Because of the emergence of drug-resistant tumor cells, successful treatments of human malignancies have been difficult to achieve in the clinic. In spite of various approaches to overcome multi drug resistance, it has remained challenging and elusive. It is, therefore, necessary to define and understand the mechanisms of drug-induced tumor cell killing for the future development of anticancer agents and for rationally designed combination chemotherapies. The clinically active antitumor drugs, topotecan, doxorubicin, etoposide, and procarbazine are currently used for the treatment of human tumors. Therefore, a great deal research has been carried to understand mechanisms of actions of these agents both in the laboratory and in the clinic. These drugs are also extensively metabolized in tumor cells to various reactive species and generate oxygen free radical species (ROS) that initiate lipid peroxidation and induce DNA damage. However, the roles of ROS in the mechanism of cytotoxicity remain unappreciated in the clinic. In addition to ROS, various reactive nitrogen species (RNS) are also formed in tumor cells and in vivo. However, the importance of RNS in cancer treatment is not clear and has remained poorly defined. This review discusses the current understanding of the formation and the significance of ROS and RNS in the mechanisms of various clinically active anticancer drugs.
{"title":"Role of Oxygen and Nitrogen Radicals in the Mechanism of Anticancer Drug Cytotoxicity.","authors":"Birandra Kumar Sinha","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Because of the emergence of drug-resistant tumor cells, successful treatments of human malignancies have been difficult to achieve in the clinic. In spite of various approaches to overcome multi drug resistance, it has remained challenging and elusive. It is, therefore, necessary to define and understand the mechanisms of drug-induced tumor cell killing for the future development of anticancer agents and for rationally designed combination chemotherapies. The clinically active antitumor drugs, topotecan, doxorubicin, etoposide, and procarbazine are currently used for the treatment of human tumors. Therefore, a great deal research has been carried to understand mechanisms of actions of these agents both in the laboratory and in the clinic. These drugs are also extensively metabolized in tumor cells to various reactive species and generate oxygen free radical species (ROS) that initiate lipid peroxidation and induce DNA damage. However, the roles of ROS in the mechanism of cytotoxicity remain unappreciated in the clinic. In addition to ROS, various reactive nitrogen species (RNS) are also formed in tumor cells and <i>in vivo</i>. However, the importance of RNS in cancer treatment is not clear and has remained poorly defined. This review discusses the current understanding of the formation and the significance of ROS and RNS in the mechanisms of various clinically active anticancer drugs.</p>","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"12 1","pages":"10-18"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7269165/pdf/nihms-1579889.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38006911","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 : 2019-05-16DOI: 10.4172/1948-5956.1000604
Bo Yang, Yaping Long, Zhibo Zhang, Yuheng Ma, Z. Cui, P. Cui, Xiao-yan Li, Y. Hu
Osimertinib (AZD9291, Tagrisso) is an irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) compound. Limited effective therapeutic regimens are recommended for patients who progress with osimertinib. We retrospectively reviewed two patients with EGFR mutations who were resistant to osimertinib and received anti-programmed cell death-1 (anti-PD-1) agents combined with Abraxane with stage IV cancer. The two patients (one male and one female) were diagnosed with EGFR mutation-positive advanced lung adenocarcinoma and received first- or second-generation EGFR-TKIs. When these patients became resistant, both received osimertinib. Both patients had disease progression after osimertinib and received combination therapy of immune checkpoint blockade (nivolumab or pembrolizumab) and albumin-bound paclitaxel (Abraxane). These patients achieved partial remission (PR), and their progression-free survival (PFS) were respectively 8.0 months and 10.0 months. The combination of immunotherapy and Abraxane could be an effective option for the treatment of patients resistant to osimertinib.
{"title":"Durable Response to Immune Checkpoint Blockade Plus Albumin-Bound Paclitaxel in Two Osimertinib-Refractory Patients with EGFR-mutated Lung Adenocarcinoma","authors":"Bo Yang, Yaping Long, Zhibo Zhang, Yuheng Ma, Z. Cui, P. Cui, Xiao-yan Li, Y. Hu","doi":"10.4172/1948-5956.1000604","DOIUrl":"https://doi.org/10.4172/1948-5956.1000604","url":null,"abstract":"Osimertinib (AZD9291, Tagrisso) is an irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) compound. Limited effective therapeutic regimens are recommended for patients who progress with osimertinib. We retrospectively reviewed two patients with EGFR mutations who were resistant to osimertinib and received anti-programmed cell death-1 (anti-PD-1) agents combined with Abraxane with stage IV cancer. The two patients (one male and one female) were diagnosed with EGFR mutation-positive advanced lung adenocarcinoma and received first- or second-generation EGFR-TKIs. When these patients became resistant, both received osimertinib. Both patients had disease progression after osimertinib and received combination therapy of immune checkpoint blockade (nivolumab or pembrolizumab) and albumin-bound paclitaxel (Abraxane). These patients achieved partial remission (PR), and their progression-free survival (PFS) were respectively 8.0 months and 10.0 months. The combination of immunotherapy and Abraxane could be an effective option for the treatment of patients resistant to osimertinib.","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"104 1","pages":"175-177"},"PeriodicalIF":0.0,"publicationDate":"2019-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80850426","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 : 2019-04-15DOI: 10.4172/1948-5956.1000596
Jianyi Zhao, Xuan Zhao, Chaoqi Zhang, Qingyi Zhang, Zhen Zhang, Zhibo Shen, Yang Yang, Xiangnan Li, Y. Qi, Zhan-feng He, Chunyang Zhang, Renyin Chen, Yi Zhang, Song Zhao
Background: Lung cancer is one of the most common cancer in the world, the role of minichromosome maintenance 10 (MCM10) in lung adenocarcinoma (ADC) is still unknown. Methods: Using TCGA (The Cancer Genome Atlas) database, MCM10 RNA-seq and patients’ clinicopathological characteristics were analyzed. The nomogram and Time-dependent area under the curve (AUC) were built from analysis of multivariate Cox regression model in TCGA database. In our patient cohort, the expression of MCM10 in gene and protein were detected, functional studies were further explored. Moreover, Gene Set Enrichment Analysis (GSEA) was performed using TCGA database.Results: In TCGA database and our patient cohort, MCM10 expression was higher in tumor tissues than normal tissues. Overall survival (OS) status revealed that high MCM10 group was poorer than low MCM10 group in TCGA database (p=0.0212) and our patient cohort (p=0.0391). Patients with higher MCM10 expression displayed shorter progression free survival (PFS) time in our patient cohort (p=0.0323). MCM10 could be a diagnostic marker due to receiver operating characteristic (ROC) curve in TCGA database (p<0.0001) and our patient cohort (p=0.0048). Univariate and multivariate cox analysis demonstrated that MCM10 was an independent prognosticator for ADC. The nomogram model combined MCM10 expression, age and pathologic stage could predict the probability of 1108 days OS and it was assessed by C-index and calibration curve in TCGA database. Time-dependent AUC showed this model in predicting OS probability was particularly effective in earlier patients. Silence of MCM10 inhibited the cell proliferation, induced the G0/G1 phase arrest in cell cycle, promoted apoptosis and decreased migration in vitro. GSEA identified that higher expression of MCM10 was positively correlated with cellular mitosis, cell cycle, chromatin assembly, DNA biosynthetic process and DNA replication. Conclusion: Our study reveals that MCM10 plays a crucial role and could be an important marker for prognosis in AD
背景:肺癌是世界上最常见的癌症之一，小染色体维持10 (MCM10)在肺腺癌(ADC)中的作用尚不清楚。方法:利用TCGA (The Cancer Genome Atlas)数据库，分析MCM10 RNA-seq和患者的临床病理特征。通过对TCGA数据库中的多变量Cox回归模型的分析，建立了nomogram和Time-dependent area under curve (AUC)。在我们的患者队列中，检测了MCM10在基因和蛋白上的表达，并进一步探讨了功能研究。利用TCGA数据库进行基因集富集分析(GSEA)。结果:在TCGA数据库和我们的患者队列中，MCM10在肿瘤组织中的表达高于正常组织。总生存(OS)状况显示，TCGA数据库(p=0.0212)和我们的患者队列(p=0.0391)中，高MCM10组低于低MCM10组。在我们的患者队列中，MCM10表达较高的患者显示出较短的无进展生存期(PFS)时间(p=0.0323)。根据TCGA数据库的受试者工作特征(ROC)曲线(p<0.0001)和我们的患者队列(p=0.0048)， MCM10可以作为诊断标志物。单因素和多因素cox分析表明MCM10是ADC的独立预后因子。结合MCM10表达、年龄和病理分期建立的nomogram模型可以预测患者1108天OS的概率，并通过TCGA数据库中的c指数和校准曲线进行评估。随时间变化的AUC表明，该模型在早期患者中预测OS概率特别有效。MCM10沉默抑制细胞增殖，诱导细胞周期G0/G1期阻滞，促进细胞凋亡，减少体外迁移。GSEA发现MCM10的高表达与细胞有丝分裂、细胞周期、染色质组装、DNA生物合成过程和DNA复制呈正相关。结论:我们的研究表明MCM10在AD中起着至关重要的作用，可能是AD预后的重要标志
{"title":"Significant Role of MCM10 in Lung Adenocarcinoma: Promote Viability and Migration","authors":"Jianyi Zhao, Xuan Zhao, Chaoqi Zhang, Qingyi Zhang, Zhen Zhang, Zhibo Shen, Yang Yang, Xiangnan Li, Y. Qi, Zhan-feng He, Chunyang Zhang, Renyin Chen, Yi Zhang, Song Zhao","doi":"10.4172/1948-5956.1000596","DOIUrl":"https://doi.org/10.4172/1948-5956.1000596","url":null,"abstract":"Background: Lung cancer is one of the most common cancer in the world, the role of minichromosome maintenance 10 (MCM10) in lung adenocarcinoma (ADC) is still unknown. Methods: Using TCGA (The Cancer Genome Atlas) database, MCM10 RNA-seq and patients’ clinicopathological characteristics were analyzed. The nomogram and Time-dependent area under the curve (AUC) were built from analysis of multivariate Cox regression model in TCGA database. In our patient cohort, the expression of MCM10 in gene and protein were detected, functional studies were further explored. Moreover, Gene Set Enrichment Analysis (GSEA) was performed using TCGA database.Results: In TCGA database and our patient cohort, MCM10 expression was higher in tumor tissues than normal tissues. Overall survival (OS) status revealed that high MCM10 group was poorer than low MCM10 group in TCGA database (p=0.0212) and our patient cohort (p=0.0391). Patients with higher MCM10 expression displayed shorter progression free survival (PFS) time in our patient cohort (p=0.0323). MCM10 could be a diagnostic marker due to receiver operating characteristic (ROC) curve in TCGA database (p<0.0001) and our patient cohort (p=0.0048). Univariate and multivariate cox analysis demonstrated that MCM10 was an independent prognosticator for ADC. The nomogram model combined MCM10 expression, age and pathologic stage could predict the probability of 1108 days OS and it was assessed by C-index and calibration curve in TCGA database. Time-dependent AUC showed this model in predicting OS probability was particularly effective in earlier patients. Silence of MCM10 inhibited the cell proliferation, induced the G0/G1 phase arrest in cell cycle, promoted apoptosis and decreased migration in vitro. GSEA identified that higher expression of MCM10 was positively correlated with cellular mitosis, cell cycle, chromatin assembly, DNA biosynthetic process and DNA replication. Conclusion: Our study reveals that MCM10 plays a crucial role and could be an important marker for prognosis in AD","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85377135","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 : 2019-04-08DOI: 10.4172/1948-5956.1000592
Andrea Brown, Sanjay Kumar, P. Tchounwou
Cisplatin (cis-diammine-dichloro-platinum II) was initially discovered to prevent the growth of Escherichia coli and was further recognized for its anti-neoplastic and cytotoxic effects on cancer cells. Administered intravenously to humans, cisplatin is used as first-line chemotherapy treatment for patients diagnosed with various types of malignancies, such as leukemia, lymphomas, breast, testicular, ovarian, head and neck, and cervical cancers, and sarcomas. Once cisplatin enters the cell it exerts its cytotoxic effect by losing one chloride ligand, binding to DNA to form intra-strand DNA adducts, and inhibiting DNA synthesis and cell growth. The DNA lesions formed from cisplatin-induced DNA damage activate DNA repair response via NER (nuclear excision repair system) by halting cisplatin-induced cell death by activation of ATM (ataxia telangiectasia mutated) pathway. Although treatment has been shown to be effective, many patients experience relapse due to drug resistance. As a result, other platinum compounds such as oxaliplatin and carboplatin have since been used and have shown some levels of effectiveness. In this review, the clinical applications of cisplatin are discussed with a special emphasis on its use in cancer chemotherapy.
{"title":"Cisplatin-Based Chemotherapy of Human Cancers","authors":"Andrea Brown, Sanjay Kumar, P. Tchounwou","doi":"10.4172/1948-5956.1000592","DOIUrl":"https://doi.org/10.4172/1948-5956.1000592","url":null,"abstract":"Cisplatin (cis-diammine-dichloro-platinum II) was initially discovered to prevent the growth of Escherichia coli and was further recognized for its anti-neoplastic and cytotoxic effects on cancer cells. Administered intravenously to humans, cisplatin is used as first-line chemotherapy treatment for patients diagnosed with various types of malignancies, such as leukemia, lymphomas, breast, testicular, ovarian, head and neck, and cervical cancers, and sarcomas. Once cisplatin enters the cell it exerts its cytotoxic effect by losing one chloride ligand, binding to DNA to form intra-strand DNA adducts, and inhibiting DNA synthesis and cell growth. The DNA lesions formed from cisplatin-induced DNA damage activate DNA repair response via NER (nuclear excision repair system) by halting cisplatin-induced cell death by activation of ATM (ataxia telangiectasia mutated) pathway. Although treatment has been shown to be effective, many patients experience relapse due to drug resistance. As a result, other platinum compounds such as oxaliplatin and carboplatin have since been used and have shown some levels of effectiveness. In this review, the clinical applications of cisplatin are discussed with a special emphasis on its use in cancer chemotherapy.","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"172 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76958388","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 : 2019-03-19DOI: 10.4172/1948-5956-C1-160
pGang Chenp
{"title":"Impact of chlorophyllin e6 photodynamic therapy in human bladder cancer cells","authors":"pGang Chenp","doi":"10.4172/1948-5956-C1-160","DOIUrl":"https://doi.org/10.4172/1948-5956-C1-160","url":null,"abstract":"","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"72 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84083845","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 : 2019-03-19DOI: 10.4172/1948-5956-C1-159
pGuoxiong Xup
{"title":"FLOT1 is a novel target of ovarian cancer for diagnosis and treatment","authors":"pGuoxiong Xup","doi":"10.4172/1948-5956-C1-159","DOIUrl":"https://doi.org/10.4172/1948-5956-C1-159","url":null,"abstract":"","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"41 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73871604","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 : 2019-03-16DOI: 10.4172/1948-5956.1000589
Shilpi Gupta, Prabhat Kumar, Jayant Maini, B. Das, M. Bhardwaj
Oral squamous cell carcinoma (OSCC) is the most prevalent cancer in Indian subcontinent with high recurrence rate, aggressive metastasis, and poor prognosis. The potential risk-factors for OSCC are tobacco smoking, alcohol intake, and persistent infection of oncogenic human papillomaviruses (HR-HPVs). HPV-positive OSCCs show distinct genetic and epigenetic changes along with distinct clinical, epidemiological and molecular characteristics. Recently, with the accumulation of large amount of genomic and epigenomic data, there is an increasing focus on epigenetic alterations playing key roles in cancer pathogenesis. Non-coding RNAs, especially the small noncoding RNAs (sncRNAs) have gained attention since they have been demonstrated to fine tune transcription via alterations in the epigenetic landscape. There are ample evidences supporting the role of small non-coding RNAs such as miRNAs and piRNAs in development and disease including cancers. PIWI-interacting RNAs (piRNAs), a class of sncRNAs are emerging players involved in transcription silencing. Its altered regulation is associated with the development of variety of tumors including oral carcinogenesis; however, their tumor specific roles are not fully understood. Therefore, identification and comprehensive characterization of oncogenic as well as tumor suppressive pi-RNAs and dissecting their roles in tumorigenesis is of great importance in the field of cancer biology. Furthermore, piRNAs may potentially serve as unique therapeutic targets and/or molecular markers for early detection and effective treatment of OSCC subtypes. In this mini review, we briefly summarize the emerging role of PIWI-RNAs in oral cancer.
{"title":"PIWI-Interacting RNAs in Oral Cancer: Paradigm Shift in Prognosis and Diagnosis","authors":"Shilpi Gupta, Prabhat Kumar, Jayant Maini, B. Das, M. Bhardwaj","doi":"10.4172/1948-5956.1000589","DOIUrl":"https://doi.org/10.4172/1948-5956.1000589","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is the most prevalent cancer in Indian subcontinent with high recurrence rate, aggressive metastasis, and poor prognosis. The potential risk-factors for OSCC are tobacco smoking, alcohol intake, and persistent infection of oncogenic human papillomaviruses (HR-HPVs). HPV-positive OSCCs show distinct genetic and epigenetic changes along with distinct clinical, epidemiological and molecular characteristics. Recently, with the accumulation of large amount of genomic and epigenomic data, there is an increasing focus on epigenetic alterations playing key roles in cancer pathogenesis. Non-coding RNAs, especially the small noncoding RNAs (sncRNAs) have gained attention since they have been demonstrated to fine tune transcription via alterations in the epigenetic landscape. There are ample evidences supporting the role of small non-coding RNAs such as miRNAs and piRNAs in development and disease including cancers. PIWI-interacting RNAs (piRNAs), a class of sncRNAs are emerging players involved in transcription silencing. Its altered regulation is associated with the development of variety of tumors including oral carcinogenesis; however, their tumor specific roles are not fully understood. Therefore, identification and comprehensive characterization of oncogenic as well as tumor suppressive pi-RNAs and dissecting their roles in tumorigenesis is of great importance in the field of cancer biology. Furthermore, piRNAs may potentially serve as unique therapeutic targets and/or molecular markers for early detection and effective treatment of OSCC subtypes. In this mini review, we briefly summarize the emerging role of PIWI-RNAs in oral cancer.","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77142557","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 : 2019-03-12DOI: 10.4172/1948-5956.1000587
S. Benkhaled, T. Dragan, S. Beauvois, A. D. Caluwé, D. V. Gestel
Background: The treatment of nasopharyngeal carcinoma (NPC) consists of radiotherapy alone (stage I) or radiotherapy concomitant with chemotherapy (stage II-V). Acute side effects management forms a major challenge for practitioners. Substantial literature is available from endemic areas, whereas data from Europe is scarce. This study examines clinical characteristics, therapeutic results, acute and late side effects of patients treated at the Jules Bordet Institute. Materials and Methods: Twenty-two consecutive non-metastatic NPC patients treated between May 2012 and September 2015 were retrospectively analyzed. All patients were treated by Intensity Modulated Radiation Therapy (IMRT) with or without chemotherapy (CT). Results: Thirteen patients have North-African ancestry while nine are of European origin. Seventy-three percent had a non-keratinizing carcinoma and 90% had an advanced stage disease (III-IVb). Ninety-five percent of the patients received concomitant CT. After a median follow-up time of 31 months, overall survival was 77%. Local, regional and distant control rates were 95%, 86% and 73%. Main acute grade 3 toxicities were swallowing disorders (91%), vomiting (82%), oropharyngeal mucositis (64%) and dermatitis (23%). Only one patient developed grade 4 dermatitis, requiring treatment discontinuation in the sixth week. In the seventh week of treatment, 86% of the patients had lost more than 10% of their starting weight. Univariate analysis identified three factors driving the weight loss: grade 3 mucositis of the soft palate (p=0.027), vomiting (p=0.019) and pre-treatment dental extraction (p=0.006). In multivariate analysis, weight loss is only linked to dental extraction (p=0.042, Odds Ratio 1.62, [95% CI: 1.16-2.80]). Late toxicities were xerostomia (68%), auditory symptoms (55%), hypothyroidism (45%) and swallowing disorders (23%). Conclusion: Our clinical characteristics outcome and toxicity are comparable to published data from endemic regions. Interestingly, weight loss of >10% is correlated to pre-treatment dental extraction. This finding should be confirmed and analyzed in a prospective manner.
{"title":"Weight Loss in Nasopharyngeal Cancer is Mainly Associated with Pre-Treatment Dental Extraction, a European Single-Center Experience","authors":"S. Benkhaled, T. Dragan, S. Beauvois, A. D. Caluwé, D. V. Gestel","doi":"10.4172/1948-5956.1000587","DOIUrl":"https://doi.org/10.4172/1948-5956.1000587","url":null,"abstract":"Background: The treatment of nasopharyngeal carcinoma (NPC) consists of radiotherapy alone (stage I) or radiotherapy concomitant with chemotherapy (stage II-V). Acute side effects management forms a major challenge for practitioners. Substantial literature is available from endemic areas, whereas data from Europe is scarce. This study examines clinical characteristics, therapeutic results, acute and late side effects of patients treated at the Jules Bordet Institute. Materials and Methods: Twenty-two consecutive non-metastatic NPC patients treated between May 2012 and September 2015 were retrospectively analyzed. All patients were treated by Intensity Modulated Radiation Therapy (IMRT) with or without chemotherapy (CT). Results: Thirteen patients have North-African ancestry while nine are of European origin. Seventy-three percent had a non-keratinizing carcinoma and 90% had an advanced stage disease (III-IVb). Ninety-five percent of the patients received concomitant CT. After a median follow-up time of 31 months, overall survival was 77%. Local, regional and distant control rates were 95%, 86% and 73%. Main acute grade 3 toxicities were swallowing disorders (91%), vomiting (82%), oropharyngeal mucositis (64%) and dermatitis (23%). Only one patient developed grade 4 dermatitis, requiring treatment discontinuation in the sixth week. In the seventh week of treatment, 86% of the patients had lost more than 10% of their starting weight. Univariate analysis identified three factors driving the weight loss: grade 3 mucositis of the soft palate (p=0.027), vomiting (p=0.019) and pre-treatment dental extraction (p=0.006). In multivariate analysis, weight loss is only linked to dental extraction (p=0.042, Odds Ratio 1.62, [95% CI: 1.16-2.80]). Late toxicities were xerostomia (68%), auditory symptoms (55%), hypothyroidism (45%) and swallowing disorders (23%). Conclusion: Our clinical characteristics outcome and toxicity are comparable to published data from endemic regions. Interestingly, weight loss of >10% is correlated to pre-treatment dental extraction. This finding should be confirmed and analyzed in a prospective manner.","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"84 1","pages":"73-79"},"PeriodicalIF":0.0,"publicationDate":"2019-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81169977","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 : 2019-03-12DOI: 10.4172/1948-5956.1000586
M. Halder, P. Roy, Abhrajyoti Ghosh
Osteosarcoma is the most common bone tumour seen in the paediatric and adolescent age group. Most osteosarcomas are highly malignant tumours arising within the bone. Several markers for diagnosis and prognosis have been proposed in osteosarcoma namely, vascular endothelial growth factor (VEGF), bone alkaline phosphatase, osteocalcin. A new family of a protein known as Vasodilator-stimulated phosphoprotein, which is known to promote cell migration may also have a role in metastasis of osteosarcoma. So this study was planned to estimate the serum concentration of VASP in patients of osteosarcoma and to find the correlation of it with serum alkaline phosphatase and compare them with controls. Fifty patients attending the Orthopaedics clinics were selected for the study and were divided into two groups. Histopathologically confirmed cases of osteosarcoma (localized without metastasis) were included in Group I and age and sex matched twenty five patients with musculoskeletal pain in Group II as controls. Serum alkaline phosphatase levels and serum vasodilator-stimulated phosphoprotein (VASP) levels were estimated and the result was analysed using standard statistical methods. It has been found that serum VASP levels were significantly decreased and serum alkaline phosphatase levels were significantly raised in patients with osteosarcoma (Group I) as compared to the controls. Serum alkaline phosphatase levels showed a positive correlation with serum VASP levels in control, which got inverted in osteosarcoma cases. VASP, a member of ENA/VASP family, has been implicated in regulating key cellular functions (namely shape change, adhesion and migration) due to its ability to modify dynamic cytoskeleton. The negative correlation between VASP and ALP in osteosarcoma patients also supported the role of VASP in bone mineralization and tumorigenesis. So, VASP in osteosarcomas may lead to improved stratification of outcome and development of novel therapeutic modalities.
{"title":"Role of Vasodilator Stimulated Phosphoprotein (VASP) in Pathogenesis of Osteosarcoma and its Association with Alkaline Phosphatase Levels","authors":"M. Halder, P. Roy, Abhrajyoti Ghosh","doi":"10.4172/1948-5956.1000586","DOIUrl":"https://doi.org/10.4172/1948-5956.1000586","url":null,"abstract":"Osteosarcoma is the most common bone tumour seen in the paediatric and adolescent age group. Most osteosarcomas are highly malignant tumours arising within the bone. Several markers for diagnosis and prognosis have been proposed in osteosarcoma namely, vascular endothelial growth factor (VEGF), bone alkaline phosphatase, osteocalcin. A new family of a protein known as Vasodilator-stimulated phosphoprotein, which is known to promote cell migration may also have a role in metastasis of osteosarcoma. So this study was planned to estimate the serum concentration of VASP in patients of osteosarcoma and to find the correlation of it with serum alkaline phosphatase and compare them with controls. Fifty patients attending the Orthopaedics clinics were selected for the study and were divided into two groups. Histopathologically confirmed cases of osteosarcoma (localized without metastasis) were included in Group I and age and sex matched twenty five patients with musculoskeletal pain in Group II as controls. Serum alkaline phosphatase levels and serum vasodilator-stimulated phosphoprotein (VASP) levels were estimated and the result was analysed using standard statistical methods. It has been found that serum VASP levels were significantly decreased and serum alkaline phosphatase levels were significantly raised in patients with osteosarcoma (Group I) as compared to the controls. Serum alkaline phosphatase levels showed a positive correlation with serum VASP levels in control, which got inverted in osteosarcoma cases. VASP, a member of ENA/VASP family, has been implicated in regulating key cellular functions (namely shape change, adhesion and migration) due to its ability to modify dynamic cytoskeleton. The negative correlation between VASP and ALP in osteosarcoma patients also supported the role of VASP in bone mineralization and tumorigenesis. So, VASP in osteosarcomas may lead to improved stratification of outcome and development of novel therapeutic modalities.","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"58 1","pages":"70-72"},"PeriodicalIF":0.0,"publicationDate":"2019-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90340124","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 : 2019-01-01DOI: 10.4172/1948-5956.1000576
R. Mahmoud, G. Hammad, T. Aboushousha, Ashraf Bakkar
Bladder cancer continues to represent a major health threat, considering the fact that it is one of the major foundations of morbidity and mortality worldwide, accounting for nearly 429,800 new incidence cases and 165,100 deaths per year, it is one of the most common malignant neoplasms in the urological system and is considered as the fourth most prevalent neoplasm in males [1,2]. In Egypt, bladder malignancies are the most common among urinary system malignant tumors (90.71%) and the third among all malignancies [3]. Bladder cancer encompasses a wide spectrum of malignancies; yet its main histological type is urothelial carcinoma, which mostly develops along two main, largely independent but rather overlapping biological pathways, commonly known as papillary and non-papillary tumors. Where, papillary tumors are usually instigated by the dispersal of flat hyperplastic urothelial alterations, also termed low-grade intraurothelial neoplasia, and are characterized by superficial non-invasive papillary protrusions [4]. Although it is very unlikely for these tumors to metastasize, they have a significantly high recurrence propensity. Whereas, Non-papillary tumors develop from Maneoplasia. Non-papillary carcinomas are usually characterized by their aggressive invasion through the bladder wall and their ability to metastasize to regional lymph [5].
{"title":"Aberrant Overexpression of Heterogeneous Nuclear Ribonucleoprotein k in Urinary Bladder Cancer Neoplasms","authors":"R. Mahmoud, G. Hammad, T. Aboushousha, Ashraf Bakkar","doi":"10.4172/1948-5956.1000576","DOIUrl":"https://doi.org/10.4172/1948-5956.1000576","url":null,"abstract":"Bladder cancer continues to represent a major health threat, considering the fact that it is one of the major foundations of morbidity and mortality worldwide, accounting for nearly 429,800 new incidence cases and 165,100 deaths per year, it is one of the most common malignant neoplasms in the urological system and is considered as the fourth most prevalent neoplasm in males [1,2]. In Egypt, bladder malignancies are the most common among urinary system malignant tumors (90.71%) and the third among all malignancies [3]. Bladder cancer encompasses a wide spectrum of malignancies; yet its main histological type is urothelial carcinoma, which mostly develops along two main, largely independent but rather overlapping biological pathways, commonly known as papillary and non-papillary tumors. Where, papillary tumors are usually instigated by the dispersal of flat hyperplastic urothelial alterations, also termed low-grade intraurothelial neoplasia, and are characterized by superficial non-invasive papillary protrusions [4]. Although it is very unlikely for these tumors to metastasize, they have a significantly high recurrence propensity. Whereas, Non-papillary tumors develop from Maneoplasia. Non-papillary carcinomas are usually characterized by their aggressive invasion through the bladder wall and their ability to metastasize to regional lymph [5].","PeriodicalId":15170,"journal":{"name":"Journal of Cancer Science & Therapy","volume":"304 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79787485","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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