Pub Date : 2007-03-01DOI: 10.1016/S1569-9056(08)60821-0
R. Kuefer, F. Genze, Waltraud Zugmaier, R. Hautmann, L. Rinnab, J. Gschwend, Marina Angelmeier, A. Estrada, B. Buechele
{"title":"Antagonistic effects of sodium butyrate and N-(4-hydroxyphenyl)-retinamide on prostate cancer.","authors":"R. Kuefer, F. Genze, Waltraud Zugmaier, R. Hautmann, L. Rinnab, J. Gschwend, Marina Angelmeier, A. Estrada, B. Buechele","doi":"10.1016/S1569-9056(08)60821-0","DOIUrl":"https://doi.org/10.1016/S1569-9056(08)60821-0","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"39 1","pages":"246-53"},"PeriodicalIF":4.8,"publicationDate":"2007-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74578350","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}
Neoplasia was launched in 1999 with the mission of providing a high-quality publication venue for the rapid dissemination of novel and exciting advances in cancer research. The journal has grown, in a very rapid fashion, from a bimonthly publication to a monthly publication by publishing a broad-based range of articles ranging from apoptosis to angiogenesis, as shown in Table 1. This table categorizes articles published by Neoplasia by general topic for publication years 2004 to 2006. Cancer genetics, cell and tumor biology, experimental therapeutics, and cancer imaging continue to be significant components of article growth published over these years. The number of submissions and published articles has continually increased over the year, and, next year, Neoplasia will enter its ninth year of publication (Vol. 9). The success of Neoplasia has affirmed to the editorial staff and editorial board that there was and continues to be a significant need for a broad-based cancer journal. During the past year, Neoplasia has further adapted and taken the lead in online peer-reviewed publication of cancer research articles. Table 1 Major Research Topics Published in Neoplasia from 2004 to 2006. In 2006, Neoplasia adopted the open access (OA) model for all articles published. This allows for all articles to be made available free to the scientific and layman communities through online electronic access. All articles are linked through PubMed (www.PubMEd.gov) to a Web-based database, which hosts all Neoplasia articles published to date. Moreover, beginning in 2007, all Neoplasia articles published in Neoplasia will also be freely available through the Biomedcentral portal (http://www.biomedcentral.com/) beginning on the day of publication, rather than after 6 to 12 months like most journals. Of 8700 selected journals currently covered in Web of Science, only 160 are available through Biomedcentral. The effect of immediate OA on the impact of Neoplasia is anticipated to dramatically improve the citation impact factor in terms of the frequency with which an article is cited in the literature (http://dlib.org/dlib/june04/harnad/06harnad.html) [301]. Overall, OA will provide for dramatically increased readership due to access to articles, which would traditionally be unavailable due to costs associated with access tolls to the journal in which it was published because their affiliated institution could not afford the price of subscription. Overall, providing OA to all past, present, and future articles published in Neoplasia should significantly improve the quality and speed at which cancer research advances will be made due to more rapid dissemination of knowledge. Neoplasia is committed to meeting the challenges and emerging needs of the cancer research scientific community. This commitment has been met through the early establishment of a rapid online peer-review system, which has facilitated review of submitted articles. Moreover, the re
《肿瘤》杂志于1999年创办，其使命是提供一个高质量的出版场所，以便快速传播癌症研究方面令人兴奋的新进展。通过发表从细胞凋亡到血管生成的广泛的文章，该杂志以非常迅速的方式从双月刊发展到月刊，如表1所示。本表按2004至2006年出版年度Neoplasia发表的文章按一般题目分类。癌症遗传学，细胞和肿瘤生物学，实验治疗学和癌症成像继续是这些年来发表的文章增长的重要组成部分。投稿和发表的文章数量在过去的一年中不断增加，明年，Neoplasia将进入其出版的第九个年头(第9卷)。Neoplasia的成功向编辑人员和编辑委员会证实了对一本基础广泛的癌症期刊的巨大需求。在过去的一年里，Neoplasia进一步适应并在在线同行评审的癌症研究文章发表方面处于领先地位。表1 2004 - 2006年肿瘤学发表的主要研究课题。2006年，Neoplasia对所有发表的文章采用开放获取(OA)模式。这使得所有的文章都可以通过在线电子访问免费提供给科学界和非专业人士。所有文章都通过PubMed (www.PubMEd.gov)链接到一个基于web的数据库，该数据库包含迄今为止发表的所有Neoplasia文章。此外，从2007年开始，所有发表在Neoplasia上的文章也将从发表当天开始通过生物中心门户网站(http://www.biomedcentral.com/)免费提供，而不是像大多数期刊那样需要6到12个月。在Web Of Science目前收录的8700种精选期刊中，只有160种可以通过Biomedcentral找到。直接开放获取对Neoplasia影响的影响预计将显著提高文献中文章被引用的频率(http://dlib.org/dlib/june04/harnad/06harnad.html)[301]。总的来说，开放获取将极大地增加读者数量，因为他们可以访问文章，而这些文章在传统上是无法获得的，因为他们的附属机构无法负担订阅费用，而这些费用与发表文章的期刊的访问费用相关。总的来说，为Neoplasia杂志上发表的所有过去、现在和未来的文章提供OA应该会显著提高癌症研究的质量和速度，因为知识的传播更加迅速。肿瘤学致力于满足癌症研究科学界的挑战和新兴需求。通过早期建立快速在线同行评议系统实现了这一承诺，该系统促进了对提交文章的评议。此外，2006年的开放获取，以及2007年扩展到生物医学中心，将最大限度地提供Neoplasia发表的所有手稿的国际传播。这种前瞻性的方法允许所有已发表文章的即时OA可用性，应该为使用Neoplasia作为其发表场所的作者提供其令人兴奋的研究成果的最大影响。
{"title":"Neoplasia: Where We Have Been and Where We Are Going","authors":"A. Rehemtulla","doi":"10.1593/NEO.08EDI","DOIUrl":"https://doi.org/10.1593/NEO.08EDI","url":null,"abstract":"Neoplasia was launched in 1999 with the mission of providing a high-quality publication venue for the rapid dissemination of novel and exciting advances in cancer research. The journal has grown, in a very rapid fashion, from a bimonthly publication to a monthly publication by publishing a broad-based range of articles ranging from apoptosis to angiogenesis, as shown in Table 1. This table categorizes articles published by Neoplasia by general topic for publication years 2004 to 2006. Cancer genetics, cell and tumor biology, experimental therapeutics, and cancer imaging continue to be significant components of article growth published over these years. The number of submissions and published articles has continually increased over the year, and, next year, Neoplasia will enter its ninth year of publication (Vol. 9). The success of Neoplasia has affirmed to the editorial staff and editorial board that there was and continues to be a significant need for a broad-based cancer journal. During the past year, Neoplasia has further adapted and taken the lead in online peer-reviewed publication of cancer research articles. \u0000 \u0000 \u0000 \u0000Table 1 \u0000 \u0000Major Research Topics Published in Neoplasia from 2004 to 2006. \u0000 \u0000 \u0000 \u0000In 2006, Neoplasia adopted the open access (OA) model for all articles published. This allows for all articles to be made available free to the scientific and layman communities through online electronic access. All articles are linked through PubMed (www.PubMEd.gov) to a Web-based database, which hosts all Neoplasia articles published to date. Moreover, beginning in 2007, all Neoplasia articles published in Neoplasia will also be freely available through the Biomedcentral portal (http://www.biomedcentral.com/) beginning on the day of publication, rather than after 6 to 12 months like most journals. Of 8700 selected journals currently covered in Web of Science, only 160 are available through Biomedcentral. The effect of immediate OA on the impact of Neoplasia is anticipated to dramatically improve the citation impact factor in terms of the frequency with which an article is cited in the literature (http://dlib.org/dlib/june04/harnad/06harnad.html) [301]. Overall, OA will provide for dramatically increased readership due to access to articles, which would traditionally be unavailable due to costs associated with access tolls to the journal in which it was published because their affiliated institution could not afford the price of subscription. Overall, providing OA to all past, present, and future articles published in Neoplasia should significantly improve the quality and speed at which cancer research advances will be made due to more rapid dissemination of knowledge. \u0000 \u0000Neoplasia is committed to meeting the challenges and emerging needs of the cancer research scientific community. This commitment has been met through the early establishment of a rapid online peer-review system, which has facilitated review of submitted articles. Moreover, the re","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"126 1","pages":"975-983"},"PeriodicalIF":4.8,"publicationDate":"2006-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88166866","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 : 2006-09-01DOI: 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
{"title":"Defining aggressive prostate cancer using a 12-gene model.","authors":"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","doi":"10.1016/S1569-9056(06)61294-3","DOIUrl":"https://doi.org/10.1016/S1569-9056(06)61294-3","url":null,"abstract":"","PeriodicalId":48716,"journal":{"name":"Neoplasia","volume":"3 1","pages":"59-68"},"PeriodicalIF":4.8,"publicationDate":"2006-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83324252","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 : 2006-07-01DOI: 10.1097/00008390-200609001-00122
J. Reiland, D. Kempf, M. Roy, Y. Denkins, D. Marchetti
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.
{"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":"2 1","pages":"596-606"},"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}
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}
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