The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
THE GENETICS OF WILMS’ TUMOR—A Case of Disrupted Development
Abstract
THE WTI GENE . . . . . . . .... . . . . .. . ........ . . . . . . . .... . . . . . . ....... . . . . . . . 526 Chromosome 11 pJ3 Deletions Led to the Isolation of the WTI Gene . . . .. . . . . . . . 526 The WTl Gelle Encodes a Transcription Factor with Four Zinc Fingers . . .... . . . 527 The WTl Gene Is Requiredfor Normal Development of the Kidney, Gonad, and Related Structures . . ...... . . . . . . ......... . . . . . . .... . . . . . . . . 528 wtl-Null Mice Fail To Develop Kidneys and Gonads . . . . . . . . . . . . . . . . . . . . . . . . . 529 Dominant-Negative WTI Mutations Are Likely To Cause the Severe Urogenital A bnormalities ill Denys-Drash Syndrome . . . . . . . . . . . . . . . . . . . . . . . 529 WTI Mutations Are Found in a Minority of Wilms' Tumors . . . . . . . .. . . . . . . . . . . 533 WTI Mutation May Play a Role in a Very Small Minority Mesotheliomas, Leukemias, and Tumors of the Gonad 536 WTl Seems To Act as a Transcriptional Repressor. . . . . . . . . . . . . . . . . . . . . . . . . . . 537 The Sigllificance of Multiple WTI lsofonns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 540 WTI Appears To Function at Three Different Stages of Nephrogenesis . ....... . . 544 ADDITIONAL WILMS' TUMOR PREDISPOSITION GENES 545 Chromosome l lp15, Genomic Imprinting, alld the Beckwith-Wiedemann Syndrome 545 Rare Familial Predisposition to Wilms' Tumor Is Not Linked To Chromosome 11 . . 549 LOH Allalysis Suggests all A dditional WT Gene 011 Chromosome 16 . . . . . . . . . . . . . 549 The p53 Tumor Suppressor Gene Is Mutated in a Very Small alld Specific Subset of Wilms' Tumors . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 550 WILMS' TUMORS IN ANIMAL MODEL SYSTEMS . . . . . . ...... . . . . .. . . . . . . . . 550 Chemically Induced Rat Wilms' Tumors A rise Through WTI Mutation . . . ... ... . . 551
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Citations
Cites
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Cited by
WT1 proteins: functions in growth and differentiation
Scharnhorst, V., van der Eb, A. J., & Jochemsen, A. G. (2001) · Gene · doi:10.1016/s0378-1119(01)00593-5 · Cited by 353
HUMAN TYPE 1 DIABETES AND THE INSULIN GENE: Principles of Mapping Polygenes
Bennett, S. T., & Todd, J. A. (1996) · Annual Review of Genetics · doi:10.1146/annurev.genet.30.1.343 · Cited by 287
Maschietto, M., de Camargo, B., Brentani, H., Grundy, P., Sredni, S. T., Torres, C., Mota, L. D., Cunha, I. W., Patrão, D. F. C., Costa, C. M. L., et al. (2008) · Oncology · doi:10.1159/000155210 · Cited by 35
Metadata
- Authors
- Hastie, N. D.
- Venue
- Annual Review of Genetics
- Publisher
- Annual Reviews
- Published
- 1994-12
- Volume
- 28
- Issue
- 1
- Pages
- 523-558
- ISSN
- 0066-4197 (ISSN-L)
- 1545-2948
- OpenAlex
- W2107863123
- Cited by
- 229
- References
- 1
- FWCI
- 5.27
- Type
- journal article
- Language
- en
- Open access
- closed
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- Hastie, N. D. (1994). THE GENETICS OF WILMS’ TUMOR—A Case of Disrupted Development. Annual Review of Genetics. https://doi.org/10.1146/annurev.ge.28.120194.002515
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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