Tumor suppressor genes: a new era for molecular genetic studies of cancer

1991 ◽  
Vol 19 (1) ◽  
pp. 3-13 ◽  
Author(s):  
Eva Y. -H. P. Lee
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Molecular Genetic ◽  
Genetic Studies ◽  
Suppressor Genes ◽  
New Era

Analysis of loss of heterozygosity on chromosomes 10q, 11, and 16 in medulloblastomas

2001 ◽  
Vol 94 (5) ◽  
pp. 799-805 ◽  
Author(s):  
Xiao-lu Yin ◽  
Jesse C. Pang ◽  
Yan-hui Liu ◽  
Edith Y. Chong ◽  
Yue Cheng ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Tumor Suppressor Genes ◽  
Molecular Genetic ◽  
Genetic Material ◽  
Suppressor Genes ◽  
Blood Samples ◽  
Content Type ◽  
Targeted Deletion ◽  
Fine Print

Object. The loss of genetic material from specific chromosome loci is a common feature in the oncogenesis of tumors and is often indicative of the presence of important tumor suppressor genes at these loci. Recent molecular genetic analyses have demonstrated frequent loss of chromosomes 10q, 11, and 16 in medulloblastomas. The aim of this study was to localize the targeted deletion regions on the three aforementioned chromosomes in medulloblastomas. Methods. Loss of heterozygosity (LOH) was examined on chromosomes 10q, 11, and 16 in a series of 22 primary and two recurrent medulloblastomas by using polymerase chain reaction—based microsatellite analysis. The DNA extracted from the tumors and corresponding normal blood samples were amplified independently in the presence of radioactively labeled microsatellite primers, resolved by denaturing gel electrophoresis and processed for autoradiography. The DNA obtained from control blood samples that displayed allelic heterozygosity at a given microsatellite locus were considered informative. Loss of heterozygosity was inferred when the allelic signal intensity of the tumor sample was reduced by at least 40%, relative to that of the constitutional control. The LOH analysis demonstrated that deletions of chromosomes 10q, 11p, and 16q are recurrent genetic events in the development of medulloblastomas. Three subchromosomal regions of loss have been identified and are localized to the deleted in malignant brain tumors 1 [DMBT1] gene site on chromosomes 10q25, 11p13–11p15.1, and 16q24.1–24.3. Conclusions. These results indicate that DMBT1 is closely associated with the oncogenesis of medulloblastomas and highlight regions of loss on chromosomes 11p and 16q for further fine mapping and cloning of candidate tumor suppressor genes that are important for the genesis of medulloblastoma.

Expression of the Tumor Suppressor Genes NF2, 4.1B, and TSLC1 in Canine Meningiomas

2009 ◽  
Vol 46 (5) ◽  
pp. 884-892 ◽  
Author(s):  
P. J. Dickinson ◽  
E. I. Surace ◽  
M. Cambell ◽  
R. J. Higgins ◽  
C. M. Leutenegger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Suppressor ◽  
Western Blotting ◽  
Tumor Suppressor Genes ◽  
Molecular Genetic ◽  
Tumor Grade ◽  
Suppressor Gene ◽  
Early Event ◽  
Rt Pcr ◽  
Suppressor Genes

Meningiomas are common primary brain tumors in dogs; however, little is known about the molecular genetic mechanisms involved in their tumorigenesis. Several tumor suppressor genes have been implicated in meningioma pathogenesis in humans, including the neurofibromatosis 2 ( NF2), protein 4.1B ( 4.1 B), and tumor suppressor in lung cancer-1 ( TSLC1) genes. We investigated the expression of these tumor suppressor genes in a series of spontaneous canine meningiomas using quantitative real-time reverse transcription polymerase chain reaction (RT-PCR) ( NF2; n = 25) and western blotting (NF2/merlin, 4.1B, TSLC1; n = 30). Decreased expression of 4.1B and TSLC1 expression on western blotting was seen in 6/30 (20%) and in 15/30 (50%) tumors, respectively, with 18/30 (60%) of meningiomas having decreased or absent expression of one or both proteins. NF2 gene expression assessed by western blotting and RT-PCR varied considerably between individual tumors. Complete loss of NF2 protein on western blotting was not seen, unlike 4.1B and TSLC1. Incidence of TSLC1 abnormalities was similar to that seen in human meningiomas, while perturbation of NF2 and 4.1B appeared to be less common than reported for human tumors. No association was observed between tumor grade, subtype, or location and tumor suppressor gene expression based on western blot or RT-PCR. These results suggest that loss of these tumor suppressor genes is a frequent occurrence in canine meningiomas and may be an early event in tumorigenesis in some cases. In addition, it is likely that other, as yet unidentified, genes play an important role in canine meningioma formation and growth.

Molecular genetic analysis of phosphatase and tensin homolog and p16 tumor suppressor genes in patients with malignant glioma

2003 ◽  
Vol 14 (4) ◽  
pp. 1-7 ◽  
Author(s):  
Jafri Malin Abdullah ◽  
Norafiza Zainuddin ◽  
Sarina Sulong ◽  
Hasnan Jaafar ◽  
Mohamad Nizam Isa
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Molecular Genetic ◽  
Malignant Gliomas ◽  
Point Mutations ◽  
Molecular Genetic Analysis ◽  
Chromosome 10 ◽  
Suppressor Genes ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog

Object Several genes have been shown to carry mutations in human malignant gliomas, including the phosphatase and tensin homolog (PTEN) deleted on chromosome 10 and p16 tumor suppressor genes. Alterations of this gene located on chromosome 10 q23 and 9p21, respectively, may contribute to gliomagenesis. In this study, the authors analyzed 20 cases of malignant gliomas obtained in patients living on the east coast of Malaysia to investigate the possibilities of involvement of the PTEN and p16 genes. Methods Samples of DNA were amplified by polymerase chain reaction (PCR), analyzed by single-stranded conformation polymorphism (SSCP), and subsequently by sequencing. Two cases of glioblastoma multiforme, three cases of anaplastic astrocytoma, one case of anaplastic pleomorphic xanthoastrocytoma, and one case of anaplastic ependymoma showed SSCP band shifts in PTEN mutational analyses. The DNA sequencing analyses of these samples revealed missense and nonsense mutations, with cluster of mutations in the region 5' to the core phosphatase motif of exon 5 and the 5'-end of exon 6. No abnormal migration shifts were detected in the glioma samples analyzed for point mutations of the p16 gene. Homozygous deletions of p16 were also not detected in all samples. Conclusions These findings indicate that mutations of the PTEN genes were likely to contribute to the tumorigenesis and morphological transformations of gliomas. In addition, the alterations of the p16 gene might not play a major role in tumorigenesis of malignant gliomas in Malaysian patients.

Molecular Genetic and Immunohistochemical Analysis of the Tumor Suppressor Genes Rb and p53 in Palmar and Aggressive Fibromatosis

1996 ◽  
Vol 5 (3) ◽  
pp. 194-200 ◽  
Author(s):  
Elkay Muller ◽  
Massimo Castagnaro ◽  
David W. Yandel ◽  
Hubert J. Wolfe ◽  
Benjamin A. Alman
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Molecular Genetic ◽  
Immunohistochemical Analysis ◽  
Aggressive Fibromatosis ◽  
Suppressor Genes
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