Loss of heterozygosity on 3p in a renal cell carcinoma in von Hippel-Lindau syndrome

Decker, Hans Joachim H.; Gemmill, Robert M.; Neumann, Hartmut P. H.; Walter, Thomas; Sandberg, Avery A.

doi:10.1016/0165-4608(89)90194-5

Cited by 26 publications

(1 citation statement)

References 16 publications

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“…Patients with von Hippel-Lindau disease (VHL) have recently been shown to have pancreatic endocrine tumors (Binkovitz et al 1990). Other tumors arising in patients with V H L have L O H on the short arm of chromosome 3 (Kovacs and Kung 1991;Decker et al 1989). We evaluated two loci on the short arm of chromosome 3 (D3S12 and D3S13) and did not find L O H .…”

Section: Resultsmentioning

confidence: 99%

Loss of heterozygosity on chromosome 11 in sporadic gastrinomas

et al. 1992

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Gastrinomas are pancreatic endocrine neoplasms that arise either sporadically or are inherited as part of the multiple endocrine neoplasia type I syndrome (MENI). Loss of heterozygosity (LOH) in the region flanking the MENI gene at chromosome 11q13 has been documented in a few sporadic and familial pancreatic endocrine tumors, but not previously in sporadic gastrinomas. It has therefore been suggested that gastrinomas develop by a mechanism different from other tumors associated with the MENI syndrome. We report LOH on chromosome 11 in 5 of 11 sporadic gastrinomas. Four of these tumors have LOH for markers flanking the MENI region. Molecular evaluation of segments of chromosomes 3, 13, and 17 known to contain cloned or putative tumor suppressor genes fail to show LOH except at one locus in one tumor. These data suggest that a tumor suppressor DNA segment exists at 11q13 that may be involved in the development of sporadic gastrinomas.

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Section: Resultsmentioning

confidence: 99%