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Prognostic Role of Human Epididymis Protein 4 (HE4) in Ovarian Cancer Treatment: Our Point of View 人附睾蛋白4 (HE4)在卵巢癌治疗中的预后作用:我们的观点
Archives of cancer biology and therapy Pub Date : 2020-12-31 DOI: 10.33696/CANCERBIOLOGY.1.012
M. Giuseppe, Plotti Francesco, Terranova Corrado, M. Roberto, DE Cicco Nardone Carlo, Guzzo Federica, Luvero Daniela, Gatti Alessandra, Schiro Teresa, Rossini Gianmarco, Deledda Cristiana, F. Fernando, M. Clara, V. Francesca, F. Laura, P. Chiara, R. Stefania, Angioli Roberto
{"title":"Prognostic Role of Human Epididymis Protein 4 (HE4) in Ovarian Cancer Treatment: Our Point of View","authors":"M. Giuseppe, Plotti Francesco, Terranova Corrado, M. Roberto, DE Cicco Nardone Carlo, Guzzo Federica, Luvero Daniela, Gatti Alessandra, Schiro Teresa, Rossini Gianmarco, Deledda Cristiana, F. Fernando, M. Clara, V. Francesca, F. Laura, P. Chiara, R. Stefania, Angioli Roberto","doi":"10.33696/CANCERBIOLOGY.1.012","DOIUrl":"https://doi.org/10.33696/CANCERBIOLOGY.1.012","url":null,"abstract":"In the last 10 years, the marker “Human Epididymis protein 4 (HE4)” for the management of gynecological tumors has entered powerfully in the world literature. At the moment, carrying out an accurate research in the main scientific portals such as PubMed, we can find more than 2,000 works concerning Cancer antigen-125 (Ca125), but those concerning HE4 are less than 400. The assessment of the prognostic significance of Ca125 has been described in more than 1000 scientific papers, whereas in the case of HE4 such works are only about 100. The HE4 gene product is an N-glycosylated protein which is secreted into the extracellular environment and can be detected in the bloodstream of patients with ovarian cancer. Diagnostic strategies for discriminate benign neoplasm from malignant Epithelial Ovarian Cancer (EOC) use tumor markers, imaging exams and combination algorithms. Ca125 is the best documented circulating marker and the most frequently recommended by clinical practice guidelines, despite its low specificity. To compensate for the low specificity of Ca125, new markers were studied: HE4 is one of the most promising; HE4 has demonstrated good sensitivity and specificity in detecting EOC, overcoming the traditional role of Ca125. So, the role currently assumed by HE4 marker has been to aid in the diagnosis of malignant ovarian neoplasm. In recent years, however, these markers (HE4 and Ca125) have assumed an important significance in the assessment of prognosis and response to chemotherapy.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78212361","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}
引用次数: 0
Role of the Gut Microbiome in the Modulation of Cancer Immunotherapy Response 肠道微生物组在癌症免疫治疗反应调节中的作用
Archives of cancer biology and therapy Pub Date : 2020-12-31 DOI: 10.33696/CANCERBIOLOGY.1.011
S. Deshmukh
{"title":"Role of the Gut Microbiome in the Modulation of Cancer Immunotherapy Response","authors":"S. Deshmukh","doi":"10.33696/CANCERBIOLOGY.1.011","DOIUrl":"https://doi.org/10.33696/CANCERBIOLOGY.1.011","url":null,"abstract":"The gut microbiome or gut flora is a vast community of microorganisms such as bacteria, viruses, protozoa, and fungi that inhabit the digestive tract of the human and other animals [1,2]. In the human body, bacterial species colonize into the oral cavity, skin, vagina, and placenta, however, the largest population of microorganisms resides in the intestine. The majority of gut microbiota belong to the phyla Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria [2]. Colonization of the gut microbiota begins during or after the birth when the neonates get exposed to the vaginal microbes as he or she passes through the birth canal of the mother [3,4]. The growth and population of the gut microbiome are influenced by multiple factors including gestational age, mode of delivery (vaginal/cesarean), infant feeding method, diet, environment, medications, exposure to antibiotics, and comorbid diseases [2,5-8]. Gut microbiota has co-evolved with humans for millions of years to form a mutually beneficial relationship. They play important role in food digestion, nutrient and mineral absorption, synthesis of amino acids, enzymes and vitamins, and production of short-chain fatty acids, thus crucial for health and wellbeing [9,10]. Also, the gut microbiota is involved in immune regulation, brain function, and neuroendocrine responses [11,12]. The human gastrointestinal tract harbor both unhealthy and healthy microbiota, that arise through a complex combination of genetic, environmental, and lifestyle factors. Their imbalance contributes to high blood sugar, high cholesterol, weight gain, and other pathological conditions [11,13]. Change in the population of normal microbiota has been suggested to associate with the development and progression of many diseases [13]. Several species of bacteria including Helicobacter pylori and Coriobacteriaceae have been identified as potential candidates associated with carcinogenesis [14,15].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88052898","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}
引用次数: 0
Synthetic Lethal Drug Combinations Targeting Proteasome and Histone Deacetylase Inhibitors in TP53-Mutated Cancers 针对蛋白酶体和组蛋白去乙酰化酶抑制剂在tp53突变癌症中的合成致死药物组合
Archives of cancer biology and therapy Pub Date : 2020-10-31 DOI: 10.33696/cancerbiology.1.009
Shaoli Das, Xiang Deng, K. Camphausen, U. Shankavaram
{"title":"Synthetic Lethal Drug Combinations Targeting Proteasome and Histone Deacetylase Inhibitors in TP53-Mutated Cancers","authors":"Shaoli Das, Xiang Deng, K. Camphausen, U. Shankavaram","doi":"10.33696/cancerbiology.1.009","DOIUrl":"https://doi.org/10.33696/cancerbiology.1.009","url":null,"abstract":"Background: We have recently published SL-BioDP, a web resource for querying, exploration and visualization of potential synthetic lethal targets and possible synergistic drug combinations for 18 cancer types. Methods: From our predictive synthetic lethality model used in SL-BioDP, we inferred TP53 mutation lead to potential synergistic drug combination of Bortezomib and Vorinostat. Here we show, how to extrapolate the drug combination results by combining drug screening data from cancer cell lines and showed the potential synergy of the drug targets, proteasome, and histone deacetylase (HDAC) pathways respectively, for patient survival advantage. Results: We found that TP53 mutation is potentially synthetic lethal with multiple genes from the proteasome and HDAC pathways exclusively in many cancer types. Also, HDAC and proteasomes were found to have potential synthetic lethal relationship. Using drug screening data in cancer cell line, the sensitivity of the HDAC inhibitor drug Vorinostat was found to be increased in TP53 mutated cells where the proteasome pathway was downregulated. Conclusions: Our in-silico pharmacogenomic study indicates that the potential synergistic drug combination of proteasome and HDAC inhibitors may be considered as potential treatment for TP53-mutant cancers.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"73 1","pages":"42 - 47"},"PeriodicalIF":0.0,"publicationDate":"2020-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86268597","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}
引用次数: 1
Lessons Learnt from COVID-19: How Can We Prepare for Another Pandemic? 从COVID-19吸取的教训:我们如何为另一场大流行做准备?
Archives of cancer biology and therapy Pub Date : 2020-01-01 DOI: 10.33696/cancerbiology.1.005
Matthew I Ehrlich, M Wasif Saif
{"title":"Lessons Learnt from COVID-19: How Can We Prepare for Another Pandemic?","authors":"Matthew I Ehrlich, M Wasif Saif","doi":"10.33696/cancerbiology.1.005","DOIUrl":"https://doi.org/10.33696/cancerbiology.1.005","url":null,"abstract":"Five months into the COVID-19 pandemic, the U.S. death toll from the virus has now surpassed 100,000 people [1]. Many more cases remain nationwide, while an unknown number of patients currently harbor the virus asymptomatically. While health officials are now optimistic regarding the decline in prevalence and number of deaths due to COVID-19 and the possibility of a vaccine by the fall, we cannot lose sight of the bigger picture: the next pandemic. In the last century, the world has seen its fair share of outbreaks, including polio, HIV/AIDS, and the previous two coronavirus outbreaks, SARS and MERS [2]. What we have learned is that pandemics don’t work on schedules – and the next one could be right around the corner [3].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"1 1","pages":"22-24"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c7/69/nihms-1607045.PMC7388647.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38206969","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}
引用次数: 4
Reduced BCR Signaling and a Metabolic Shift Accompanies Malignant Progression of Follicular Lymphoma: A Lesson from Transcriptomics 减少BCR信号和代谢转移伴随滤泡性淋巴瘤恶性进展:转录组学的教训
Archives of cancer biology and therapy Pub Date : 2020-01-01 DOI: 10.33696/CANCERBIOLOGY.1.007
C. Sala, A. Arcangeli
{"title":"Reduced BCR Signaling and a Metabolic Shift Accompanies Malignant Progression of Follicular Lymphoma: A Lesson from Transcriptomics","authors":"C. Sala, A. Arcangeli","doi":"10.33696/CANCERBIOLOGY.1.007","DOIUrl":"https://doi.org/10.33696/CANCERBIOLOGY.1.007","url":null,"abstract":"In the manuscript entitled “The ion channels and transporters gene expression profile indicates a shift in excitability and metabolisms during malignant progression of Follicular Lymphoma” [1], we reported recent advances in our understanding of how the gene expression profile of ion channels and transporters (ICT-GEP) contributes to identify specific signatures associated with Follicular Lymphoma (FL), with those FL that acquire chemoresistance after a relapsing-remitting course, and with the more aggressive Diffuse Large Cell Lymphoma (DLBCL), which may represent the evolution of FLs. From the analysis of how ICT-GEP changes during FL malignant progression emerged the progressive decrease in the expression of genes encoding those channels which are responsible for the maintenance of the ionic homeostasis and the driving force for Ca2+ entry, upon cell activation, as well as a shift from a glycolytic to an oxidative metabolism.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"75 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83600139","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}
引用次数: 4
Impact of Cisplatin Dosing Regimens on Mammary Tumor Growth in an Animal Model. 顺铂剂量方案对动物模型乳腺肿瘤生长的影响
Archives of cancer biology and therapy Pub Date : 2020-01-01 Epub Date: 2020-06-15 DOI: 10.33696/cancerbiology.1.004
James A Koziol, Theresa J Falls, Jan E Schnitzer
{"title":"Impact of Cisplatin Dosing Regimens on Mammary Tumor Growth in an Animal Model.","authors":"James A Koziol, Theresa J Falls, Jan E Schnitzer","doi":"10.33696/cancerbiology.1.004","DOIUrl":"10.33696/cancerbiology.1.004","url":null,"abstract":"<p><strong>Background: </strong>We have recently introduced a modification of the seminal Simeoni model for tumor growth, the modification entailing the incorporation of delay differential equations into its formulation. We found that the modification was competitive with the Simeoni construct in modeling mammary tumor growth under cisplatin treatment in an animal model.</p><p><strong>Methods: </strong>In our original study, we had two cohorts of animals: untreated, and treatment with bolus injection of cisplatin on day 0. We here explore how modifications in the cisplatin dosing scheme affect tumor growth in our model.</p><p><strong>Results: </strong>We found that modest fractionation dosing schemes have little ultimate impact on tumor growth. In contrast, metronomic dosing schemes seem quite efficacious, and might yield effective control over tumor progression.</p><p><strong>Conclusions: </strong>With regard to cisplatin as single agent chemotherapy, a minimum level of drug for a prolonged period of time seems more critical than rapid achievement of a very high dose for a shorter time frame for deterring tumor growth or progression. Exploration of tumor dose schedules with mathematical models can provide valuable insights into potentially effective therapeutic regimens.</p>","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"1 1","pages":"18-21"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38206968","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}
引用次数: 0
Synthetic Lethal Drug Combinations Targeting Proteasome and Histone Deacetylase Inhibitors in TP53-Mutated Cancers. 针对蛋白酶体和组蛋白去乙酰化酶抑制剂在tp53突变癌症中的合成致死药物组合。
Shaoli Das, Xiang Deng, Kevin Camphausen, Uma Shankavaram
{"title":"Synthetic Lethal Drug Combinations Targeting Proteasome and Histone Deacetylase Inhibitors in TP53-Mutated Cancers.","authors":"Shaoli Das,&nbsp;Xiang Deng,&nbsp;Kevin Camphausen,&nbsp;Uma Shankavaram","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>We have recently published SL-BioDP, a web resource for querying, exploration and visualization of potential synthetic lethal targets and possible synergistic drug combinations for 18 cancer types.</p><p><strong>Methods: </strong>From our predictive synthetic lethality model used in SL-BioDP, we inferred TP53 mutation lead to potential synergistic drug combination of Bortezomib and Vorinostat. Here we show, how to extrapolate the drug combination results by combining drug screening data from cancer cell lines and showed the potential synergy of the drug targets, proteasome, and histone deacetylase (HDAC) pathways respectively, for patient survival advantage.</p><p><strong>Results: </strong>We found that TP53 mutation is potentially synthetic lethal with multiple genes from the proteasome and HDAC pathways exclusively in many cancer types. Also, HDAC and proteasomes were found to have potential synthetic lethal relationship. Using drug screening data in cancer cell line, the sensitivity of the HDAC inhibitor drug Vorinostat was found to be increased in TP53 mutated cells where the proteasome pathway was downregulated.</p><p><strong>Conclusions: </strong>Our in-silico pharmacogenomic study indicates that the potential synergistic drug combination of proteasome and HDAC inhibitors may be considered as potential treatment for TP53-mutant cancers.</p>","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"1 2","pages":"42-47"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7644110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38684373","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}
引用次数: 0
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