Neoplasia最新文献_第2页

Defining aggressive prostate cancer using a 12-gene model. 用12基因模型定义侵袭性前列腺癌。

IF 4.8 2区医学

Neoplasia Pub Date : 2006-09-01 DOI: 10.1016/S1569-9056(06)61294-3

T. Bismar, F. Demichelis, A. Riva, R. Kim, S. Varambally, Le He, J. Kutok, J. Aster, Jeffery Tang, R. Kuefer, M. Hofer, P. Febbo, A. Chinnaiyan, M. Rubin

引用次数: 106

FGF2 binding, signaling, and angiogenesis are modulated by heparanase in metastatic melanoma cells. 肝素酶在转移性黑色素瘤细胞中调节FGF2的结合、信号传导和血管生成。

IF 4.8 2区医学

Neoplasia Pub Date : 2006-07-01 DOI: 10.1097/00008390-200609001-00122

J. Reiland, D. Kempf, M. Roy, Y. Denkins, D. Marchetti

{"title":"FGF2 binding, signaling, and angiogenesis are modulated by heparanase in metastatic melanoma cells.","authors":"J. Reiland, D. Kempf, M. Roy, Y. Denkins, D. Marchetti","doi":"10.1097/00008390-200609001-00122","DOIUrl":"https://doi.org/10.1097/00008390-200609001-00122","url":null,"abstract":"Heparanase (HPSE) and fibroblast growth factor-2 (FGF2) are critical regulators of melanoma angiogenesis and metastasis. Elevated HPSE expression contributes to melanoma progression; however, further augmentation of HPSE presence can inhibit tumorigenicity. HPSE enzymatically cleaves heparan sulfate glycosaminoglycan chains (HS) from proteoglycans. HS act as both low-affinity FGF2 receptors and coreceptors in the formation of high-affinity FGF2 receptors. We have investigated HPSE's ability to modulate FGF2 activity through HS remodeling. Extensive HPSE degradation of human metastatic melanoma cells (70W) inhibited FGF2 binding. Unexpectedly, treatment of 70W cells with low HPSE concentrations enhanced FGF2 binding. In addition, HPSE-unexposed cells did not phosphorylate extracellular signal-related kinase (ERK) or focal adhesion kinase (FAK) in response to FGF2. Conversely, in cells treated with HPSE, FGF2 stimulated ERK and FAK phosphorylation. Secondly, the presence of soluble HPSE-degraded HS enhanced FGF2 binding and ERK phosphorylation at low HS concentrations. Higher concentrations of soluble HS inhibited FGF2 binding, but FGF2 signaling through ERK remained enhanced. Soluble HS were unable to support FGF2-stimulated FAK phosphorylation irrespective of HPSE treatment. Finally, cell exposure to HPSE or to HPSE-degraded HS modulated FGF2-induced angiogenesis in melanoma. In conclusion, these effects suggest relevant mechanisms for the HPSE modulation of melanoma growth factor responsiveness and tumorigenicity.","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79422870","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}

引用次数: 77

Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinoma. 抑制c-Met作为食管癌的治疗策略。

IF 4.8 2区医学

Neoplasia Pub Date : 2005-09-01 DOI: 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

引用次数: 22

CF101, an agonist to the A3 adenosine receptor, enhances the chemotherapeutic effect of 5-fluorouracil in a colon carcinoma murine model. CF101是A3腺苷受体的激动剂，可增强5-氟尿嘧啶在结肠癌小鼠模型中的化疗效果。

IF 4.8 2区医学

Neoplasia Pub Date : 2004-09-01 DOI: 10.1016/s1359-6349(04)80396-3

S. Bar‐Yehuda, L. Madi, D. Silberman, Slosman Gery, Maya Shkapenuk, P. Fishman

引用次数: 46

Tax-independent constitutive IkappaB kinase activation in adult T-cell leukemia cells. 成人t细胞白血病细胞中不依赖税收的IkappaB激酶激活。

IF 4.8 2区医学

Neoplasia Pub Date : 2004-05-01 DOI: 10.1593/NEO.03388

N. Hironaka, K. Mochida, N. Mori, M. Maeda, N. Yamamoto, S. Yamaoka

{"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":null,"pages":null},"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}

引用次数: 85

High-resolution analysis of gene copy number alterations in human prostate cancer using CGH on cDNA microarrays: impact of copy number on gene expression. 利用cDNA微阵列上的CGH对人前列腺癌基因拷贝数变化的高分辨率分析:拷贝数对基因表达的影响。

IF 4.8 2区医学

Neoplasia Pub Date : 2004-05-01 DOI: 10.1593/NEO.03439

M. Wolf, S. Mousses, S. Hautaniemi, R. Karhu, P. Huusko, M. Allinen, A. Elkahloun, O. Monni, Yidong Chen, A. Kallioniemi, O. Kallioniemi

{"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":null,"pages":null},"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}

引用次数: 141

CREB regulates AChE-R-induced proliferation of human glioblastoma cells. CREB调控ache - r诱导的人胶质母细胞瘤细胞增殖。

IF 4.8 2区医学

Neoplasia Pub Date : 2004-05-01 DOI: 10.1593/NEO.03424

C. Perry, E. Sklan, H. Soreq

引用次数: 67

The Association for International Cancer Research 国际癌症研究协会

IF 4.8 2区医学

Neoplasia Pub Date : 2002-11-01 DOI: 10.1038/SJ.NEO.7900273

D. Napier

引用次数: 10

Kidney Cancer Association 肾癌协会