Institution
Eppley Institute for Research in Cancer and Allied Diseases
About: Eppley Institute for Research in Cancer and Allied Diseases is a based out in . It is known for research contribution in the topics: Pancreatic cancer & Cancer. The organization has 965 authors who have published 1396 publications receiving 58994 citations.
Topics: Pancreatic cancer, Cancer, DNA, Gene, Cancer cell
Papers published on a yearly basis
Papers
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TL;DR: The successful application to the expression of the 66-residue cytoplasmic tail of human MUC1 indicates that the system can be applied to other peptides as well, and indicates a broader application of formic acid than cyanogen bromide in cleaving fusion proteins.
72 citations
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TL;DR: Investigation of basal activation of Stat5 in mammary epithelium of virgin wild-type mice indicated a role of this transcription factor in normal, nonpregnant breast epithelial cells, and may shed new light on Stat5 involvement in breast tumor promotion.
Abstract: Transcription factor Stat5 (signal transducer and activator of transcription) is essential for PRL-induced terminal differentiation of mouse mammary epithelial cells during pregnancy and lactation and has been implicated in mammary tumorigenesis. A new and sensitive immunological method to detect active, tyrosine phosphorylated Stat5 in situ revealed that Stat5 is continuously activated in luminal epithelial cells of mouse and human breast, not only during pregnancy and lactation, but also outside of pregnancy. Examination of virgin Stat5a or Stat5b null mice suggested that Stat5a was the primary isoform activated in mammary epithelial cells. Basal activation of Stat5 in mammary epithelium of virgin wild-type mice was continuous throughout estrous cycle and was also detected in 17 of 17 normal human breast tissue specimens analyzed. PRL was identified as the principal factor maintaining basal activation of Stat5 in mammary epithelium of nonpregnant mice based on several lines of evidence. First, administration of PRL, but not GH or epidermal growth factor, uniformly enhanced basal activation of Stat5 in luminal mammary epithelial cells. Second, hypophysectomy disrupted basal activation of Stat5, an effect that was completely reversed by administration of PRL, but only partially by GH. Third, knock-out of the PRL receptor gene markedly reduced basal activation of Stat5, an effect that was maintained in a normalized endocrine environment after transplanting PRL receptor null mammary epithelium into wild-type mice. Continuous activation of Stat5 indicates a role of this transcription factor in normal, nonpregnant breast epithelial cells, and may shed new light on Stat5 involvement in breast tumor promotion.
72 citations
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TL;DR: A stabilization model in which interruptions contribute in cis to reduce hairpin formation during TNR replication and thus inhibit expansion rates is supported, suggesting that expansion in yeast cells can proceed without loss of the interruption.
Abstract: In most trinucleotide repeat (TNR) diseases, the primary factor determining the likelihood of expansions is the length of the TNR. In some diseases, however, stable alleles contain one to three base pair substitutions that interrupt the TNR tract. The unexpected stability of these alleles compared to the frequent expansions of perfect TNRs suggested that interruptions somehow block expansions and that expansions occur only upon loss of at least one interruption. The work in this study uses a yeast genetic assay to examine the mechanism of stabilization conferred by two interruptions of a 25-repeat tract. Expansion rates are reduced up to 90-fold compared to an uninterrupted allele. Stabilization is greatest when the interruption is replicated early on the lagging strand, relative to the rest of the TNR. Although expansions are infrequent, they are often polar, gaining new DNA within the largest available stretch of perfect repeats. Surprisingly, interruptions are always retained and sometimes even duplicated, suggesting that expansion in yeast cells can proceed without loss of the interruption. These findings support a stabilization model in which interruptions contribute in cis to reduce hairpin formation during TNR replication and thus inhibit expansion rates.
72 citations
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TL;DR: The expression of prostate‐derived factor is significantly elevated in human prostate tumors and this work investigates the functional role and signaling of PDF in androgen receptor (AR)‐positive human prostate cancer cells.
Abstract: BACKGROUND
The expression of prostate-derived factor (PDF) is significantly elevated in human prostate tumors. We investigate the functional role and signaling of PDF in androgen receptor (AR)-positive human prostate cancer cells.
METHODS
Transient or stable expression of PDF by cDNA transfection, antisense-mediated gene silencing, media conditioned by PDF-elevated cells, and antibody (Ab) neutralization were employed.
RESULTS
Elevated endogenous and exogenous expression of PDF and treatment of PDF-enriched media were associated with increased proliferation and clonogenic growth of the cells. On the contrary, knockdown of PDF or addition of PDF neutralizing Ab resulted in diminished proliferation and reduced anchorage-independent growth. Further, ERK1/2 and p90RSK, but not Smad2/3, were activated in PDF-elevated cells as well as in cells treated with PDF-enriched media, while inhibition of ERK1/2 decreased the growth of those cells.
CONCLUSION
PDF promotes AR-positive prostate tumor progression through upregulating cell proliferation via ERK1/2 signal pathway. Prostate 67: 557–571, 2007. © 2007 Wiley-Liss, Inc.
71 citations
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TL;DR: The discovery that Sox proteins are regulated differentially at multiple levels, including transactivation, protein partnerships with Pit-Oct-Unc transcription factors, and DNA binding autoregulation is found, and a conserved domain of Sox-11 has the novel capability of autoinhibiting its ability to bind DNA in vitro and to activate gene expression in vivo.
71 citations
Authors
Showing all 965 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael R. Green | 126 | 537 | 57447 |
Henrik Clausen | 109 | 520 | 49820 |
Howard E. Gendelman | 101 | 567 | 39460 |
James O. Armitage | 97 | 558 | 59171 |
Surinder K. Batra | 87 | 564 | 30653 |
Michael L. Gross | 82 | 701 | 27140 |
Michael A. Hollingsworth | 76 | 249 | 24460 |
Peter M. J. Burgers | 73 | 167 | 16123 |
Patrick L. Iversen | 68 | 319 | 13707 |
J. Alan Diehl | 67 | 168 | 19966 |
Samuel M. Cohen | 65 | 421 | 15940 |
Kenneth H. Cowan | 64 | 178 | 14094 |
Gangning Liang | 60 | 150 | 18081 |
Michael G. Brattain | 59 | 199 | 13199 |
Thomas E. Smithgall | 57 | 184 | 8904 |