Indoleamine 2,3-dioxygenase as a modifier of pathogenic inflammation in cancer and other inflammation-associated diseasesG C Prendergast
Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA
Curr Med Chem 18:2257-62. 2011
..We propose that IDO induction in a chronically inflamed tissue may shape the inflammatory state to support, or in some cases retard, pathogenesis and disease severity...
Towards a genetic definition of cancer-associated inflammation: role of the IDO pathwayGeorge C Prendergast
Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA
Am J Pathol 176:2082-7. 2010
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BAR the door: cancer suppression by amphiphysin-like genesGeorge C Prendergast
Lankenau Institute for Medical Research, Wynnewood PA, USA
Biochim Biophys Acta 1795:25-36. 2009
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Immune escape as a fundamental trait of cancer: focus on IDOG C Prendergast
Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA
Oncogene 27:3889-900. 2008
..New modalities in this area offer promising ways to broaden the combinatorial attack on advanced cancers, where immune escape mechanisms likely provide pivotal support...
Chasing cancer: from genes to drugsGeorge C Prendergast
Lankenau Institute for Medical Research, Wynnewood, Pennsylvania 19096, USA
Cancer Biol Ther 4:901-5. 2005
RhoB in cancer suppressionM Huang
Lankenau Institute for Medical Research, Jefferson Medical School, Thomas Jefferson University, Philadelphia, PA, USA
Histol Histopathol 21:213-8. 2006
..How RhoB acts to suppress different aspects of cancer pathophysiology has emerged as a question of significant interest...
RhoB facilitates c-Myc turnover by supporting efficient nuclear accumulation of GSK-3M Huang
Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA
Oncogene 25:1281-9. 2006
..The ability of RhoB to support GSK-3-dependent turnover of c-Myc offers a mechanism by which RhoB acts to limit the proliferation of neoplastically transformed cells...
Bin1 mediates apoptosis by c-Myc in transformed primary cellsJ B DuHadaway
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Cancer Res 61:3151-6. 2001
..Loss of Bin1 in human tumors may promote malignant progression in part by helping to stanch the death penalty associated with c-Myc activation...
The c-Myc-interacting adaptor protein Bin1 activates a caspase-independent cell death programK Elliott
The Wistar Institute, Philadelphia, PA, USA
Oncogene 19:4669-84. 2000
..Our findings suggest that the tumor suppressor activity of Bin1 reflects engagement of a unique cell death program. We propose that loss of Bin1 may promote malignancy by blunting death penalties associated with oncogene activation...
Bin2, a functionally nonredundant member of the BAR adaptor gene familyK Ge
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Genomics 67:210-20. 2000
..Thus, Bin2 appears to encode a nonredundant function in the BAR adaptor gene family...
Loss of heterozygosity and tumor suppressor activity of Bin1 in prostate carcinomaK Ge
The Wistar Institute, Philadelphia, Pennsylvania, USA
Int J Cancer 86:155-61. 2000
..Ectopic expression of Bin1 suppressed the growth of prostate cancer lines in vitro. Our findings support the candidacy of Bin1 as the chromosome 2q prostate tumor suppressor gene...
The Bin1 gene localizes to human chromosome 2q14 by PCR analysis of somatic cell hybrids and fluorescence in situ hybridizationD Negorev
Medical College of Pennsylvania, Philadelphia, USA
Genomics 33:329-31. 1996
Losses of the tumor suppressor BIN1 in breast carcinoma are frequent and reflect deficits in programmed cell death capacityK Ge
The Wistar Institute, Philadelphia, PA, USA
Int J Cancer 85:376-83. 2000
..We propose that loss of BIN1 may contribute to breast cancer progression by eliminating a mechanism that restrains the ability of activated MYC to drive cell division inappropriately...
Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanomaK Ge
The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA
Proc Natl Acad Sci U S A 96:9689-94. 1999
..Our findings suggest that aberrant splicing of Bin1 may contribute to melanoma progression, and they define a mechanism by which the activity of a tumor suppressor can be eliminated in cells...
BIN1 is a novel MYC-interacting protein with features of a tumour suppressorD Sakamuro
Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Nat Genet 14:69-77. 1996
..Deficits were functionally significant because ectopic expression of BIN1 inhibited the growth of tumour cells lacking endogenous message. We conclude that BIN1 is an MYC-interacting protein with features of a tumour suppressor...
Structural analysis of the human BIN1 gene. Evidence for tissue-specific transcriptional regulation and alternate RNA splicingR Wechsler-Reya
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
J Biol Chem 272:31453-8. 1997
..This study lays the foundation for genetic and epigenetic investigations into the role of BIN1 in normal and neoplastic cell regulation...
The murine Bin1 gene functions early in myogenesis and defines a new region of synteny between mouse chromosome 18 and human chromosome 2N C Mao
The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania, 19104, USA
Genomics 56:51-8. 1999
..Since the human gene was mapped previously to chromosome 2q14, the location of Bin1 defines a previously unrecognized region of synteny between human chromosome 2 and mouse chromosome 18...
A role for the putative tumor suppressor Bin1 in muscle cell differentiationR J Wechsler-Reya
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Mol Cell Biol 18:566-75. 1998
..Taken together, the results indicated that Bin1 expression, structure, and localization are tightly regulated during muscle differentiation and suggested that Bin1 plays a functional role in the differentiation process...
A key in vivo antitumor mechanism of action of natural product-based brassinins is inhibition of indoleamine 2,3-dioxygenaseT Banerjee
NewLink Genetics Corporation, Ames, IA, USA
Oncogene 27:2851-7. 2008
..The natural product brassinin thus provides the structural basis for a new class of compounds with in vivo anticancer activity that is mediated through the inhibition of IDO...
BAP1: a novel ubiquitin hydrolase which binds to the BRCA1 RING finger and enhances BRCA1-mediated cell growth suppressionD E Jensen
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Oncogene 16:1097-112. 1998
..BAP1 may be a new tumor suppressor gene which functions in the BRCA1 growth control pathway...
Actin' up: RhoB in cancer and apoptosisG C Prendergast
The DuPont Pharmaceuticals Company, Glenolden Laboratory, Pennsylvania 19004, USA
Nat Rev Cancer 1:162-8. 2001
..Genetic analysis in mice indicates that RhoB is dispensable for normal cell physiology, but that it has a suppressor or negative modifier function in stress-associated processes, including cancer...
RhoB is dispensable for mouse development, but it modifies susceptibility to tumor formation as well as cell adhesion and growth factor signaling in transformed cellsA X Liu
The Wistar Institute, Philadelphia, Pennsylvania, USA
Mol Cell Biol 21:6906-12. 2001
..Our findings suggest that RhoB is a negative regulator of integrin and growth factor signals that are involved in neoplastic transformation and possibly other stress or disease states...
RhoB alteration is necessary for apoptotic and antineoplastic responses to farnesyltransferase inhibitorsA X Liu
The Wistar Institute, Philadelphia, Glenolden, Pennsylvania, USA
Mol Cell Biol 20:6105-13. 2000
..Significantly, the apoptotic defect of -/- cells compromised the antitumor efficacy of FTI in xenograft assays. This study offers genetic proof of the hypothesis that RhoB-GG is a crucial mediator of the antineoplastic effects of FTIs...
Mbh 1: a novel gelsolin/severin-related protein which binds actin in vitro and exhibits nuclear localization in vivoG C Prendergast
Department of Biochemistry, New York University Medical Center, NY 10016
EMBO J 10:757-66. 1991
..The data suggest that Mbh1 may play a role in regulating cytoplasmic and/or nuclear architecture through potential interactions with actin...