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ABSTRACT: Sugarcane mosaic virus (SCMV) is one of the devastating virus diseases of maize in the world. Understanding the genetic of
resistance gene(s) is the basis for effective selection in resistance breeding program. In this study, analyses were conducted
to determine the genetic basis in line Siyi with tropic germplasm conferring complete resistance to SCMV. Based on the responses
of parents and F1, F2 and backcross populations in three successive years’ field trails, two dominant complementary genes, were found to condition
the resistance by Mendelian genetic analysis. The two genes were mapped on chromosome 3 and chromosome 6, respectively using
microsatellite markers. The resistance gene on chromosome 3 (bin 3.04/05) was flanked by simple sequence repeat markers umc1527
and phi053 with the genetic distances of 1.8 and 2.1cM, respectively; whereas the genetic distances between the two flanking
markers umc2311 and bnlg1371 and resistance gene on chromosome 6 (bin 6.00/01) was 2.1 and 1.5cM, respectively. Genotypic
analysis of the plants from backcross and F3 populations also validated the two genes with the unique genetic model. For further confirming the interaction between the
two genes, a set of near isogenic lines (NILs) carrying different number of the resistance genes were developed, genotypic
analysis of NILs clearly show that two dominant complementary genes cooperatively control the resistance to SCMV in maize.
Euphytica 04/2012; 156(3):355-364. · 1.55 Impact Factor
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Zhi-Min Li,
Jun-Qiang Ding,
Rui-Xia Wang,
Jia-Fa Chen,
Xiao-Dong Sun,
Wei Chen,
Wei-Bin Song,
Hua-Fang Dong,
Xiao-Dong Dai,
Zong-Liang Xia, Jian-Yu Wu
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ABSTRACT: Understanding the inheritance of resistance to Fusarium ear rot is a basic prerequisite for an efficient resistance breeding in maize. In this study, 250 recombinant inbred lines (RILs) along with their resistant (BT-1) and susceptible (N6) parents were planted in Zhengzhou with three replications in 2007 and 2008. Each line was artificially inoculated using the nail-punch method. Significant genotypic variation in response to Fusarium ear rot was detected in both years. Based on a genetic map containing 207 polymorphic simple sequence repeat (SSR) markers with average genetic distances of 8.83 cM, the ear rot resistance quantitative trait loci (QTL) were analyzed by composite interval mapping with a mixed model (MCIM) across the environments. In total, four QTL were detected on chromosomes 3, 4, 5, and 6. The resistance allele at each of these four QTL was contributed by resistant parent BT-1, and accounted for 2.5-10.2% of the phenotypic variation. However, no significant epistasis interaction effect was detected after a two-dimensional genome scan. Among the four QTL, one QTL with the largest effect on chromosome 4 (bin 4.06) can be suggested to be a new locus for resistance to Fusarium ear rot, which broadens the genetic base for resistance to the disease and can be used for further genetic improvement in maize-breeding programs.
Journal of applied genetics 05/2011; 52(4):403-6. · 1.66 Impact Factor
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ABSTRACT: To evaluate the efficacy and safety of bevacizumab plus capecitabine in treating metastatic colorectal cancer(mCRC).
Eleven patients with mCRC (6 females and 5 males) were enrolled in this study. Bevacizumab was given with 5 mg/kg every two weeks in five patients, 10 mg/kg every two weeks in four patients and 15 mg/kg every three weeks in two patients. All patients received capecitabine 2000 mg/m2 per day for 14 days.
Five of 11 patients had partial response and five patients had stable disease and two patients had progressive disease. The disease control rate was 90.9%. The progress-free survival were 4 months and the median overall survival time were 15 months. The adverse events related to bevacizumab were grade 2 hypertension in 3 patients (27.3%) and grade 1 or 2 proteinuria in 4 patients (36.4%). Other adverse events such as mucositis, fatigue, subcutaneous haemorrhage were also observed. No thromboembolism or severe haemorrhage happened. No other grade 3 or 4 adverse events were observed.The adverse events in the combined therapy were hand-foot-syndrome (54.6%), diarrhea (27.3%), and neutropenia (18.2%), mainly due to capecitabine.
The combination of bevacizumab plus capecitabine has definite benefit in patients with mCRC. However,these benefits can not be maintained after the withdrawal of bevacizumab. The adverse drug reactions are well tolerated.
Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 08/2010; 32(4):417-20.
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ABSTRACT: Test weight is an important trait in maize breeding. Understanding the genetic mechanism of test weight is important for effective selection of maize test weight improvement. In this study, quantitative trait loci (QTL) for maize test weight were identified. In the years 2007 and 2008, a F(2:3) population along with the parents Chang7-2 and Zheng58 were planted in Zhengzhou, People's Republic of China. Significant genotypic variation for maize test weight was observed in both years. Based on the genetic map containing 180 polymorphic SSR markers with an average linkage distance of 11.0 cM, QTL for maize test weight were analysed by mixed-model composite interval mapping. Five QTL, including four QTL with only additive effects, were identified on chromosomes 1, 2, 3, 4 and 5, and together explained 25.2% of the phenotypic variation. Seven pairs of epistatic interactions were also detected, involving 11 loci distributed on chromosomes 1, 2, 3, 4, 5 and 7, respectively, which totally contributed 18.2% of the phenotypic variation. However, no significant QTL x environment (QxE) interaction and epistasis x environment interaction effects were detected. The results showed that besides the additive QTL, epistatic interactions also formed an important genetic basis for test weight in maize.
Journal of Genetics 04/2010; 90(1):75-80. · 1.09 Impact Factor
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ABSTRACT: bevacizumab is a humanized recombinant vascular endothelial growth factor (VEGF) monoclonal antibody, which specifically binds to VEGF and inhibits tumor cell growth, proliferation and metastasis. We aimed to investigate the safety and pharmacokinetics of bevacizumab in Chinese patients with advanced cancer.
Thirty-nine Chinese patients with metastatic or relapsed cancers who failed prior therapy were enrolled in this phase I study of bevacizumab. Bevacizumab was infused by a calculated pump at doses from 5 mg/kg to 15 mg/kg in 90 minutes. Patients underwent serial pharmacokinetic evaluations. Patients that received at least one infusion of bevacizumab were included in the safety study.
Thirty-five patients finished all 5 infusions following protocol. One patient withdrew after 3 infusions due to grade 3 proteinuria. Common adverse events possibly related to the study drug were proteinuria (17/39, 43.6%), hypertension (13/39, 33.3%), gingival bleeding (7/39, 17.9%), epistaxis (6/39, 15.4%), pharyngeal inflammation (6/39, 15.4%), fatigue (6/39, 15.4%) and stomatitis (4/39, 10.3%). Bevacizumab pharmacokinetics was linear within the range of 5 mg/kg q2w--10 mg/kg q2w and 15 mg/kg q3w. CL (clearance), Vd (volume of distribution at elimination) and Vss (volume of distribution at steady state) were similar after single and multiple doses at 5, 10 and 15 mg/kg.
Bevacizumab is well tolerated in Chinese patients. No unexpected adverse events were observed. There is no racial difference in the pharmacokinetics.
Chinese medical journal 04/2010; 123(7):901-6. · 0.86 Impact Factor
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ABSTRACT: Mutations in tumor-suppressor gene BARD1 have been found in inherited and spontaneous breast, ovarian and uterine cancers. BARD1 plays a critical role in DNA repair and ubiquitination as binding partner of BRCA1, with which it colocalizes to nuclear dots. Independently of BRCA1, BARD1 can induce p53-dependent apoptosis in response to genotoxic stress. Therefore, BARD1 or p53 might be defective in cancer cells spared from apoptosis. We investigated BARD1 and p53 expression in ovarian, breast and non-small-cell lung cancers. BARD1 expression was highly upregulated and cytoplasmic in most cancer cells, while weak nuclear staining was observed in the surrounding normal tissue. Maximal BARD1 expression was associated with the most malignant ovarian cancer, clear cell carcinoma. In breast cancer, BARD1 expression was correlated with poor differentiation and large tumor size, established factors of poor prognosis, as well as short disease-free survival. In contrast to breast and ovarian cancers, no correlation of BARD1 expression with either grade or stage could be determined for lung cancer. RT-PCR, performed on 10 ovarian cancers, revealed absence of the 5' portion of the BARD1 transcript in 7 tumors, and sequencing of the remaining 3 identified a missense mutation (A1291G) resulting in an amino acid change of glutamine 406 to arginine. These data suggest that genetic and epigenetic changes might lead to elevated cytoplasmic expression of BARD1 and that cytoplasmic BARD1 might be a poor prognostic factor for breast and ovarian cancers.
International Journal of Cancer 04/2006; 118(5):1215-26. · 5.44 Impact Factor
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ABSTRACT: The BRCA1-associated RING domain protein BARD1 acts with BRCA1 in double-strand break repair and ubiquitination. BARD1 plays a role as mediator of apoptosis by binding to and stabilizing p53, and BARD1-repressed cells are resistant to apoptosis. We therefore investigated the mechanism by which BARD1 induces p53 stability and apoptosis. The apoptotic activity of p53 is regulated by phosphorylation. We demonstrate that BARD1 binds to unphosphorylated and serine-15 phosphorylated forms of p53 in several cell types and that the region required for binding comprises the region sufficient for apoptosis induction. In addition, BARD1 binds to Ku-70, the regulatory subunit of DNA-PK, suggesting that the mechanism of p53-induced apoptosis requires BARD1 for the phosphorylation of p53. Upregulation of BARD1 alone is sufficient for stabilization of p53 and phosphorylation on serine-15, as shown in nonmalignant epithelial cells and ovarian cancer cells, NuTu-19, which are defective in apoptosis induction and express aberrant splice variants of BARD1. Stabilization and phosphorylation of p53 in NuTu-19 cells, as well as apoptosis, can be induced by the exogenous expression of wild-type BARD1, suggesting that BARD1, by binding to the kinase and its substrate, catalyses p53 phosphorylation.
Oncogene 06/2005; 24(23):3726-36. · 6.37 Impact Factor
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ABSTRACT: Maize dwarf mosaic is one of the devastating and widespread viral diseases in the world. So far, only a few genes were identified and mapped in the resistant materials. A new resistant elite inbred line Siyi was identified with resistance to maize dwarf mosaic virus strain B at early and adult stage. Two complementary dominant genes conditioned the resistance, with a new genetic model, of the maize inbred line were found at adult stage by the genetic analysis based on parents, F1, F2 and backcrosses in two years. The microsatellite analysis of a F2 population from the cross between Siyi and Mo17 was used to identify the two resistance genes on chromosome 3 and 6 respectively by 87 pairs of microsatellite markers. The linkage distance between phi029 and the one resistance gene on chromosome 3 is 14.5 cM, and phi126 to the other on chromosome 6 is 7.2 cM.
Acta Genetica Sinica 01/2003; 29(12):1095-9.
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Jian-Yu Wu
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ABSTRACT: Le complexe BARD1-BRCA1 joue un rôle dans la réparation de l'ADN et dans l'ubiquitination. BARD1 seule peut induire l'apoptose en présence de p53. Comme la réparation de l'ADN et l'apoptose sont des fonctions anti-tumorales qui sont souvent défectueuses dans des cellules cancéreuses, nous avons déterminé les niveaux d'expression de BARD1 et de p53 dans des tissus de cancer d'ovaire et du sein. BARD1 est sur-exprimée dans des cellules cancéreuses et localisée dans le cytoplasme. L'expression maximale de BARD1 est associée au cancer ovarien le plus invasif, le "carcinome des cellules claires". Dans le cancer du sein, l'expression de BARD1 est corrélée avec une tumeur peu différentiée, de grande taille et une baisse de la survie des patientes. Nos données suggèrent que des cancers expriment une forme de BARD1 ayant perdu sa fonction "suppresseur de tumeurs" et la présence cytoplasmique de BARD1 est un facteur pronostique défavorable pour les cancers du sein et de l'ovaire.
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Jian-Yu. Wu
