Gene delivery systems for gene therapy provide a great opportunity for treating diseases from genetic disorders, cancer, and other infections. The recent development of gene delivery system has reviewed for viral delivery systems and non-viral delivery systems. The viral delivery systems have discussed for DNA-based vectors and RNA-based vectors, and the non-viral delivery systems have summarized on the bases of physical approaches and chemical methods. In the application of gene delivery systems, viral vector systems for gene therapy and polymeric gene delivery systems have briefly reviewed. *Correspondence to: Sung Wan Kim, Center for Controlled Chemical Delivery (CCCD), Department of Pharmaceutics and Pharmaceutical Chemistry, University of Utah, BPRB, Room 205, Salt Lake City, UT 84112, USA, E-mail: sw.kim@pharm.utah.edu
用于基因治疗的基因传递系统为治疗遗传性疾病、癌症和其他感染疾病提供了巨大的机会。综述了近年来基因传递系统的研究进展，包括病毒传递系统和非病毒传递系统。讨论了基于dna的载体和基于rna的载体的病毒传递系统，总结了基于物理途径和化学方法的非病毒传递系统。在基因传递系统的应用方面，综述了用于基因治疗的病毒载体系统和聚合基因传递系统。*通讯:Sung Wan Kim，受控化学输送中心，美国犹他大学药物与药物化学系，BPRB，盐湖城，UT 84112, USA, 205室，E-mail: sw.kim@pharm.utah.edu
{"title":"The practical application of gene vectors in cancer therapy","authors":"Y. Sung, S. W. Kim","doi":"10.15761/ICST.1000287","DOIUrl":"https://doi.org/10.15761/ICST.1000287","url":null,"abstract":"Gene delivery systems for gene therapy provide a great opportunity for treating diseases from genetic disorders, cancer, and other infections. The recent development of gene delivery system has reviewed for viral delivery systems and non-viral delivery systems. The viral delivery systems have discussed for DNA-based vectors and RNA-based vectors, and the non-viral delivery systems have summarized on the bases of physical approaches and chemical methods. In the application of gene delivery systems, viral vector systems for gene therapy and polymeric gene delivery systems have briefly reviewed. *Correspondence to: Sung Wan Kim, Center for Controlled Chemical Delivery (CCCD), Department of Pharmaceutics and Pharmaceutical Chemistry, University of Utah, BPRB, Room 205, Salt Lake City, UT 84112, USA, E-mail: sw.kim@pharm.utah.edu","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67475443","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}
Masaru Takemae, Michiko Harao, N. Hoshi, T. Inada, M. Wada, J. Ando
{"title":"Feasibility study of clipped node resections with Crystal crystal Violet violet dye marking in patientswith biopsy provenwho underwent biopsies for metastatic lymph nodes:Targeted tTargeted Axillary axillary Dissection dissections in Japann","authors":"Masaru Takemae, Michiko Harao, N. Hoshi, T. Inada, M. Wada, J. Ando","doi":"10.15761/icst.1000264","DOIUrl":"https://doi.org/10.15761/icst.1000264","url":null,"abstract":"","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67474124","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}
T. Namiki, Rintaro Harada, Natsuko Nozaki-Tagucuhi, Y. Hirasaki, Sho Takahashi, Ryo Takamura
{"title":"Study protocol for a phase IVsingle-center, randomized trial to evaluate theefficacy and safety of orento (AJapanese herbal (Kampo) medicines)for oral mucositis in patients withhead and neck cancer receivingchemoradiationtherapy","authors":"T. Namiki, Rintaro Harada, Natsuko Nozaki-Tagucuhi, Y. Hirasaki, Sho Takahashi, Ryo Takamura","doi":"10.15761/icst.1000266","DOIUrl":"https://doi.org/10.15761/icst.1000266","url":null,"abstract":"","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67474329","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}
Received: June 03, 2018; Accepted: June 22, 2018; Published: June 25, 2018 Cancer stem cells are the most important targets for cancer therapy. Prince et al. report CD44 is the cancer stem cell marker in HNSCC [1]. But various isoforms can be found in CD44, so it is unclear that which variant is the most important. One of characteristic of cancer stem cell is the radio-resistance. Various HNSCC cell lines are irradiated and we established radio-resistant cell line. After irradiation, the expression of CD44v9 increased in all HNSCC cell lines [2]. At present, the importance of CD44v9 is being studies. CD44v9 is expressed in cancer stem cells and functions to enhance the oxidative stress avoidance mechanism that causes resistance to treatment. This indicates that oxidative stress is important for the survival and proliferation of tumor cells, such stress has dual effects of inducing not only differentiation but also cell death when a certain threshold value is exceeded. In addition, in cell membranes, CD44v9 binds to xCT, which is a light chain subunit system xc-, a transporter that takes cysteine into cells.
{"title":"CD44v9 and CD98hc is the marker of cancer stem cells in HNSCC","authors":"Y. Kawasaki, Y. Omori","doi":"10.15761/icst.1000279","DOIUrl":"https://doi.org/10.15761/icst.1000279","url":null,"abstract":"Received: June 03, 2018; Accepted: June 22, 2018; Published: June 25, 2018 Cancer stem cells are the most important targets for cancer therapy. Prince et al. report CD44 is the cancer stem cell marker in HNSCC [1]. But various isoforms can be found in CD44, so it is unclear that which variant is the most important. One of characteristic of cancer stem cell is the radio-resistance. Various HNSCC cell lines are irradiated and we established radio-resistant cell line. After irradiation, the expression of CD44v9 increased in all HNSCC cell lines [2]. At present, the importance of CD44v9 is being studies. CD44v9 is expressed in cancer stem cells and functions to enhance the oxidative stress avoidance mechanism that causes resistance to treatment. This indicates that oxidative stress is important for the survival and proliferation of tumor cells, such stress has dual effects of inducing not only differentiation but also cell death when a certain threshold value is exceeded. In addition, in cell membranes, CD44v9 binds to xCT, which is a light chain subunit system xc-, a transporter that takes cysteine into cells.","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67475098","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}
Received: September 28, 2018; Accepted: October 12, 2018; Published: October 16, 2018 Tumor-associated macrophages (TAMs) are stromal cells in the tumor microenvironment that affect the progression of tumor development. Macrophages can be divided into different subsets based on their functions. A simplistic model is that M1 (or classically activated) macrophages favor the immunosurveillance of malignant cells and M2 (or alternatively activated) macrophages exert immunosuppressive effects and perform protumoral functions. TAMs are not a single uniform population. They exhibit features that are intermediate between the M1 and M2 macrophage phenotypes. In some cancer types such as lung cancer, extensive accumulation of TAMs is often associated with poor prognosis. In addition to the regulation of immunological responses, TAMs promote tumor progression through the regulation of cancer cell proliferation, invasion, and metastasis. Therefore, the molecular mechanisms underlying the interaction between macrophages and cancer cells to build a protumoral microenvironment were investigated with the goal of developing antitumor strategies [1-4].
{"title":"Macrophages promote progression of lung cancer by regulating ubiquitin-specific peptidase 17 in cancer cells","authors":"Chih-hao Lu, Chao-Yang Lai, T. Chuang","doi":"10.15761/ICST.1000290","DOIUrl":"https://doi.org/10.15761/ICST.1000290","url":null,"abstract":"Received: September 28, 2018; Accepted: October 12, 2018; Published: October 16, 2018 Tumor-associated macrophages (TAMs) are stromal cells in the tumor microenvironment that affect the progression of tumor development. Macrophages can be divided into different subsets based on their functions. A simplistic model is that M1 (or classically activated) macrophages favor the immunosurveillance of malignant cells and M2 (or alternatively activated) macrophages exert immunosuppressive effects and perform protumoral functions. TAMs are not a single uniform population. They exhibit features that are intermediate between the M1 and M2 macrophage phenotypes. In some cancer types such as lung cancer, extensive accumulation of TAMs is often associated with poor prognosis. In addition to the regulation of immunological responses, TAMs promote tumor progression through the regulation of cancer cell proliferation, invasion, and metastasis. Therefore, the molecular mechanisms underlying the interaction between macrophages and cancer cells to build a protumoral microenvironment were investigated with the goal of developing antitumor strategies [1-4].","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"70 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67475166","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}
Y. Hayashi, K. Fujita, Takahiro Yoshida, T. Kato, A. Kawashima, T. Ujike, A. Nagahara, M. Uemura, M. Inoue, H. Fushimi, R. Imamura, S. Yamaguchi, H. Miyamoto, N. Nonomura
TP63 is a key regulator of epithelial development and homeostasis, but its role in cancer progression remains unclear. In this study, we assessed the usefulness of ΔNp63 (predominant isoform of TP63) as a prognostic biomarker of upper tract urothelial carcinoma (UTUC) that is a relatively uncommon cancer and is often associated with poor outcome. We investigated the immunoreactivity of ΔNp63 in radical nephroureterectomy specimens on tissue microarrays containing samples from 83 patients with UTUC. There were no significant associations between ΔNp63 expression and tumor grade/stage, disease progression, or cancer-specific survival (CSS). However, in subgroup analysis of 32 patients who experienced disease recurrence after radical nephroureterectomy and subsequently received platinum-based chemotherapy showed that high ΔNp63 expression was associated with better CSS (P<0.05). Our study indicated that ΔNp63 expression could be a significant prognostic biomarker and a promising factor for predicting chemo-sensitivity in patients with UTUC. Correspondence to: Kazutoshi Fujita, Department of Urology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan, Tel: +81-6-6879-3531, Fax: +81-6-6879-3539, E-mail: kazufujita2@gmail.com Received: February 02, 2018; Accepted: February 21, 2018; Published: February 24, 2018 Introduction Upper tract urothelial carcinoma (UTUC) is a relatively rare malignancy and accounts for only a small number of urothelial carcinoma [1-3]. Because patients with UTUC often exhibit only mild symptoms, it is difficult to diagnose at the early stage. Indeed, about 60% of UTUCs are invasive at diagnosis compared with 1525% of bladder tumors [4,5]. Radical nephroureterectomy is offered as a standard treatment for localized tumors. Systemic chemotherapy is administered for patients who have metastasis at diagnosis or experience recurrence after surgery, but the prognosis is poor in most cases [6]. Although pathological stage and tumor grade are associated with tumor progression and poor survival [7,8], it is difficult for physicians guided only by these histopathological factors to predict prognosis and decide whether to offer adjuvant chemotherapy in a precise manner for individual UTUC patients. A greater understanding of the biological behavior of tumors is necessary for the realization of precision medicine and improvement of patient outcomes. TP63 is a member of the TP53 family, and this gene is composed of 15 exons, spanning over 270,000 bp on chromosome 3q27 [9,10]. The Tp63 gene has two transcriptional start sites: one contains an N-terminal transactivation (TA) domain (TAp63), and the others don’t (ΔNp63). Both genes can be alternatively spliced to generate proteins with three types of C-termini (α, β, and γ). TP63 is constitutively expressed in the nuclei of epithelial cells and acts as a key regulator of development and homeostasis of epithelium, but the role of TP63 in cancer progression
TP63是上皮发育和体内平衡的关键调节因子，但其在癌症进展中的作用尚不清楚。在这项研究中，我们评估了ΔNp63 (TP63的主要亚型)作为上路尿路上皮癌(UTUC)的预后生物标志物的有效性，UTUC是一种相对罕见的癌症，通常与不良预后相关。我们在含有83例UTUC患者样本的组织微阵列上研究了ΔNp63在根治性肾输尿管切除术标本中的免疫反应性。ΔNp63表达与肿瘤分级/分期、疾病进展或癌症特异性生存(CSS)之间没有显著关联。然而，对32例根治性肾输尿管切除术后疾病复发并随后接受铂类化疗的患者进行亚组分析显示，高ΔNp63表达与较好的CSS相关(P为中位数，低组:H评分≤中位数)。统计分析使用JMP®Pro 13.2.0 (SAS Institute Inc.， Cary, NC)进行统计分析。采用Mann-Whitney U检验和χ2检验比较患者特征。生存率采用Kaplan-Meier法测定，并与log-rank检验进行比较。结果表1显示了83例患者的特征。该队列包括47名男性和36名女性患者，年龄48至87岁(中位:71岁)，患有低级别尿路上皮癌(11例)和高级别尿路上皮癌(72例)。31例为非肌肉侵袭性肿瘤(pTa或pT1)， 52例为肌肉侵袭性肿瘤(pT2、pT3或pT4)。11例患者出现病理性淋巴结转移(pN+)。随访时间(从根治性肾输尿管切除术之日至最后一次随访时间)为2至139个月。中位癌症特异性生存期(CSS)为46个月。在此期间，34例(41.0%)患者出现局部或远处肿瘤复发，22例(26.5%)患者出现膀胱复发(图1)。具有代表性的免疫表达模式如图1所示。ΔNp63染色强22例(26.5%)，中度33例(39.8%)，弱17例(20.5%)，缺席11例(13.2%)。ΔNp63免疫反应性与病理分期或肿瘤分级无关。为了评估ΔNp63表达在UTUC中的预后价值，我们进行了Kaplan-Meier分析和logrank检验。在整个队列中，ΔNp63的表达与癌症特异性死亡率或淋巴结或远处转移的疾病复发无关(图2A,2B)。然而，在32例根治性肾输尿管切除术后疾病复发并随后接受铂类化疗的患者(包括8例辅助铂类化疗患者)的亚组分析中，ΔNp63高表达与更好的CSS相关(图2C)。在本研究中，我们发现根治性肾输尿管切除术标本中ΔNp63的表达与术后复发并接受铂类化疗的患者的CSS显著相关，而在整个队列中ΔNp63的表达与癌症特异性死亡率、淋巴结疾病复发或远处转移无关。然而，已有许多研究表明ΔNp63表达与尿路上皮性膀胱癌的疾病侵袭性和预后相关[11-18]，而在我们的UTUC队列中，ΔNp63表达与癌症特异性死亡率无显著相关性。这可能是由于上尿路和膀胱肿瘤在治疗策略(如淋巴结切除术、围手术期化疗)、胚胎学和癌症生物学上的差异。需要进一步的研究来澄清这种差异。ΔNp63在根治性肾输尿管切除术标本中的表达与术后复发并随后接受铂类化疗的患者的CSS有显著相关性。在肌肉浸润性膀胱癌中，Choi等报道以p63激活为特征的“基底肿瘤”具有良好的应答特征ΔNp63高ΔNp63低
{"title":"DeltaNp63 expression is a biomarker to predict survival after recurrence of upper urinary tract urothelial carcinoma","authors":"Y. Hayashi, K. Fujita, Takahiro Yoshida, T. Kato, A. Kawashima, T. Ujike, A. Nagahara, M. Uemura, M. Inoue, H. Fushimi, R. Imamura, S. Yamaguchi, H. Miyamoto, N. Nonomura","doi":"10.15761/ICST.1000265","DOIUrl":"https://doi.org/10.15761/ICST.1000265","url":null,"abstract":"TP63 is a key regulator of epithelial development and homeostasis, but its role in cancer progression remains unclear. In this study, we assessed the usefulness of ΔNp63 (predominant isoform of TP63) as a prognostic biomarker of upper tract urothelial carcinoma (UTUC) that is a relatively uncommon cancer and is often associated with poor outcome. We investigated the immunoreactivity of ΔNp63 in radical nephroureterectomy specimens on tissue microarrays containing samples from 83 patients with UTUC. There were no significant associations between ΔNp63 expression and tumor grade/stage, disease progression, or cancer-specific survival (CSS). However, in subgroup analysis of 32 patients who experienced disease recurrence after radical nephroureterectomy and subsequently received platinum-based chemotherapy showed that high ΔNp63 expression was associated with better CSS (P<0.05). Our study indicated that ΔNp63 expression could be a significant prognostic biomarker and a promising factor for predicting chemo-sensitivity in patients with UTUC. Correspondence to: Kazutoshi Fujita, Department of Urology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan, Tel: +81-6-6879-3531, Fax: +81-6-6879-3539, E-mail: kazufujita2@gmail.com Received: February 02, 2018; Accepted: February 21, 2018; Published: February 24, 2018 Introduction Upper tract urothelial carcinoma (UTUC) is a relatively rare malignancy and accounts for only a small number of urothelial carcinoma [1-3]. Because patients with UTUC often exhibit only mild symptoms, it is difficult to diagnose at the early stage. Indeed, about 60% of UTUCs are invasive at diagnosis compared with 1525% of bladder tumors [4,5]. Radical nephroureterectomy is offered as a standard treatment for localized tumors. Systemic chemotherapy is administered for patients who have metastasis at diagnosis or experience recurrence after surgery, but the prognosis is poor in most cases [6]. Although pathological stage and tumor grade are associated with tumor progression and poor survival [7,8], it is difficult for physicians guided only by these histopathological factors to predict prognosis and decide whether to offer adjuvant chemotherapy in a precise manner for individual UTUC patients. A greater understanding of the biological behavior of tumors is necessary for the realization of precision medicine and improvement of patient outcomes. TP63 is a member of the TP53 family, and this gene is composed of 15 exons, spanning over 270,000 bp on chromosome 3q27 [9,10]. The Tp63 gene has two transcriptional start sites: one contains an N-terminal transactivation (TA) domain (TAp63), and the others don’t (ΔNp63). Both genes can be alternatively spliced to generate proteins with three types of C-termini (α, β, and γ). TP63 is constitutively expressed in the nuclei of epithelial cells and acts as a key regulator of development and homeostasis of epithelium, but the role of TP63 in cancer progression","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67474281","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}
Received: June 03, 2018; Accepted: June 20, 2018; Published: June 23, 2018 Increasing body of evidence ascribes tumorigenesis to the emergence of cancer stem cells (CSCs). The two main theories predicting the origin of CSCs are either transformation of adult stem cells, or dedifferentiation of mature cells that is accompanied by the induction of the epithelial to mesenchymal transition (EMT) program [1]. Yet, both are associated with the accumulation of genetic and epigenetic aberrations that underlies cell plasticity [2]. Since accumulating data link mutations in the tumor-suppressor p53 with both CSCs formation and cancer-associated EMT, it is tempting to hypothesize that mutant p53 might facilitate CSCs formation by inducing EMT and cell plasticity. Here, we will evaluate the latter hypothesis by analyzing recent publications, and supporting it by our new data pertaining prostate cancer.
{"title":"Mutant p53 hinges between epithelial-mesenchymal transition and cancer stem cells","authors":"H. Solomon, I. Kogan, V. Rotter","doi":"10.15761/icst.1000278","DOIUrl":"https://doi.org/10.15761/icst.1000278","url":null,"abstract":"Received: June 03, 2018; Accepted: June 20, 2018; Published: June 23, 2018 Increasing body of evidence ascribes tumorigenesis to the emergence of cancer stem cells (CSCs). The two main theories predicting the origin of CSCs are either transformation of adult stem cells, or dedifferentiation of mature cells that is accompanied by the induction of the epithelial to mesenchymal transition (EMT) program [1]. Yet, both are associated with the accumulation of genetic and epigenetic aberrations that underlies cell plasticity [2]. Since accumulating data link mutations in the tumor-suppressor p53 with both CSCs formation and cancer-associated EMT, it is tempting to hypothesize that mutant p53 might facilitate CSCs formation by inducing EMT and cell plasticity. Here, we will evaluate the latter hypothesis by analyzing recent publications, and supporting it by our new data pertaining prostate cancer.","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67474958","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":"Persistent Risk for Hepatocellular carcinoma in patients on antiviral treatment: A Need for HBV cure","authors":"Joseph Yoo, Grace Park, R. S. Hann, H. Hann","doi":"10.15761/ICST.1000275","DOIUrl":"https://doi.org/10.15761/ICST.1000275","url":null,"abstract":"","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67475010","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}
M. Tesson, C. Rae, Donna L. Nile, M. Gaze, R. Mairs
Received: October 15, 2017; Accepted: November 10, 2017; Published: November 13, 2017 Neuroblastoma is a malignancy predominantly of infancy. It originates most commonly in the adrenal gland and affects a hundred individuals per year in the UK. Half of neuroblastomas are highly aggressive, disseminated throughout the body of the patient and characterised by unresponsiveness to therapy or early relapse if remission is achieved. High-risk neuroblastoma is responsible for 12% of paediatric cancer fatalities and new treatments are urgently needed [1].
{"title":"Targeted radiotherapy of neuroblastoma: future directions","authors":"M. Tesson, C. Rae, Donna L. Nile, M. Gaze, R. Mairs","doi":"10.15761/ICST.1000260)","DOIUrl":"https://doi.org/10.15761/ICST.1000260)","url":null,"abstract":"Received: October 15, 2017; Accepted: November 10, 2017; Published: November 13, 2017 Neuroblastoma is a malignancy predominantly of infancy. It originates most commonly in the adrenal gland and affects a hundred individuals per year in the UK. Half of neuroblastomas are highly aggressive, disseminated throughout the body of the patient and characterised by unresponsiveness to therapy or early relapse if remission is achieved. High-risk neuroblastoma is responsible for 12% of paediatric cancer fatalities and new treatments are urgently needed [1].","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47847318","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 : 2017-10-01Epub Date: 2017-10-23DOI: 10.15761/icst.1000255
Priya Kumthekar, Vaibhav Patel, Carly Bridge, Alfred Rademaker, Irene Helenowski, Maciej M Mrugala, Jason K Rockhill, Sean Grimm, Kristin R Swanson, Jeffrey Raizer
Introduction: Clinical behavior, treatment parameters, and prognostic factors are less well defined in older adults with low-grade gliomas (LGG). We conducted a two-institution retrospective review of older patients with LGG to better understand disease characteristics and prognosis in this population.
Methods: Northwestern University (NU) and The University of Washington (UW) clinical research databases were queried for patients ≥ 50 years of age with a diagnosis of WHO grade II glioma between January 1, 2000 and December 2012 (UW). Medical records were reviewed and data relevant to diagnosis, treatment and outcomes were collected. PFS and OS with respect to prognostic factors were calculated. Log-rank test and multivariate proportional hazards models were calculated for multiple tumor characteristics.
Results: Thirty-five patients with a diagnosis of LGG (WHO grade II) were identified; 15 women and 20 men had a median age of 55 (range 50-78). Fourteen had astrocytomas, fourteen had oligodendrogliomas and seven had oligoastrocytomas. Eight patients had contrast enhancement on neuroimaging, 9 of 21 tested had 1p19q co-deletion and 5 of 14 tested had an IDH1 mutation. Five year PFS was 21% with median PFS of 17 months; 20 patients had died (5 year OS=43%, median OS=48 months). On univariate analysis There was a statistically significant improvement in OS for patients with mixed histology (p=0.001), no midline shift at diagnosis (p=0.002) and with IDH1 mutation (p=0.003).
Conclusion: LGG appear more aggressive in older patients. Treatment following surgical resection should be considered; ongoing studies may clarify the most appropriate treatments for this age group.
{"title":"Prognosis of older patients with low-grade glioma: A retrospective study.","authors":"Priya Kumthekar, Vaibhav Patel, Carly Bridge, Alfred Rademaker, Irene Helenowski, Maciej M Mrugala, Jason K Rockhill, Sean Grimm, Kristin R Swanson, Jeffrey Raizer","doi":"10.15761/icst.1000255","DOIUrl":"https://doi.org/10.15761/icst.1000255","url":null,"abstract":"<p><strong>Introduction: </strong>Clinical behavior, treatment parameters, and prognostic factors are less well defined in older adults with low-grade gliomas (LGG). We conducted a two-institution retrospective review of older patients with LGG to better understand disease characteristics and prognosis in this population.</p><p><strong>Methods: </strong>Northwestern University (NU) and The University of Washington (UW) clinical research databases were queried for patients ≥ 50 years of age with a diagnosis of WHO grade II glioma between January 1, 2000 and December 2012 (UW). Medical records were reviewed and data relevant to diagnosis, treatment and outcomes were collected. PFS and OS with respect to prognostic factors were calculated. Log-rank test and multivariate proportional hazards models were calculated for multiple tumor characteristics.</p><p><strong>Results: </strong>Thirty-five patients with a diagnosis of LGG (WHO grade II) were identified; 15 women and 20 men had a median age of 55 (range 50-78). Fourteen had astrocytomas, fourteen had oligodendrogliomas and seven had oligoastrocytomas. Eight patients had contrast enhancement on neuroimaging, 9 of 21 tested had 1p19q co-deletion and 5 of 14 tested had an IDH1 mutation. Five year PFS was 21% with median PFS of 17 months; 20 patients had died (5 year OS=43%, median OS=48 months). On univariate analysis There was a statistically significant improvement in OS for patients with mixed histology (p=0.001), no midline shift at diagnosis (p=0.002) and with IDH1 mutation (p=0.003).</p><p><strong>Conclusion: </strong>LGG appear more aggressive in older patients. Treatment following surgical resection should be considered; ongoing studies may clarify the most appropriate treatments for this age group.</p>","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"4 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523685/pdf/nihms-946500.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38540963","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}
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