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Haisheng You - One of the best experts on this subject based on the ideXlab platform.
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association between loss of heterozygosity of Chromosome 16q and survival in wilms tumor a meta analysis
Pathology Research and Practice, 2018Co-Authors: Di Fan, Zhenyu Pan, Jun Lyu, Haisheng YouAbstract:BACKGROUND Wilms' tumor (WT) is the most common pediatric renal tumor. Despite its high survival rate, the potential prognostic factors should further be studied to reduce the intensity of the treatment. A few studies have found LOH of 16q is associated with worse survival in patients with WT, but it is still contradictory. This study aimed to performed a meta-analysis to clarify this. METHODS Databases including the Wanfang, PubMed, Chinese National Knowledge Infrastructure, Embase, and Cochrane Library databases were searched July 2018. The meta-analysis was done using Stata (version 14.0). Publication bias was evaluated by funnel plots, Begg's test, and Egger's test. The trim-and-fill method was applied if significant publication bias existed. Sensitivity analysis was performed to evaluate the stability of the results. RESULTS This meta-analysis identified 9 cohort studies encompassing 3266 cases. The pooled relative risk when comparing LOH of 16q groups with control groups was 2.22 [95% confidence interval (CI) = 1.64-3.00, P < 0.001], and the pooled hazard ratio was 1.92 (95%CI = 1.32-2.80, P = 0.001). The results were stable after correcting for publication bias and performing a leave-one-out sensitivity analysis. CONCLUSIONS This meta-analysis indicated that LOH of 16q was significantly associated with worse survival in WT. Further studies need to identify this conclusion because the overall quality of the included studies is not high, investigate the impact of LOH of 16q on the survival of WT patients in different subgroups and identify better treatments for WT patients with LOH of 16q in order to lengthen their survival.
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Association between loss of heterozygosity of Chromosome 16q and survival in Wilms' tumor: A meta-analysis.
Pathology - Research and Practice, 2018Co-Authors: Di Fan, Zhenyu Pan, Jun Lyu, Haisheng YouAbstract:BACKGROUND Wilms' tumor (WT) is the most common pediatric renal tumor. Despite its high survival rate, the potential prognostic factors should further be studied to reduce the intensity of the treatment. A few studies have found LOH of 16q is associated with worse survival in patients with WT, but it is still contradictory. This study aimed to performed a meta-analysis to clarify this. METHODS Databases including the Wanfang, PubMed, Chinese National Knowledge Infrastructure, Embase, and Cochrane Library databases were searched July 2018. The meta-analysis was done using Stata (version 14.0). Publication bias was evaluated by funnel plots, Begg's test, and Egger's test. The trim-and-fill method was applied if significant publication bias existed. Sensitivity analysis was performed to evaluate the stability of the results. RESULTS This meta-analysis identified 9 cohort studies encompassing 3266 cases. The pooled relative risk when comparing LOH of 16q groups with control groups was 2.22 [95% confidence interval (CI) = 1.64-3.00, P
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Loss of heterozygosity on Chromosome 16q increases relapse risk in Wilms’ tumor: a meta-analysis
Oncotarget, 2017Co-Authors: Zhenyu Pan, Lina Tang, Hua Cheng, Anmin Wang, Jun Lyu, Haisheng YouAbstract:// Zhenyu Pan 1, 2, * , Hairong He 1, * , Lina Tang 3 , Qingting Bu 4 , Hua Cheng 2 , Anmin Wang 2 , Jun Lyu 1 and Haisheng You 3 1 Clinical Research Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi’an, Shaanxi, 710061, China 2 Department of Pharmacy, Xi’an Jiaotong University Affiliated Children’s Hospital, Xi’an, Shaanxi, 710003, China 3 Department of Pharmacy, The First Affiliated Hospital of Xi'an Jiaotong University, Xi’an, Shaanxi, 710061, China 4 Department of Genetics, Northwest Women’s and Children’s Hospital, Xi’an, Shaanxi, 710061, China * Authors contributed equally to this work Correspondence to: Haisheng You, email: haishengyou77@163.com Jun Lyu, email: lujun2006@xjtu.edu.cn Keywords: Wilms’ tumor, LOH 16q, relapse, meta-analysis Received: June 28, 2017 Accepted: August 06, 2017 Published: August 11, 2017 ABSTRACT Wilms’ tumor (WT) is the most frequent malignant renal tumor in children. The survival rate is lower in patients with recurrence, and the factors that influence relapse in WT are not fully understood. Loss of heterozygosity on Chromosome 16q (LOH 16q) has been reported to be associated with the relapse in WT, but this remains controversial. We performed a meta-analysis to clarify this. PUBMED, EMBASE, and the Cochrane Library were searched up to March 17, 2017. Ten studies involving 3385 patients were ultimately included in the meta-analysis. The meta-analysis showed that LOH 16q was significantly associated with the relapse in WT (relative risk [RR] = 1.74, 95% confidence interval [CI] = 1.43–2.13, P < 0.00001; hazard ratio [HR] = 1.76, 95% CI = 1.38–2.24, P < 0.00001). No significant heterogeneity among studies or publication bias was found. Sensitivity analysis showed omitting one study in each turn could not change the results. Subgroup analysis based on two studies indicated LOH 16q was more effective on elevated replase risk in patients with favorable-histology WT (RR = 2.52, 95% CI = 1.68–3.78, P < 0.00001; HR = 2.99, 95% CI = 1.84–4.88, P < 0.0001) but further work are needed to confirm this. These findings confirm that LOH 16q increased the relapse risk in WT, but more studies are required to further assess the association between LOH 16q and WT relapse among different subgroups.
H Tsuda - One of the best experts on this subject based on the ideXlab platform.
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Loss of heterozygosity on Chromosome 16q suggests malignancy in core needle biopsy specimens of intraductal papillary breast lesions
Virchows Archiv, 2012Co-Authors: Miwa Yoshida, H Tsuda, Sadako Akashi-tanaka, Sohei Yamamoto, Takayuki Kinoshita, Takashi Hojo, Takashi FukutomiAbstract:It is often difficult to make a definitive diagnosis of papillary breast lesions using core needle biopsy (CNB) specimens. We studied loss of heterozygosity (LOH) on Chromosome 16q in order to assess its diagnostic use for papillary breast lesions in CNB specimens. Of 25 patients with intraductal papillary breast tumors, we extracted DNA from paired samples of tumor cells from CNB specimens and non-tumor cells from subsequent excision specimens and analyzed LOH at the D16S419 and D16S514 loci on Chromosome 16q. LOH analysis results were compared with final diagnoses based on pathological features of the resected specimens. On the CNB specimens, 21 tumors were histologically diagnosed as indeterminate or suspicious for malignancy, while four tumors were unambiguously malignant. Of the 21 indeterminate or suspicious tumors, 11 were finally diagnosed as benign and ten as malignant, and on these, LOH analyses were informative for 8 of the 11 benign tumors and 7 of the 10 malignant tumors. LOH was also informative on two of the four tumors unambiguously malignant on CNB. None of the eight informative benign tumors showed LOH on 16q. Six of the eleven informative malignant tumors showed LOH on 16q. LOH on 16q was significantly different between CNB specimens of benign and malignant intraductal papillary tumors ( P = 0.007). Analysis of LOH on 16q may be helpful in making a definitive diagnosis in cases of papillary breast lesions, in both excised and CNB specimens.
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Intracystic invasive papillary carcinoma of the male breast with analyses of loss of heterozygosity on Chromosome 16q.
Breast Cancer, 2009Co-Authors: Miwa Yoshida, Takashi Fukutomi, Sohei Yamamoto, Yukako Mouri, Kyoko Yorozuya, Kimihito Fujii, Shogo Nakano, Kazuo Hara, H TsudaAbstract:A 64-year-old man noticed a right subareolar mass in May 2005. On physical examination, an oval-shaped, well-circumscribedthe tumor (6.0 × 5.5 cm in size) was located just beneath the right nipple. The tumor was elastic, firm and freely movable. Neither axillary nor supraclavicular lymph nodes were palpable. Mammography demonstrated a 5 × 5-cm, relatively distinct and dense mass without microcalcifications or spiculations. There were no findings of concurrent gynecomastia. Ultrasonography revealed a large multilocular cyst with a mural hypoechoic protruding lesion exhibiting wide-based morphology with an irregular margin. On contrast-enhanced computed tomography, the inner lesion enhanced, but direct invasion of the tumor to the major pectoral muscle was not found. An intracystic papillary lesion, possibly papillary carcinoma, was suspected. In December 2007, wide excision of the tumor was performed. On histopathological examination, the tumor had a papillary pattern with a small cribriform component in the cystic wall with microinvasion of the stroma. Marginal status was negative. The final diagnosis of the disease was a microinvasive intracystic papillary carcinoma of low grade without axillary lymph node metastases. Immunohistochemically, estrogen receptor and progesterone receptor were both positive, but negative for HER-2 protein. No LOH on 16q could be detected. The prognosis of the disease was unclear; however, the malignant potential of this condition may be more clearly determined by studying the LOH on Chromosome 16q.
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Pattern of Chromosome 16q loss differs between an atypical proliferative lesion and an intraductal or invasive ductal carcinoma occurring subsequently in the same area of the breast.
Modern Pathology, 2001Co-Authors: H Tsuda, Takashi Fukutomi, Teruko Takarabe, Sadako Akashi-tanaka, Setsuo HirohashiAbstract:Pattern of Chromosome 16q Loss Differs between an Atypical Proliferative Lesion and an Intraductal or Invasive Ductal Carcinoma Occurring Subsequently in the Same Area of the Breast
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Pattern of Chromosome 16q Loss Differs between an Atypical Proliferative Lesion and an Intraductal or Invasive Ductal Carcinoma Occurring Subsequently in the Same Area of the Breast
Modern Pathology, 2001Co-Authors: H Tsuda, Takashi Fukutomi, Teruko Takarabe, Sadako Akashi-tanaka, Setsuo HirohashiAbstract:Atypical proliferative lesions of the breast, such as atypical ductal hyperplasia and atypical papilloma, are considered to be precursors of breast carcinomas and have frequently been shown to have loss of heterozygosity (LOH) on Chromosome 16q at the DNA level. We evaluated whether an atypical proliferative lesion and a carcinoma that subsequently occurred in the same area of the ipsilateral breast were of identical clonal origin in seven patients. Using DNA isolated from microdissected archival tissue of epithelial components of both the biopsy specimen of the atypical proliferative lesion and the mastectomy specimen of the carcinoma, the pattern of LOH on 16q was compared between these two lesions using polymerase chain reaction –microsatellite LOH analysis. As a control, LOH on 16q was examined in 13 cases of usual ductal hyperplasia, 10 usual papillomas, and 6 atypical ductal hyperplasias. In the seven cases, LOH on 16q was detected in three of the six atypical proliferative lesions and in five of the seven carcinomas, but the allele with LOH or a deleted region always differed between the two. LOH was detected in both atypical proliferative lesions and carcinomas in one case, only in the atypical proliferative lesion in two cases, and only in carcinomas in three cases. In the controls, LOH on 16q was absent in usual ductal hyperplasias or usual papillomas but was detected in two of six atypical ductal hyperplasias. Although atypical proliferative lesions were frequently confirmed to be of clonal nature with LOH on 16q, these lesions and carcinomas were considered to be clones, probably originated from a field with these clones.
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Detection of Allele Loss on Chromosome 16q in DNA Isolated from Fine Needle Aspiration Specimens of Breast Tumors
Acta Cytologica, 1996Co-Authors: H Tsuda, Chinami Sakamaki, Kayako Shimamura, Setsuo HirohashiAbstract:OBJECTIVE: To clarify whether analysis of loss of heterozygosity (LOH) on Chromosome 16q is possible using DNA isolated from fine needle aspiration specimens, a simulation study was performed using resected biopsy or mastectomy specimens of 37 breast carcinomas and 3 fibroadenomas. STUDY DESIGN: A highly polymorphic (AC) n repeat region on the D16S305 locus on Chromosome 16q24 was amplified in the DNA samples by the polymerase chain reaction (PCR) using 32 P-labeled oligonucleotide primers, and the PCR products were electrophoresed in dematuring gel for detection of LOH by autoradiography. RESULTS: PCR was successful in 34 cases, and LOH was detected in 10 (71%) of 14 carcinomas but not in the 3 fibroadenomas. These results were almost always compatible with the data obtained by restriction fragment length polymorphism analysis on Chromosome 16q using Southern blotting. CONCLUSION: Examination of LOH on 16q by (AC) n polymorphism analysis using fine needle aspiration specimens is suggested as a supportive tool for preoperative diagnosis of breast tumors
Setsuo Hirohashi - One of the best experts on this subject based on the ideXlab platform.
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Pattern of Chromosome 16q loss differs between an atypical proliferative lesion and an intraductal or invasive ductal carcinoma occurring subsequently in the same area of the breast.
Modern Pathology, 2001Co-Authors: H Tsuda, Takashi Fukutomi, Teruko Takarabe, Sadako Akashi-tanaka, Setsuo HirohashiAbstract:Pattern of Chromosome 16q Loss Differs between an Atypical Proliferative Lesion and an Intraductal or Invasive Ductal Carcinoma Occurring Subsequently in the Same Area of the Breast
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Pattern of Chromosome 16q Loss Differs between an Atypical Proliferative Lesion and an Intraductal or Invasive Ductal Carcinoma Occurring Subsequently in the Same Area of the Breast
Modern Pathology, 2001Co-Authors: H Tsuda, Takashi Fukutomi, Teruko Takarabe, Sadako Akashi-tanaka, Setsuo HirohashiAbstract:Atypical proliferative lesions of the breast, such as atypical ductal hyperplasia and atypical papilloma, are considered to be precursors of breast carcinomas and have frequently been shown to have loss of heterozygosity (LOH) on Chromosome 16q at the DNA level. We evaluated whether an atypical proliferative lesion and a carcinoma that subsequently occurred in the same area of the ipsilateral breast were of identical clonal origin in seven patients. Using DNA isolated from microdissected archival tissue of epithelial components of both the biopsy specimen of the atypical proliferative lesion and the mastectomy specimen of the carcinoma, the pattern of LOH on 16q was compared between these two lesions using polymerase chain reaction –microsatellite LOH analysis. As a control, LOH on 16q was examined in 13 cases of usual ductal hyperplasia, 10 usual papillomas, and 6 atypical ductal hyperplasias. In the seven cases, LOH on 16q was detected in three of the six atypical proliferative lesions and in five of the seven carcinomas, but the allele with LOH or a deleted region always differed between the two. LOH was detected in both atypical proliferative lesions and carcinomas in one case, only in the atypical proliferative lesion in two cases, and only in carcinomas in three cases. In the controls, LOH on 16q was absent in usual ductal hyperplasias or usual papillomas but was detected in two of six atypical ductal hyperplasias. Although atypical proliferative lesions were frequently confirmed to be of clonal nature with LOH on 16q, these lesions and carcinomas were considered to be clones, probably originated from a field with these clones.
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Detection of Allele Loss on Chromosome 16q in DNA Isolated from Fine Needle Aspiration Specimens of Breast Tumors
Acta Cytologica, 1996Co-Authors: H Tsuda, Chinami Sakamaki, Kayako Shimamura, Setsuo HirohashiAbstract:OBJECTIVE: To clarify whether analysis of loss of heterozygosity (LOH) on Chromosome 16q is possible using DNA isolated from fine needle aspiration specimens, a simulation study was performed using resected biopsy or mastectomy specimens of 37 breast carcinomas and 3 fibroadenomas. STUDY DESIGN: A highly polymorphic (AC) n repeat region on the D16S305 locus on Chromosome 16q24 was amplified in the DNA samples by the polymerase chain reaction (PCR) using 32 P-labeled oligonucleotide primers, and the PCR products were electrophoresed in dematuring gel for detection of LOH by autoradiography. RESULTS: PCR was successful in 34 cases, and LOH was detected in 10 (71%) of 14 carcinomas but not in the 3 fibroadenomas. These results were almost always compatible with the data obtained by restriction fragment length polymorphism analysis on Chromosome 16q using Southern blotting. CONCLUSION: Examination of LOH on 16q by (AC) n polymorphism analysis using fine needle aspiration specimens is suggested as a supportive tool for preoperative diagnosis of breast tumors
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Identification of Multiple Breast Cancers of Multicentric Origin by Histological Observations and Distribution of Allele Loss on Chromosome 16q
Cancer research, 1995Co-Authors: H Tsuda, Setsuo HirohashiAbstract:Breast cancer is often detected as multiple lesions clinically and/or histopathologically. To examine if the origin of such lesions can be identified objectively by comparison of their loss of heterozygosity (LOH) patterns, LOH on Chromosome 16q was analyzed in a total of 60 cases of multiple breast cancer by Southern blot analysis. Based on continuity among tumors and satellite nodule features, 30 cases of unilateral multiple cancer were classified morphologically into 3 groups: A, multicentric origin (11 cases); B, multifocal invasion of one intraductal carcinoma (15 cases); and C, intramammary metastases (4 cases). As controls, group D, synchronously bilateral breast cancers (11 cases), and group E, sets of a primary tumor and a lymph node metastasis (19 cases), were also examined. On a highly probable assumption that LOH on 16q occurs randomly in 50% of breast cancer cases at an early stage, the number of cases showing a concordant LOH pattern on 16q among tumors was compared between observed data, and the value was estimated from a normal distribution model in each group. In groups A and D, the allele pattern on 16q among tumors was concordant in 5 of 11 cases each, thus supporting their independent occurrence and multicentric origin, whereas the LOH pattern among tumors was identical in all of the cases in groups B, C, and E, thus supporting their monocentric origin. This comparison of the LOH pattern in multiple breast cancer was shown to yield results compatible with the morphological classification and was suggested to be of diagnostic value.
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Different incidence of loss of heterozygosity on Chromosome 16q between intraductal papilloma and intracystic papillary carcinoma of the breast.
Japanese Journal of Cancer Research, 1994Co-Authors: H Tsuda, Yoshio Uei, Takashi Fukutomi, Setsuo HirohashiAbstract:Loss of heterozygosity (LOH) on Chromosome 16q was examined in DNA isolated from 11 intraductal papillomas and 12 intracystic papillary adenocarcinomas of the breast. Such LOH was detected in 8 (67%) out of 12 intracystic papillary adenocarcinomas, and in 7 (64%) of 11 of these adenocarcinomas of low grade atypia (Grade 1), whereas it was not detected in 11 intraductal papillomas. Therefore, inactivation of tumor-suppressor genes on Chromosome 16q was suggested to be involved in acquisition of malignant phenotype rather than in tumorigenesis in mammary gland epithelial cell. Examination of LOH on 16q should be helpful for differential diagnosis of intracystic papillary tumors.
James E. Hixson - One of the best experts on this subject based on the ideXlab platform.
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A Quantitative Trait Locus on Chromosome 16q Influences Variation in Plasma HDL-C Levels in Mexican Americans
Arteriosclerosis Thrombosis and Vascular Biology, 2003Co-Authors: Michael C. Mahaney, Laura Almasy, David L. Rainwater, John L. Vandeberg, Shelley A. Cole, James E. Hixson, John Blangero, Jean W. MaccluerAbstract:Objective— We conducted a whole-genome, multipoint linkage screen to localize a previously reported major locus accounting for 56% to 67% of the additive genetic effects on covariate-adjusted plasma HDL cholesterol (HDL-C) levels in Mexican Americans from the San Antonio Family Heart Study (SAFHS). Methods and Results— After using complex segregation analysis to recover the major locus in 472 SAFHS participants from 10 genotyped families, we incorporated covariates required to detect that major locus, including plasma levels of triglycerides and apolipoprotein A-I, in a maximum-likelihood-based variance-components linkage screen. Only Chromosome 16 exhibited convincing evidence for a quantitative trait locus (QTL), with a peak multipoint log of the odds (LOD)=3.73 ( P =0.000034). Subsequent penetrance model-based linkage analysis, incorporating genotypes at the marker locus nearest the multipoint peak (D16S518) into the segregation model, detected linkage with the previously detected major locus (LOD=2.73, P =0.000642). Initial estimates place this QTL within a 15-cM region of Chromosome 16q near the structural loci for lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). Conclusions— A QTL influencing plasma levels of HDL-C in Mexican Americans from San Antonio maps to a region of human Chromosome 16q near LCAT and CETP .
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Genes influencing variation in serum osteocalcin concentrations are linked to markers on Chromosomes 16q and 20q
Journal of Clinical Endocrinology & Metabolism, 2000Co-Authors: Braxton D. Mitchell, Shelley A. Cole, John Blangero, Jean W. Maccluer, Richard L. Bauer, Stephen J. Iturria, Edgar A. Rodriguez, James E. HixsonAbstract:Osteocalcin (OC) is an important constituent of bone that is synthesized by osteoblasts. Serum levels of OC have been used as a biochemical marker of bone turnover. To identify the genes influencing variation in serum OC levels, we conducted a genome-wide scan in 429 individuals comprising 10 large multigenerational families. OC levels were measured by immunoassay, and genetic markers were typed at approximately 10-cM intervals across the genome. Quantitative trait linkage was tested using a multipoint analysis based on variance component methodology, adjusting for the effects of age, sex, and oral contraceptive use. Significance levels for linkage were obtained empirically, by Monte Carlo simulation. The heritability of OC levels in this population was 62 ± 8%. We detected significant evidence for linkage between a quantitative trait locus influencing serum OC levels and markers on Chromosome 16q, and suggestive evidence for linkage of OC levels with markers on Chromosome 20q. The multipoint lod scores p...
Perry E. Telzerow - One of the best experts on this subject based on the ideXlab platform.
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Loss of heterozygosity for Chromosomes 16q and 1p in Wilms' tumors predicts an adverse outcome
Cancer Research, 1994Co-Authors: Paul E Grundy, Perry E. Telzerow, Norman Breslow, Jamie Moksness, Vicki Huff, Malcolm C. PatersonAbstract:Abstract We have prospectively analyzed Wilms9 tumors from 232 patients registered on the National Wilms9 Tumor Study for loss of heterozygosity (LOH) on Chromosomes 11p, 16q, and 1p. These chromosomal aberrations were found in 70 (33%), 35 (17%), and 21 (12%) of the informative cases, respectively. LOH for two of these regions occurred in only 25 cases, and only one tumor harbored LOH at all three sites. There was no statistically significant association between LOH at any of the three regions and either the stage or histological classification of the tumor. Patients with tumorspecific LOH for Chromosome 16q had relapse rates 3.3 times higher ( P = 0.01) and mortality rates 12 times higher ( P
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A Third Wilms' Tumor Locus on Chromosome 16q
Cancer Research, 1992Co-Authors: Paul E Grundy, Lynn J. Millow, Michael R. Eccles, Roseanne S. Dunn, Malcolm C. Paterson, Andrew P. Feinberg, Peter J Smith, Perry E. TelzerowAbstract:Abstract Loss of heterozygosity studies have been used to identify chromosomal regions which are frequently deleted and thus indicate areas which may harbor tumor suppressor genes. As a result, both the WT1 gene located in Chromosome 11p13 and an unidentified gene(s) within Chromosome 11p15 have been implicated in Wilms9 tumorigenesis. Cytogenetic and linkage studies suggest that additional non-Chromosome 11 sites are involved in Wilms9 tumor. Because these sites may also involve loss of heterozygosity, loci on 33 autosomal arms were screened for allele loss in a series of Wilms9 tumors. We found that in addition to loss on Chromosome 11p (11 of 25 informative tumors) there was significant loss on Chromosome 16q (9 of 45 informative tumors), while the total frequency of allele loss excluding these loci was low (9 of 426 total informative loci). These data indicate that losses of both Chromosome 11p and 16q alleles are nonrandom events and suggest that 16q is the location of a third tumor suppressor gene underlying Wilms9 tumorigenesis. The parental origin of the lost Chromosome 16q allele was determined in eight sporadic tumors. Alleles of paternal and of maternal origin were each lost in four sporadic tumors indicating that, unlike Chromosome 11p, alleles of either parental origin are lost on 16q.