ArticleProceedings of the National Academy of Sciences of the United States of America1994
Genome-wide search for loss of heterozygosity in transgenic mouse tumors reveals candidate tumor suppressor genes on chromosomes 9 and 16.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 73 citations in OpenAlex.
- A whole-genome mouse BAC microarray with 1-Mb resolution for analysis of DNA copy number changes by array comparative genomic hybridization.Genome research · 2004Article
- Of mice and MEN1: Insulinomas in a conditional mouse knockout.Molecular and cellular biology · 2003Article
- Recurrent allelic deletions at mouse chromosomes 4 and 14 in Myc-induced liver tumors.Oncogene · 2002Article
- A PCR-based clonal analysis of radiation-induced loss of heterozygosity in haemopoietic stem cells.Leukemia · 2001Article
- Loss of heterozygosity at the Ink4a/Arf locus facilitates Abelson virus transformation of pre-B cells.Journal of virology · 2000Article
- MCG10, a novel p53 target gene that encodes a KH domain RNA-binding protein, is capable of inducing apoptosis and cell cycle arrest in G(2)-M.Molecular and cellular biology · 2000Article
- Review
- Genetic differences in endocrine pancreatic tumor subtypes detected by comparative genomic hybridization.The American journal of pathology · 1999Article
- Homozygous deletions and point mutations of the Ikaros gene in gamma-ray-induced mouse thymic lymphomas.Oncogene · 1999Article
- Allelic loss mapping and physical delineation of a region harboring a putative thymic lymphoma suppressor gene on mouse chromosome 12.Oncogene · 1999Article
- Human Insulinomas: Clinical, Cellular, and Molecular Aspects.Endocrine pathology · 1999Article
- The Rasgrf1-repeat sequence (D9Ncvs53) maps between Mod1 and Rbp1 on mouse chromosome 9 and may define a putative imprinted region.Mammalian genome : official journal of the International Mammalian Genome Society · 1998Article
- Article
- Mouse mammary tumor virus/v-Ha-ras transgene-induced mammary tumors exhibit strain-specific allelic loss on mouse chromosome 4.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Low-frequency loss of heterozygosity in Moloney murine leukemia virus-induced tumors in BRAKF1/J mice.Journal of virology · 1997Article
- The role of the laboratory mouse in the human genome project.American journal of human genetics · 1996Review
- Dlgh1, a mouse homolog of the drosophila discs-large gene, is located on chromosome 16.Mammalian genome : official journal of the International Mammalian Genome Society · 1996Article
- Tumor angiogenesis: a physiological process or genetically determined?Cancer metastasis reviews · 1996Review
- Generation and mapping of Mus spretus strain-specific markers for rapid genomic scanning.Mammalian genome : official journal of the International Mammalian Genome Society · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A genome-wide scan for loss of heterozygosity (LOH) in tumors provides a powerful route to the identification of genes involved in tumorigenesis. This approach has not previously been applied to transgenic mice, despite the considerable advantages they afford for genetic dissection. Here, we report a genome-wide LOH analysis of insulinomas and carcinoid tumors in transgenic mice expressing the simian virus 40 large tumor oncogene. Although the overall genome-wide rate of LOH was quite low, chromosomes 9 and 16 showed high rates of allelic loss. About one-third of tumors showed partial LOH, allowing localization of the likely tumor suppressor genes to intervals of approximately 11 centimorgans. The locus on chromosome 9, named Loh-1, lies in a region with synteny conservation to human chromosomes 3q, 6q12, 15q24, and 3p21, while the locus on chromosome 16, named Loh-2, lies in a region corresponding to human chromosomes 3q and 22q. Of particular note is the synteny conservation with human 3p21, which shows frequent loss in human cancers. These regions do not encode two tumor suppressors, pRB and p53, known to interact with large tumor oncoprotein, suggesting the presence of new genes whose loss of function contributes to multistage tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.