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W. K. A. Yung

Bio: W. K. A. Yung is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Gene & Gene mapping. The author has an hindex of 3, co-authored 4 publications receiving 2729 citations.

Papers
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Journal ArticleDOI
TL;DR: The results identify a strong candidate tumour suppressor gene at chromosome 10q23.3, whose loss of function appears to be associated with the oncogenesis of multiple human cancers.
Abstract: Deletions involving regions of chromosome 10 occur in the vast majority (> 90%) of human glioblastoma multiformes. A region at chromosome 10q23-24 was implicated to contain a tumour suppressor gene and the identification of homozygous deletions in four glioma cell lines further refined the location. We have identified a gene, designated MMAC1, that spans these deletions and encodes a widely expressed 5.5-kb mRNA. The predicted MMAC1 protein contains sequence motifs with significant homology to the catalytic domain of protein phosphatases and to the cytoskeletal proteins, tensin and auxilin. MMAC1 coding-region mutations were observed in a number of glioma, prostate, kidney and breast carcinoma cell lines or tumour specimens. Our results identify a strong candidate tumour suppressor gene at chromosome 10q23.3, whose loss of function appears to be associated with the oncogenesis of multiple human cancers.

2,777 citations

Journal ArticleDOI
06 Mar 1997-Oncogene
TL;DR: The differential expression pattern, tissue distribution and chromosomal location of RIG suggests it serves as a molecular marker for or may play a role in the malignant progression of GBMs.
Abstract: Genetic deletions to chromosome 10 have been extensively documented for human glioblastomas (GBMs). To identify gene products that may be involved in malignant progression, a subtractive hybridization was performed between GBM cells and hybrid cells suppressed for tumorigenicity following microcell transfer of chromosome 10. One novel cDNA isolated from this subtraction showed consistent upregulation (approximately 4 to 10-fold) that correlated with the nontumorigenic phenotype of the hybrid cells. Subsequent analysis resulted in the identification of a full length cDNA (2,569 bp) termed RIG (regulated in glioma). RIG expression was either not detected or detected only at low levels in cultured glioma cells and primary glioblastoma specimens compared to normal brain cells. The 2.6 kb RIG mRNA was expressed predominantly in normal brain with lower levels in heart and lung. Sequence analysis showed no significant homology to known gene products. Genomic alterations of RIG were present in approximately 25% of glioma cell lines examined. Also, RIG mapped to chromosome 11p15.1, a region that is known to be altered in malignant astrocytomas. The differential expression pattern, tissue distribution and chromosomal location of RIG suggests it serves as a molecular marker for or may play a role in the malignant progression of GBMs.

12 citations


Cited by
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Journal ArticleDOI
TL;DR: Small-molecule therapeutics that block PI3K signalling might deal a severe blow to cancer cells by blocking many aspects of the tumour-cell phenotype.
Abstract: One signal that is overactivated in a wide range of tumour types is the production of a phospholipid, phosphatidylinositol (3,4,5) trisphosphate, by phosphatidylinositol 3-kinase (PI3K) This lipid and the protein kinase that is activated by it — AKT — trigger a cascade of responses, from cell growth and proliferation to survival and motility, that drive tumour progression Small-molecule therapeutics that block PI3K signalling might deal a severe blow to cancer cells by blocking many aspects of the tumour-cell phenotype

5,654 citations

Journal ArticleDOI
TL;DR: The authors found that approximately 5% of patients with malignant gliomas have a family history of glioma and most of these familial cases are associated with rare genetic syndromes, such as neurofibromatosis types 1 and 2, the Li−Fraumeni syndrome (germ-line p53 mutations associated with an increased risk of several cancers), and Turcot's syndrome (intestinal polyposis and brain tumors).
Abstract: Approximately 5% of patients with malignant gliomas have a family history of gliomas. Some of these familial cases are associated with rare genetic syndromes, such as neurofibromatosis types 1 and 2, the Li−Fraumeni syndrome (germ-line p53 mutations associated with an increased risk of several cancers), and Turcot’s syndrome (intestinal polyposis and brain tumors). 10 However, most familial cases have

3,823 citations

Journal ArticleDOI
17 May 2001-Nature
TL;DR: Deregulated cell proliferation provides a minimal 'platform' necessary to support further neoplastic progression and should be targeted withroit targeting to have potent and specific therapeutic consequences.
Abstract: Beneath the complexity and idiopathy of every cancer lies a limited number of 'mission critical' events that have propelled the tumour cell and its progeny into uncontrolled expansion and invasion One of these is deregulated cell proliferation, which, together with the obligate compensatory suppression of apoptosis needed to support it, provides a minimal 'platform' necessary to support further neoplastic progression Adroit targeting of these critical events should have potent and specific therapeutic consequences

3,151 citations

Journal ArticleDOI
TL;DR: It is demonstrated that overexpression of PTEN, a putative tumor suppressor, reduced insulin-induced PtdIns(3,4,5)P3 production in human 293 cells without effecting insulin- induced phosphoinositide 3-kinase activation.

3,069 citations

Journal ArticleDOI
TL;DR: In light of the recent advances in understanding of the function of PI3Ks in the pathogenesis of diabetes and cancer, the exciting therapeutic opportunities for targeting this pathway to treat these diseases are discussed.
Abstract: Phosphatidylinositol 3-kinases (PI3Ks) evolved from a single enzyme that regulates vesicle trafficking in unicellular eukaryotes into a family of enzymes that regulate cellular metabolism and growth in multicellular organisms. In this review, we examine how the PI3K pathway has evolved to control these fundamental processes, and how this pathway is in turn regulated by intricate feedback and crosstalk mechanisms. In light of the recent advances in our understanding of the function of PI3Ks in the pathogenesis of diabetes and cancer, we discuss the exciting therapeutic opportunities for targeting this pathway to treat these diseases.

2,935 citations