Physical and Transcriptional Mapping of the 17p13.3 Region That Is Frequently Deleted in Human Cancer

Hoff, Céline; Seranski, Peter; Mollenhauer, Jan; Korn, Bernhard; Detzel, Tanja; Reinhardt, Richard; Ramser, Juliane; Poustka, Annemarie

doi:10.1006/geno.2000.6353

Cited by 16 publications

(12 citation statements)

References 27 publications

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“…We therefore suggest that these adjacent deletions may have occurred prior to the deletion of the TP53 locus, providing evidence for ongoing deletional events on 17p. Interestingly, loss of heterozygosity has been described at 17p13.3, distal to the TP53 locus, in lymphomas and leukemias [23] and other malignancies [24]. ArrayCGH also identified chromosomal losses on 18p and 20p.…”

Section: Discussionmentioning

confidence: 95%

Characterising the TP53-deleted subgroup of chronic lymphocytic leukemia: an analysis of additional cytogenetic abnormalities detected by interphase fluorescencein situhybridisation and array-based comparative genomic hybridisation

Rudenko

Else²,

Dearden³

et al. 2008

Leukemia & Lymphoma

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Deletion of the TP53 gene on chromosome 17p13.1 is the prognostic factor associated with the shortest survival in CLL. We used array-based comparative genomic hybridisation (arrayCGH) to identify additional DNA copy number changes in peripheral blood samples from 74 LRF CLL4 trial patients, 37 with >or=5% and 37 without TP53-deleted cells. ArrayCGH reliably detected deletions on 17p, including the TP53 locus, in cases with >or=50%TP53-deleted cells detected by fluorescence in situ hybridisation, plus seven additional cases with deleted regions on 17p excluding TP53. Losses on chromosomal regions 18p and/or 20p were found exclusively in cases with >or=5%TP53-deleted cells (p<0.001), 38% having one or both losses. The incidence of additional cytogenetic abnormalities, reflecting an increased chromosomal instability, was higher in >or=5%TP53-deleted cases (p=0.02). In particular, amplification of 2p and deletion of 6q were both more frequent. Cases with >20%TP53-deleted cells had the worst prognosis in the LRF CLL4 trial.

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Section: Discussionmentioning

confidence: 95%

Characterising the TP53-deleted subgroup of chronic lymphocytic leukemia: an analysis of additional cytogenetic abnormalities detected by interphase fluorescencein situhybridisation and array-based comparative genomic hybridisation

Rudenko

Else²,

Dearden³

et al. 2008

Leukemia & Lymphoma

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“…These results also raise the possibility that Mnt may function as a tumor suppressor in human breast cancer. Indeed the MNT gene resides at17p13.3, a hotspot for LOH in breast and other cancers (Cornelis et al ., 1994; Hoff et al ., 2000). However, a previous study of nine sporadic breast cancers showing LOH specifically at the MNT locus failed to identify mutations in the remaining allele (Nigro et al ., 1998).…”

Section: Discussionmentioning

confidence: 99%

Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

et al. 2003

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Mnt is a Max‐interacting transcriptional repressor that has been hypothesized to function as a Myc antagonist. To investigate Mnt function we deleted the Mnt gene in mice. Since mice lacking Mnt were born severely runted and typically died within several days of birth, mouse embryo fibroblasts (MEFs) derived from these mice and conditional Mnt knockout mice were used in this study. In the absence of Mnt, MEFs prematurely entered the S phase of the cell cycle and proliferated more rapidly than Mnt+/+ MEFs. Defective cell cycle control in the absence of Mnt is linked to upregulation of Cdk4 and cyclin E and the Cdk4 gene appears to be a direct target of Mnt–Myc antagonism. Like MEFs that overexpress Myc, Mnt−/− MEFs were prone to apoptosis, efficiently escaped senescence and could be transformed with oncogenic Ras alone. Consistent with Mnt functioning as a tumor suppressor, conditional inactivation of Mnt in breast epithelium led to adenocarinomas. These results demonstrate a unique negative regulatory role for Mnt in governing key Myc functions associated with cell proliferation and tumorigenesis.

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“…The TP53 tumor-suppressor gene (TSG) at 17p13.1 is one of the most frequently mutated genes in EOC (Okamoto et al, 1991). However, LOH analysis suggests the location of novel TSGs on the short arm of chromosome 17 at or close to the TP53 locus (Okamoto et al, 1991;Tsao et al, 1991;Eccles et al, 1992;Cliby et al, 1993;Foulkes et al, 1993;Yang-Feng et al, 1993) and at a more telomeric region, 17p13.3 (Phillips et al, 1993;Konishi et al, 1998;Phelan et al, 1998;Hoff et al, 2000). A number of genes on the long arm of chromosome 17 also have been shown to be implicated in EOC: the ERBB2 oncogene at 17q21.1 (Slamon et al, 1989), the hereditary breast/ ovarian cancer TSG BRCA1 at 17q21.1 (Miki et al, 1994;Merajver et al, 1995) and the NME1 tumor metastasis marker gene at 17q21.3 (Mandai et al, 1994;Leary et al, 1995;Schneider et al, 1996Schneider et al, , 2000.…”

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confidence: 99%

Patterns of expression of chromosome 17 genes in primary cultures of normal ovarian surface epithelia and epithelial ovarian cancer cell lines

Presneau

Mes-Masson

et al. 2003

Oncogene

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Physical and Transcriptional Mapping of the 17p13.3 Region That Is Frequently Deleted in Human Cancer

Cited by 16 publications

References 27 publications

Characterising the TP53-deleted subgroup of chronic lymphocytic leukemia: an analysis of additional cytogenetic abnormalities detected by interphase fluorescencein situhybridisation and array-based comparative genomic hybridisation

Characterising the TP53-deleted subgroup of chronic lymphocytic leukemia: an analysis of additional cytogenetic abnormalities detected by interphase fluorescencein situhybridisation and array-based comparative genomic hybridisation

Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

Patterns of expression of chromosome 17 genes in primary cultures of normal ovarian surface epithelia and epithelial ovarian cancer cell lines

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