Tumor Suppressor Genes

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Maria Del Mar Alonso - One of the best experts on this subject based on the ideXlab platform.

  • Cloning of Tumor Suppressor Genes Involved in Solid Tumor Development
    Archives of otolaryngology--head & neck surgery, 1993
    Co-Authors: David I. Smith, Maria Del Mar Alonso
    Abstract:

    Objective: The homozygous inactivation of Tumor Suppressor Genes is a common event in the multistep process of TumoriGenesis. The identification of most Tumor Suppressor Genes known to date has come from the study of individuals with a defective copy of such a gene that increases their predisposition to malignancy. Although much is still to be learned about the function of these Genes, they all seem to play a role in cell growth regulation. Karyotypic and molecular studies of several solid Tumors suggest the presence of at least three Tumor Suppressor Genes on the short arm of human chromosome 3. We present an overview on the progress made in the identification of Tumor Suppressor Genes involved in solid Tumor development. Conclusion: The explosive effort to map the human genome fueled by the Human Genome Project will facilitate the identification of Tumor Suppressor Genes on chromosome 3 and on other chromosomes within

Chao Zhang - One of the best experts on this subject based on the ideXlab platform.

  • derepression of co silenced Tumor Suppressor Genes by nanoparticle loaded circular ssdna reduces Tumor malignancy
    Science Translational Medicine, 2018
    Co-Authors: Jing Meng, Shuang Chen, Jingxia Han, Qiang Tan, Xiaorui Wang, Hongzhi Wang, Weilong Zhong, Yuan Qin, Kailiang Qiao, Chao Zhang
    Abstract:

    The co-silencing of multiple Tumor Suppressor Genes can lead to escalated malignancy in cancer cells. Given the limited efficacy of anticancer therapies targeting single Tumor Suppressor Genes, we developed small circular single-stranded DNA (CSSD) that can up-regulate the expression of co-silenced Tumor Suppressor Genes by sequestering microRNAs (miRNAs) that negatively regulate these Genes. We found that cancer patients with low Tumor expression of the Tumor Suppressor Genes KLF17, CDH1, and LASS2 had shortened survival times. The up-regulation of these Genes upon transfection of artificial CSSD-9 inhibited Tumor proliferation and metastasis and promoted apoptosis in vitro as well as in ex vivo and patient-derived xenograft models. In addition, CSSD is more stable and effective than current miRNA inhibitors, and transfecting CSSDs via nanoparticles substantially improved delivery efficiency. The use of a single CSSD can promote the inhibition of multiple Tumor Suppressor Genes. This study provides evidence for the possibility of using CSSDs as therapeutic miRNA inhibitors to target the co-silencing of multiple Tumor Suppressor Genes.

Ilana Zalcberg Renault - One of the best experts on this subject based on the ideXlab platform.

  • Methylation status of nine Tumor Suppressor Genes in multiple myeloma
    International Journal of Hematology, 2010
    Co-Authors: Esteban Braggio, Angelo Maiolino, Maria E. Gouveia, Roberto Magalhães, João T. Souto Filho, Márcia Garnica, Marcio Nucci, Ilana Zalcberg Renault
    Abstract:

    Aberrant methylation in promoter-associated CpG islands has been recognized as a major mechanism for Tumor Suppressor gene silencing in several malignancies. We determined the methylation status of nine Tumor Suppressor Genes in 68 newly diagnosed MM patients by methylation-specific PCR. The frequency of promoter hypermethylation for individual Genes was: CDH 1, 50%; p16 ^ INK4a , 42.8%; p15 ^ INK4b , 16.2%; SHP 1, 14.7%; ER and BNIP 3, 13.2%; RAR β, 11.8%; DAPK 5.9%; and MGMT 0%. Overall, 79% of patients presented at least one hypermethylated gene. By univariate analysis, hypermethylation of DAPK ( P  

Maartje G Noordhuis - One of the best experts on this subject based on the ideXlab platform.

  • key Tumor Suppressor Genes inactivated by greater promoter methylation and somatic mutations in head and neck cancer
    Epigenetics, 2014
    Co-Authors: Rafael Guerreropreston, Christina Michailidi, Luigi Marchionni, Curtis R Pickering, Mitchell J Frederick, Jeffrey N Myers, Srinivasan Yegnasubramanian, Tal Hadar, Maartje G Noordhuis
    Abstract:

    Tumor Suppressor Genes (TSGs) are commonly inactivated by somatic mutation and/or promoter methylation; yet, recent high-throughput genomic studies have not identified key TSGs inactivated by both mechanisms. We pursued an integrated molecular analysis based on methylation binding domain sequencing (MBD-seq), 450K Methylation arrays, whole exome sequencing, and whole genome gene expression arrays in primary head and neck squamous cell carcinoma (HNSCC) Tumors and matched uvulopalatopharyngoplasty tissue samples (UPPPs). We uncovered 186 downregulated Genes harboring cancer specific promoter methylation including PAX1 and PAX5 and we identified 10 key Tumor Suppressor Genes (GABRB3, HOXC12, PARP15, SLCO4C1, CDKN2A, PAX1, PIK3AP1, HOXC6, PLCB1, and ZIC4) inactivated by both promoter methylation and/or somatic mutation. Among the novel Tumor Suppressor Genes discovered with dual mechanisms of inactivation, we found a high frequency of genomic and epigenomic alterations in the PAX gene family of transcription...

Robert A. Weinberg - One of the best experts on this subject based on the ideXlab platform.

  • OncoGenes and Tumor Suppressor Genes
    CA: a cancer journal for clinicians, 1994
    Co-Authors: Robert A. Weinberg
    Abstract:

    In the past 15 years, many of the mechanisms underlying the molecular origins of cancer have been uncovered, and a clear picture of the role of oncoGenes and Tumor Suppressor Genes in carcinoGenesis has developed. This article reviews the mechanisms by which oncoGenes and Tumor Suppressor Genes participate in the creation of Tumors.

  • Tumor Suppressor Genes
    Current Opinion in Genetics & Development, 1994
    Co-Authors: Philip W Hinds, Robert A. Weinberg
    Abstract:

    The mutation of Tumor Suppressor Genes is thought to contribute to Tumor growth by inactivating proteins that normally act to limit cell proliferation. Several Tumor Suppressor proteins have been identified in recent years, but only two of them, p53 and pRb, are understood in detail. In the past year, a role has become apparent for both of these proteins in transcription and phosphorylation events required for passage of a cell from G1 to S phase. The pRb protein appears to prevent the function of transcription factors and other proteins needed for S phase until its inactivation by cyclin-dependent kinases in late G1. Induction of p53 by DNA damage may act to cause cell cycle arrest or cell death by altering the transcription program of damaged cells. A detailed molecular understanding of these growth regulators is now emerging, and is the subject of this review.

  • Tumor Suppressor Genes
    Neuron, 1993
    Co-Authors: Robert A. Weinberg
    Abstract:

    For the past two decades, oncoGenes have captured the lion’s share of attention among those interested in the molecular and genetic bases of cell transformation. These Genes have presented a powerful paradigm of how cell transformation takes place when triggered by viral infections or somatic mutation. Yet we now realize that there is an equally important second side of the coin, presented by a distinct class of Genes known variously as Tumor Suppressor Genes or anti-oncoGenes. The existence of Tumor Suppressor Genes could have been predicted from first principles, but few had the temerity to do so. The logic of their function is simple and straightforward. Cellular oncoGenes represent deregulated, hyperactive forms of normal cellular growth-promoting Genes (proto-oncoGenes). The activation of an oncogene in the genome of a normal cell results in the release of a steady stream of mitogenie signals that forces a cell and its descendants through unrelenting rounds of division. Logic dictates an equally elaborate array of growthconstraining elements in the cell’s signaling circuitry that serve as a counterweight to the growth-promoting proto-oncoGenes. Their loss through mutational inactivation might lead to runaway cell growth. We now know that Tumor cell growth often depends on the confluence of both types of genetic change, yielding hyperactivegrowth-promotingGenes(oncoGenes) on the one hand and inactive versions of the growthconstraining Genes (Tumor Suppressors) on the other. The very existence of such Suppressor Genes becomes apparent only when they are lost from the cell genome. This experimental difficulty has kept progress in the field studying these Genes a decade behind that devoted to research on oncoGenes. But this substantial inconvenience has been swept aside by new and powerful means of detecting Tumor Suppressor Genes and isolating them through molecular cloning. We now have a collection of more than a half dozen of these Genes in cloned form. Inactivated versions of each can be found in the genomes of a variety of Tumor cell types (see Table 1).

  • Tumor Suppressor Genes
    Science (New York N.Y.), 1991
    Co-Authors: Robert A. Weinberg
    Abstract:

    For the past decade, cellular oncoGenes have attracted the attention of biologists intent on understanding the molecular origins of cancer. As the present decade unfolds, oncoGenes are yielding their place at center stage to a second group of actors, the Tumor Suppressor Genes, which promise to teach us equally important lessons about the molecular mechanisms of cancer pathoGenesis.