The scientist’s investigation covers issues in Telomere, Telomerase, Genetics, Carcinogenesis and Cancer research. His work deals with themes such as Shelterin, Telomere-binding protein, DNA damage, Molecular biology and Cell biology, which intersect with Telomere. His work carried out in the field of Telomerase brings together such families of science as Liver function, Cirrhosis and Endocrinology, Ratón.
His Cancer research study incorporates themes from Tumor suppressor gene and Senescence. His studies in Tumor suppressor gene integrate themes in fields like Gene expression, Chromosomal translocation, KRAS and Metastatic carcinoma, Carcinoma. His Genome instability research integrates issues from Telomerase RNA component and DNA repair.
Sandy Chang spends much of his time researching Telomere, Genetics, DNA damage, Telomerase and Cell biology. The Telomere study combines topics in areas such as Telomere-binding protein, Shelterin, Cancer research, Genome instability and Molecular biology. He has included themes like Low Molecular Weight Cyclin E, Carcinogenesis, Tumor suppressor gene, Cyclin E and KRAS in his Cancer research study.
In his work, Gene expression is strongly intertwined with Chromosomal translocation, which is a subfield of Tumor suppressor gene. His study in the field of Cancer, Chromosome, Telomere dysfunction and Genome stability is also linked to topics like Context. Sandy Chang interconnects Cancer cell, Tumor progression, Cell culture and DNA polymerase in the investigation of issues within Telomerase.
His primary areas of investigation include Telomere, Cell biology, DNA repair, Genetics and Telomere-binding protein. His biological study spans a wide range of topics, including Shelterin, DNA damage, Mutation, Senescence and Telomerase. His studies deal with areas such as Carcinogenesis, G2-M DNA damage checkpoint and Binding site as well as DNA damage.
His Telomerase study combines topics from a wide range of disciplines, such as DNA, Mutant and Cas9. His Cell biology research includes elements of Protein structure and Repeated sequence. His Genetics research is mostly focused on the topic Genome instability.
His main research concerns DNA repair, Telomere, Telomere-binding protein, Homologous recombination and Genome instability. Much of his study explores DNA repair relationship to Gene silencing. Sandy Chang has researched Telomere in several fields, including Nucleoprotein, Homology, Protein structure, Repeated sequence and Cell biology.
His Telomere-binding protein research is multidisciplinary, incorporating perspectives in Plasma protein binding and Telomere end protection. His Homologous recombination research incorporates elements of Cancer research, Polymerase and DNA mismatch repair. His Genome instability research is included under the broader classification of Genetics.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice
Sunil R. Hingorani;Lifu Wang;Asha S. Multani;Chelsea Combs.
Cancer Cell (2005)
Longevity, stress response, and cancer in aging telomerase-deficient mice.
Karl Lenhard Rudolph;Sandy Chang;Han Woong Lee;Maria Blasco.
Cell (1999)
Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
Steven E. Artandi;Sandy Chang;Sandy Chang;Shwu-Luan Lee;Scott Alson.
Nature (2000)
Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects
David A Tuveson;Alice T Shaw;Alice T Shaw;Alice T Shaw;Nicholas A Willis;Daniel P Silver.
Cancer Cell (2004)
Inhibition of experimental liver cirrhosis in mice by telomerase gene delivery.
Karl Lenhard Rudolph;Sandy Chang;Melissa Millard;Nicole Schreiber-Agus.
Science (2000)
Essential role of limiting telomeres in the pathogenesis of Werner syndrome.
Sandy Chang;Asha S Multani;Noelia G Cabrera;Maria L Naylor.
Nature Genetics (2004)
The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations.
David O. Ferguson;JoAnn M. Sekiguchi;Sandy Chang;Karen M. Frank.
Proceedings of the National Academy of Sciences of the United States of America (2000)
Pot1 deficiency initiates DNA damage checkpoint activation and aberrant homologous recombination at telomeres.
Ling Wu;Asha S. Multani;Hua He;Wilfredo Cosme-Blanco.
Cell (2006)
Telomere dysfunction and tumour suppression: the senescence connection
Yibin Deng;Suzanne S. Chan;Sandy Chang.
Nature Reviews Cancer (2008)
Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice.
Geng Liu;John M Parant;Gene Lang;Patty Chau.
Nature Genetics (2004)
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