Involvement of 3p Deletions in Sporadic and Hereditary Forms of Renal Cell Carcinoma

Ferenc Boldog, Kristina Arheden, Stephan Imreh, Bodil Strombeck, Laszlo Szekely, Rikard Erlandsson, Zoltan Marcsek, Janos Sumegi, Felix Mitelman, George Klein

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Deletions of the short arm of chromosome 3 and associated allele losses have been reported in the majority of sporadic renal cell carcinomas (RCC). On the basis of the combined cytogenetic and molecular data, it is reasonable to assume that a putative RCC locus, which contributes to tumor development by its loss, is located telomerically of the D3F15S2 site. Using H3E4, a D3F1SS2‐specific probe, we have isolated a cDNA clone (c1.4–2), and a sequence comparison revealed that the cDNA clone corresponds to the human acyl‐peptide hydrolase gene. The gene is fairly universally expressed, but in RCC biopsies its expression is severely reduced, compared to the normal kidney. Cl.4–2 was used for in situ hybridization on metaphase chromosomes prepared from an Epstein‐Barr virus (EBV) transformed lymphoblastoid cell line, derived from a t(3;8) (p14.2;q24.1) carrying member of the RCC family described by Cohen et al. in 1979 (N Engl J Med: 301:592–595). Carriers of this translocation regularly develop RCC by middle age. We now report that D3F15S2 is localized on the telomeric side of the constitutional breakpoint, in 3p21. The region of 3p affected by this familial translocation is thus not identical with the region of 3p most frequently deleted in sporadic RCC.

Original languageEnglish (US)
Pages (from-to)403-406
Number of pages4
JournalGenes, Chromosomes and Cancer
Issue number5
StatePublished - Sep 1991
Externally publishedYes

ASJC Scopus subject areas

  • Genetics
  • Cancer Research


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