Pub Date : 2020-12-01DOI: 10.13189/COR.2020.060301
R. Bhalla, S. Bhalla, Duleep D. Bhonsale, D. Pawar
Oral cancer is a major health problem in India. The use of tobacco in various forms has escalated the problem to be the leading cause of cancer in males in India. Many patients postpone surgery for fear of facial mutilation and therefore present with Late stage Buccal Cancer. The management of Late stage buccal cancer has very few options. Conventional surgery, chemotherapy and radiation give very little relief to patients. The occurrence of inevitable recurrence after surgery due to Field cancerisation makes the surgery a futile exercise in controlling the spread of the tumor. The treatment in unresectable tumors which is given as palliation is often limited to pain control and bypassing of oral functions by inserting a nasogastric tube. The mortality rate has remained changed over last 10 years. Therefore Quality of life in these patients has become a discussion matter in most cancer forums. The main cause of the suffering of the patient is the bulk of the tumour. Intralesional Laser ablation offers an alternative way to destroy the bulk of the tumor. The reduction in tumor volume allows good restitution of oral function and pain. There were 49 patients observed in this study. Many patients went into remission after laser ablation and Chemotherapy. The ensuing results were analyzed taking into account Quality and Quantity of life and the resulting Quality index was applied on the patients. Most patients had a good Quality Index post-procedure. All patients were highly satisfied with the procedure. There was an enhanced benefit noted in the quality of life and the expected overall survival time of the patients. Conclusion: Laser Ablation offers an alternative treatment in late-stage Oral Cancer for palliation as well as remission.
{"title":"Laser Ablation Surgery in Late Stage Buccal Cancer","authors":"R. Bhalla, S. Bhalla, Duleep D. Bhonsale, D. Pawar","doi":"10.13189/COR.2020.060301","DOIUrl":"https://doi.org/10.13189/COR.2020.060301","url":null,"abstract":"Oral cancer is a major health problem in India. The use of tobacco in various forms has escalated the problem to be the leading cause of cancer in males in India. Many patients postpone surgery for fear of facial mutilation and therefore present with Late stage Buccal Cancer. The management of Late stage buccal cancer has very few options. Conventional surgery, chemotherapy and radiation give very little relief to patients. The occurrence of inevitable recurrence after surgery due to Field cancerisation makes the surgery a futile exercise in controlling the spread of the tumor. The treatment in unresectable tumors which is given as palliation is often limited to pain control and bypassing of oral functions by inserting a nasogastric tube. The mortality rate has remained changed over last 10 years. Therefore Quality of life in these patients has become a discussion matter in most cancer forums. The main cause of the suffering of the patient is the bulk of the tumour. Intralesional Laser ablation offers an alternative way to destroy the bulk of the tumor. The reduction in tumor volume allows good restitution of oral function and pain. There were 49 patients observed in this study. Many patients went into remission after laser ablation and Chemotherapy. The ensuing results were analyzed taking into account Quality and Quantity of life and the resulting Quality index was applied on the patients. Most patients had a good Quality Index post-procedure. All patients were highly satisfied with the procedure. There was an enhanced benefit noted in the quality of life and the expected overall survival time of the patients. Conclusion: Laser Ablation offers an alternative treatment in late-stage Oral Cancer for palliation as well as remission.","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"38 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90604178","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}
Pub Date : 2020-05-01DOI: 10.13189/cor.2020.060201
F. Najjar, M. Alammar, G. Al-Massarani, Abdulmonem Japawe, Nissreen Alamalla, I. Banat, A. Ikhtiar
Increased values of circulating microparticles (MPs) have been reported in solid tumors including non-small cell lung cancer (NSCLC). We therefore investigated the utility of baseline MPs in the clinical setting of patients with NSCLC. Quantification of MPs in the plasma was performed by flowcytometry. Baseline MP values were correlated with clinical patients' characteristics, estimated tumor volume (ETV) and treatment response. Receiver operating characteristics (ROC) curves were plotted to discriminate between patients and controls in order to determine the diagnostic value of circulating MPs in NSCLC. Our prospective study included 134 NSCLC patients (98 at initial diagnosis, ID and 36 at relapse, R) and 30 healthy individuals. The mean of baseline MP numbers was significantly higher in patients presented either at ID or R than in controls (p<0.0001). Basal MP numbers were inversely correlated with ETV values (p=0.04). In addition, the difference in MP levels at diagnosis was significant according to tumor histology (p=0.02) and primary tumor size (p=0.0007). Using ROC analysis, the optimal cutoff value for baseline MPs was 1307 events/µL with a sensitivity and a specificity of 67.3% and 90.0%, respectively. High MPs expression was significantly associated with low-level smoking degree (p=0.001), non-squamous cell types (p=0.017) and decreased tumor size (p=0.003). Our results suggest that high baseline MP values could be an indicator of tumor growth inhibition in NSSLC. Furthermore, high expression of circulating MPs at diagnosis might predict good prognosis in NSCLC patients.
{"title":"Expression of Circulating Microparticles for the Diagnosis of Non-small Cell Lung Cancer: Clinicopathological Correlations and Prognostic Value","authors":"F. Najjar, M. Alammar, G. Al-Massarani, Abdulmonem Japawe, Nissreen Alamalla, I. Banat, A. Ikhtiar","doi":"10.13189/cor.2020.060201","DOIUrl":"https://doi.org/10.13189/cor.2020.060201","url":null,"abstract":"Increased values of circulating microparticles (MPs) have been reported in solid tumors including non-small cell lung cancer (NSCLC). We therefore investigated the utility of baseline MPs in the clinical setting of patients with NSCLC. Quantification of MPs in the plasma was performed by flowcytometry. Baseline MP values were correlated with clinical patients' characteristics, estimated tumor volume (ETV) and treatment response. Receiver operating characteristics (ROC) curves were plotted to discriminate between patients and controls in order to determine the diagnostic value of circulating MPs in NSCLC. Our prospective study included 134 NSCLC patients (98 at initial diagnosis, ID and 36 at relapse, R) and 30 healthy individuals. The mean of baseline MP numbers was significantly higher in patients presented either at ID or R than in controls (p<0.0001). Basal MP numbers were inversely correlated with ETV values (p=0.04). In addition, the difference in MP levels at diagnosis was significant according to tumor histology (p=0.02) and primary tumor size (p=0.0007). Using ROC analysis, the optimal cutoff value for baseline MPs was 1307 events/µL with a sensitivity and a specificity of 67.3% and 90.0%, respectively. High MPs expression was significantly associated with low-level smoking degree (p=0.001), non-squamous cell types (p=0.017) and decreased tumor size (p=0.003). Our results suggest that high baseline MP values could be an indicator of tumor growth inhibition in NSSLC. Furthermore, high expression of circulating MPs at diagnosis might predict good prognosis in NSCLC patients.","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87072180","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}
Pub Date : 2020-04-09DOI: 10.17303/jcrto.2020.8.204
P. Xing, Yuxin Mu, Shouzheng Wang, Jing Lin, Hao Liu, A. Lizaso, Han-Zhang Han, Jianxing, Xiang, X. Mao, X. Hao, Junling Li
with
与
{"title":"Survival outcomes Associated with Various Resistance Mechanisms of Osimertinib in Chinese Advanced Non-Small Cell Lung Cancer Patients","authors":"P. Xing, Yuxin Mu, Shouzheng Wang, Jing Lin, Hao Liu, A. Lizaso, Han-Zhang Han, Jianxing, Xiang, X. Mao, X. Hao, Junling Li","doi":"10.17303/jcrto.2020.8.204","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.204","url":null,"abstract":"with","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"54 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85661440","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}
Pub Date : 2020-04-01Epub Date: 2020-12-29DOI: 10.17303/jcrto.2020.8.206
Christopher DeAngelo, Megan Burnett Tarasiewicz, Athena Strother, Heather Taggart, Caron Gray, Meaghan Shanahan, Christopher Glowacki, Jimmy Khandalavala, Erin Talaska, Andrea Kinnan, John Joseph Coté, Adrienne Perfilio Edwards, Gina Harper-Harrison, Murray Joseph Casey, Traci-Lynn Hirai, Sarah Schultz, Lynnea Stines, Roma Vora, Dominique Boudreau, Jennifer Burgart, Meredith Shama, Trevor Watson, Lisa Strasheim, Rachel Thompson, Rachel Lawlor, Kayleen Joyce, Claire M Magnuson, Jane Driano, Breanna Elger, Anne Lentino, Margaret Driscoll, Elise Tidwell, Apoorva Sharma, Sarah R Walker, Gretchen Jones, Poonam Sharma, Holly Stessman, Yanyuan Wu, Jay Vadgama, Dana Chase, Lesley Conrad, Srinivasa T Reddy, Robin Farias-Eisner
Background: Endometriosis is complex, but identifying the novel biomarkers, inflammatory molecules, and genetic links holds the key to the enhanced detection, prediction and treatment of both endometriosis and endometriosis related malignant neoplasia. Here we review the literature relating to the specific molecular mechanism(s) mediating tumorigenesis arising within endometriosis.
Methods: Guidance (e.g. Cochrane) and published studies were identified. The Published studies were identified through PubMed using the systematic review methods filter, and the authors' topic knowledge. These data were reviewed to identify key and relevant articles to create a comprehensive review article to explore the molecular fingerprint associated with in endometriosis-driven tumorigenesis.
Results: An important focus is the link between C3aR1, PGR, ER1, SOX-17 and other relevant gene expression profiles and endometriosis-driven tumorigenesis. Further studies should also focus on the combined use of CA-125 with HE-4, and the role for OVA1/MIA as clinically relevant diagnostic biomarkers in the prediction of endometriosis-driven tumorigenesis.
Conclusions: Elucidating endometriosis' molecular fingerprint is to understand the molecular mechanisms that drive the endometriosis-associated malignant phenotype. A better understanding of the predictive roles of these genes and the value of the biomarker proteins will allow for the derivation of unique molecular treatment algorithms to better serve our patients.
{"title":"Endometriosis: A Malignant Fingerprint.","authors":"Christopher DeAngelo, Megan Burnett Tarasiewicz, Athena Strother, Heather Taggart, Caron Gray, Meaghan Shanahan, Christopher Glowacki, Jimmy Khandalavala, Erin Talaska, Andrea Kinnan, John Joseph Coté, Adrienne Perfilio Edwards, Gina Harper-Harrison, Murray Joseph Casey, Traci-Lynn Hirai, Sarah Schultz, Lynnea Stines, Roma Vora, Dominique Boudreau, Jennifer Burgart, Meredith Shama, Trevor Watson, Lisa Strasheim, Rachel Thompson, Rachel Lawlor, Kayleen Joyce, Claire M Magnuson, Jane Driano, Breanna Elger, Anne Lentino, Margaret Driscoll, Elise Tidwell, Apoorva Sharma, Sarah R Walker, Gretchen Jones, Poonam Sharma, Holly Stessman, Yanyuan Wu, Jay Vadgama, Dana Chase, Lesley Conrad, Srinivasa T Reddy, Robin Farias-Eisner","doi":"10.17303/jcrto.2020.8.206","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.206","url":null,"abstract":"<p><strong>Background: </strong>Endometriosis is complex, but identifying the novel biomarkers, inflammatory molecules, and genetic links holds the key to the enhanced detection, prediction and treatment of both endometriosis and endometriosis related malignant neoplasia. Here we review the literature relating to the specific molecular mechanism(s) mediating tumorigenesis arising within endometriosis.</p><p><strong>Methods: </strong>Guidance (e.g. Cochrane) and published studies were identified. The Published studies were identified through PubMed using the systematic review methods filter, and the authors' topic knowledge. These data were reviewed to identify key and relevant articles to create a comprehensive review article to explore the molecular fingerprint associated with in endometriosis-driven tumorigenesis.</p><p><strong>Results: </strong>An important focus is the link between C3aR1, PGR, ER1, SOX-17 and other relevant gene expression profiles and endometriosis-driven tumorigenesis. Further studies should also focus on the combined use of CA-125 with HE-4, and the role for OVA1/MIA as clinically relevant diagnostic biomarkers in the prediction of endometriosis-driven tumorigenesis.</p><p><strong>Conclusions: </strong>Elucidating endometriosis' molecular fingerprint is to understand the molecular mechanisms that drive the endometriosis-associated malignant phenotype. A better understanding of the predictive roles of these genes and the value of the biomarker proteins will allow for the derivation of unique molecular treatment algorithms to better serve our patients.</p>","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"8 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7909468/pdf/nihms-1661598.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25414873","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}
Pub Date : 2020-03-20DOI: 10.17303/jcrto.2020.8.203
{"title":"Critical Review on Role of Some Nutritional Components in Prevention of Cancer In India: An Educators Role","authors":"","doi":"10.17303/jcrto.2020.8.203","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.203","url":null,"abstract":"","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73546130","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}
Pub Date : 2020-02-05DOI: 10.17303/jcrto.2020.8.202
{"title":"Epigenetics Meets CRISPR/Cas to Fight Cancer","authors":"","doi":"10.17303/jcrto.2020.8.202","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.202","url":null,"abstract":"","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80993113","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}
Pub Date : 2020-01-28DOI: 10.17303/jcrto.2020.8.102
E. Alexander, Allyson R. Minton, M. Peters, J. Ryn, S. Gilmour
and Cisplatin Co-Treatment Enhances the Antitumor Efficacy of Immune Checkpoint Blockade in A Model of Resistant Ovarian Cancer. Abstract The standard treatment for ovarian cancer is surgical debulking followed by platinum- taxane-based chemotherapy. Although most patients are initially responsive to this therapy, patients in advanced stages eventually relapse and die. New therapeutic approaches using immune checkpoint blockade (ICB) have been less promising in ovarian cancer compared to other tumor types, resulting in durable tumor regression in only a small subset of ovarian cancer patients. Because previous studies showed immunomodulatory effects following co-treatment with cisplatin and the thrombin inhibitor dabigatran etexilate (C/D) in a preclinical animal model of ovarian cancer, we explored to what extent this co-treatment may enhance the anti-tumor efficacy of ICB in the ID8 tumor model that is resistant to ICB. Whereas cisplatin or dabigatran treatment alone or co-treatment with cisplatin and anti-PD-1 monoclonal antibody (mAb) demonstrated little significant effect on tumor spread, co-treatment with C/D with or without anti-PD-1 mAb significantly reduced ID8 tumor burden and increased peritoneal INF-γ producing CD8+ T-cells after only 2 weeks of treatment. Moreover, C/D cotreatment with ICB conferred a durable survival advantage over C/D or ICB alone. The enhanced anti-tumor effect and survival with C/D co-treatment and ICB compared to that with C/D or ICB alone was accompanied by decreases in immunosuppressive M2- macrophages, decreases in pro-tumorigenic cytokines, and corresponding increases in tumor-infiltrating, IFN-γ-producing CD8+ T-cells. Our findings provide proof-of-concept evidence that the addition of ICB with thrombin inhibition in frontline platinum-based chemotherapy may be a potential new therapeutic treatment combination for advanced ovarian cancer.
{"title":"Dabigatran and Cisplatin Co-Treatment Enhances the Antitumor Efficacy of Immune Checkpoint Blockade in A Murine Model of Resistant Ovarian Cancer","authors":"E. Alexander, Allyson R. Minton, M. Peters, J. Ryn, S. Gilmour","doi":"10.17303/jcrto.2020.8.102","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.102","url":null,"abstract":"and Cisplatin Co-Treatment Enhances the Antitumor Efficacy of Immune Checkpoint Blockade in A Model of Resistant Ovarian Cancer. Abstract The standard treatment for ovarian cancer is surgical debulking followed by platinum- taxane-based chemotherapy. Although most patients are initially responsive to this therapy, patients in advanced stages eventually relapse and die. New therapeutic approaches using immune checkpoint blockade (ICB) have been less promising in ovarian cancer compared to other tumor types, resulting in durable tumor regression in only a small subset of ovarian cancer patients. Because previous studies showed immunomodulatory effects following co-treatment with cisplatin and the thrombin inhibitor dabigatran etexilate (C/D) in a preclinical animal model of ovarian cancer, we explored to what extent this co-treatment may enhance the anti-tumor efficacy of ICB in the ID8 tumor model that is resistant to ICB. Whereas cisplatin or dabigatran treatment alone or co-treatment with cisplatin and anti-PD-1 monoclonal antibody (mAb) demonstrated little significant effect on tumor spread, co-treatment with C/D with or without anti-PD-1 mAb significantly reduced ID8 tumor burden and increased peritoneal INF-γ producing CD8+ T-cells after only 2 weeks of treatment. Moreover, C/D cotreatment with ICB conferred a durable survival advantage over C/D or ICB alone. The enhanced anti-tumor effect and survival with C/D co-treatment and ICB compared to that with C/D or ICB alone was accompanied by decreases in immunosuppressive M2- macrophages, decreases in pro-tumorigenic cytokines, and corresponding increases in tumor-infiltrating, IFN-γ-producing CD8+ T-cells. Our findings provide proof-of-concept evidence that the addition of ICB with thrombin inhibition in frontline platinum-based chemotherapy may be a potential new therapeutic treatment combination for advanced ovarian cancer.","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89897094","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}
Pub Date : 2020-01-04DOI: 10.17303/jcrto.2020.8.105
Maria Patrizia Mongiardi, R. Pallini, A. Levi, M. Falchetti
Glioblastoma, the most aggressive brain tumor, is associated with invariably poor prognosis in spite of extensive surgical resection, radiotherapy, and concomitant and adjuvant chemotherapy. The histological landmarks of glioblastoma are massive necrosis and prominent angiogenesis. Glioblastoma vasculature is structurally and function-ally aberrant, characterized by tortuous and leaky vessels, with an increased diameter and significantly thickened basement membranes. This altered vasculature enhances tumor hypoxia and affects the possibility of effective drug delivery to the tumor. Many efforts have been spent in developing therapeutic strategies targeting glioblastoma neo-angiogen-esis, with the dual aim of inhibiting tumor growth and stabilizing tumor vasculature, therefore improving chemotherapy delivery to the tumor. Bevacizumab, a humanized monoclonal antibody targeting Vascular Endothelial Growth Factor (VEGF), has been approved by Food and Drug Administration (FDA) for recurrent glioblastoma, but unfortunately it seems to have limited efficacy in terms of overall survival. Here, we review literature data both from molecular and clinical studies and analyze the state of the art and the future perspectives of antiangiogenic therapies for glioblastoma.
{"title":"Current Status and Future Perspectives of Anti-Angiogenic Therapeutic Attempts for Glioblastoma","authors":"Maria Patrizia Mongiardi, R. Pallini, A. Levi, M. Falchetti","doi":"10.17303/jcrto.2020.8.105","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.105","url":null,"abstract":"Glioblastoma, the most aggressive brain tumor, is associated with invariably poor prognosis in spite of extensive surgical resection, radiotherapy, and concomitant and adjuvant chemotherapy. The histological landmarks of glioblastoma are massive necrosis and prominent angiogenesis. Glioblastoma vasculature is structurally and function-ally aberrant, characterized by tortuous and leaky vessels, with an increased diameter and significantly thickened basement membranes. This altered vasculature enhances tumor hypoxia and affects the possibility of effective drug delivery to the tumor. Many efforts have been spent in developing therapeutic strategies targeting glioblastoma neo-angiogen-esis, with the dual aim of inhibiting tumor growth and stabilizing tumor vasculature, therefore improving chemotherapy delivery to the tumor. Bevacizumab, a humanized monoclonal antibody targeting Vascular Endothelial Growth Factor (VEGF), has been approved by Food and Drug Administration (FDA) for recurrent glioblastoma, but unfortunately it seems to have limited efficacy in terms of overall survival. Here, we review literature data both from molecular and clinical studies and analyze the state of the art and the future perspectives of antiangiogenic therapies for glioblastoma.","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89236592","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}
Pub Date : 2020-01-01Epub Date: 2020-01-17DOI: 10.17303/jcrto.2020.8.101
Feng Su, Anantharamaiah Gm, Mayakonda N Palgunachari, C Roger White, Holly Stessman, Yanyuan Wu, Jay Vadgama, Richard Pietras, Dorothy Nguyen, Srinivasa T Reddy, Robin Farias-Eisner
A growing body of literature supports the role of apolipoproteins present in HDL in the treatment of pro-inflammatory diseases including cancer. We examined whether bovine HDL (bHDL) and three dual-domain peptides, namely AEM-28 and its analog AEM-28-2, and HM-10/10, affect tumor growth and development in mouse models of ovarian and colon cancer. We demonstrate that bHDL inhibits mouse colorectal cancer cell line CT26-mediated lung tumor development, and mouse ovarian cancer cell line ID8-mediated tumor burden. We also demonstrate that, although to different degrees, dual-domain peptides inhibit cell viability of mouse and human ovarian and colon cancer cell lines, but not that of normal human colonic epithelial cells or NIH3T3 mouse fibroblasts. Dual-domain peptides administered subcutaneously or in a chow diet decrease CT26 cell-mediated tumor burden, tumor growth, and tumor dissemination in BALB/c mice. Plasma levels of lysophosphatidic acid (LPA) are significantly reduced in mice that received bHDL and the dual-domain peptides, suggesting that reduction by effecting accumulation and/or synthesis of pro-inflammatory lipids may be one of the mechanisms for the inhibition of tumor development by bHDL and the dual-domain peptides. Our studies suggest that therapeutics based on apolipoproteins present in HDL may be novel agents for the treatment of epithelial adenocarcinomas of the ovary and colon.
{"title":"Bovine HDL and Dual Domain HDL-Mimetic Peptides Inhibit Tumor Development in Mice.","authors":"Feng Su, Anantharamaiah Gm, Mayakonda N Palgunachari, C Roger White, Holly Stessman, Yanyuan Wu, Jay Vadgama, Richard Pietras, Dorothy Nguyen, Srinivasa T Reddy, Robin Farias-Eisner","doi":"10.17303/jcrto.2020.8.101","DOIUrl":"https://doi.org/10.17303/jcrto.2020.8.101","url":null,"abstract":"<p><p>A growing body of literature supports the role of apolipoproteins present in HDL in the treatment of pro-inflammatory diseases including cancer. We examined whether bovine HDL (bHDL) and three dual-domain peptides, namely AEM-28 and its analog AEM-28-2, and HM-10/10, affect tumor growth and development in mouse models of ovarian and colon cancer. We demonstrate that bHDL inhibits mouse colorectal cancer cell line CT26-mediated lung tumor development, and mouse ovarian cancer cell line ID8-mediated tumor burden. We also demonstrate that, although to different degrees, dual-domain peptides inhibit cell viability of mouse and human ovarian and colon cancer cell lines, but not that of normal human colonic epithelial cells or NIH3T3 mouse fibroblasts. Dual-domain peptides administered subcutaneously or in a chow diet decrease CT26 cell-mediated tumor burden, tumor growth, and tumor dissemination in BALB/c mice. Plasma levels of lysophosphatidic acid (LPA) are significantly reduced in mice that received bHDL and the dual-domain peptides, suggesting that reduction by effecting accumulation and/or synthesis of pro-inflammatory lipids may be one of the mechanisms for the inhibition of tumor development by bHDL and the dual-domain peptides. Our studies suggest that therapeutics based on apolipoproteins present in HDL may be novel agents for the treatment of epithelial adenocarcinomas of the ovary and colon.</p>","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37980897","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}
Pub Date : 2019-12-04DOI: 10.17303/JCRTO.2014.2.102
G. Banfalvi
{"title":"Tumor Cell Fusion and Multipolar Trivision","authors":"G. Banfalvi","doi":"10.17303/JCRTO.2014.2.102","DOIUrl":"https://doi.org/10.17303/JCRTO.2014.2.102","url":null,"abstract":"","PeriodicalId":15189,"journal":{"name":"Journal of Cancer Research and Therapeutic Oncology","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86212205","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}
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