There are two aspects of this Core. In the first we will exploit a newly developed procedure to make chromosome-specific and chromosome region- specific probes for fluorescent in-situ hybridization. The new procedure, based on inter-Alu-PCR of DNA from hybrid cells containing localized regions of the human genome results in probe specific for painting those regions of the genome in human normal and cancer cells. Probes will be made for the various candidate regions of the human genome implicated in human pediatric cancer. This methodology will then be combined with a new approach for making direct cytogenetic preparations from pediatric tumors, and tumors cultured in nude mice, in order to investigate primary chromosomal events associated with those cancers. Probes will also be applied to tumor cell lines derived from Li-Fraumeni patients and families to once again identify non-random chromosomal changes associated with that syndrome. Pediatric cancer patients presenting with congenital abnormalities will have their lymphocytes studied by traditional G-band cytogenetics in order to identify candidate regions for further analyses. For any chromosomal regions so identified, painting probe will be produced as above for in depth analysis and confirmation of the suspected chromosomal abnormalities. The second aspect of the Core is to provide isozyme genetic signature analysis on tumors grown in nude mice to rapidly and unambiguously verify their human origin. To a lesser extent this aspect of the Core will also help verify the genetic origin of cell lines and nude mouse tumors developed from pediatric cancer patients.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA034936-12
Application #
5207220
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
12
Fiscal Year
1996
Total Cost
Indirect Cost
Peng, Gang; Bojadzieva, Jasmina; Ballinger, Mandy L et al. (2017) Estimating TP53 Mutation Carrier Probability in Families with Li-Fraumeni Syndrome Using LFSPRO. Cancer Epidemiol Biomarkers Prev 26:837-844
Maturu, Paramahamsa; Jones, Devin; Ruteshouser, E Cristy et al. (2017) Role of Cyclooxygenase-2 Pathway in Creating an Immunosuppressive Microenvironment and in Initiation and Progression of Wilms' Tumor. Neoplasia 19:237-249
Huang, Le; Mokkapati, Sharada; Hu, Qianghua et al. (2016) Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with ?-Catenin Activation or Wt1 Ablation and Igf2 Upregulation. Neoplasia 18:71-81
Palculict, Timothy Blake; Ruteshouser, E Cristy; Fan, Yu et al. (2016) Identification of germline DICER1 mutations and loss of heterozygosity in familial Wilms tumour. J Med Genet 53:385-8
Liu, Changlu; Ma, Jianzhong; Amos, Christopher I (2015) Bayesian variable selection for hierarchical gene-environment and gene-gene interactions. Hum Genet 134:23-36
Mokkapati, Sharada; Niopek, Katharina; Huang, Le et al. (2014) ?-catenin activation in a novel liver progenitor cell type is sufficient to cause hepatocellular carcinoma and hepatoblastoma. Cancer Res 74:4515-25
Quintás-Cardama, Alfonso; Post, Sean M; Solis, Luisa M et al. (2014) Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer. J Pathol 234:108-19
Maturu, Paramahamsa; Overwijk, Willem W; Hicks, John et al. (2014) Characterization of the inflammatory microenvironment and identification of potential therapeutic targets in wilms tumors. Transl Oncol 7:484-92
Shahidul Makki, Mohammad; Cristy Ruteshouser, E; Huff, Vicki (2013) Ubiquitin specific protease 18 (Usp18) is a WT1 transcriptional target. Exp Cell Res 319:612-22
Kaftanovskaya, Elena M; Neukirchner, Giselle; Huff, Vicki et al. (2013) Left-sided cryptorchidism in mice with Wilms' tumour 1 gene deletion in gubernaculum testis. J Pathol 230:39-47

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