Crystal structure of tris(pyridine)(salicylaldehyde semicarbazonato(2-))cobalt(III)-trichloropyridinecobaltate(II) at 293 and 120 K

The crystal structure of [CoIII(L)(py)3][CoIICl3(py)[ (H2L = salicylaldehyde semicarbazone)was determined by X-ray analysis based on two single crystal X-ray experiments performed at 120 K and 293 K, respectively. It was found that the pyridine ligand of the complex anion is disordered over two positions. The preferential position of this pyridine found at120Kwas explained in terms of the C–H...Cl intermolecular interaction between the tetrahedral [CoII(py)Cl3]- anions. The mer-octahedral geometry of the cation in the presented crystal structure was compared with previously published structures of similar composition, [CoIII(L1)(py)3]+[CoIICl3(py)]-·EtOH and [CoIII(LI)(py)3]+I3- (H2LI = salicylaldehyde S-methylisothiosemicarbazone). Although the tetrahedral [CoIICl3(py)]- anions possess the same charge, they mutually form different intermolecular interactions which can be realized either by C–H...Cl hydrogen bonds or by p-p interactions between the pyridine rings

Characteristics of novel myeloid precursor cell line, PC-MDS, established from a bone marrow of the patient with therapy-related myelodysplastic syndrome

We report on characteristics of the first human cell line, PC-MDS, derived from a bone marrow of a patient with therapy-related myelodysplastic syndrome (t-MDS) who had no overt post-MDS leukemia. Classic cytology analyses, immunophenotyping, cytogenetic and molecular genetic procedures were used for characterization of the cell line. PC-MDS cells are positive for the expression of CD13, CD15, CD30, CD33, and CD45 antigen. Positive cytochemical staining and immunophenotype analyses indicated that PC-MDS cells have some characteristics of the early myeloid precursor cell. The karyotype analysis of PC-MDS cell line revealed various numerical and structural changes including those typically associated with t-MDS: del(5)(q13)[7], der(5)t(5;11)(p11;q11)[13], -7[6], del(7)(q31)[2], +20[3], -20[4]. Evaluation of methylation status in a promoter region of p 15, p 16 and MGMT genes showed biallelic hypermethylation pattern of 5 promoter region only in MGMT gene. PC-MDS is the first t-MDS derived cell line, and based on its immunological, cytogenetic and molecular characterization could be a new tool in evaluation of complex biology of MDS and a model for methylation studies. (c) 2007 Elsevier Ltd. All rights reserved

Combined GSTM1-Null, GSTT1-Active, GSTA1 Low-Activity and GSTP1-Variant Genotype Is Associated with Increased Risk of Clear Cell Renal Cell Carcinoma.

The aim of this study was to evaluate specific glutathione S-transferase (GST) gene variants as determinants of risk in patients with clear cell renal cell carcinoma (cRCC), independently or simultaneously with established RCC risk factors, as well as to discern whether phenotype changes reflect genotype-associated risk. GSTA1, GSTM1, GSTP1 and GSTT1 genotypes were determined in 199 cRCC patients and 274 matched controls. Benzo(a)pyrene diolepoxide (BPDE)-DNA adducts were determined in DNA samples obtained from cRCC patients by ELISA method. Significant association between GST genotype and risk of cRCC development was found for the GSTM1-null and GSTP1-variant genotype (p = 0.02 and p<0.001, respectively). Furthermore, 22% of all recruited cRCC patients were carriers of combined GSTM1-null, GSTT1-active, GSTA1-low activity and GSTP1-variant genotype, exhibiting 9.32-fold elevated cRCC risk compared to the reference genotype combination (p = 0.04). Significant association between GST genotype and cRCC risk in smokers was found only for the GSTP1 genotype, while GSTM1-null/GSTP1-variant/GSTA1 low-activity genotype combination was present in 94% of smokers with cRCC, increasing the risk of cRCC up to 7.57 (p = 0.02). Furthermore, cRCC smokers with GSTM1-null genotype had significantly higher concentration of BPDE-DNA adducts in comparison with GSTM1-active cRCC smokers (p = 0.05). GSTM1, GSTT1, GSTA1 and GSTP1 polymorphisms might be associated with the risk of cRCC, with special emphasis on GSTM1-null and GSTP1-variant genotypes. Combined GSTM1-null, GSTT1-active, GSTA1 low activity and GSTP1-variant genotypes might be considered as "risk-carrying genotype combination" in cRCC

<i>GST</i> genotypes in relation to the risk of cRCC.

<p><i>GST</i> genotypes in relation to the risk of cRCC.</p

Baseline characteristic of patients with cRCC and respective controls.

<p>Baseline characteristic of patients with cRCC and respective controls.</p

Combined effect of <i>GST</i> genotypes on risk of cRCC.

<p>Combined effect of <i>GST</i> genotypes on risk of cRCC.</p

<i>GST</i> genotypes in relation to the risk of cRCC.

<p><i>GST</i> genotypes in relation to the risk of cRCC.</p

The association between <i>GST</i> genotypes and the levels of BPDE-DNA adducts in cRCC smokers.

<p>The association between <i>GST</i> genotypes and the levels of BPDE-DNA adducts in cRCC smokers.</p

Combined <i>GSTM1-Null</i>, <i>GSTT1-Active</i>, <i>GSTA1 Low-Activity</i> and <i>GSTP1-Variant</i> Genotype Is Associated with Increased Risk of Clear Cell Renal Cell Carcinoma

<div><p>The aim of this study was to evaluate specific glutathione S-transferase (GST) gene variants as determinants of risk in patients with clear cell renal cell carcinoma (cRCC), independently or simultaneously with established RCC risk factors, as well as to discern whether phenotype changes reflect genotype-associated risk. <i>GSTA1</i>, <i>GSTM1</i>, <i>GSTP1</i> and <i>GSTT1</i> genotypes were determined in 199 cRCC patients and 274 matched controls. Benzo(a)pyrene diolepoxide (BPDE)-DNA adducts were determined in DNA samples obtained from cRCC patients by ELISA method. Significant association between <i>GST</i> genotype and risk of cRCC development was found for the <i>GSTM1-null</i> and <i>GSTP1-variant</i> genotype (p = 0.02 and p<0.001, respectively). Furthermore, 22% of all recruited cRCC patients were carriers of combined <i>GSTM1-null</i>, <i>GSTT1-active</i>, <i>GSTA1-low activity</i> and <i>GSTP1-variant</i> genotype, exhibiting 9.32-fold elevated cRCC risk compared to the reference genotype combination (p = 0.04). Significant association between <i>GST</i> genotype and cRCC risk in smokers was found only for the <i>GSTP1</i> genotype, while <i>GSTM1-null/GSTP1-variant/GSTA1 low-activity</i> genotype combination was present in 94% of smokers with cRCC, increasing the risk of cRCC up to 7.57 (p = 0.02). Furthermore, cRCC smokers with <i>GSTM1-null</i> genotype had significantly higher concentration of BPDE-DNA adducts in comparison with <i>GSTM1-active</i> cRCC smokers (p = 0.05). <i>GSTM1</i>, <i>GSTT1</i>, <i>GSTA1</i> and <i>GSTP1</i> polymorphisms might be associated with the risk of cRCC, with special emphasis on <i>GSTM1-null</i> and <i>GSTP1-variant</i> genotypes. Combined <i>GSTM1-null</i>, <i>GSTT1-active</i>, <i>GSTA1 low activity</i> and <i>GSTP1-variant</i> genotypes might be considered as “risk-carrying genotype combination” in cRCC.</p></div