Receptor protein-tyrosine phosphatase gamma is a candidate tumor suppressor gene at human chromosome region 3p21.

LaForgia, Sal; Morse, B; Levy, Joan; Barnea, Gilad; Cannizzaro, Linda A.; Li, F; Nowell, PC; Boghosian-Sell, Leslie; Glick, Joseph; Weston, Ainsley

doi:10.1073/pnas.88.11.5036

Cited by 182 publications

(95 citation statements)

References 25 publications

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“…In breast cancer, LOH ranging from 30% to 47% were observed at two separate regions, 3p13Ðp14 and 3p21Ðp25 (Chen et al, 1994) or 3p14.3Ðp21.1 and 3p24.3Ðp25.1 (Matsumoto et al, 1997), suggesting the involvement of several tumour-suppressor genes. PTPRG, a protein-tyrosine phosphatase gene, and FHIT that encodes the human diadenosine triphosphate hydrolase (Barnes et al, 1996), both localized within the 3p13Ðp14 region, are potential candidates as targets of deletions in primary breast tumours (LaForgia et al, 1991;Negrini et al, 1996;Ohta et al, 1996). Furthermore, a 3p21.3 region (SCLC) was shown to be homozygously deleted in SCLC cell lines (Daly et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Frequent loss of heterozygosity at the DNA mismatch-repair loci hMLH1 and hMSH3 in sporadic breast cancer

et al. 1999

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SummaryTo study the involvement of DNA mismatch-repair genes in sporadic breast cancer, matched normal and tumoral DNA samples of 22 patients were analysed for genetic instability and loss of heterozygosity (LOH) with 42 microsatellites at or linked to hMLH1 (3p21), hMSH2 (2p16), hMSH3 (5q11-q13), hMSH6 (2p16), hPMS1 (2q32) and hPMS2 (7p22) loci. Chromosomal regions 3p21 and 5q11-q13 were found hemizygously deleted in 46% and 23% of patients respectively. Half of the patients deleted at hMLH1 were also deleted at hMSH3. The shortest regions of overlapping (SRO) deletions were delimited by markers D3S1298 and D3S1266 at 3p21 and by D5S647 and D5S418 at 5q11-q13. Currently, the genes hMLH1 (3p21) and hMSH3 (5q11-q13) are the only known candidates located within these regions. The consequence of these allelic losses is still unclear because none of the breast cancers examined displayed microsatellite instability, a hallmark of mismatch-repair defect during replication error correction. We suggest that hMLH1 and hMSH3 could be involved in breast tumorigenesis through cellular functions other than replication error correction.

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Section: Discussionmentioning

confidence: 99%

Frequent loss of heterozygosity at the DNA mismatch-repair loci hMLH1 and hMSH3 in sporadic breast cancer

et al. 1999

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“…In a search for the candidate tumor suppressor gene for RCC, the 3p14.2 locus has been intensively studied (Yamakawa et al, 1992;Boghosian-Sell and Cannizzaro, 1992;LaForgia et al, 1991LaForgia et al, , 1993Atchison et al, 1995;Gnarra et al, 1995, Shi andCannizzaro, 1996). Even though multiple markers which span this breakpoint region have been isolated, a gene has yet to be identi®ed in RCC, with altered expression as a result of the 3;8 rearrangement.…”

Section: Introductionmentioning

confidence: 99%

The FHIT gene is alternatively spliced in normal kidney and renal cell carcinoma

et al. 1997

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“…This gene is located on the short arm of chromosome 3 in a region carrying multiple tumour suppressor genes presumably involved in cancer development (LaForgia et al, 1991;. Genetic studies have defined this locus as unstable.…”

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Different gene expression of MDM2, GAGE-1, –2 and FHIT in hepatocellular carcinoma and focal nodular hyperplasia

et al. 1999

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SummaryOverexpression and/or mutations of oncogenes, tumour suppressor genes and tumour rejection genes have been observed in several human malignancies. Their analyses might be of diagnostic importance. Therefore, malignant hepatocytes derived from hepatocellular carcinoma (HCC) tissue as well as non-malignant hepatocytes derived from focal nodular hyperplasia (FNH) were studied. Samples containing normal human hepatocytes (HC) served as controls. Cellular material was obtained by fine-needle aspiration biopsy guided by ultrasound. Cells were analysed for expression and mutation of the oncogene MDM2, the genes GAGE-1, -2 coding for tumourassociated antigens and the candidate tumour suppressor gene FHIT. Different patterns of non-mutant FHIT transcripts including precise deletion of exons were found in 7/10 HCC, 2/10 FNH and 2/10 HC. However, expression of non-mutant GAGE-1, -2 RNA was demonstrated exclusively in 6/10 HCC samples. Further genetic features specific of HCC were point mutations in a zinc-finger motif of MDM2 (3/10 HCC samples). Neither GAGE-1, -2 expression nor MDM2 mutations were observed in the FNH samples, or in normal hepatocytes. Our findings suggest that occurrence of variable FHIT transcripts is not restricted to hepatic malignant tumours. In contrast, MDM2 mutations and GAGE-1, -2 expression were associated with HCC specimens. Therefore, the RT-PCR assays for GAGE-1, -2 and MDM2 might be useful adjuncts in cytodiagnosis of liver neoplasms.

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Receptor protein-tyrosine phosphatase gamma is a candidate tumor suppressor gene at human chromosome region 3p21.

Cited by 182 publications

References 25 publications

Frequent loss of heterozygosity at the DNA mismatch-repair loci hMLH1 and hMSH3 in sporadic breast cancer

Frequent loss of heterozygosity at the DNA mismatch-repair loci hMLH1 and hMSH3 in sporadic breast cancer

The FHIT gene is alternatively spliced in normal kidney and renal cell carcinoma

Different gene expression of MDM2, GAGE-1, –2 and FHIT in hepatocellular carcinoma and focal nodular hyperplasia

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