Molecular biology of ependymoma is being extensively studied in recent years, providing insights into newer therapeutic strategies. The different anatomic subgroups of ependymoma, namely supratentorial, posterior fossa (PF), and spinal, pose entirely different clinical behavior and prognosis. Recently, nine molecular subgroups of ependymoma have been identified, one of which has been incorporated into the WHO classification. Further understanding of the molecular biology of ependymoma is vital to expand its clinical utility. Here, we performed a review of the literature on the molecular biology of ependymoma. Therapeutic avenues include: (1) targeted agents against – (a) chromothripsis-induced nuclear factor-kappa beta signaling, (b) gene silencing by DNA methylation, (c) increased telomerase activity, and (d) microRNA and (2) de-escalating treatment in good prognostic subgroup such as PFB. The prognostic value of different chromosomal gain or loss is being better understood and may serve as prognostic signatures in future. Faster adoption of molecular classification into clinical practice requires simpler identification techniques using immunohistochemical surrogates for molecular subgroups, for example, cell adhesion molecule L1 for v-rel reticuloendotheliosis viral oncogene homolog A (RELA) fusion, laminin subunit alpha 2, tenascin-C, and neural epidermal growth factor-like 2 for PFA and PFB. Identification of poor prognostic markers such as RELA fusion and PFA has necessitated future research impetus to be directed to find more efficacious treatment approach in these groups.
{"title":"Molecular insights turning game for management of ependymoma: A review of literature","authors":"A. Sasidharan, R. Krishnatry","doi":"10.4103/ctm.ctm_40_17","DOIUrl":"https://doi.org/10.4103/ctm.ctm_40_17","url":null,"abstract":"Molecular biology of ependymoma is being extensively studied in recent years, providing insights into newer therapeutic strategies. The different anatomic subgroups of ependymoma, namely supratentorial, posterior fossa (PF), and spinal, pose entirely different clinical behavior and prognosis. Recently, nine molecular subgroups of ependymoma have been identified, one of which has been incorporated into the WHO classification. Further understanding of the molecular biology of ependymoma is vital to expand its clinical utility. Here, we performed a review of the literature on the molecular biology of ependymoma. Therapeutic avenues include: (1) targeted agents against – (a) chromothripsis-induced nuclear factor-kappa beta signaling, (b) gene silencing by DNA methylation, (c) increased telomerase activity, and (d) microRNA and (2) de-escalating treatment in good prognostic subgroup such as PFB. The prognostic value of different chromosomal gain or loss is being better understood and may serve as prognostic signatures in future. Faster adoption of molecular classification into clinical practice requires simpler identification techniques using immunohistochemical surrogates for molecular subgroups, for example, cell adhesion molecule L1 for v-rel reticuloendotheliosis viral oncogene homolog A (RELA) fusion, laminin subunit alpha 2, tenascin-C, and neural epidermal growth factor-like 2 for PFA and PFB. Identification of poor prognostic markers such as RELA fusion and PFA has necessitated future research impetus to be directed to find more efficacious treatment approach in these groups.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"44 1","pages":"123 - 128"},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85129132","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}
Michael Zhang, Kelvin Zheng, M. Choudhury, J. Phillips, S. Konno
Aim: Mushroom extract, PDF, is a bioactive proteoglucan with anticancer/antitumor activity, and Vitamin K3 (VK3) is a synthetic VK derivative with antitumor activity as well. An unconventional approach using these two agents was tested to see their anticancer effects on bladder cancer cells in vitro. Methods: Human bladder cancer T24 cells were treated with PDF, VK3, or their combination, and cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. To explore the anticancer mechanism, cell cycle and epigenetic alterations were specifically studied. Results: PDF ≥ 500 μg/mL led to a ~ 35% reduction in cell viability while VK3 had little effects. However, when PDF (300 μg/mL) was combined with VK3 (5 μM), a ~ 75% cell viability reduction was attained. This specific combination induced a G1 cell cycle arrest with the downregulation of G1-specific regulators. In addition, histone deacetylase was inactivated while histones 3 and 4 were highly acetylated. Two apoptotic regulators were significantly activated with PDF/VK3 combination as well. Conclusion: The specific combination of PDF and VK3 appears to potentiate anticancer effect on T24 cells. This is primarily attributed to a G1 cell cycle arrest with chromatin modifications, ultimately leading to apoptosis. Thus, the PDF/VK3 combination may offer a potential therapeutic option for bladder cancer.
{"title":"Enhanced anticancer effect by combination of proteoglucan and Vitamin K3 on bladder cancer cells","authors":"Michael Zhang, Kelvin Zheng, M. Choudhury, J. Phillips, S. Konno","doi":"10.4103/ctm.ctm_25_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_25_18","url":null,"abstract":"Aim: Mushroom extract, PDF, is a bioactive proteoglucan with anticancer/antitumor activity, and Vitamin K3 (VK3) is a synthetic VK derivative with antitumor activity as well. An unconventional approach using these two agents was tested to see their anticancer effects on bladder cancer cells in vitro. Methods: Human bladder cancer T24 cells were treated with PDF, VK3, or their combination, and cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. To explore the anticancer mechanism, cell cycle and epigenetic alterations were specifically studied. Results: PDF ≥ 500 μg/mL led to a ~ 35% reduction in cell viability while VK3 had little effects. However, when PDF (300 μg/mL) was combined with VK3 (5 μM), a ~ 75% cell viability reduction was attained. This specific combination induced a G1 cell cycle arrest with the downregulation of G1-specific regulators. In addition, histone deacetylase was inactivated while histones 3 and 4 were highly acetylated. Two apoptotic regulators were significantly activated with PDF/VK3 combination as well. Conclusion: The specific combination of PDF and VK3 appears to potentiate anticancer effect on T24 cells. This is primarily attributed to a G1 cell cycle arrest with chromatin modifications, ultimately leading to apoptosis. Thus, the PDF/VK3 combination may offer a potential therapeutic option for bladder cancer.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"4 1","pages":"117 - 122"},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78903379","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}
J. Zhong, K. Chen, B. Ahir, Qi Huang, Y. Wu, C. Liao, Rong-Rong Jia, B. Xiang, Lequn Li
Hepatocellular adenoma (HCAs) is a rare benign tumor in the liver. Bleeding and malignant transformation are the two severe outcomes of HCAs. Transarterial embolization (TAE) is used to treat HCAs; however, its role in an elective setting is uncertain. Here, we report a case with HCA treated by TAE in an elective setting, followed by resection after 2 months, because of stable disease. Further, we performed a comprehensive review of PubMed database for studies published between January 2000 and June 2018 involving TAE to treat HCA. The review included 22 studies involving 1504 patients with HCA, of whom 89.4% were female. Only 171/1504 (11.4%) patients received TAE, among whom resection was avoided in 80 (46.8%) patients, of whom 31 (38.7%) were bleeding before TAE and 49 (61.3%) were not. Based on data of 115 tumors reviewed, the rate of complete and partial response were 9.6% and 74.8%, respectively, with an overall (complete + partial) response of 84.3%. No mortality or adverse side effects were noted. Therefore, both in elective setting and in the setting of bleeding, TAE can be considered safe in the management of HCAs and may be regarded as reasonable alternative management to hepatic resection.
{"title":"Transarterial embolization for hepatocellular adenomas: Case report and literature review","authors":"J. Zhong, K. Chen, B. Ahir, Qi Huang, Y. Wu, C. Liao, Rong-Rong Jia, B. Xiang, Lequn Li","doi":"10.4103/ctm.ctm_24_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_24_18","url":null,"abstract":"Hepatocellular adenoma (HCAs) is a rare benign tumor in the liver. Bleeding and malignant transformation are the two severe outcomes of HCAs. Transarterial embolization (TAE) is used to treat HCAs; however, its role in an elective setting is uncertain. Here, we report a case with HCA treated by TAE in an elective setting, followed by resection after 2 months, because of stable disease. Further, we performed a comprehensive review of PubMed database for studies published between January 2000 and June 2018 involving TAE to treat HCA. The review included 22 studies involving 1504 patients with HCA, of whom 89.4% were female. Only 171/1504 (11.4%) patients received TAE, among whom resection was avoided in 80 (46.8%) patients, of whom 31 (38.7%) were bleeding before TAE and 49 (61.3%) were not. Based on data of 115 tumors reviewed, the rate of complete and partial response were 9.6% and 74.8%, respectively, with an overall (complete + partial) response of 84.3%. No mortality or adverse side effects were noted. Therefore, both in elective setting and in the setting of bleeding, TAE can be considered safe in the management of HCAs and may be regarded as reasonable alternative management to hepatic resection.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"33 1","pages":"102 - 108"},"PeriodicalIF":0.0,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83804370","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}
Shazima Sheereen, F. Lobo, Waseemoddin Patel, S. Sheereen, A. Nayyar, Mubeen Khan
Aim: Breast cancer therapy causes morphological alterations in the cancerous as well as the surrounding healthy tissue. The histopathological interpretation in such cases, thus, requires a thorough knowledge of the cytological and stromal changes rendered by the therapy during and posttherapy. The aim of the present study was to evaluate such cytological and stromal changes rendered by the therapy in breast cancer cases. Methods: The present study was a combined retrospective and prospective study, wherein clinical and histopathological details were collected from a total of 39 cases of breast carcinoma before and posttherapy, and the changes induced by the therapy were correlated. Results: Stage II breast carcinoma was found to be the most predominant stage, while invasive ductal carcinoma-not otherwise specified (IDC-NOS) of tumor was the most common histologic type both before (94.87%) and after (76.92%) therapy. Pathologic complete response (pCR) was observed in 18% of the cases while 15% showed pathologic partial response (pPR) and 66.7% cases had a stable disease. Intracellular changes commonly noted after chemotherapy included nuclear enlargement, hyperchromasia, and increased nuclear: cytoplasmic ratio while predominant stromal changes included necrosis (74.4%), fibrosis (64.1%), and desmoplasia (59%). Conclusion: Breast cancer therapy causes morphological alterations in the cancerous as well as the surrounding healthy tissue. The histopathological interpretation in such cases, thus, requires a thorough knowledge of the cytological and stromal changes rendered by the therapy.
{"title":"Therapy-induced histopathological changes in breast cancers: The changing role of pathology in breast cancer diagnosis and treatment","authors":"Shazima Sheereen, F. Lobo, Waseemoddin Patel, S. Sheereen, A. Nayyar, Mubeen Khan","doi":"10.4103/ctm.ctm_23_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_23_18","url":null,"abstract":"Aim: Breast cancer therapy causes morphological alterations in the cancerous as well as the surrounding healthy tissue. The histopathological interpretation in such cases, thus, requires a thorough knowledge of the cytological and stromal changes rendered by the therapy during and posttherapy. The aim of the present study was to evaluate such cytological and stromal changes rendered by the therapy in breast cancer cases. Methods: The present study was a combined retrospective and prospective study, wherein clinical and histopathological details were collected from a total of 39 cases of breast carcinoma before and posttherapy, and the changes induced by the therapy were correlated. Results: Stage II breast carcinoma was found to be the most predominant stage, while invasive ductal carcinoma-not otherwise specified (IDC-NOS) of tumor was the most common histologic type both before (94.87%) and after (76.92%) therapy. Pathologic complete response (pCR) was observed in 18% of the cases while 15% showed pathologic partial response (pPR) and 66.7% cases had a stable disease. Intracellular changes commonly noted after chemotherapy included nuclear enlargement, hyperchromasia, and increased nuclear: cytoplasmic ratio while predominant stromal changes included necrosis (74.4%), fibrosis (64.1%), and desmoplasia (59%). Conclusion: Breast cancer therapy causes morphological alterations in the cancerous as well as the surrounding healthy tissue. The histopathological interpretation in such cases, thus, requires a thorough knowledge of the cytological and stromal changes rendered by the therapy.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"112 1","pages":"89 - 94"},"PeriodicalIF":0.0,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80790611","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}
The nicotinamide adenine dinucleotide (NAD+) pool is an important electron exchanger in tumor biology. The salvage pathway plays an important role in the regulation of the levels of cellular NAD+ biosynthesis and the nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme of this pathway. Thus, NAMPT plays a key role in the levels of the NAD+ pool. NAMPT levels in several types of cancer, both solid and hematological cancers, are found to be high compared to the normal tissue. In these tumors, NAMPT overexpression induces an increase in tumorigenic properties. Increased transcription levels of NAMPT result in an increased rate of growth, resistance to cell death, and epidermal-to-mesenchymal transition imparting cancer stem cell-like properties in tumorigenic cells. Main stemness signaling pathways such as Notch, Hippo, Sonic, and Wnt are associated with increased NAMPT transcription levels. NAMPT-induced oncogenic phenotype is also associated with worse prognosis and resistance to therapy in human tumors. Therefore, NAMPT could be an interesting enzyme to consider as probable therapeutic target.
{"title":"Nicotinamide phosphoribosyltransferase: Biology, role in cancer, and novel drug target","authors":"Antonio Lucena-Cacace, A. Carnero","doi":"10.4103/ctm.ctm_20_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_20_18","url":null,"abstract":"The nicotinamide adenine dinucleotide (NAD+) pool is an important electron exchanger in tumor biology. The salvage pathway plays an important role in the regulation of the levels of cellular NAD+ biosynthesis and the nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme of this pathway. Thus, NAMPT plays a key role in the levels of the NAD+ pool. NAMPT levels in several types of cancer, both solid and hematological cancers, are found to be high compared to the normal tissue. In these tumors, NAMPT overexpression induces an increase in tumorigenic properties. Increased transcription levels of NAMPT result in an increased rate of growth, resistance to cell death, and epidermal-to-mesenchymal transition imparting cancer stem cell-like properties in tumorigenic cells. Main stemness signaling pathways such as Notch, Hippo, Sonic, and Wnt are associated with increased NAMPT transcription levels. NAMPT-induced oncogenic phenotype is also associated with worse prognosis and resistance to therapy in human tumors. Therefore, NAMPT could be an interesting enzyme to consider as probable therapeutic target.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"6 1","pages":"109 - 116"},"PeriodicalIF":0.0,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73428399","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}
Glioma is the most common type of malignant tumor of the central nervous system. Studies of the biological mechanism behind its occurrence and development have significant importance in better understanding glioma. In the era of multiomics and big data, glioma research is undergoing a paradigm shift from traditional standardized medical models to precision medicine. Big data in glioma research is in its infancy, and as such, there are exciting opportunities to take advantage of. However, there are also major challenges that must be addressed. This review introduces a series of changes in glioma research brought about by medical big data. It further elaborates on how big data bioinformatic analyzes can contribute to the identification of molecular targets, leading to molecular pathological diagnosis and the promotion of precision medicine of glioma.
{"title":"Glioma Research in the era of medical big data","authors":"Feiyifan Wang, Christopher J. Pirozzi, Xue-Jun Li","doi":"10.4103/ctm.ctm_26_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_26_18","url":null,"abstract":"Glioma is the most common type of malignant tumor of the central nervous system. Studies of the biological mechanism behind its occurrence and development have significant importance in better understanding glioma. In the era of multiomics and big data, glioma research is undergoing a paradigm shift from traditional standardized medical models to precision medicine. Big data in glioma research is in its infancy, and as such, there are exciting opportunities to take advantage of. However, there are also major challenges that must be addressed. This review introduces a series of changes in glioma research brought about by medical big data. It further elaborates on how big data bioinformatic analyzes can contribute to the identification of molecular targets, leading to molecular pathological diagnosis and the promotion of precision medicine of glioma.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"177 1","pages":"95 - 101"},"PeriodicalIF":0.0,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74323279","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 : 2018-05-01Epub Date: 2018-06-29DOI: 10.4103/ctm.ctm_22_18
Sulin Zeng, Wen H Shen, Li Liu
Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP). At least, three types of cellular stress such as activation of oncogenes, loss of tumor suppressor genes, and chemo/radiotherapy can induce cell senescence. Oncogene-induced senescence can be intertwiningly associated with the replicative senescence. Early-stage senescence may protect cell from transformation, while prolonged senescence often promotes cancer development. This review will focus on the characteristics of senescence, discuss the regulation of senescence during cancer development, and highlight the complexity of senescence that makes cancer treatment challenging.
{"title":"Senescence and Cancer.","authors":"Sulin Zeng, Wen H Shen, Li Liu","doi":"10.4103/ctm.ctm_22_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_22_18","url":null,"abstract":"<p><p>Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP). At least, three types of cellular stress such as activation of oncogenes, loss of tumor suppressor genes, and chemo/radiotherapy can induce cell senescence. Oncogene-induced senescence can be intertwiningly associated with the replicative senescence. Early-stage senescence may protect cell from transformation, while prolonged senescence often promotes cancer development. This review will focus on the characteristics of senescence, discuss the regulation of senescence during cancer development, and highlight the complexity of senescence that makes cancer treatment challenging.</p>","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"4 3","pages":"70-74"},"PeriodicalIF":0.0,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6372122/pdf/nihms-984426.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36559842","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}
Aim: Magnetic resonance imaging (MRI) has been widely used in radiation therapy (RT) treatment planning. The current practice to capture clinical indications like tumor from MRI is to review multiple types of MRI separately, which can be inefficient and the tumor contrast is limited by existing images. This study presented a novel approach to effectively integrate clinical meaningful information of multiple MRI to produce a set of fused MRI with versatile image contrasts. A multisource adaptive fusion technique was developed in this approach using limited number of standard MR images as input. Methods: The multisource adaptive MRI fusion technique is designed with five key components: input multiple MRI, image preprocessing, fusion algorithm, adaptation methods, and output-fused MRI. A linear-weighting fusion algorithm is used to demonstrate the proof of concept. Fusion options (weighting parameters and image features) are precalculated and saved in a database for fast fusion operation. Input- and output-driven approaches are developed for MRI contrast adaptation. The technique is tested in human digital phantom 4D extended cardiac-torso (XCAT) for versatile contrast MRI generation. Results: A graphic user interface was developed in Matlab environment. Input- and output-driven adaptation methods were implemented for interactive user operation to achieve different clinical goals. Using four input MR images (T1W, T2W, T2/T1W, and diffusion weighted), the fusion technique generated hundreds of fused MR images with versatile image contrasts. Conclusion: A novel multisource adaptive image fusion technique capable of generating versatile contrast MRI from a limited number of standard MR images was demonstrated. This method has the potential to enhance the effectiveness and efficiency of MR applications in RT.
{"title":"A multisource adaptive magnetic resonance image fusion technique for versatile contrast magnetic resonance imaging","authors":"Lei Zhang, F. Yin, B. Moore, Silu Han, Jing Cai","doi":"10.4103/ctm.ctm_21_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_21_18","url":null,"abstract":"Aim: Magnetic resonance imaging (MRI) has been widely used in radiation therapy (RT) treatment planning. The current practice to capture clinical indications like tumor from MRI is to review multiple types of MRI separately, which can be inefficient and the tumor contrast is limited by existing images. This study presented a novel approach to effectively integrate clinical meaningful information of multiple MRI to produce a set of fused MRI with versatile image contrasts. A multisource adaptive fusion technique was developed in this approach using limited number of standard MR images as input. Methods: The multisource adaptive MRI fusion technique is designed with five key components: input multiple MRI, image preprocessing, fusion algorithm, adaptation methods, and output-fused MRI. A linear-weighting fusion algorithm is used to demonstrate the proof of concept. Fusion options (weighting parameters and image features) are precalculated and saved in a database for fast fusion operation. Input- and output-driven approaches are developed for MRI contrast adaptation. The technique is tested in human digital phantom 4D extended cardiac-torso (XCAT) for versatile contrast MRI generation. Results: A graphic user interface was developed in Matlab environment. Input- and output-driven adaptation methods were implemented for interactive user operation to achieve different clinical goals. Using four input MR images (T1W, T2W, T2/T1W, and diffusion weighted), the fusion technique generated hundreds of fused MR images with versatile image contrasts. Conclusion: A novel multisource adaptive image fusion technique capable of generating versatile contrast MRI from a limited number of standard MR images was demonstrated. This method has the potential to enhance the effectiveness and efficiency of MR applications in RT.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"1 1","pages":"65 - 69"},"PeriodicalIF":0.0,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73103681","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}
Glioma is the most frequent malignant neoplasm of the central nervous system with high recurrence and extremely poor prognosis. Hexokinase 2 (HK2) is the key enzyme in Warburg effect that has been proved to promote tumorigenesis and is found highly expressed in several tumors. However, the HK2 function in glioma was reported only in a few studies. In this review, we will summarize the changes in the energy metabolism in glioma and the critical function of HK2 in the process. Further, the recent research progress and perspective of HK2 in the diagnosis and treatment of glioma will be discussed.
{"title":"The contribution of hexokinase 2 in glioma","authors":"Hui Liu, Hongwei Yang, Xin Wang, Y. Tu","doi":"10.4103/ctm.ctm_11_18","DOIUrl":"https://doi.org/10.4103/ctm.ctm_11_18","url":null,"abstract":"Glioma is the most frequent malignant neoplasm of the central nervous system with high recurrence and extremely poor prognosis. Hexokinase 2 (HK2) is the key enzyme in Warburg effect that has been proved to promote tumorigenesis and is found highly expressed in several tumors. However, the HK2 function in glioma was reported only in a few studies. In this review, we will summarize the changes in the energy metabolism in glioma and the critical function of HK2 in the process. Further, the recent research progress and perspective of HK2 in the diagnosis and treatment of glioma will be discussed.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"62 1","pages":"54 - 58"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77725340","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}
Akiko Sasaki, Y. Tsunoda, K. Furuya, H. Oyamada, Mayumi Tsuji, Yuko Udaka, M. Hosonuma, Haruna Shirako, Nana Ichimura, Y. Kiuchi
Aim: This study aims to examine the role of microRNAs (miRNAs) in regulating the expression of p21, a cyclin-dependent kinase inhibitor, and in inducing resistance to cisplatin, an anticancer drug. Methods: Human breast cancer cell line MDA-MB231 cells were separated into two subpopulations, cancer stem-like cells (CSCs) and cancer cells, based on the expression of cell surface antigens CD44 and CD24. Results: p21 protein expression was higher in CSCs than in cancer cells. Exposure of MDA-MB-231 cells to cisplatin increased p21 protein expression. However, p21 expression was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, suggesting that p21-dependent cell cycle suppression was lower in CSCs than in cancer cells. Moreover, caspase-3 activity was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, indicating that CSCs were more resistant to cisplatin-induced apoptosis than cancer cells. Treatment with miR-93 inhibitors increased p21 expression in CSCs, suggesting that miR-93 suppressed p21 expression. Conclusion: The results of the present study indicate that CSCs contribute to cisplatin resistance of MDA-MB231 cells and suggest that miR-93 inhibits the expression of p21, a factor involved in drug resistance.
{"title":"Cancer stem-like cells have cisplatin resistance and miR-93 regulate p21 expression in breast cancer","authors":"Akiko Sasaki, Y. Tsunoda, K. Furuya, H. Oyamada, Mayumi Tsuji, Yuko Udaka, M. Hosonuma, Haruna Shirako, Nana Ichimura, Y. Kiuchi","doi":"10.4103/ctm.ctm_41_17","DOIUrl":"https://doi.org/10.4103/ctm.ctm_41_17","url":null,"abstract":"Aim: This study aims to examine the role of microRNAs (miRNAs) in regulating the expression of p21, a cyclin-dependent kinase inhibitor, and in inducing resistance to cisplatin, an anticancer drug. Methods: Human breast cancer cell line MDA-MB231 cells were separated into two subpopulations, cancer stem-like cells (CSCs) and cancer cells, based on the expression of cell surface antigens CD44 and CD24. Results: p21 protein expression was higher in CSCs than in cancer cells. Exposure of MDA-MB-231 cells to cisplatin increased p21 protein expression. However, p21 expression was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, suggesting that p21-dependent cell cycle suppression was lower in CSCs than in cancer cells. Moreover, caspase-3 activity was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, indicating that CSCs were more resistant to cisplatin-induced apoptosis than cancer cells. Treatment with miR-93 inhibitors increased p21 expression in CSCs, suggesting that miR-93 suppressed p21 expression. Conclusion: The results of the present study indicate that CSCs contribute to cisplatin resistance of MDA-MB231 cells and suggest that miR-93 inhibits the expression of p21, a factor involved in drug resistance.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"27 1","pages":"48 - 53"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89903908","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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