Differential DNA sequence deletions from chromosomes 3, 11, 13, and 17 in squamous-cell carcinoma, large-cell carcinoma, and adenocarcinoma of the human lung.

Weston, Ainsley; Willey, James C.; Modali, Rama; Sugimura, Haruhiko; McDowell, Elizabeth M.; Resau, James H.; Light, B; Haugen, Aage; Mann, Dean L.; Trump, Benjamin F.

doi:10.1073/pnas.86.13.5099

Cited by 199 publications

(88 citation statements)

References 30 publications

(36 reference statements)

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“…Our polymorphic marker and STS scan of a large number of lung cancer cell lines is in agreement with previous publications, which have described frequent allele loss but no homozygous deletion in the region (Ali et al, 1987;Bepler and Garcia-Blanco, 1994;Fearon et al, 1985;Fong et al, 1994;Karnik et al, 1998;Lu et al, 1997;Ludwig et al, 1991;Ranzani et al, 1993;Shibagaki et al, 1994;Shiraishi et al, 1987;Skinner et al, 1990;Tran and Newsham, 1996;Viel et al, 1992;Weston et al, 1989;Winqvist et al, 1993). We found a lower than expected frequency of heterozygosity for the polymorphic markers D11S4932 and RRI9, which suggests that allele loss has occurred in a substantial number of cell lines.…”

Section: Discussionsupporting

confidence: 91%

“…The minimal region of LOH was 650 kb and¯anked by the markers D11S988 (centromeric) and D11S860 (telomeric). Numerous investigators have reported LOH in this region for non-SCLC with frequencies ranging from 17% to 82% (Bepler and Garcia-Blanco, 1994;Fong et al, 1994;Ludwig et al, 1991;Shiraishi et al, 1987;Skinner et al, 1990;Tran and Newsham, 1996;Weston et al, 1989). LOH in or near this region has also been described for breast, ovarian, esophageal, stomach, and other cancers arising in adults (Ali et al, 1987;Fearon et al, 1985;Karnik et al, 1998;Lu et al, 1997;Ranzani et al, 1993;Shibagaki et al, 1994;Tran and Newsham, 1996;Viel et al, 1992;Winqvist et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Transcript map and complete genomic sequence for the 310 kb region of minimal allele loss on chromosome segment 11p15.5 in non-small-cell lung cancer

Zhao

Bepler

2001

Oncogene

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Molecular, functional, and clinical analyses strongly suggest that chromosome segment 11p15.5 contains a gene involved in lung cancer pathogenesis. The critical region of allele loss is 310 kb in size. We used our contig of P1-phage arti®cial chromosome (PAC) clones together with newly identi®ed bacterial arti®cial chromosome (BAC) clones and the draft human genome sequence to complete a contiguous string of 380 407 bp. Three PAC clones that span the region were used to identify transcripts by exon trapping. Computational gene prediction algorithms were used to query the sequence for potential genes and exons. Screening for expression was performed with tissue-speci®c and cell line derived mRNA arrays. The region contains the complete SSA/Ro52 and RRM1 genes, exons 7 ± 12 of the GOK gene, and the crad pseudo-gene. A cluster of six nearly identical genes with an intact open reading frame (ORF) of 585 bp that share 75% identity with the HSPC182 gene was found. In addition, ®ve putative novel genes were identi®ed. Sequence tagged sites (STS) and polymorphic markers were used to screen 117 lung cancer cell lines for homozygous deletions and none were identi®ed. These data provide the basis for the identi®cation of a lung cancer suppressor gene on 11p15.5. Oncogene (2001) 20, 8154 ± 8164.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Transcript map and complete genomic sequence for the 310 kb region of minimal allele loss on chromosome segment 11p15.5 in non-small-cell lung cancer

Zhao

Bepler

2001

Oncogene

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“…Loss of DNA sequences from chromosome 3 may be one of the leading events in the development of RCCs (Zbar et al, 1987;Anglard et al, 1994;Ogawa et al, 1991), but allele loss from other chromosomal regions points to the involvement of additional tumor suppressor genes in the pathogenesis of RCCs, as it is in several other solid tumors including those of colon, breast, lung, and bladder (Fearon et al, 1990a;Callahan et al, 1989;Tsai et al, 1990;Weston et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Loss of heterozygosity on the long arm of human chromosome 7 in sporadic renal cell carcinomas

et al. 1997

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Cytogenetic and molecular analysis of DNA sequences with highly polymorphic microsatellite markers have implicated allele loss in several chromosomal regions including 3p, 6p, 6q, 8p, 9p, 9q, 11p and 14q in the pathogenesis of sporadic renal cell carcinomas (RCCs). Deletions involving the long arm of chromosome 7 have not been described in RCCs although they have been seen in several other tumor types. However, there have been no detailed analysis of loss of heterozygosity (LOH) of 7q sequences in sporadic RCCs. We therefore studied LOH for DNA sequences on 7q with 10 highly polymorphic markers in 92 matched normal/tumor samples representing sporadic RCCs including papillary, nonpapillary, and oncocytomas in order to determine whether allelic loss could be detected in a tumor type with no visible 7q rearrangements at the cytogenetic level. We found chromosome 7q allele loss in 59 of 92 cases (64%) involving one, two, or more microsatellite markers. The most common allele loss included loci D7S522 (24%) and D7S649 (30%) at 7q31.1-31.2, a region that contains one of the common fragile sites, FRA7G. By comparative multiplex PCR analysis, we detected a homozygous deletion of one marker in the 7q 31.1-31.2 region in one tumor, RC21. These results support the idea that a tumor suppressor gene in 7q31 is involved in the pathogenesis of sporadic renal cell carcinomas.

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“…In these cases, other lesions such as amplifications of the growth factor int-2 gene, c-myc, and/or alterations ofthe tumorsuppressor genes p53 and Rb, which are often found (36), may be important determinants of metastatic potential. In human lung cancer, numerous different genetic alterations have been found within single tumors (37). In small cell as well as nonsmall cell carcinomas, mutations have been found frequently in K-ras, Rb, and p53.…”

Section: Summary and Studies On Human Tumorsmentioning

confidence: 99%

Molecular determinants of metastatic transformation.

Egan

Wright

Greenberg

1991

Environ Health Perspect

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In recent years, experimental systems have developed to analyze genetic and epigenetic regulation of the metastatic phenotype. Numerous studies have uncovered a potent role for transforming oncogenes in metastatic conversion. In addition, it has been shown that oncoprotein products operate in a dose-dependent fashion. The continued expression of oncoproteins is required to induce and regulate metastatic dissemination of tumor cells and, consequently, many of the signal transduction pathways that are controlled by the oncogene products can regulate metastasis. Exogenous growth factors that act through these same pathways also alter metastatic potential. Some primary and immortalized cells can be transformed by oncogenes but remain completely benign and nonmetastatic. Malignant transformation can be achieved in these cells through the cooperative interaction of specific oncogenes or loss of active suppression regulated by recessive genetic determinants. Therefore, it is likely that tumor cells acquire the metastatic phenotype through the cooperative interaction of dominant and recessive genetic alterations. This model is consistent with the correlative data accumulating in studies of human tumor specimens where more malignant carcinomas often contain both activating mutations in oncogenes and either inactivating mutations or loss of tumor-suppressor genes.

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Differential DNA sequence deletions from chromosomes 3, 11, 13, and 17 in squamous-cell carcinoma, large-cell carcinoma, and adenocarcinoma of the human lung.

Cited by 199 publications

References 30 publications

Transcript map and complete genomic sequence for the 310 kb region of minimal allele loss on chromosome segment 11p15.5 in non-small-cell lung cancer

Transcript map and complete genomic sequence for the 310 kb region of minimal allele loss on chromosome segment 11p15.5 in non-small-cell lung cancer

Loss of heterozygosity on the long arm of human chromosome 7 in sporadic renal cell carcinomas

Molecular determinants of metastatic transformation.

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