Pub Date : 2005-09-01DOI: 10.1016/J.JAMCOLLSURG.2005.06.198
G. Watson, Xinglu Zhang, M. Stang, Ryan M. Levy, Pierre E Queiroz de Oliveira, W. Gooding, J. Christensen, S. Hughes
{"title":"Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinoma.","authors":"G. Watson, Xinglu Zhang, M. Stang, Ryan M. Levy, Pierre E Queiroz de Oliveira, W. Gooding, J. Christensen, S. Hughes","doi":"10.1016/J.JAMCOLLSURG.2005.06.198","DOIUrl":"https://doi.org/10.1016/J.JAMCOLLSURG.2005.06.198","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"18 1","pages":"949-55"},"PeriodicalIF":4.8,"publicationDate":"2005-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90308980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2004-09-01DOI: 10.1016/s1359-6349(04)80396-3
S. Bar‐Yehuda, L. Madi, D. Silberman, Slosman Gery, Maya Shkapenuk, P. Fishman
{"title":"CF101, an agonist to the A3 adenosine receptor, enhances the chemotherapeutic effect of 5-fluorouracil in a colon carcinoma murine model.","authors":"S. Bar‐Yehuda, L. Madi, D. Silberman, Slosman Gery, Maya Shkapenuk, P. Fishman","doi":"10.1016/s1359-6349(04)80396-3","DOIUrl":"https://doi.org/10.1016/s1359-6349(04)80396-3","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"17 1","pages":"85-90"},"PeriodicalIF":4.8,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75514465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Hironaka, K. Mochida, N. Mori, M. Maeda, N. Yamamoto, S. Yamaoka
Adult T-cell leukemia (ATL) is a fatal T-cell malignancy that arises long after infection with human T-cell leukemia virus type I (HTLV-I). We reported previously that nuclear factor-kappaB (NF-kappaB) was constitutively activated in ATL cells, although expression of the viral proteins was barely detectable, including Tax, which was known to persistently activate NF-kappaB. Here we demonstrate that ATL cells that do not express detectable Tax protein exhibit constitutive IkappaB kinase (IKK) activity. Transfection studies revealed that a dominant-negative form of IKK1, and not of IKK2 or NF-kappaB essential modulator (NEMO), suppressed constitutive NF-kappaB activity in ATL cells. This IKK activity was accompanied by elevated expression of p52, suggesting that the recently described noncanonical pathway of NF-kappaB activation operates in ATL cells. We finally show that specific inhibition of NF-kappaB by a super-repressor form of IkappaBalpha (SR-IkappaBalpha) in HTLV-I-infected T cells results in cell death regardless of Tax expression, providing definitive evidence of an essential role for NF-kappaB in the survival of ATL cells. In conclusion, the IKK complex is constitutively activated in ATL cells through a cellular mechanism distinct from that of Tax-mediated IKK activation. Further elucidation of this cellular mechanism should contribute to establishing a rationale for treatment of ATL.
{"title":"Tax-independent constitutive IkappaB kinase activation in adult T-cell leukemia cells.","authors":"N. Hironaka, K. Mochida, N. Mori, M. Maeda, N. Yamamoto, S. Yamaoka","doi":"10.1593/NEO.03388","DOIUrl":"https://doi.org/10.1593/NEO.03388","url":null,"abstract":"Adult T-cell leukemia (ATL) is a fatal T-cell malignancy that arises long after infection with human T-cell leukemia virus type I (HTLV-I). We reported previously that nuclear factor-kappaB (NF-kappaB) was constitutively activated in ATL cells, although expression of the viral proteins was barely detectable, including Tax, which was known to persistently activate NF-kappaB. Here we demonstrate that ATL cells that do not express detectable Tax protein exhibit constitutive IkappaB kinase (IKK) activity. Transfection studies revealed that a dominant-negative form of IKK1, and not of IKK2 or NF-kappaB essential modulator (NEMO), suppressed constitutive NF-kappaB activity in ATL cells. This IKK activity was accompanied by elevated expression of p52, suggesting that the recently described noncanonical pathway of NF-kappaB activation operates in ATL cells. We finally show that specific inhibition of NF-kappaB by a super-repressor form of IkappaBalpha (SR-IkappaBalpha) in HTLV-I-infected T cells results in cell death regardless of Tax expression, providing definitive evidence of an essential role for NF-kappaB in the survival of ATL cells. In conclusion, the IKK complex is constitutively activated in ATL cells through a cellular mechanism distinct from that of Tax-mediated IKK activation. Further elucidation of this cellular mechanism should contribute to establishing a rationale for treatment of ATL.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"35 1","pages":"266-78"},"PeriodicalIF":4.8,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85590162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The cyclic adenosine monophosphate (AMP) response element-binding protein, CREB, often modulates stress responses. Here, we report that CREB suppresses the glioblastoma proliferative effect of the stress-induced acetylcholinesterase variant, AChE-R. In human U87MG glioblastoma cells, AChE-R formed a triple complex with protein kinase C (PKC) epsilon and the scaffold protein RACK1, enhanced PKCepsilon phosphorylation, and facilitated BrdU incorporation. Either overexpressed CREB, or antisense destruction of AChE-R mRNA, PKC, or protein kinase A (PKA) inhibitors-but not CREB combined with PKC inhibition suppressed-this proliferation, suggesting that CREB's repression of this process involves a PKC-mediated pathway, whereas impaired CREB regulation allows AChE-R-induced, PKA-mediated proliferation of glioblastoma tumors.
{"title":"CREB regulates AChE-R-induced proliferation of human glioblastoma cells.","authors":"C. Perry, E. Sklan, H. Soreq","doi":"10.1593/NEO.03424","DOIUrl":"https://doi.org/10.1593/NEO.03424","url":null,"abstract":"The cyclic adenosine monophosphate (AMP) response element-binding protein, CREB, often modulates stress responses. Here, we report that CREB suppresses the glioblastoma proliferative effect of the stress-induced acetylcholinesterase variant, AChE-R. In human U87MG glioblastoma cells, AChE-R formed a triple complex with protein kinase C (PKC) epsilon and the scaffold protein RACK1, enhanced PKCepsilon phosphorylation, and facilitated BrdU incorporation. Either overexpressed CREB, or antisense destruction of AChE-R mRNA, PKC, or protein kinase A (PKA) inhibitors-but not CREB combined with PKC inhibition suppressed-this proliferation, suggesting that CREB's repression of this process involves a PKC-mediated pathway, whereas impaired CREB regulation allows AChE-R-induced, PKA-mediated proliferation of glioblastoma tumors.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"104 1","pages":"279-86"},"PeriodicalIF":4.8,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86261480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Wolf, S. Mousses, S. Hautaniemi, R. Karhu, P. Huusko, M. Allinen, A. Elkahloun, O. Monni, Yidong Chen, A. Kallioniemi, O. Kallioniemi
Identification of target genes for genetic rearrangements in prostate cancer and the impact of copy number changes on gene expression are currently not well understood. Here, we applied high-resolution comparative genomic hybridization (CGH) on cDNA microarrays for analysis of prostate cancer cell lines. CGH microarrays identified most of the alterations detected by classic chromosomal CGH, as well as a number of previously unreported alterations. Specific recurrent regions of gain (28) and loss (18) were found, and their boundaries defined with sub-megabasepair accuracy. The most common changes included copy number decreases at 13q, and gains at 1q and 5p. Refined mapping identified several sites, such as at 13q (33-44, 49-51, and 74-76 Mbp from the p-telomere), which matched with minimal regions of loss seen in extensive loss of heterozygosity mapping studies of large numbers of tumors. Previously unreported recurrent changes were found at 2p, 2q, 3p, and 17q (losses), and at 3q, 5p, and 6p (gains). Integration of genomic and transcriptomic data revealed the role of individual candidate target genes for genomic alterations as well as a highly significant (P <.0001) overall association between copy number levels and the percentage of differentially expressed genes. Across the genome, the overall impact of copy number on gene expression levels was, to a large extent, attributable to low-level gains and losses of copy number, corresponding to common deletions and gains of often large chromosomal regions.
{"title":"High-resolution analysis of gene copy number alterations in human prostate cancer using CGH on cDNA microarrays: impact of copy number on gene expression.","authors":"M. Wolf, S. Mousses, S. Hautaniemi, R. Karhu, P. Huusko, M. Allinen, A. Elkahloun, O. Monni, Yidong Chen, A. Kallioniemi, O. Kallioniemi","doi":"10.1593/NEO.03439","DOIUrl":"https://doi.org/10.1593/NEO.03439","url":null,"abstract":"Identification of target genes for genetic rearrangements in prostate cancer and the impact of copy number changes on gene expression are currently not well understood. Here, we applied high-resolution comparative genomic hybridization (CGH) on cDNA microarrays for analysis of prostate cancer cell lines. CGH microarrays identified most of the alterations detected by classic chromosomal CGH, as well as a number of previously unreported alterations. Specific recurrent regions of gain (28) and loss (18) were found, and their boundaries defined with sub-megabasepair accuracy. The most common changes included copy number decreases at 13q, and gains at 1q and 5p. Refined mapping identified several sites, such as at 13q (33-44, 49-51, and 74-76 Mbp from the p-telomere), which matched with minimal regions of loss seen in extensive loss of heterozygosity mapping studies of large numbers of tumors. Previously unreported recurrent changes were found at 2p, 2q, 3p, and 17q (losses), and at 3q, 5p, and 6p (gains). Integration of genomic and transcriptomic data revealed the role of individual candidate target genes for genomic alterations as well as a highly significant (P <.0001) overall association between copy number levels and the percentage of differentially expressed genes. Across the genome, the overall impact of copy number on gene expression levels was, to a large extent, attributable to low-level gains and losses of copy number, corresponding to common deletions and gains of often large chromosomal regions.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"48 1","pages":"240-7"},"PeriodicalIF":4.8,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88163352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Association for International Cancer Research","authors":"D. Napier","doi":"10.1038/SJ.NEO.7900273","DOIUrl":"https://doi.org/10.1038/SJ.NEO.7900273","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"1944 1","pages":"558-559"},"PeriodicalIF":4.8,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91208297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of alpha(v)beta(3) in prostate cancer progression.","authors":"C. Cooper, C. Chay, K. Pienta","doi":"10.1038/SJ/NEO/7900224","DOIUrl":"https://doi.org/10.1038/SJ/NEO/7900224","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"1 1","pages":"191-4"},"PeriodicalIF":4.8,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80420768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-01-01DOI: 10.4135/9781412953979.n49
Claudia Winograd
Prostate Cancer Prostate cancer is the second leading cause of cancer death in men. In 2002, an estimated 189,000 men will be diagnosed with prostate cancer and almost 30,000 men will lose their lives to the disease. Prostate cancer frequently causes few, if any, symptoms in its early stages. Yet, prostate cancer is the most commonly occurring non–skin cancer in men, affecting one man in every six during his lifetime. More men will be at risk as the 76 million members of the baby boom generation continue to age.
{"title":"CaP CURE: Association for the Cure of Cancer of the Prostate.","authors":"Claudia Winograd","doi":"10.4135/9781412953979.n49","DOIUrl":"https://doi.org/10.4135/9781412953979.n49","url":null,"abstract":"Prostate Cancer Prostate cancer is the second leading cause of cancer death in men. In 2002, an estimated 189,000 men will be diagnosed with prostate cancer and almost 30,000 men will lose their lives to the disease. Prostate cancer frequently causes few, if any, symptoms in its early stages. Yet, prostate cancer is the most commonly occurring non–skin cancer in men, affecting one man in every six during his lifetime. More men will be at risk as the 76 million members of the baby boom generation continue to age.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"20 1","pages":"369-71"},"PeriodicalIF":4.8,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90179306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Breast Cancer Research Foundation; a cure in our lifetime.","authors":"","doi":"10.1038/sj.neo.7900240","DOIUrl":"https://doi.org/10.1038/sj.neo.7900240","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"38 1","pages":"275-7"},"PeriodicalIF":4.8,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82205250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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