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Cheng Huang - One of the best experts on this subject based on the ideXlab platform.
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risk factors affecting prognosis in metachronous liver metastases from who classification g1 and g2 gastroenteropancreatic neuroendocrine Tumors after initial r0 surgical resection
BMC Cancer, 2019Co-Authors: Yang Lv, Yu-hong Zhou, Jian Zhou, Cheng Huang, Xuefeng Xu, Yuan JiAbstract:Here we describe the treatments and prognosis for metachronous metastases from gastroenteropancreatic neuroendocrine Tumors (GEP-NETs) after initial R0 surgical resection at a large center in China. The clinicopathological data and survival outcomes for 108 patients (median age, 54.0 years) with metachronous hepatic metastatic GEP-NETs disease who were initially treated using R0 surgical resection between August 2003 and July 2014 were analyzed using one-way comparisons, survival analysis, and a predictive nomogram. Fifty-five (50.9%) patients had pancreatic NETs and 92 (85.2%) had G2 primary Tumors. For treatment of the hepatic metastases, 48 (44.4%) patients received liver-directed local treatment (metastasectomy, radiofrequency ablation, transcatheter arterial chemoembolization, etc.), 15 (13.9%) received systemic treatment (interferon, somatostatin analogs, etc.), and 45 (41.7%) received both treatments. Multivariable analyses revealed that OS was associated with hepatic Tumor Number (P < 0.001), treatment modality (P = 0.045), and elevated Ki-67 index between the metastatic and primary lesions (P = 0.027). The predictive nomogram C-index was 0.63. A higher Ki-67 index in metastases compared to primary Tumor was an independent factor for poor prognosis. Local treatment was associated with prolonged survival of hepatic metastatic GEP-NET patients. Optimal treatment strategies based on clinicopathological characteristics should be developed.
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Risk factors affecting prognosis in metachronous liver metastases from WHO classification G1 and G2 gastroenteropancreatic neuroendocrine Tumors after initial R0 surgical resection
BMC, 2019Co-Authors: Xu Han, Yu-hong Zhou, Hui-chuan Sun, Jian Zhou, Jia Fan, Wen-hui Lou, Cheng HuangAbstract:Abstract Background Here we describe the treatments and prognosis for metachronous metastases from gastroenteropancreatic neuroendocrine Tumors (GEP-NETs) after initial R0 surgical resection at a large center in China. Methods The clinicopathological data and survival outcomes for 108 patients (median age, 54.0 years) with metachronous hepatic metastatic GEP-NETs disease who were initially treated using R0 surgical resection between August 2003 and July 2014 were analyzed using one-way comparisons, survival analysis, and a predictive nomogram. Results Fifty-five (50.9%) patients had pancreatic NETs and 92 (85.2%) had G2 primary Tumors. For treatment of the hepatic metastases, 48 (44.4%) patients received liver-directed local treatment (metastasectomy, radiofrequency ablation, transcatheter arterial chemoembolization, etc.), 15 (13.9%) received systemic treatment (interferon, somatostatin analogs, etc.), and 45 (41.7%) received both treatments. Multivariable analyses revealed that OS was associated with hepatic Tumor Number (P
William F Dove - One of the best experts on this subject based on the ideXlab platform.
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identification of mom7 a novel modifier of apcmin on mouse chromosome 18
Genetics, 2007Co-Authors: Lawrence N Kwong, Alexandra Shedlovsky, Bryan S Biehl, Linda Clipson, Cheri A Pasch, William F DoveAbstract:The ApcMin mouse model of colorectal cancer provides a discrete, quantitative measurement of Tumor multiplicity, allowing for robust quantitative trait locus analysis. This advantage has previously been used to uncover polymorphic modifiers of the Min phenotype: Mom1, which is partly explained by Pla2g2a; Mom2, a spontaneous mutant modifier; and Mom3, which was discovered in an outbred cross. Here, we describe the localization of a novel modifier, Mom7, to the pericentromeric region of chromosome 18. Mom7 was mapped in crosses involving four inbred strains: C57BL/6J (B6), BTBR/Pas (BTBR), AKR/J (AKR), and A/J. There are at least two distinct alleles of Mom7: the recessive, enhancing BTBR, AKR, and A/J alleles and the dominant, suppressive B6 allele. Homozygosity for the enhancing alleles increases Tumor Number by approximately threefold in the small intestine on both inbred and F1 backgrounds. Congenic line analysis has narrowed the Mom7 region to within 7.4 Mb of the centromere, 28 Mb proximal to Apc. Analysis of SNP data from various genotyping projects suggests that the region could be as small as 4.4 Mb and that there may be five or more alleles of Mom7 segregating among the many strains of inbred mice. This has implications for experiments involving ApcMin and comparisons between different or mixed genetic backgrounds.
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n ethyl n nitrosourea treatment of multiple intestinal neoplasia min mice age related effects on the formation of intestinal adenomas cystic crypts and epidermoid cysts
Cancer Research, 1995Co-Authors: Alex R Shoemaker, Amy R. Moser, William F DoveAbstract:The timing of intestinal Tumor initiation in B6- Min /+ mice has been examined by treating mice at 5–35 days of age with a single i.p. injection of the direct-acting alkylating agent N -ethyl- N -nitrosourea (ENU). Treatment of Min /+ mice at 5–14 days of age resulted in a 3.8-fold increase in intestinal Tumor multiplicity over untreated mice. Mice treated at 20–35 days of age showed only a 1.6-fold increase in Tumor Number. These results, in conjunction with examination of Tumor multiplicities of untreated Min /+ mice as a function of age, suggest that the majority of intestinal Tumors in Min /+ mice are initiated relatively early in life. Min /+ mice treated with ENU also showed an increase in the Number of cystic intestinal crypts. However, the relationship between age at ENU treatment and cystic crypt multiplicity was distinct from that seen for intestinal adenomas. Mice treated at 5–9 days of age showed only a 1.9-fold increase in cystic crypts over untreated animals. By contrast, the increase in average cystic crypt multiplicity for mice treated at 10–35 days of age was 4.5-fold. In addition, 60% of Min /+ mice treated with ENU before 25 days of age developed epidermoid cysts, an extracolonic manifestation commonly associated with familial adenomatous polyposis in humans.
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genetic identification of mom 1 a major modifier locus affecting min induced intestinal neoplasia in the mouse
Cell, 1993Co-Authors: William F Dietrich, Amy R. Moser, Karen A. Gould, Eric S Lander, Jennifer S Smith, Cindy Luongo, Natalie Borenstein, William F DoveAbstract:Abstract Mutations in the human APC gene cause various familial colon cancer syndromes. The Multiple intestinal neoplasia (Min) mouse provides an excellent model for familial colon cancer: it carries a mutant mouse Apc gene and develops many intestinal adenomas. Here, we analyze how this Tumor phenotype is dramatically modified by genetic background. We report the genetic mapping of a locus that strongly modifies Tumor Number in Min /+ animals. This gene, Mom-1 (Modifier of Min-1), maps to distal chromosome 4 and controls about 50% of genetic variation in Tumor Number in two intraspecific backcrosses. The mapping is supported by a LOD score exceeding 14. Interestingly, Mom-1 lies in a region of synteny conservation with human chromosome 1p35–36, a region of frequent somatic loss of heterozygosity in a variety of human Tumors, including colon Tumors. These results provide evidence of a major modifier affecting expression of an inherited cancer syndrome.
Jian Zhou - One of the best experts on this subject based on the ideXlab platform.
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risk factors affecting prognosis in metachronous liver metastases from who classification g1 and g2 gastroenteropancreatic neuroendocrine Tumors after initial r0 surgical resection
BMC Cancer, 2019Co-Authors: Yang Lv, Yu-hong Zhou, Jian Zhou, Cheng Huang, Xuefeng Xu, Yuan JiAbstract:Here we describe the treatments and prognosis for metachronous metastases from gastroenteropancreatic neuroendocrine Tumors (GEP-NETs) after initial R0 surgical resection at a large center in China. The clinicopathological data and survival outcomes for 108 patients (median age, 54.0 years) with metachronous hepatic metastatic GEP-NETs disease who were initially treated using R0 surgical resection between August 2003 and July 2014 were analyzed using one-way comparisons, survival analysis, and a predictive nomogram. Fifty-five (50.9%) patients had pancreatic NETs and 92 (85.2%) had G2 primary Tumors. For treatment of the hepatic metastases, 48 (44.4%) patients received liver-directed local treatment (metastasectomy, radiofrequency ablation, transcatheter arterial chemoembolization, etc.), 15 (13.9%) received systemic treatment (interferon, somatostatin analogs, etc.), and 45 (41.7%) received both treatments. Multivariable analyses revealed that OS was associated with hepatic Tumor Number (P < 0.001), treatment modality (P = 0.045), and elevated Ki-67 index between the metastatic and primary lesions (P = 0.027). The predictive nomogram C-index was 0.63. A higher Ki-67 index in metastases compared to primary Tumor was an independent factor for poor prognosis. Local treatment was associated with prolonged survival of hepatic metastatic GEP-NET patients. Optimal treatment strategies based on clinicopathological characteristics should be developed.
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Risk factors affecting prognosis in metachronous liver metastases from WHO classification G1 and G2 gastroenteropancreatic neuroendocrine Tumors after initial R0 surgical resection
BMC, 2019Co-Authors: Xu Han, Yu-hong Zhou, Hui-chuan Sun, Jian Zhou, Jia Fan, Wen-hui Lou, Cheng HuangAbstract:Abstract Background Here we describe the treatments and prognosis for metachronous metastases from gastroenteropancreatic neuroendocrine Tumors (GEP-NETs) after initial R0 surgical resection at a large center in China. Methods The clinicopathological data and survival outcomes for 108 patients (median age, 54.0 years) with metachronous hepatic metastatic GEP-NETs disease who were initially treated using R0 surgical resection between August 2003 and July 2014 were analyzed using one-way comparisons, survival analysis, and a predictive nomogram. Results Fifty-five (50.9%) patients had pancreatic NETs and 92 (85.2%) had G2 primary Tumors. For treatment of the hepatic metastases, 48 (44.4%) patients received liver-directed local treatment (metastasectomy, radiofrequency ablation, transcatheter arterial chemoembolization, etc.), 15 (13.9%) received systemic treatment (interferon, somatostatin analogs, etc.), and 45 (41.7%) received both treatments. Multivariable analyses revealed that OS was associated with hepatic Tumor Number (P
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metroticket 2 0 model for analysis of competing risks of death after liver transplantation for hepatocellular carcinoma
Gastroenterology, 2018Co-Authors: Vincenzo Mazzaferro, Jian Zhou, Jia Fan, Carlo Sposito, Antonio Daniele Pinna, Luciano De Carlis, Matteo Cescon, Stefano Di Sandro, He Yifeng, Andrea LauterioAbstract:Background & Aims Outcomes of liver transplantation for hepatocellular carcinoma (HCC) are determined by cancer-related and non-related events. Treatments for hepatitis C virus infection have reduced non-cancer events among patients receiving liver transplants, so reducing HCC-related death might be an actionable end point. We performed a competing-risk analysis to evaluate factors associated with survival of patients with HCC and developed a prognostic model based on features of HCC patients before liver transplantation. Methods We performed multivariable competing-risk regression analysis to identify factors associated with HCC-specific death of patients who underwent liver transplantation. The training set comprised 1018 patients who underwent liver transplantation for HCC from January 2000 through December 2013 at 3 tertiary centers in Italy. The validation set comprised 341 consecutive patients who underwent liver transplantation for HCC during the same period at the Liver Cancer Institute in Shanghai, China. We collected pretransplantation data on etiology of liver disease, Number and size of Tumors, patient level of α-fetoprotein (AFP), model for end-stage liver disease score, Tumor stage, Numbers and types of treatment, response to treatments, Tumor grade, microvascular invasion, dates, and causes of death. Death was defined as HCC-specific when related to HCC recurrence after transplantation, disseminated extra- and/or intrahepatic Tumor relapse and worsened liver function in presence of Tumor spread. The cumulative incidence of death was segregated for hepatitis C virus status. Results In the competing-risk regression, the sum of Tumor Number and size and of log 10 level of AFP were significantly associated with HCC-specific death ( P P P = .044) to predict which patients will survive for 5 years after liver transplantation. Conclusions We developed a model based on level of AFP, Tumor size, and Tumor Number, to determine risk of death from HCC-related factors after liver transplantation. This model might be used to select end points and refine selection criteria for liver transplantation for patients with HCC. To predict 5-year survival and risk of HCC-related death using an online calculator, please see www.hcc-olt-metroticket.org/. ClinicalTrials.gov ID NCT02898415.
Margaret R. Wallace - One of the best experts on this subject based on the ideXlab platform.
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nf1 patient missense variants predict a role for atm in modifying neurofibroma initiation
Acta Neuropathologica, 2020Co-Authors: Kwangmin Choi, Jose A Cancelas, Paul R Andreassen, Phillip J Dexheimer, Mehdi Keddache, Hilde Brems, Robert J Spinner, Lisa J Martin, Margaret R. WallaceAbstract:In Neurofibromatosis type 1, NF1 gene mutations in Schwann cells (SC) drive benign plexiform neurofibroma (PNF), and no additional SC changes explain patient-to-patient variability in Tumor Number. Evidence from twin studies suggests that variable expressivity might be caused by unidentified modifier genes. Whole exome sequencing of SC and fibroblast DNA from the same resected PNFs confirmed biallelic SC NF1 mutations; non-NF1 somatic SC variants were variable and present at low read Number. We identified frequent germline variants as possible neurofibroma modifier genes. Genes harboring variants were validated in two additional cohorts of NF1 patients and by variant burden test. Genes including CUBN, CELSR2, COL14A1, ATR and ATM also showed decreased gene expression in some neurofibromas. ATM-relevant DNA repair defects were also present in a subset of neurofibromas with ATM variants, and in some neurofibroma SC. Heterozygous ATM G2023R or homozygous S707P variants reduced ATM protein expression in heterologous cells. In mice, genetic Atm heterozygosity promoted Schwann cell precursor self-renewal and increased Tumor formation in vivo, suggesting that ATM variants contribute to neurofibroma initiation. We identify germline variants, rare in the general population, overrepresented in NF1 patients with neurofibromas. ATM and other identified genes are candidate modifiers of PNF pathogenesis.
Jose A Cancelas - One of the best experts on this subject based on the ideXlab platform.
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nf1 patient missense variants predict a role for atm in modifying neurofibroma initiation
Acta Neuropathologica, 2020Co-Authors: Kwangmin Choi, Jose A Cancelas, Paul R Andreassen, Phillip J Dexheimer, Mehdi Keddache, Hilde Brems, Robert J Spinner, Lisa J Martin, Margaret R. WallaceAbstract:In Neurofibromatosis type 1, NF1 gene mutations in Schwann cells (SC) drive benign plexiform neurofibroma (PNF), and no additional SC changes explain patient-to-patient variability in Tumor Number. Evidence from twin studies suggests that variable expressivity might be caused by unidentified modifier genes. Whole exome sequencing of SC and fibroblast DNA from the same resected PNFs confirmed biallelic SC NF1 mutations; non-NF1 somatic SC variants were variable and present at low read Number. We identified frequent germline variants as possible neurofibroma modifier genes. Genes harboring variants were validated in two additional cohorts of NF1 patients and by variant burden test. Genes including CUBN, CELSR2, COL14A1, ATR and ATM also showed decreased gene expression in some neurofibromas. ATM-relevant DNA repair defects were also present in a subset of neurofibromas with ATM variants, and in some neurofibroma SC. Heterozygous ATM G2023R or homozygous S707P variants reduced ATM protein expression in heterologous cells. In mice, genetic Atm heterozygosity promoted Schwann cell precursor self-renewal and increased Tumor formation in vivo, suggesting that ATM variants contribute to neurofibroma initiation. We identify germline variants, rare in the general population, overrepresented in NF1 patients with neurofibromas. ATM and other identified genes are candidate modifiers of PNF pathogenesis.
