” every 3-5 fractions. This study examined the effectiveness of the “after-first” physics check with respect to improving patient safety and clinical efficiency. Methods and Materials : A shared spreadsheet was created to record errors discovered during patient-specific chart review following the first fraction of treatment and before the second fraction. First, entries were recorded and categorized from August 2014 through February 2015. Frequencies were assessed month-to-month. Next, utilizing these results, a continuous quality improvement (CQI) process following Deming’s Plan-Do-Study-Act (PDSA) methodology was generated. The first iteration of this PDSA was adding a dose tracking checklist item in the pre-treatment plan check assessment. A two-sided Fisher’s exact test was used to determine if there was a nonrandom association between the checklist implementation and incidence of dose tracking errors. Results : Analysis of recorded errors indicated an overall error rate of 3.4% over the 13 month period. The majority of errors related to discrepancies in documentation, followed by prescription, plan deficiency, and dose tracking-related errors. A two-sided Fisher’s exact test revealed a statistically significant decrease in dose tracking-related errors after implementing the checklist item (p = 0.0322, significance level = 0.05). Conclusions : This work indicates that this redundant secondary check is an effective QA process in our department. The first month spike in rates could be due to the Hawthorne/observer effect, but the consistent 3% error rate suggests the need for continuous quality improvement and periodical re-training on errors noted as frequent to improve awareness and quality of the initial chart review process, which may lead to improved treatment quality, patient safety and increased clinical efficiency.","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 1","pages":"19-24"},"PeriodicalIF":0.0,"publicationDate":"2017-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41860349","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":"Inorganic Nanoplatforms for Simultaneous Cancer Imaging and Therapy: Status and Challenges","authors":"Mian Chen","doi":"10.6000/1929-2279.2017.06.01.1","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.01.1","url":null,"abstract":"Functional nanomaterials have inspired revolutionary methods for cancer early diagnosis, treatment, and prevention. For instance, the imaging property of nanomaterials with high resolution and sensitivity can be used for noninvasive detection of cancer and visualization of drug transport. Meanwhile, the therapeutic property of nanomaterials with controllable fashion will increase therapy efficacy and decrease adverse side effect. Thus, compared to traditional treatment approaches, the nanomaterials which combines imaging and therapeutic functionalities, will be more suitable for cancer theranostics. This review introduces several types of inorganic nanoparticles, including silica nanoparticles, upconversion nanoparticles, iron oxide nanoparticles and gold nanoparticles, which can been explored as theranostic nanoplatforms for simultaneous cancer imaging and therapy. We also cover the ongoing challenges of these nanoparticles in clinical applications.","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2017-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41682855","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":"Short Communication: Studying the Role of Smart Flare Gold Nano Particles in Studying Micro RNA and Oncogene Differential Expression in Prostate Cancer Cell Lines.","authors":"Hirendra Banerjee,&nbsp;Jamel Joyner,&nbsp;Monet Stevenson,&nbsp;William Kaha,&nbsp;Christopher Krauss,&nbsp;Sasha Hodges,&nbsp;Eduardo Santos,&nbsp;Myla Worthington,&nbsp;Jeffferey Rousch,&nbsp;Gloria Payne,&nbsp;Vinod Manglik,&nbsp;Narendra Banerjee,&nbsp;Brianna Morris,&nbsp;Dayton Bell,&nbsp;Santosh Mandal","doi":"10.6000/1929-2279.2017.06.02.1","DOIUrl":"https://doi.org/10.6000/1929-2279.2017.06.02.1","url":null,"abstract":"<p><p>Nano technology is a cutting edge science which is now effectively used in the field of cancer biology. Smart Flare gold nanoparticles are now used often for differential gene expression analysis. In this manuscript we are reporting the use of micro RNA miR 146a and onco gene EZH2 Smart Flare probes to study their expression in different prostate cancer cell lines and the effect of novel Rhenium compounds on these genes using a flow cytometer and a Fluorescence microscope. Our results showed this novel nanotechnology can be effectively used in cancer biology to successfully detect the effect of novel drugs on oncogenes and could be a very useful tool for next generation of cancer researchers.</p>","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"6 2","pages":"25-28"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6000/1929-2279.2017.06.02.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35386619","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":"lincRNA HOTAIR as a novel promoter of cancer progression.","authors":"Gregory Loewen,&nbsp;Ying Zhuo,&nbsp;Yan Zhuang,&nbsp;Janarthanan Jayawickramarajah,&nbsp;Bin Shan","doi":"10.6000/1929-2279.2014.03.03.3","DOIUrl":"https://doi.org/10.6000/1929-2279.2014.03.03.3","url":null,"abstract":"<p><p>Large intergenic non-coding RNAs (lincRNA) regulate development and disease <i>via</i> interactions with their protein partners. Expression of the lincRNA HOX transcript antisense RNA (HOTAIR) is elevated in a variety of malignancies and linked to metastasis and poor prognosis. HOTAIR promotes proliferation, invasion, and metastasis in the preclinical studies of cancer through modulation of chromatin modifying complexes. In the current review we discuss the molecular mechanisms of HOTAIR-mediated aggressive phenotypes of cancer, HOTAIR's potential in cancer intervention, and challenges in exploration of HOTAIR in cancer biology.</p>","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"3 3","pages":"134-140"},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318250/pdf/nihms653912.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33038934","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":"Drug Resistance Mechanisms in Non-Small Cell Lung Carcinoma.","authors":"Janet Wangari-Talbot,&nbsp;Elizabeth Hopper-Borge","doi":"10.6000/1929-2279.2013.02.04.5","DOIUrl":"https://doi.org/10.6000/1929-2279.2013.02.04.5","url":null,"abstract":"<p><p>Lung cancer is the most commonly diagnosed cancer in the world. \"Driver\" and \"passenger\" mutations identified in lung cancer indicate that genetics play a major role in the development of the disease, progression, metastasis and response to therapy. Survival rates for lung cancer treatment have remained stagnant at ~15% over the past 40 years in patients with disseminated disease despite advances in surgical techniques, radiotherapy and chemotherapy. Resistance to therapy; either intrinsic or acquired has been a major hindrance to treatment leading to great interest in studies seeking to understand and overcome resistance. Genetic information gained from molecular analyses has been critical in identifying druggable targets and tumor profiles that may be predictors of therapeutic response and mediators of resistance. Mutated or overexpressed epidermal growth factor receptor (EGFR) and translocations in the echinoderm microtubule-associated protein-like 4 (<i>EML4</i>)-anaplastic lymphoma kinase (<i>ALK</i>) genes (EML4-ALK) are examples of genetic aberrations resulting in targeted therapies for both localized and metastatic disease. Positive clinical responses have been noted in patients harboring these genetic mutations when treated with targeted therapies compared to patients lacking these mutations. Resistance is nonetheless a major factor contributing to the failure of targeted agents and standard cytotoxic agents. In this review, we examine molecular mechanisms that are potential drivers of resistance in non-small cell lung carcinoma, the most frequently diagnosed form of lung cancer. The mechanisms addressed include resistance to molecular targeted therapies as well as conventional chemotherapeutics through the activity of multidrug resistance proteins.</p>","PeriodicalId":89799,"journal":{"name":"Journal of cancer research updates","volume":"2 4","pages":"265-282"},"PeriodicalIF":0.0,"publicationDate":"2013-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/aa/7d/nihms-557320.PMC3952141.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32180442","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}