Chromosome 11p15 deletions in human malignant astrocytomas and primitive neuroectodermal tumors

Fults, Dan; Petronio, Joseph; Noblett, Bradley D.; Pedone, Carolyn A.

doi:10.1016/s0888-7543(05)80191-0

Cited by 51 publications

(35 citation statements)

References 8 publications

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“…Allelic deletion of the chromosome 11 p-arm occurs in approximately 30% of high-grade astrocytomas and rarely occurs in low-grade astrocytomas (121,(132)(133)(134)(135) , suggesting the presence of a tumor suppressor gene involved in the malignant progression of astrocytic gliomas. Based on a limited number of mapping studies, the common deletion interval has been localized to a 21-cM region on 11p15.5-pter (133,134).…”

Section: Chromosome Arm 11pmentioning

confidence: 99%

Genetic alterations in adult diffuse glioma: occurrence, significance, and prognostic implications

Smith

Jenkins²

2000

Front Biosci

146

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Our understanding of diffuse glioma development and progression has expanded remarkably over the past decade. As the genetic alterations responsible for these tumors are identified, molecular models of glioma pathogenesis are emerging and hold great promise to explain the biologic mechanisms of these neoplasms. Although these models continue to evolve and remain highly simplified, some of the genetic alterations that they encompass appear to be prognostically useful. Among the astrocytic gliomas, age and tumor grade are the most powerful indicators of patient survival, however, a wide range of variability remains, particularly among the lowgrade and anaplastic astrocytomas. Recent reports indicate that alterations of the PTEN tumor suppressor gene are independent predictors of overall survival for anaplastic astrocytoma patients, helping to distinguish the cases with behavior resembling their more malignant counterparts, the glioblastomas.Among the oligodendroglial tumors, alterations of the 1p and 19q chromosome arms have emerged as potentially powerful predictors of overall patient survival and in vivo chemotherapeutic response, while alterations of the p16/CDKN2A tumor suppressor gene suggest shorter overall survival. As our molecular models continue to improve, through functional analyses and the identification of additional genetic contributors, we will expand our capacity to more effectively prognose these patients and to design rational therapeutic strategies. INTRODUCTIONDiffuse gliomas exhibit an inherent tendency to progress to more malignant phenotypes and a broad range of clinical behavior. Classification of diffuse gliomas by histologic subtype (figure 1) and malignancy grade (figure 2),

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Section: Chromosome Arm 11pmentioning

confidence: 99%

Genetic alterations in adult diffuse glioma: occurrence, significance, and prognostic implications

Smith

Jenkins²

2000

Front Biosci

146

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“…Loss of heterozygosity studies have previously implicated chromosome 11p15 in the genesis of multiple cancers, including Wilms tumor, small cell lung carcinoma, non-small cell lung carcinoma, bladder carcinoma, breast carcinoma and astrocytoma (Fults et al, 1992;Sonoda et al, 1995;Weston et al, 1989;Ludwig et al, 1991;Hao et al, 1993;Wingvist et al, 1993). Since most allelic deletion studies of astrocytomas have implicated the region 11p15.5 and not 11p15.1, it appears unlikely that RIG would be deleted in astrocytomas.…”

Section: Discussionmentioning

confidence: 99%

“…Since most allelic deletion studies of astrocytomas have implicated the region 11p15.5 and not 11p15.1, it appears unlikely that RIG would be deleted in astrocytomas. However, allelic deletions around 11p15.1 were not investigated in most studies (Fults et al, 1992;Sonoda et al, 1995). We identi®ed structural alterations of RIG in three cultured GBM cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…A number of chromosomal abnormalities are observed during the formation of GBM including ampli®cations of chromosome 7, speci®cally the EGF-R gene, and deletions of chromosomes 9p, 10p, 10q, 11p, 13, 17p and 22 (Wong et al, 1987;James et al, 1988;Bigner et al, 1990;Fults et al, 1992;Rasheed et al, 1992Rasheed et al, , 1995Ransom et al, 1992;Steck et al, 1995). Although candidate genes corresponding to some of these genetic losses have been identi®ed (Fults et al, 1989;James et al, 1989;Kamb et al, 1994;Henson et al, 1994), the speci®c genes mapping to the remaining loci remain elusive.…”

Section: Introductionmentioning

confidence: 99%

“…Although candidate genes corresponding to some of these genetic losses have been identi®ed (Fults et al, 1989;James et al, 1989;Kamb et al, 1994;Henson et al, 1994), the speci®c genes mapping to the remaining loci remain elusive. For instance, loss of heterozygosity on chromosome 11 has been shown to occur in 30 ± 40% of astrocytic tumors, yet no gene has been identi®ed as the target of this loss (Fults et al, 1992;Sonoda et al, 1995). By far the most frequent cytogenetic and molecular abnormality observed in GBM is the deletion of large regions of chromosome 10, however no speci®c region critical to the development of GBM has been identi®ed on this chromosome (Bigner et al, 1988;James et al, 1988;Ransom et al, 1992;Karlbom et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

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