Cancer therapy最新文献

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PML: An emerging tumor suppressor and a target with therapeutic potential. PML:一种新兴的肿瘤抑制因子和具有治疗潜力的靶点。
Cancer therapy Pub Date : 2009-09-01
Erin L Reineke, Hung-Ying Kao
{"title":"PML: An emerging tumor suppressor and a target with therapeutic potential.","authors":"Erin L Reineke,&nbsp;Hung-Ying Kao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Though originally discovered as a tumor suppressor in Acute Promyelocytic Leukemia (APL), the importance of promyelocytic leukemia protein (PML) in cancers of other origins has not been widely studied. Recent studies have shown that multiple types of cancers show decreased expression of PML protein, though the mechanisms leading to this down-regulation are unknown. Decreased expression of PML can result in loss of cell cycle control and prevention of apoptosis and is likely a key event in the promotion of oncogenesis. Many of these effects are due to changes in the transcriptional profile of the cell as a result of decreased size and number of PML nuclear bodies. Several mouse studies confirm the contribution of PML to oncogenesis and cancer progression. It is important to not only further define a role for PML as a tumor suppressor, but also to begin to develop strategies to target PML therapeutically.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743178/pdf/nihms115742.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28404020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Chemokine signaling in cancer: Implications on the tumor microenvironment and therapeutic targeting. 趋化因子信号在癌症中的作用:对肿瘤微环境和治疗靶向的影响。
Cancer therapy Pub Date : 2009-04-14
Stacey L Hembruff, Nikki Cheng
{"title":"Chemokine signaling in cancer: Implications on the tumor microenvironment and therapeutic targeting.","authors":"Stacey L Hembruff,&nbsp;Nikki Cheng","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chemokines are soluble factors shown to play important roles in regulating immune cell recruitment during inflammatory responses and defense against foreign pathogens. De-regulated expression and activity of several chemokine signaling pathways have been implicated in cancer progression, including: CCL2, CCL5, CXCL1 and CXCL12. While studies in the past have focused the role of these chemokine signaling pathways in regulating immune responses, emerging studies show that these molecules regulate diverse cellular processes including angiogenesis, and regulation of epithelial cell growth and survival. New evidence indicates that chemokines are critical for cancer progression and indicate complex and diverse functions in the tumor microenvironment. This review will focus on the contributions of chemokine signaling in regulating cancer microvironment and discuss the utility of targeting or delivering chemokines in cancer therapeutics.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907742/pdf/nihms124893.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29138930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Stress sensor Gadd45 genes as therapeutic targets in cancer. 应激传感器Gadd45基因作为癌症治疗靶点。
Cancer therapy Pub Date : 2009-01-01
Alexandra Cretu, Xiaojin Sha, Jennifer Tront, Barbara Hoffman, Dan A Liebermann
{"title":"Stress sensor Gadd45 genes as therapeutic targets in cancer.","authors":"Alexandra Cretu,&nbsp;Xiaojin Sha,&nbsp;Jennifer Tront,&nbsp;Barbara Hoffman,&nbsp;Dan A Liebermann","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Gadd45 genes have been implicated in stress signaling responses to various physiological or environmental stressors, resulting in cell cycle arrest, DNA repair, cell survival and senescence, or apoptosis. Evidence accumulated up to date suggests that Gadd45 proteins function as stress sensors, mediating their activity through a complex interplay of physical interactions with other cellular proteins that are implicated in cell cycle regulation and the response of cells to stress. These include PCNA, p21, cdc2/cyclinB1, and the p38 and JNK stress response kinases. Disregulated expression of Gadd45 has been observed in multiple types of solid tumors as well as in hematopoietic malignancies. Also, evidence has accumulated that Gadd45 proteins are intrinsically associated with the response of tumor cells to a variety of cancer therapeutic agents. Thus, Gadd45 proteins may represent a novel class of targets for therapeutic intervention in cancer. Additional research is needed to better understand which of the Gadd45 stress response functions may be targeted for chemotherapeutic drug design in cancer therapy.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696386/pdf/nihms-116240.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40009686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Phage L5 integrating vectors are present within the Mycobacterial Cell in an equilibrium between integrated and excised states. 噬菌体L5整合载体存在于分枝杆菌细胞内,处于整合和切除状态之间的平衡状态。
Cancer therapy Pub Date : 2009-01-01
Beatrice Saviola
{"title":"Phage L5 integrating vectors are present within the Mycobacterial Cell in an equilibrium between integrated and excised states.","authors":"Beatrice Saviola","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Integrating mycobacterial plasmids containing the phage L5 attachment site (attP) are able to insert into the mycobacterial chromosome attB site. Plasmids containing the attP site and chromosome containing the attB site are present in equilibrium between the inserted and the excised states in the presence of the phage L5 integrase.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548942/pdf/nihms107390.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34026348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
siRNA Down-regulation of the PATZ1 Gene in Human Glioma Cells Increases Their Sensitivity to Apoptotic Stimuli. 人胶质瘤细胞中siRNA下调PATZ1基因增加其对凋亡刺激的敏感性。
Cancer therapy Pub Date : 2008-01-01
Richard Tritz, Barbara M Mueller, Michelle J Hickey, Amy H Lin, German G Gomez, Philipp Hadwiger, Dinah W Y Sah, Leslie Muldoon, Edward A Neuwelt, Carol A Kruse
{"title":"siRNA Down-regulation of the PATZ1 Gene in Human Glioma Cells Increases Their Sensitivity to Apoptotic Stimuli.","authors":"Richard Tritz,&nbsp;Barbara M Mueller,&nbsp;Michelle J Hickey,&nbsp;Amy H Lin,&nbsp;German G Gomez,&nbsp;Philipp Hadwiger,&nbsp;Dinah W Y Sah,&nbsp;Leslie Muldoon,&nbsp;Edward A Neuwelt,&nbsp;Carol A Kruse","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The PATZ1 gene encodes a transcription factor that belongs to the BTB/POZ group of transcriptional regulators and has been implicated as a transcriptional repressor. We cloned cDNA from glioma cell lines and found they expressed transcript variant 2 of PATZ1. We designed a specific siRNA against PATZ1 and showed that this siRNA, but not a control randomized siRNA, reduced PATZ1 expression in glioma cells as determined by quantitative PCR. In a panel of human glioma cell lines incubated with proapoptotic FasL, those transfected with PATZ1 siRNA displayed reduced cell numbers by the MTT colorimetric assay, relative to those transfected with randomized siRNA. Further studies showed that in 10-08-MG, U-251MG, U-87MG, and T98G cells PATZ1 siRNA significantly increased apoptosis in response to incubation with soluble FasL, as shown by a morphologic acridine orange/ethidium bromide apoptotic assay. Using an apoptosis specific cDNA microarray we further demonstrated that down-regulation of PATZ1 by siRNA resulted in the upregulation of death receptor pro-apoptotic genes including caspase 8 and Death Receptor 5 (DR5) in U-373MG cells. Since DR5 is the receptor for TRAIL we tested whether PATZ1 downregulation also sensitized cells to TRAIL-induced apoptosis and found that PATZ1 siRNA, but not control siRNA, sensitized U-251MG and T98G glioma cells to TRAIL-induced apoptosis. Altogether, these data demonstrate a previously unknown role for the transcription factor PATZ1 in conferring resistance to apoptosis and indicate that modulation of PATZ1 expression may be a therapeutic strategy for gliomas.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600477/pdf/nihms-73909.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27899159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Disruption of Survivin in K562 cells elevates telomerase activity and protects cells against apoptosis induced by the Bcr-abl kinase inhibitor STI571. 破坏K562细胞中的Survivin可提高端粒酶活性,保护细胞免受Bcr-abl激酶抑制剂STI571诱导的凋亡。
Cancer therapy Pub Date : 2008-01-01
Zhanxiang Wang, Louis M Pelus
{"title":"Disruption of Survivin in K562 cells elevates telomerase activity and protects cells against apoptosis induced by the Bcr-abl kinase inhibitor STI571.","authors":"Zhanxiang Wang,&nbsp;Louis M Pelus","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The Bcr-abl kinase inhibitor STI571 produces clinical responses in most patients with Chronic Myeloid Leukemia (CML); however, development of resistance limits utility. One strategy to overcome STI571 resistance is to decrease the level/activity of Bcr-abl. We reported that disruption of the anti-apoptotic protein Survivin promoted STI571-induced apoptosis in Bcr-abl(+) K562 cells, through caspase-dependent Bcr-abl degradation. To investigate the utility of Survivin disruption in drug-resistant CML cells, we generated STI571-resistant K562 cells by long-term culture with STI571. In contrast to parental cells, where Survivin disruption enhances STI571-induced apoptosis, Survivin disruption in STI571-resistant cells failed to promote STI571-induced apoptosis; rather it protected cells from STI571 and other apoptosis-inducing compounds. Even though Survivin levels were similar in parental and STI571-resistant K562 cells, Survivin disruption in STI571-resistant cells increased telomerase activity, likely due to Bcr-abl/c-abl degradation. Our results indicate that emergence of STI571 resistance in Bcr-abl(+) K562 cells results from induction of additional pathways that circumvent STI571-responsiveness.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600525/pdf/nihms70570.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27897293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thiazolidinediones as anti-cancer agents. 噻唑烷二酮类抗癌药物。
Cancer therapy Pub Date : 2008-01-01
Carmelo Blanquicett, Jesse Roman, C Michael Hart
{"title":"Thiazolidinediones as anti-cancer agents.","authors":"Carmelo Blanquicett,&nbsp;Jesse Roman,&nbsp;C Michael Hart","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The PPAR-gamma (PPAR-γ) activating thiazolidinedione (TZD) medications are a class of drugs used to improve lipid and glucose metabolism in type-2 diabetes. In addition to their known insulin sensitization action, these drugs have been shown to suppress tumor development in several in vitro and in vivo models. Among the proposed mechanisms for the anti-tumor effects of TZDs, apoptosis induction, cell cycle arrest, and differentiation have been extensively reported. Interestingly, some of the observed anti-tumor effects are independent of PPAR-γ activation. The following review will discuss studies employing TZDs as anti-cancer therapies for the most common types of cancers including, lung, breast, and colon and will explore the principal PPAR-γ-dependent and -independent mechanisms by which TZDs exert their anti-tumor effects.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600565/pdf/nihms-57085.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27898104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
From here to eternity - the secret of Pharaohs: Therapeutic potential of black cumin seeds and beyond. 从这里到永恒-法老的秘密:黑孜然种子的治疗潜力和超越。
Cancer therapy Pub Date : 2008-01-01
Subhash Padhye, Sanjeev Banerjee, Aamir Ahmad, Ramzi Mohammad, Fazlul H Sarkar
{"title":"From here to eternity - the secret of Pharaohs: Therapeutic potential of black cumin seeds and beyond.","authors":"Subhash Padhye,&nbsp;Sanjeev Banerjee,&nbsp;Aamir Ahmad,&nbsp;Ramzi Mohammad,&nbsp;Fazlul H Sarkar","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Over many centuries humans have been mining the bounties of nature for discovering substances that have been used for the treatment of all human diseases; many such remedies are useful even today as modern day medicine. Emerging evidence also suggests that the search is still continuing for harnessing active compounds from nature in combating human illnesses although pharmaceutical industries are equally active for synthesizing small molecule compounds as novel therapeutics. The lesson learned over many centuries clearly suggests that further sophisticated search for finding compounds from natural resources together with robust characterization and chemical synthesis will lead to the discovery of novel drugs that may have high therapeutic efficacy against all human diseases including cancer. Black cumin seed (Nigella sativa) oil extracts have been used for many centuries for the treatment of many human illnesses, and more recently the active compound found in black seed oil, viz. thymoquinone (TQ) has been tested for its efficacy against several diseases including cancer. However, further research is needed in order to assess the full potential of TQ as a chemopreventive and/or therapeutic agent against cancers. Here, we have summarized what is known regarding the value of black seed oil and its active compound TQ, and how this knowledge will help us to advance further research in this field by creating awareness among scientists and health professionals in order to appreciate the medicinal value of TQ and beyond.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583426/pdf/nihms-73138.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27846703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Needle-like morphology of H2K4b polyplexes associated with increases in transfection in vitro. H2K4b多聚体的针状形态与体外转染增加有关。
Cancer therapy Pub Date : 2007-06-01
Qixin Leng, Jason Kahn, Jingsong Zhu, Puthapparampil Scaria, James Mixson
{"title":"Needle-like morphology of H2K4b polyplexes associated with increases in transfection in vitro.","authors":"Qixin Leng,&nbsp;Jason Kahn,&nbsp;Jingsong Zhu,&nbsp;Puthapparampil Scaria,&nbsp;James Mixson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>SUMMARY: Several synthetic histidine-lysine (HK) polymers have been screened for their efficacy as carriers of nucleic acids in vitro. One branched HK polymer, H2K4b (and its derivatives), has been particularly effective as an in vitro carrier of plasmids. In this study, we investigated whether various salt conditions during formation of the H2K4b/plasmid DNA polyplex affected transfection. We compared the transfection ability of H2K4b polyplexes prepared under three conditions: 1) water, 2) water and then Opti-MEM (or 300 mM NaCl), or 3) Opti-MEM (or 150 mM NaCl). The milieu in which the H2K4b polyplexes were prepared significantly affected in vitro transfection, and conditions that resulted in highest to lowest transfection levels were as follows: water and then Opti-MEM > Opti-MEM (or 150 mM NaCl)>> water. Several biophysical properties (size and shape of polyplex, surface charge, stability) were examined for their correlation with the level of transfection by the HK carrier. Strikingly, electron micrographs showed that HK polyplexes, first formed in water and then in salt, had a needle-like morphology with a mean length of 170 nm and a width of 53 nm; these needle-like polyplexes were observed intracellularly and absorbed to the cell surface, which was in marked contrast to the spherical HK polyplexes formed in water or in Opti-MEM. Notably, these needle-like HK polyplexes entered the cell through clathrin-mediated endocytosis, in contrast to spherical polyplexes, which entered primarily through non clathrin-mediated endocytosis.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950327/pdf/nihms24405.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26898573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neutrophil gelatinase-associated lipocalin: new paths for an old shuttle. 中性粒细胞明胶酶相关脂钙蛋白:旧穿梭的新途径。
Cancer therapy Pub Date : 2007-01-01
Prasad Devarajan
{"title":"Neutrophil gelatinase-associated lipocalin: new paths for an old shuttle.","authors":"Prasad Devarajan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a lipocalin that is well known for its functions as a shuttle for iron and siderophores, which comprises a critical component of innate immunity to exogenous bacterial infections. However, several lines of recent evidence have added new dimensions of functionality that have attracted the interest of cancer biologists and oncologists. This review will highlight the exciting new paths and roles that are emerging for NGAL in human cancers, in the tissue response to anticancer therapy, and in the acute kidney injuries that commonly complicate the care of patients with cancer. The evidence for NGAL induction and its role in various human cancers will be explored. The current status of NGAL as a predictive non-invasive biomarker of acute kidney injuries will also be examined.</p>","PeriodicalId":87393,"journal":{"name":"Cancer therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361391/pdf/nihms37280.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27416725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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