ArticleMolecular and cellular biology2001
Efficiency alleles of the Pctr1 modifier locus for plasmacytoma susceptibility.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 84 citations in OpenAlex.
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- Activated gp130 signaling selectively targets B cell differentiation to induce mature lymphoma and plasmacytoma.JCI insight · 2019Article
- Early Generated B-1-Derived B Cells Have the Capacity To Progress To Become Mantle Cell Lymphoma-like Neoplasia in Aged Mice.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Canine Mammary Carcinomas: A Comparative Analysis of Altered Gene Expression.Veterinary sciences · 2015Review
- Preclinical validation of interleukin 6 as a therapeutic target in multiple myeloma.Immunologic research · 2014Review
- TORC1 and class I HDAC inhibitors synergize to suppress mature B cell neoplasms.Molecular oncology · 2014Article
- A novel rapid-onset high-penetrance plasmacytoma mouse model driven by deregulation of cMYC cooperating with KRAS12V in BALB/c mice.Blood cancer journal · 2013Article
- Waldenström macroglobulinemia: clinical and immunological aspects, natural history, cell of origin, and emerging mouse models.ISRN hematology · 2013Review
- Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer.Cancer research · 2010Article
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- Defining the oncogenic function of the TEL/AML1 (ETV6/RUNX1) fusion protein in a mouse model.Oncogene · 2005Article
- Cell cycle in mouse development.Oncogene · 2005Review
- Increased gene dosage of Ink4a/Arf results in cancer resistance and normal aging.Genes & development · 2004Article
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9 authors at 4 institutions in 3 countries.
Funding
Abstract
The susceptibility of BALB/c mice to pristane-induced plasmacytomas is a complex genetic trait involving multiple loci, while DBA/2 and C57BL/6 strains are genetically resistant to the plasmacytomagenic effects of pristane. In this model system for human B-cell neoplasia, one of the BALB/c susceptibility and modifier loci, Pctr1, was mapped to a 5.7-centimorgan (cM) chromosomal region that included Cdkn2a, which encodes p16(INK4a) and p19(ARF), and the coding sequences for the BALB/c p16(INK4a) and p19(ARF) alleles were found to be polymorphic with respect to their resistant Pctr1 counterparts in DBA/2 and C57BL/6 mice (45). In the present study, alleles of Pctr1, Cdkn2a, and D4Mit15 from a resistant strain (BALB/cDAG) carrying DBA/2 chromatin were introgressively backcrossed to the susceptible BALB/c strain. The resultant C.DAG-Pctr1 Cdkn2a D4Mit15 congenic was more resistant to plasmacytomagenesis than BALB/c, thus narrowing Pctr1 to a 1.5-cM interval. Concomitantly, resistant C57BL/6 mice, from which both gene products of the Cdkn2a gene have been eliminated, developed pristane-induced plasma cell tumors over a shorter latency period than the traditionally susceptible BALB/cAn strain. Biological assays of the p16(INK4a) and p19(ARF) alleles from BALB/c and DBA/2 indicated that the BALB/c p16(INK4a) allele was less active than its DBA/2 counterpart in inducing growth arrest of mouse plasmacytoma cell lines and preventing ras-induced transformation of NIH 3T3 cells, while the two p19(ARF) alleles displayed similar potencies in both assays. We propose that the BALB/c susceptibility/modifier locus, Pctr1, is an "efficiency" allele of the p16(INK4a) gene.
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