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Article ; Online: RAC1: an emerging therapeutic option for targeting cancer angiogenesis and metastasis.

Bid, Hemant K / Roberts, Ryan D / Manchanda, Parmeet K / Houghton, Peter J

2013 Volume 12, Issue 10, Page(s) 1925–1934

Abstract: Angiogenesis and metastasis are well recognized as processes fundamental to the development of malignancy. Both processes involve the coordination of multiple cellular and chemical activities through myriad signaling networks, providing a mass of ... ...

Abstract	Angiogenesis and metastasis are well recognized as processes fundamental to the development of malignancy. Both processes involve the coordination of multiple cellular and chemical activities through myriad signaling networks, providing a mass of potential targets for therapeutic intervention. This review will focus on one master regulator of cell motility, RAC1, and the existing data with regard to its role in cell motility, including particular roles for tumor angiogenesis and invasion/metastasis. We also emphasize the preclinical investigations carried out with RAC1 inhibitors to evaluate the therapeutic potential of this target. Herein, we explore potential future directions as well as the challenges of targeting RAC1 in the treatment of cancer. Recent insights at the molecular and cellular levels are paving the way for a more directed and detailed approach to target mechanisms of RAC1 regulating angiogenesis and metastasis. Understanding these mechanisms may provide insight into RAC1 signaling components as alternative therapeutic targets for tumor angiogenesis and metastasis.
MeSH term(s)	Cell Movement/genetics ; Humans ; Molecular Targeted Therapy ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/genetics ; Signal Transduction ; rac1 GTP-Binding Protein/genetics
Chemical Substances	RAC1 protein, human ; rac1 GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2013-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-13-0164
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Zs.A 5750: Show issues

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Article ; Online: Protein kinase A activation enhances β-catenin transcriptional activity through nuclear localization to PML bodies.

Zhang, Mei / Mahoney, Emilia / Zuo, Tao / Manchanda, Parmeet K / Davuluri, Ramana V / Kirschner, Lawrence S

PloS one

2014 Volume 9, Issue 10, Page(s) e109523

Abstract: The Protein Kinase A (PKA) and Wnt signaling cascades are fundamental pathways involved in cellular development and maintenance. In the osteoblast lineage, these pathways have been demonstrated functionally to be essential for the production of ... ...

Abstract	The Protein Kinase A (PKA) and Wnt signaling cascades are fundamental pathways involved in cellular development and maintenance. In the osteoblast lineage, these pathways have been demonstrated functionally to be essential for the production of mineralized bone. Evidence for PKA-Wnt crosstalk has been reported both during tumorigenesis and during organogenesis, and the nature of the interaction is thought to rely on tissue and cell context. In this manuscript, we analyzed bone tumors arising from mice with activated PKA caused by mutation of the PKA regulatory subunit Prkar1a. In primary cells from these tumors, we observed relocalization of β-catenin to intranuclear punctuate structures, which were identified as PML bodies. Cellular redistribution of β-catenin could be recapitulated by pharmacologic activation of PKA. Using 3T3-E1 pre-osteoblasts as a model system, we found that PKA phosphorylation sites on β-catenin were required for nuclear re-localization. Further, β-catenin's transport to the nucleus was accompanied by an increase in canonical Wnt-dependent transcription, which also required the PKA sites. PKA-Wnt crosstalk in the cells was bi-directional, including enhanced interactions between β-catenin and the cAMP-responsive element binding protein (CREB) and transcriptional crosstalk between the Wnt and PKA signaling pathways. Increases in canonical Wnt/β-catenin signaling were associated with a decrease in the activity of the non-canonical Wnt/Ror2 pathway, which has been shown to antagonize canonical Wnt signaling. Taken together, this study provides a new understanding of the complex regulation of the subcellular distribution of β-catenin and its differential protein-protein interaction that can be modulated by PKA signaling.
MeSH term(s)	Animals ; Bone Neoplasms/genetics ; Bone Neoplasms/metabolism ; Bone Neoplasms/pathology ; Bone and Bones/metabolism ; Bone and Bones/pathology ; Cell Line, Tumor ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/genetics ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/metabolism ; Cytosol/drug effects ; Cytosol/metabolism ; Gene Expression Regulation, Neoplastic ; Mice ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Phosphorylation ; Protein Binding ; Protein Transport ; Receptor Tyrosine Kinase-like Orphan Receptors/genetics ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Signal Transduction ; Transcription, Genetic ; Wnt3A Protein/genetics ; Wnt3A Protein/metabolism ; Wnt3A Protein/pharmacology ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	CTNNB1 protein, human ; Creb1 protein, mouse ; Cyclic AMP Response Element-Binding Protein ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Prkar1a protein, mouse ; Wnt3A Protein ; Wnt3a protein, mouse ; beta Catenin ; Receptor Tyrosine Kinase-like Orphan Receptors (EC 2.7.10.1) ; Ror2 protein, mouse (EC 2.7.10.1)
Language	English
Publishing date	2014-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0109523
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Article ; Online: Knockdown of PRKAR1A, the gene responsible for Carney complex, interferes with differentiation in osteoblastic cells.

Zhang, Mei / Manchanda, Parmeet K / Wu, Dayong / Wang, Qianben / Kirschner, Lawrence S

Molecular endocrinology (Baltimore, Md.)

2014 Volume 28, Issue 3, Page(s) 295–307

Abstract: PRKAR1A is the gene encoding the type 1A regulatory subunit of protein kinase A, and it is the cause of the inherited human tumor syndrome Carney complex. Data from our laboratory has demonstrated that Prkar1a loss causes tumors in multiple cell lineages, ...

Abstract	PRKAR1A is the gene encoding the type 1A regulatory subunit of protein kinase A, and it is the cause of the inherited human tumor syndrome Carney complex. Data from our laboratory has demonstrated that Prkar1a loss causes tumors in multiple cell lineages, including neural crest cells and osteoblasts. We have proposed that one mechanism by which tumorigenesis occurs is through the failure of terminal differentiation. In the present study, we directly test the effects of Prkar1a reduction on osteogenic differentiation in mouse and human cells in vitro. We found that Prkar1a levels noticeably increased during osteoblastic differentiation, indicating a positive correlation between the expression of Prkar1a and osteogenic potential. To validate this hypothesis, we generated stable Prkar1a knockdown in both mouse and human cells. These cells displayed significantly suppressed bone nodule formation and decreased expression of osteoblast markers such as osteocalcin and osteopontin. These observations imply that the antiosteogenic effect of Prkar1a ablation is not species or cell line specific. Furthermore, because Runt-related transcription factor-2 (Runx2) is a key mediator of osteoblast differentiation, we reasoned that the function of this transcription factor may be inhibited by Prkar1a knockdown. Chromatin immunoprecipitation and luciferase assays demonstrated that Prkar1a ablation repressed DNA binding and function of Runx2 at its target genes. Additionally, we determined that this effect is likely due to reductions in the Runx2-cooperating transcription factors forkhead box O1 and activating transcription factor 4. Taken together, this study provides direct evidence that ablation of Prkar1a interferes with signaling pathways necessary for osteoblast differentiation.
MeSH term(s)	3T3 Cells ; Animals ; Carney Complex/genetics ; Cell Differentiation ; Cell Line, Tumor ; Core Binding Factor Alpha 1 Subunit/physiology ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/genetics ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Humans ; Mesenchymal Stem Cells/physiology ; Mice ; Osteoblasts/physiology ; Osteocalcin/genetics ; Osteocalcin/metabolism ; Osteopontin/genetics ; Osteopontin/metabolism ; Promoter Regions, Genetic ; RNA, Small Interfering/genetics ; Signal Transduction ; Transcription, Genetic
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Prkar1a protein, mouse ; RNA, Small Interfering ; Osteocalcin (104982-03-8) ; Osteopontin (106441-73-0)
Language	English
Publishing date	2014-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2013-1152
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Zs.A 2261: Show issues

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Article: Genotype and haplotype determination of IL1B (g. -511C>T and g. +3954C>T) and (IL1RN) in pediatric nephrolithiasis.

Mittal, Rama D / Bid, Hemant K / Manchanda, Parmeet K

Clinica chimica acta; international journal of clinical chemistry

2007 Volume 379, Issue 1-2, Page(s) 42–47

Abstract: Background: Nephrolithiasis is a multifactorial and polygenic disorder characterized by presence of stones in urinary tract. Interleukin1 (IL1) plays role in process of bone loss/hypercalciuria and is involved in formation of kidney stones. We ... ...

Abstract	Background: Nephrolithiasis is a multifactorial and polygenic disorder characterized by presence of stones in urinary tract. Interleukin1 (IL1) plays role in process of bone loss/hypercalciuria and is involved in formation of kidney stones. We investigated the association between IL1B promoter region and exon-5 (g.-511C>T and g. +3954C>T) polymorphism and variable number of tandem repeats in IL1 receptor antagonist, IL1RN (IVS2) with risk of stone formation in childhood nephrolithiasis in north Indian population. Methods: Control group of 60 healthy pediatric individuals (age range =4-16 y) and 50 pediatric nephrolithiasis patients (age range =2-14 y) were studied. Polymorphism was detected by PCR based restriction analysis. Haplotypes for IL1B and IL1RN were constructed using Arlequin v2.0 software. Results: Distribution of IL1RN gene polymorphism demonstrated significant difference (p=0.023). Pediatric patients had significantly higher frequency of allele I in IL1RN (16% vs. 1.7%). The distribution of IL1B (g. -511C>T and g. +3954C>T) genotypes in patients and controls were similar (p=0.263 and 0.694 respectively). There was a significant difference in haplotype frequencies between pediatric patients and control group (p<0.05). Haplotype T-E1-I showed>7-folds risk for nephrolithiasis (p=0.033; OR=7.07, 95% CI=1.16-42.84). Conclusions: Significant association was observed for allele I(*) of IL1RN however, no association was observed for IL1B. Haplotype T-E1-I was significantly associated with higher risk of pediatric nephrolithiasis. These findings suggest that the IL1RN and haplotyping may be an influential marker for susceptibility to pediatric nephrolithiasis.
MeSH term(s)	Adolescent ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Haplotypes ; Humans ; Interleukin-1beta/genetics ; Male ; Nephrolithiasis/genetics ; Polymorphism, Genetic
Chemical Substances	IL1B protein, human ; Interleukin-1beta
Language	English
Publishing date	2007-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2006.12.004
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Ud II Zs.173: Show issues

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Article: Predisposition of genetic polymorphism with the risk of urolithiasis.

Mittal, Rama D / Bid, Hemant K / Manchanda, Parmeet K / Kapoor, Rakesh

Indian journal of clinical biochemistry : IJCB

2008 Volume 23, Issue 2, Page(s) 106–116

Abstract: Urolithiasis is a relevant clinical problem with a subsequent burden for health system. The aim of this review is to provide recent progress made using genetic polymorphisms to define pathophysiology, to identify persons at risk for kidney stone disease ... ...

Abstract	Urolithiasis is a relevant clinical problem with a subsequent burden for health system. The aim of this review is to provide recent progress made using genetic polymorphisms to define pathophysiology, to identify persons at risk for kidney stone disease and to predict treatment response. Population case-control studies are useful both as an alternative and an adjunct as compared to family studies. These involve either whole genome scanning or candidate gene approaches. While whole genome scanning is likely to be widely used in future, at present, candidate gene studies are more feasible. When performing candidate gene case-control studies factors such as study design, methods for recruitment of case and controls, selection of candidate genes, functional significance of polymorphisms chosen for study and statistical analysis require close attention to ensure that only genuine associations are detected. Some of the significant genes that play role in stone formation include calcitonin receptor gene (CTR), vitamin D receptor (VDR), Urokinase, Interleukin, (IL-1β, IL-Ra), E-Cadherin, Androgen & oestrogen receptor gene, vascular endothelial growth factor (VEGF) and Arginine p21. In our case-control study we studied CTR, VDR, Urokinase, IL-1β(-511 and +3954), IL-Ra from north India and predict that VDR, IL-β (-511) and IL-1Ra gene may be used as a possible genetic marker for earlier detection in patients who are at risk for calcium oxalate stone disease. Further, linkage disequilibrium and haplotype structure of a certain candidate gene is important for association analysis. When a certain polymorphic allele has been found to be associated with disease, it is further explained on basis of LD and haplotype structure by one or more other alleles. Once it is determined which haplotype carries the risk allele, by means of molecular biological functional analyses, the variants on that haplotype allele truly causing the effect can be determined.
Language	English
Publishing date	2008-06-11
Publishing country	India
Document type	Journal Article
ZDB-ID	1033583-3
ISSN	0974-0422 ; 0970-1915
ISSN (online)	0974-0422
ISSN	0970-1915
DOI	10.1007/s12291-008-0027-1
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Zs.A 2949: Show issues

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Article: Association of interleukin-1beta gene and receptor antagonist polymorphisms with calcium oxalate urolithiasis.

Mittal, Rama D / Bid, Hemant K / Manchanda, Parmeet K / Kapoor, Rakesh

Journal of endourology

2007 Volume 21, Issue 12, Page(s) 1565–1570

Abstract: Background and purpose: Genetic polymorphisms of the interleukin-1beta (IL-1beta) promoter region (-511) and exon 5 +3954 and a variable number of tandem repeats in the IL receptor antagonist (IL-1RA) gene have been proposed as markers for calcium ... ...

Abstract	Background and purpose: Genetic polymorphisms of the interleukin-1beta (IL-1beta) promoter region (-511) and exon 5 +3954 and a variable number of tandem repeats in the IL receptor antagonist (IL-1RA) gene have been proposed as markers for calcium oxalate urolithiasis. Because the prevalence of these polymorphisms could be influenced by racial variation/ethnicity, we explored the association of IL-1 gene-cluster polymorphisms with stone formation in a north India population. Patients and methods: The case-control study involved 150 stone-free control subjects (mean age 46.5 +/- 10.5 years) and 130 patients (mean age 40.0 +/- 11.5 years) with calcium oxalate urolithiasis. Biallelic polymorphisms of two loci, IL-1beta (-511) and IL-1beta (+3954), as well as the penta-allelic variable number of tandem repeats of IL-1RA, were genotyped by polymerase chain reaction-based restriction analysis. Haplotypes were constructed for the IL-1 gene cluster using SNP Analyzer software. Results: We observed a significant association between stone disease and IL-1beta -511 and IL-1RA polymorphisms (P < 0.001 and P = 0.039, respectively), whereas no association was observed for IL-1beta +3954 (P = 0.408). The frequency of the TT (-511) and I/II (410/240; IL-1RA) genotypes was higher in patients than in control subjects (50/130 v 16/150 and 55/130 v 38/150, respectively), whereas the frequencies of the haplotypes were similar (P = 0.485). Significant linkage disequilibrium showed that three genes were strongly linked (P < 0.0001). Patients with a combination of high IL-1beta (-511 and +3954) and low IL-1RA genotypes were at significantly higher risk for urolithiasis (P < 0.001; odds ratio = 5.448, 0.013, and 2.560, respectively). Conclusion: Our study demonstrated a strong association of IL-1RA and IL-1beta-511 and suggested that differences in the IL-1 gene cluster could be linked to the risk of urolithiasis. A combination of IL-1beta and IL-1RA associations exhibiting gene-gene interaction further substantiates the finding of risk.
MeSH term(s)	Adult ; Calcium Oxalate/urine ; DNA/genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Interleukin 1 Receptor Antagonist Protein/blood ; Interleukin 1 Receptor Antagonist Protein/genetics ; Interleukin-1beta/blood ; Interleukin-1beta/genetics ; Interleukin-1beta/urine ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Retrospective Studies ; Urolithiasis/blood ; Urolithiasis/genetics ; Urolithiasis/urine
Chemical Substances	Interleukin 1 Receptor Antagonist Protein ; Interleukin-1beta ; Calcium Oxalate (2612HC57YE) ; DNA (9007-49-2)
Language	English
Publishing date	2007-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	356931-7
ISSN	1557-900X ; 0892-7790
ISSN (online)	1557-900X
ISSN	0892-7790
DOI	10.1089/end.2007.0071
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Zs.A 2628: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Analysis of polymorphisms of tumor necrosis factor-alpha and polymorphic xenobiotic metabolizing enzymes in inflammatory bowel disease: study from northern India.

Mittal, Rama D / Manchanda, Parmeet K / Bid, Hemant K / Ghoshal, Uday C

Journal of gastroenterology and hepatology

2007 Volume 22, Issue 6, Page(s) 920–924

Abstract: Background: Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine associated with inflammatory diseases, while GSTM1 and T1 enzymes catalyze detoxification of products of oxidative stress and hence reduce inflammation. Thus, both may play ... ...

Abstract	Background: Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine associated with inflammatory diseases, while GSTM1 and T1 enzymes catalyze detoxification of products of oxidative stress and hence reduce inflammation. Thus, both may play important roles in the pathogenesis of inflammatory bowel disease (IBD). The present study aimed to evaluate the effect of polymorphism of the TNF-alpha promoter at the -308 site, GSTM1 and GSTT1 in patients with IBD and healthy controls from northern India. Method: Genotyping was performed in 114 patients with IBD (22 Crohn's disease [CD] and 92 ulcerative colitis [UC]) in TNF-alpha and 105 (20 CD and 85 UC) in GSTM1 and T1 and 164 healthy controls using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and multiplex PCR methods. Results: Patients with IBD were comparable to healthy controls in relation to age and gender. Genotypic and allelic frequencies of TNF-alpha were comparable among patients with IBD and healthy controls. GSTM1 null genotype was more frequent in UC than in healthy controls (52/85 vs 49/164; P < 0.001) and GSTT1 null genotype was more frequent both in UC and CD as compared to healthy controls (77/85 and 18/20 vs 26/164, respectively; P < 0.001 for both). Frequency of combined null genotype in GSTM1 and T1 was more frequently associated with IBD than healthy controls (4/20 vs 8/164; P = 0.029, OR = 4.875 and 28/85 vs 8/164; P < 0.001, OR = 9.579, respectively). Conclusions: 'Null' genotypes of GSTM1 and T1 are associated with IBD and the combination of the two GST genotypes further increases the risk, possibly due to gene-gene interaction. TNF-alpha is unlikely to be an important determinant of susceptibility to IBD in the Indian population.
MeSH term(s)	Alleles ; Case-Control Studies ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Glutathione Transferase/genetics ; Humans ; India ; Inflammatory Bowel Diseases/enzymology ; Inflammatory Bowel Diseases/genetics ; Male ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Risk Factors ; Tumor Necrosis Factor-alpha/genetics
Chemical Substances	Tumor Necrosis Factor-alpha ; glutathione S-transferase T1 (EC 2.5.1.-) ; Glutathione Transferase (EC 2.5.1.18) ; glutathione S-transferase M1 (EC 2.5.1.18)
Language	English
Publishing date	2007-06
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632882-9
ISSN	0815-9319
ISSN	0815-9319
DOI	10.1111/j.1440-1746.2006.04538.x
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Zs.A 2180: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 299: Show issues

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Article: Association of vitamin-D receptor (Fok-I) gene polymorphism with bladder cancer in an Indian population.

Mittal, Rama D / Manchanda, Parmeet K / Bhat, Sanjay / Bid, Hemant K

BJU international

2007 Volume 99, Issue 4, Page(s) 933–937

Abstract: Objective: To explore the association of vitamin-D receptor (VDR) genotypes and haplotypes (variants at the Fok-I, and Taq-I sites) with the risk of bladder cancer, as vitamin D is antiproliferative and reported to induce apoptosis in human bladder ... ...

Abstract	Objective: To explore the association of vitamin-D receptor (VDR) genotypes and haplotypes (variants at the Fok-I, and Taq-I sites) with the risk of bladder cancer, as vitamin D is antiproliferative and reported to induce apoptosis in human bladder tumour cells in vitro. Patients, subjects and methods: A case-control study using polymerase chain reaction-restriction fragment length polymorphism was conducted in 130 patients with bladder cancer and 346 normal healthy individuals in a north Indian population. Patients were also categorized according to grade and stage of tumour. Results: There was a significant difference in genotype and allelic distribution of VDR (Fok-I) polymorphism in the patients (P = 0.033 and = 0.017, respectively). The FF genotype was associated with twice the risk for bladder cancer (odds ratio 2.042, 95% confidence interval, CI, 0.803-5.193). There was no significant difference in genotypic distribution or allelic frequencies of the VDR (Taq-I) polymorphism (P = 0.477 and 0.230) when compared with the controls. The stage and grade of the bladder tumours had no association with VDR (Fok-I and Taq-I) genotypes. There was a significant difference in the frequency distribution of the haplotypes FT and fT (P < 0.001); these haplotypes had a protective effect in the control group (odds ratio 0.167, 95% CI 0.096-0.291, and 0.079, 0.038-0.164). Conclusion: These data suggest that VDR (Fok-I) polymorphism is associated with the risk of bladder cancer. Further, the results for the haplotype FT and fT indicate that patients with this haplotype have a lower risk of developing bladder cancer than those with other haplotypes.
MeSH term(s)	Aged ; Case-Control Studies ; Female ; Genetic Predisposition to Disease/genetics ; Genotype ; Haplotypes/genetics ; Humans ; India/ethnology ; Male ; Middle Aged ; Polymerase Chain Reaction/methods ; Polymorphism, Genetic/genetics ; Receptors, Calcitriol/genetics ; Risk Factors ; Urinary Bladder Neoplasms/ethnology ; Urinary Bladder Neoplasms/genetics
Chemical Substances	Receptors, Calcitriol
Language	English
Publishing date	2007-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1462191-5
ISSN	1464-410X ; 1464-4096 ; 1358-8672
ISSN (online)	1464-410X
ISSN	1464-4096 ; 1358-8672
DOI	10.1111/j.1464-410X.2007.06657.x
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Ui VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Mouse models of endocrine tumours.

Jones, Georgette N / Manchanda, Parmeet K / Pringle, Daphne R / Zhang, Mei / Kirschner, Lawrence S

Best practice & research. Clinical endocrinology & metabolism

2010 Volume 24, Issue 3, Page(s) 451–460

Abstract: Since the onset of the genomic era, there has been tremendous progress in identifying the genetic causes of endocrine tumours. Although this knowledge is valuable in its own right, understanding the molecular basis of tumourigenesis allows the ... ...

Abstract	Since the onset of the genomic era, there has been tremendous progress in identifying the genetic causes of endocrine tumours. Although this knowledge is valuable in its own right, understanding the molecular basis of tumourigenesis allows the development of new therapies targeted at the causative defects. Understanding the connection between genotype and phenotype is a complex process, which can only be partially understood from the analysis of primary tumours or from the studies of cells in vitro. To bridge this gap, genetically modified mice have been developed to allow molecular dissection of the relevant defects in an intact organism. In this article, we discuss the status of genetic modelling for hereditary and sporadic endocrine tumourigenesis with a goal towards providing a view of how this technology will be of future benefit to clinicians developing specifically targeted therapies for endocrine tumours.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Disease Models, Animal ; Endocrine Gland Neoplasms/genetics ; Endocrine Gland Neoplasms/pathology ; Humans ; Mice/genetics
Language	English
Publishing date	2010-09-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2010.01.004
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Article ; Online: Influence of genetic polymorphisms in GSTM1, GSTM3, GSTT1 and GSTP1 on allograft outcome in renal transplant recipients.

Singh, Ranjana / Manchanda, Parmeet K / Kesarwani, Pravin / Srivastava, Aneesh / Mittal, Rama D

Clinical transplantation

2009 Volume 23, Issue 4, Page(s) 490–498

Abstract: Introduction: Glutathione S-transferases (GSTs) are important in protection against xenobiotic compounds and toxicity caused by immunosuppressants in renal transplant recipients. In the present study we hypothesize that genetic variability in GSTM1, ... ...

Abstract	Introduction: Glutathione S-transferases (GSTs) are important in protection against xenobiotic compounds and toxicity caused by immunosuppressants in renal transplant recipients. In the present study we hypothesize that genetic variability in GSTM1, GSTM3, GSTP1 and GSTT1 genes may be associated with allograft outcome. Methods: The study included 223 controls and 273 transplant recipients categorized into 184 stable graft function (SGF), 57 rejection episodes (RE) and 32 delayed graft function (DGF). The polymorphism was studied using multiplex PCR and PCR-RFLP. Results: GSTM1 null genotype showed a 3.35-fold higher risk for rejection in SGF vs. RE category [95% confidence interval (CI) 1.27-8.84, p = 0.014]. Mutant (G) allele of GSTP1 was associated with a 5.52-fold risk for DGF (95% CI 1.37-22.17, p = 0.016). Kaplan-Meier analysis revealed significantly lower mean time to first RE in null genotype as compared with GSTM1 present patients (Log p = 0.002). The dose adjusted C(2) levels in null genotype was higher as compared with GSTM1 present patients at one (p = 0.007) and three months (p = 0.027) post transplantation. Conclusion: Patients with variant genotype of GSTM1 and GSTP1 were at higher risk for rejection and delayed functioning of the allograft, respectively, supporting the hypothesis for involvement of GST isoform variants in allograft outcome in renal transplant recipients.
MeSH term(s)	Adult ; Case-Control Studies ; Delayed Graft Function/genetics ; Female ; Gene Frequency ; Glutathione S-Transferase pi/genetics ; Glutathione Transferase/genetics ; Graft Rejection/genetics ; Graft Survival/genetics ; Humans ; India ; Kaplan-Meier Estimate ; Kidney Transplantation/immunology ; Living Donors ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics
Chemical Substances	glutathione S-transferase T1 (EC 2.5.1.-) ; GSTM3 protein, human (EC 2.5.1.18) ; GSTP1 protein, human (EC 2.5.1.18) ; Glutathione S-Transferase pi (EC 2.5.1.18) ; Glutathione Transferase (EC 2.5.1.18) ; glutathione S-transferase M1 (EC 2.5.1.18)
Language	English
Publishing date	2009-08
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639001-8
ISSN	1399-0012 ; 0902-0063
ISSN (online)	1399-0012
ISSN	0902-0063
DOI	10.1111/j.1399-0012.2009.00985.x
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