A Transcript Map of the Chromosome 19q-Arm Glioma Tumor Suppressor Region

Smith, Justin S.; Tachibana, Issei; Pohl, Ute; Lee, Hyun K.; Thanarajasingam, Uma; Portier, Bryce P.; Ueki, Keisuke; Ramaswamy, Shivapriya; Billings, Stephanie; Mohrenweiser, Harvey W.; Louis, David N.; Jenkins, Robert B.

doi:10.1006/geno.1999.6101

Cited by 117 publications

(80 citation statements)

References 31 publications

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“…In addition, this region is in the near vicinity of the region affected in Prader-Willi and Angelman syndromes 44 and the deletion of DNA in 15q13-14 (region 2) may cause additional clinical features in these patients. 45 Region 3 is estimated as 4.7 Mb and contains 15 known genes including one (LOC440311) similar to glioma tumor suppressor candidate gene 2 (GLTSCR2 46 ). GLTSCR2 has been localized in a common deletion region for human diffuse gliomas on chromosome 19, together with other genes like GLTSCR1.…”

Section: Discussionmentioning

confidence: 99%

Loss of heterozygosity at 15q21.3 correlates with occurrence of metastases in head and neck cancer

Poetsch

Kleist

2006

Modern Pathology

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Deletions on the long arm of chromosome 15 suggesting the presence of potential tumor suppressor genes have been found in several tumors including carcinomas of the colorectum, urinary bladder, breast, lung, and head and neck. Here, we analyzed allelic imbalance on chromosome 15q in head and neck carcinomas and corresponding lymph node metastases to define common regions of aberrations with potential involvement in development and progression of these tumors. We studied a panel of 40 polymorphic microsatellite markers, spanning 15q13-15q26, in 63 head and neck carcinomas and 38 lymph node metastases. Loss of heterozygosity (LOH) could be demonstrated in 34 primary tumors (54%) and 35 metastases (92%). Aberration mapping defined three minimum regions of aberrations: a region between the markers D15S106 and D15S1029 in 15q21.3 (estimated as 3.9 Mb; region 1) was affected in the majority of tumors, whereas two other regions between D15S144 and D15S1040 in 15q13.3-14 (estimated as 2.4 Mb; region 2) and between D15S130 and D15S985 in 15q26.2-26.3 (estimated as 4.7 Mb; region 3) were less often involved. Allelic loss in region 1 correlated with T stages (P ¼ 0.0029) and metastatic potential (P ¼ 0.0018). LOH in regions 2 and 3 occurred predominantly in metastases (P ¼ 0.0129 and P ¼ 0.0013, respectively). No correlation with grading, localization, or clinical outcome could be established for any of the affected regions. Our data hint at aberrations in 15q21.3 as a possible important characteristic for head and neck squamous cell carcinomas with risk of progression.

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Section: Discussionmentioning

confidence: 99%

Loss of heterozygosity at 15q21.3 correlates with occurrence of metastases in head and neck cancer

Poetsch

Kleist

2006

Modern Pathology

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“…56) An accumulating body of evidence has revealed that the 19q13.3 locus is frequently altered in certain types of human tumors, such as glioma and neuroblastoma, indicating that a yet unidentified tumor suppressor gene(s) specifically encoded in this region may participate in the tumorigenesis. [56][57][58][59] Our group has demonstrated that PICT-1 facilitates the C-tail phosphorylation and plays an essential role in stabilizing PTEN protein in cells. 52,55,60) Forced downregulation of PICT-1 in cells by the RNA interference decreased both PTEN C-tail phosphorylation and PTEN protein levels, leading to the hyperactivation of PI3K/PIP3 signals.…”

Section: Pten Regulators Involved In Human Tu-morigenensismentioning

confidence: 99%

PTEN: Its Deregulation and Tumorigenesis

Maehama

2007

Biological & Pharmaceutical Bulletin

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The tumor suppressor phosphatase and tensin homolog (PTEN) functions as a phosphoinositide 3-phosphatase, that antagonizes phosphatidylinositol 3-kinase action, and negatively regulates cell proliferation and survival signals. Inactivation of PTEN by loss-of-function mutations gives rise to deregulated hyperproliferation of cells, leading to oncogenic transformation. Recent studies have identified a number of upstream regulatory factors for PTEN and unveiled that the impairment in the PTEN regulatory system potentially becomes a causal factor for oncogenic transformation of cells. This article will review the PTEN inactivation mechanism which is linked to human tumorigenesis, particularly focusing on recent research progress in PTEN regulators.

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“…Recent finer deletion mapping have identified two overlapping regions, flanked by markers D19S241 and STD, with high frequency of allelic loss (Rosenberg et al, 1996;Smith et al, 2000a). A partial transcript map has been constructed for this deletion region (Smith et al, 2000b) and it remains to be determined if any of these genes is the tumour suppressor for gliomas.…”

Section: Genetics and Genomicsmentioning

confidence: 99%

High-resolution genome-wide allelotype analysis identifies loss of chromosome 14q as a recurrent genetic alteration in astrocytic tumours

Pang

Tong

et al. 2002

Br J Cancer

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Diffusely infiltrative astrocytic tumours are the most common neoplasms in the human brain. To localise putative tumour suppressor loci that are involved in low-grade astrocytomas, we performed high-resolution genome-wide allelotype analysis on 17 fibrillary astrocytomas. Non-random allelic losses were identified on chromosomal arms 10p (29%), 10q (29%), 14q (35%), 17p (53%), and 19q (29%), with their respective common regions of deletions delineated at 10p14-15.1, 10q25.1-qter, 14q212.2-qer, 17p11.2-pter and 19q12-13.4. These results suggest that alterations of these chromosomal regions play important roles in the development of astrocytoma. We also allelotyped 21 de novo glioblastoma multiforme with an aim to unveil genetic changes that are common to both types of astrocytic tumours. Non-random allelic losses were identified on 9p (67%), 10p (62%), 10q (76%), 13q (60%), 14q (50%), and 17p (65%). Allelic losses of 10p, 10q, 14q and 17p were common genetic alterations detectable in both fibrillary astrocytomas and glioblastoma multiforme. In addition, two common regions of deletions on chromosome 14 were mapped to 14q22.3-32.1 and 14q32.1-qter, suggesting the presence of two putative tumour suppressor genes. In conclusion, our comprehensive allelotype analysis has unveiled several critical tumour suppressor loci that are involved in the development of fibrillary astrocytomas and glioblastoma multiforme. Although these two types of brain tumours are believed to evolve from different genetic pathways, they do share some common genetic changes. Our results indicate that deletions of chromosome 14q is a recurrent genetic event in the development of astrocytoma and highlight the subchromosomal regions on this chromosome that are likely to contain putative tumour suppressor genes involved in the oncogenesis of astrocytic tumours.

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A Transcript Map of the Chromosome 19q-Arm Glioma Tumor Suppressor Region

Cited by 117 publications

References 31 publications

Loss of heterozygosity at 15q21.3 correlates with occurrence of metastases in head and neck cancer

Loss of heterozygosity at 15q21.3 correlates with occurrence of metastases in head and neck cancer

PTEN: Its Deregulation and Tumorigenesis

High-resolution genome-wide allelotype analysis identifies loss of chromosome 14q as a recurrent genetic alteration in astrocytic tumours

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