Neoplasia (New York, N.Y.)最新文献_第4页

Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with β-Catenin Activation or Wt1 Ablation and Igf2 Upregulation1 β-Catenin激活或Wt1消融和Igf2上调小鼠模型中肾素祖细胞而非间质祖细胞可引起肾母细胞瘤1

Neoplasia (New York, N.Y.) Pub Date : 2016-02-01 DOI: 10.1016/j.neo.2015.12.001

Le Huang, Sharada Mokkapati, Q. Hu, E. Ruteshouser, M. Hicks, V. Huff

引用次数: 25

Signaling from p53 to NF-kappa B determines the chemotherapy responsiveness of neuroblastoma. 从p53到nf - κ B的信号传导决定了神经母细胞瘤的化疗反应性。

Neoplasia (New York, N.Y.) Pub Date : 2006-11-01

Michael B Armstrong, Xin Bian, Yihong Liu, Chitra Subramanian, Anthony B Ratanaproeksa, Feng Shao, Victor C Yu, Roland P S Kwok, Anthony W Opipari, Valerie P Castle

{"title":"Signaling from p53 to NF-kappa B determines the chemotherapy responsiveness of neuroblastoma.","authors":"Michael B Armstrong, Xin Bian, Yihong Liu, Chitra Subramanian, Anthony B Ratanaproeksa, Feng Shao, Victor C Yu, Roland P S Kwok, Anthony W Opipari, Valerie P Castle","doi":"","DOIUrl":"","url":null,"abstract":"Neuroblastic (N) type neuroblastoma (NB) is the predominant cell type in NB tumors. Previously, we determined that activated nuclear factor kappaB (NF-kappaB) is required for doxorubicin and etoposide to kill N-type NB cells. This study was undertaken to determine how NF-kappaB is activated by these agents. The results show that p53 protein levels increase within 15 to 30 minutes of treatment. This increase occurs before the degradation of inhibitor of NF-kappaB (I-KB) alpha and the NF-kappaB-dependent activation of gene transcription. Moreover, p53 is necessary for NF-kappaB activation because cells with inactive p53 were resistant to NF-kappaB-mediated cell death. This pathway was further defined to show that p53 leads to the activation of MAPK/ERK activity kinase (MEK) 1 through a process that depends on protein synthesis and H-Ras. MEK1, in turn, mediates I-kappaB kinase activation. Together, these results demonstrate for the first time how NF-kappaB is activated in NB cells in response to conventional drugs. Furthermore, these findings provide an explanation as to why H-Ras expression correlates with a favorable prognosis in NB and identify intermediary signaling molecules that are targets for discovering treatments for NB that is resistant to conventional agents.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"8 11","pages":"964-74"},"PeriodicalIF":0.0,"publicationDate":"2006-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764827/pdf/neo0811_0964.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26482932","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

Phosphorylated epidermal growth factor receptor on tumor-associated endothelial cells in human renal cell carcinoma is a primary target for therapy by tyrosine kinase inhibitors. 磷酸化的表皮生长因子受体在肿瘤相关的内皮细胞在人肾细胞癌是酪氨酸激酶抑制剂治疗的主要目标。

Neoplasia (New York, N.Y.) Pub Date : 2006-06-01 DOI: 10.1593/neo.06172

Cheryl H Baker, Maria S Pino, Isaiah J Fidler

{"title":"Phosphorylated epidermal growth factor receptor on tumor-associated endothelial cells in human renal cell carcinoma is a primary target for therapy by tyrosine kinase inhibitors.","authors":"Cheryl H Baker, Maria S Pino, Isaiah J Fidler","doi":"10.1593/neo.06172","DOIUrl":"https://doi.org/10.1593/neo.06172","url":null,"abstract":"We determined whether therapy for human renal cell carcinoma (HRCC) that grows in the kidney of nude mice by the specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, PKI166, is directed against phosphorylated EGFR on tumor cells or on tumor-associated endothelial cells. EGFR+/transforming growth factor alpha (TGF-alpha)- SN12-PM6 HRCC cells were transfected with full-length sense TGF-alpha cDNA or vector control. SN12-PM6 cells expressing low or high levels of TGF-alpha were implanted into the kidney of nude mice. Only tumors produced by TGF-alpha+ HRCC cells contained tumor-associated endothelial cells expressing activated EGFR. Oral administration of PKI166 produced significant therapy only in TGF-alpha+ tumors, which correlated with apoptosis of tumor-associated endothelial cells. These data suggest that the production of TGF-alpha by HRCC cells leads to the activation of EGFR on tumor-associated endothelial cells that serve as an essential target for therapy with tyrosine kinase inhibitors.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"8 6","pages":"470-6"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1601465/pdf/neo0806_0470.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26125802","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: 22

Prostate-Specific Antigen Modulates the Expression of Genes Involved in Prostate Tumor Growth. 前列腺特异性抗原调控前列腺肿瘤生长相关基因的表达。

Neoplasia (New York, N.Y.) Pub Date : 2005-05-01

B Bindukumar, Stanley A Schwartz, Madhavan P N Nair, Ravikumar Aalinkeel, Elzbieta Kawinski, Kailash C Chadha

引用次数: 0

Tumor-targeted hyaluronan nanoliposomes increase the antitumor activity of liposomal Doxorubicin in syngeneic and human xenograft mouse tumor models. 肿瘤靶向透明质酸纳米脂质体增加阿霉素脂质体在同体和人异种移植小鼠肿瘤模型中的抗肿瘤活性。

Neoplasia (New York, N.Y.) Pub Date : 2004-07-01 DOI: 10.1593/neo.03460

Dan Peer, Rimona Margalit

{"title":"Tumor-targeted hyaluronan nanoliposomes increase the antitumor activity of liposomal Doxorubicin in syngeneic and human xenograft mouse tumor models.","authors":"Dan Peer, Rimona Margalit","doi":"10.1593/neo.03460","DOIUrl":"https://doi.org/10.1593/neo.03460","url":null,"abstract":"Naturally occurring high-Mr hyaluronan, bound to the surface of nanoliposomes (denoted targeted hyaluronan liposomes, or tHA-LIP), is a candidate for active targeting to tumors, many of which overexpress the hyaluronan receptors CD44 and RHAMM. The surface-bound hyaluronan also provides a hydrophilic coat that, similar to polyethylene glycol, may promote long-term circulation. We recently reported the successful targeting of mitomycin C, mediated by tHA-LIP, in tumor-bearing syngeneic mice. Hypothesizing that this targeting is carrier-specific, rather than drug-specific, we report here studies with doxorubicin (DXR)-loaded tHA-LIP, in syngeneic and human xenograft models. Saline, free DXR, DXR-loaded nontargeted liposomes (nt-LIP), and Doxil served as controls. The tHA-LIP were long-circulating, more than all controls, in healthy and tumor-bearing (C57BL/6/B16F10.9; BALB/c/C-26) mice. Mediated by tHA-LIP, DXR accumulation in tumor-bearing lungs was 30-, 6.7-, and 3.5-fold higher than free DXR, nt-LIP, and Doxil, respectively. Key indicators of therapeutic responses--tumor progression, metastatic burden, and survival--were superior (P < .001) in animals receiving DXR-loaded tHA-LIP compared with controls, in tumor-bearing syngeneic mice (BDF1/P388/ADR ascites, C57BL/6/B16F10.9 lung metastasis, and BALB/c/C-26 solid tumors), and in nude mice bearing PANC-1 solid tumors. In conclusion, tHA-LIP, performing as tumor-targeted carriers, have the potential to join the arsenal of carrier-formulated anticancer drugs.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"6 4","pages":"343-53"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1593/neo.03460","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24617611","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: 206

Aberrant methylation of the maspin promoter is an early event in human breast cancer. maspin启动子的异常甲基化是人类乳腺癌的早期事件。

Neoplasia (New York, N.Y.) Pub Date : 2004-07-01 DOI: 10.1593/neo.04115

Bernard W Futscher, Megan M O'Meara, Christina J Kim, Margaret A Rennels, Di Lu, Lynn M Gruman, Richard E B Seftor, Mary J C Hendrix, Frederick E Domann

{"title":"Aberrant methylation of the maspin promoter is an early event in human breast cancer.","authors":"Bernard W Futscher, Megan M O'Meara, Christina J Kim, Margaret A Rennels, Di Lu, Lynn M Gruman, Richard E B Seftor, Mary J C Hendrix, Frederick E Domann","doi":"10.1593/neo.04115","DOIUrl":"https://doi.org/10.1593/neo.04115","url":null,"abstract":"The maspin gene functions as a tumor suppressor in human breasts, and its expression is frequently lost during breast cancer progression. In vitro models of human breast cancer indicate that the loss of maspin expression is closely linked to aberrant methylation of the maspin promoter. We conducted a study on 30 archival ductal carcinoma in situ (DCIS) specimens to determine if aberrant methylation of the maspin promoter occurred in vivo, and whether it occurred early in breast cancer evolution. Healthy tissue obtained from reduction mammoplasty was used as normal control. Results from immunohistochemical analysis indicate that maspin expression is lost in a substantial fraction of DCIS specimens (57%). Bisulfite sequencing of DNA isolated from laser capture-microdissected normal and neoplastic ducts showed that loss of maspin expression was often, but not always, linked to aberrant methylation of the maspin promoter, suggesting that other mechanisms, in addition to aberrant methylation, participate and/or cooperate to silence maspin gene expression. Taken together, these results indicate that aberrant methylation of the maspin promoter is an early event in human breast cancer.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"6 4","pages":"380-9"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1502109/pdf/neo0604_0380.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24617612","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: 81

CREB regulates AChE-R-induced proliferation of human glioblastoma cells. CREB 调节 AChE-R 诱导的人类胶质母细胞瘤细胞增殖。

Neoplasia (New York, N.Y.) Pub Date : 2004-05-01 DOI: 10.1593/neo.3424

Chava Perry, Ella H Sklan, Hermona Soreq

引用次数: 0

Spontaneous immortalization of clinically normal colon-derived fibroblasts from a familial adenomatous polyposis patient. 家族性腺瘤性息肉病患者临床正常结肠来源成纤维细胞的自发永生化。

Neoplasia (New York, N.Y.) Pub Date : 2004-05-01 DOI: 10.1593/neo.4103

Nicholas R Forsyth, Carmela P Morales, Shirish Damle, Bruce Boman, Woodring E Wright, Levy Kopelovich, Jerry W Shay

{"title":"Spontaneous immortalization of clinically normal colon-derived fibroblasts from a familial adenomatous polyposis patient.","authors":"Nicholas R Forsyth, Carmela P Morales, Shirish Damle, Bruce Boman, Woodring E Wright, Levy Kopelovich, Jerry W Shay","doi":"10.1593/neo.4103","DOIUrl":"https://doi.org/10.1593/neo.4103","url":null,"abstract":"Normal human diploid cells do not spontaneously immortalize in culture, but instead enter replicative senescence after a finite number of population doublings. Ablation of key checkpoint arrest or cancer-suppressor genes, through dominantly inherited germline mutation (p53+/-, Li-Fraumeni) or viral oncogene expression (SV40 large T, HPV16/18, and E6/E7) can lead to escape from senescence, additional doublings, and entrance into crisis phase, where immortal clones emerge at low frequency. In the vast majority of cases, telomerase is reactivated and telomeres are stabilized. Here we describe the spontaneous immortalization of clinically normal fibroblasts derived from colonic stroma of a familial adenomatous polyposis (FAP) patient. The preimmortal (C26C) and the spontaneously immortalized derivative (C26Ci) cells are heterozygous for a characterized germline mutation in exon 15 of the adenomatous polyposis coli gene. Immortalization was accompanied by spontaneous reactivation of endogenous telomerase and establishment of telomeres at presenescent lengths. Normal checkpoint behavior is retained and a diploid karyotype is maintained. These cells provide a valuable new addition to the limited number of spontaneously immortalized human cell types, particularly fibroblast cells, and will be useful in experimentally determining the functional pathways in neoplastic development and in the identification of potential molecular targets for cancer chemoprevention.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"6 3","pages":"258-65"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1502101/pdf/neo0603_0258.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24527516","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

Glutathione depletion induced by c-Myc downregulation triggers apoptosis on treatment with alkylating agents. c-Myc下调引起的谷胱甘肽耗竭可触发烷基化剂处理后的细胞凋亡。

Neoplasia (New York, N.Y.) Pub Date : 2004-05-01 DOI: 10.1593/neo.3370

Annamaria Biroccio, Barbara Benassi, Francesco Fiorentino, Gabriella Zupi

{"title":"Glutathione depletion induced by c-Myc downregulation triggers apoptosis on treatment with alkylating agents.","authors":"Annamaria Biroccio, Barbara Benassi, Francesco Fiorentino, Gabriella Zupi","doi":"10.1593/neo.3370","DOIUrl":"https://doi.org/10.1593/neo.3370","url":null,"abstract":"Here we investigate the mechanism(s) involved in the c-Myc-dependent drug response of melanoma cells. By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line. On the contrary, topoisomerase inhibitors, adriamycin and camptothecin, induce apoptosis to the same extent regardless of c-Myc expression. Because we previously demonstrated that c-Myc downregulation decreases glutathione (GSH) content, we evaluated the role of GSH in the apoptosis induced by the different drugs. In control cells treated with one of the alkylating agents or the others, GSH depletion achieved by L-buthionine-sulfoximine preincubation opens the apoptotic pathway. The apoptosis proceeded through early Bax relocalization, cytochrome c release, and concomitant caspase-9 activation, whereas reactive oxygen species production and alteration of mitochondria membrane potential were late events. That GSH was determining in the c-Myc-dependent drug-induced apoptosis was demonstrated by altering the intracellular GSH content of the c-Myc low-expressing cells up to the level of controls. Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution. The relationship among c-Myc, GSH content, and the response to alkylating agent has been also evaluated in the M14 Myc overexpressing clones as well as in the melanoma JR8 c-Myc antisense transfectants. All together, these results demonstrate that GSH plays a key role in governing c-Myc-dependent drug-induced apoptosis.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"6 3","pages":"195-206"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1502103/pdf/neo0603_0195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24527642","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

The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells. 乙酰转移酶p300/ cbp相关因子是乳腺肿瘤细胞中p53的靶基因。

Neoplasia (New York, N.Y.) Pub Date : 2004-05-01 DOI: 10.1593/neo.3292

George S Watts, Marc M Oshiro, Damian J Junk, Ryan J Wozniak, Summer Watterson, Frederick E Domann, Bernard W Futscher

{"title":"The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells.","authors":"George S Watts, Marc M Oshiro, Damian J Junk, Ryan J Wozniak, Summer Watterson, Frederick E Domann, Bernard W Futscher","doi":"10.1593/neo.3292","DOIUrl":"https://doi.org/10.1593/neo.3292","url":null,"abstract":"p300/CBP-associated factor (PCAF) is a coactivator of the tumor suppressor, p53. PCAF participates in p53's transactivation of target genes through acetylation of both bound p53 and histones within p53 target promoters. Using microarrays, we discovered that PCAF itself is induced by p53 in a panel of breast tumor cell lines. Two p53 mutant breast tumor cell lines, BT-549 and UACC-1179, were chosen for further study of PCAF induction by wild-type p53. PCAF induction following adenoviral transduction of p53 expression was confirmed with real-time polymerase chain reaction in a time course experiment. Chromatin immunoprecipitation experiments then showed that PCAF induction was associated with increased p53 binding to the PCAF promoter, which contains p53 consensus-binding sites. PCAF induction by p53 activity was further demonstrated in wild-type p53 MCF10A cells when PCAF expression was induced following activation of endogenous wild-type p53 with doxorubicin in a dose- and time-dependent manner. Furthermore, the doxorubicin-induced increase in PCAF expression was blocked by pretreatment of the MCF10A cells with siRNA (small interfering RNA) targeted against p53 mRNA. Taken together, the results show that PCAF expression can be induced by wild-type p53.","PeriodicalId":18888,"journal":{"name":"Neoplasia (New York, N.Y.)","volume":"6 3","pages":"187-94"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1502105/pdf/neo0603_0187.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24527641","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: 46