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Dr. Qing-Bin Guo

Ph.D.
Interests

Genomic Alterations in Solid Tumors and Myelodysplastic Syndromes

Titles

Assistant Profesor of Oncology, Johns Hopkins University, Baltimore, MD

Schools\Degrees

Ph.D., Biochemistry, Ohio State University, Columbus, Ohio

Training

Postdoctoral Fellow, Lab of J. Michael Bishop, University of California at San Francisco, San Francisco, CA

Senior Staff Fellow, National Cancer Institute, Bethesda, MD

Research Summary

Research GoalsDr. Guo has been interested in how the cell can precisely control its growth, differentiation or death, and how the failure to control these processes can result in cancer. His current work is focused on how the tumorigenic cell growth can be caused by the overexpression of Myc and how the genetic instability caused by the abnormal behavior of centrosomes can lead to cancers. His research goal is to understand the mechanism of tumorigenesis by combining technologies in genomics with genetic, molecular and cellular biological approaches.

Overall Research Summary and SignificanceDr. Guo is interested in understanding the mechanism of tumorigenesis. His current research has focused on the following two lines of investigation. The first line of investigation is to study how the proto-oncogene myc functions in the proliferation of normal or neoplastic cells. Deregulated Myc expression is among the most commonly found aberrations in human cancers. Extensive studies on myc in the past twenty years have demonstrated that myc plays an important role in cell growth, differentiation, and apoptosis. However, the mechanism by which Myc induces tumorigenic growth remains largely unknown. As a transcription factor, Myc contributes to the proliferation of the cell by turning on or off its target genes. Using cDNA microarray technology, Dr. Guo has discovered 198 genes regulated by physiologically expressed Myc. They also found that over-expressed Myc regulates an additional set of genes that are not regulated by the physiologically expressed Myc. These genes have provided a comprehensive road map to further decipher the signaling pathways regulated by Myc. The microarray study of the genes regulated by overexpressed Myc in human cancer cells should provide new avenues to develop diagnostic tools for the cancers related to Myc overexpression. The second line of investigation is to study the genetic instability caused by the abnormal centrosomes. Recent studies have shown that genetic instability is one of the most important causes for tumorigenesis. A centrosome, which is the microtubule organization center in metazoa, has to duplicate once and only once per cell cycle to organize a bipolar spindle for accurate chromosome segregation. Abnormal centrosomal duplication, which has been rarely studied for its contribution to tumorigenesis, can cause multiple centrosomes, multi-polar spindle in cell division. This could lead to genetic instability, aneuploidy and cancers. Dr. Guo’s lab is now searching for genetic changes that can cause abnormal centrosomal duplication and multiple centrosomes. They hope that the studies of these genetic changes can help to understand the mechanism of tumorigenesis.

Highlights of One or Two Published Scientific AccomplishmentsThe nuclear oncogene myc is a master regulator of cell growth and the activation of myc is among the most commonly found aberrations in human cancer. Myc-target genes have been the focus in the field for many years, and are considered the key for understanding Myc’s function. The functionally defined and relevant Myc target genes were essentially unknown due to the lack of a good cellular system and effective method. Using cDNA microarray analysis of genetically defined cellular systems, Dr. Guo has identified 198 Myc target genes, which are regulated by a physiological level of Myc and might be important for Myc’s function in the growth of normal cells. Using similar approaches, Dr. Guo has also found 51 genes specifically regulated by overexpressed Myc, not by the physiologically expressed Myc. Since physiological expression of Myc is necessary and essential for the normal cell growth, whereas overexpression of Myc can cause tumorigenic growth, the overexpressed Myc must behave differently from the physiologically expressed Myc. The overexpressed Myc may turn on or turn off the transcription of an additional set of genes, when compared to the physiologically expressed c-Myc. These abnormally expressed genes caused by Myc overexpression could in turn activate or suppress certain signaling pathways and eventually lead to neoplastic transformation of the cell. These work have been published recently (Guo et al., Cancer Research 60, 5922-5928, November 1, 2000).

Future Directions

The future research direction of Dr. Guo’s lab is to understand the mechanism of tumorigenesis by combining the technologies in genomics and molecular biology. More specifically, Dr. Guo’s lab will focus on the following questions: (1) How the overexpressed Myc functions in apoptosis in order to contribute to the tumorigenesis process; (2) What are the checkpoints regulating the coupling of DNA replication and centrosome duplication; (3) How these checkpoint genes function in the cell to segregate chromosomes correctly to avoid aneuploidy.

Description of Research Activities

Dr. Guo’s research aims to understand mechanism of tumorigenesis by combining technologies in genomics with genetic and molecular biological approaches.

Journal Citations

Qingbin M. Guo (2003), DNA Microarrays and Cancer, Current Opinion in Oncology 15, issue 1, in press.



R. L Malek, R. B. Irby, Qingbin M. Guo, K. Lee, S. Wong, M. He, J. Tsai, B. Frank, E. T. Liu, J. Quackenbush, R. Jove, T. J. Yeatman, N. H. Lee (2002), Identification of Src transformation fingerprint in human colon cancer, Oncogene 21, 7256-7265.



L. D. Miller, K. S. Park, Qingbin M. Guo, N. W. Alkharouf, R. L. Malek, N. H. Lee, E. T. Liu, and S-y. Cheng (2001). Silencing of Wnt signaling and activation of multiple metabolic pathways in response to thyroid hormone-stimulated cell proliferation. Molecular and Cellular Biology 21, 6626-6639.

 

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