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[Cancer Research 59, 2182-2189, May 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 2182-2189, May 1, 1999]
© 1999 American Association for Cancer Research

Molecular Biology and Genetics

The Genetic Locus NRC-1 within Chromosome 3p12 Mediates Tumor Suppression in Renal Cell Carcinoma Independently of Histological Type, Tumor Microenvironment, and VHL Mutation1

Mercedes Lovell, Steven Trent Lott, Patricia Wong, Adel El-Naggar, Susan Tucker and Ann McNeill Killary2

Section of Experimental Laboratory Medicine, Departments of Laboratory Medicine [M. L., S. T. L., P. W., A. M. K.] and Pathology [A. E-N.], Division of Pathology and Laboratory Medicine and Department of Biomathematics [S. T.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030-4095

Human chromosome 3p cytogenetic abnormalities and loss of heterozygosity have been observed at high frequency in the nonpapillary form of sporadic renal cell carcinoma (RCC). The von Hippel-Lindau (VHL) gene has been identified as a tumor suppressor gene for RCC at 3p25, and functional studies as well as molecular genetic and cytogenetic analyses have suggested as many as two or three additional regions of 3p that could harbor tumor suppressor genes for sporadic RCC. We have previously functionally defined a novel genetic locus nonpapillary renal carcinoma-1 (NRC-1) within chromosome 3p12, distinct from the VHL gene, that mediates tumor suppression and rapid cell death of RCC cells in vivo. We now report the suppression of tumorigenicity of RCC cells in vivo after the transfer of a defined centric 3p fragment into different histological types of RCC. Results document the functional involvement of NRC-1 in not only different cell types of RCC (i.e., clear cell, mixed granular cell/clear cell, and sarcomatoid types) but also in papillary RCC, a less frequent histological type of RCC for which chromosome 3p LOH and genetic aberrations have only rarely been observed. We also report that the tumor suppression observed in functional genetic screens was independent of the microenvironment of the tumor, further supporting a role for NRC-1 as a more general mediator of in vivo growth control. Furthermore, this report demonstrates the first functional evidence for a VHL-independent pathway to tumorigenesis in the kidney via the genetic locus NRC-1.




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