Pulivarthi H. Rao, PhD
- Cancer and Blood Disorders
Director, Cancer Cytogenetics Core Laboratory, Texas Children’s Cancer Center, Professor, Department of Pediatrics, Section of Hematology-Oncology, Baylor College of Medicine
Departments:
Office locations:
1102 Bates Avenue
Houston, TX 77030
Get to know Pulivarthi H. Rao, PhD
Education
| School | Education | Degree | Year |
|---|---|---|---|
| Memorial Sloan Kettering Cancer Center, Department of Human Genetics | Post-doctoral Fellowship | 1988 | |
| Nagarjuna University, India | PhD | Doctor of Philosophy | 1988 |
Organizations
| Organization Name | Role |
|---|---|
| American Association for Advancement of Science (AAAS) | Member |
| American Association for Cancer Research (AACR) | Member |
| American Society for Human Genetics (ASHG) | Member |
| American Society of Hematology (ASH) | Member |
| Children’s Oncology Group (COG) | Associate Member |
* Texas Children’s Hospital physicians’ licenses and credentials are reviewed prior to practicing at any of our facilities. Sections titled From the Doctor, Professional Organizations and Publications were provided by the physician’s office and were not verified by Texas Children’s Hospital.
Research Area:
Bone Tumors
Dr. Pulivarthi Rao is Director of the Cancer Cytogenetics Core Laboratory and a principal investigator for the Cancer Genetics and Genomics Program at Texas Children's Cancer and Hematology Center. He is certified with a Clinical Laboratory Cytogenetics Director License by the New York State Department of Health.
The main goals of the Rao laboratory are to identify oncogenes from the amplified chromosomal regions and the role of genomic instability in osteosarcoma (OS). Osteosarcoma is the most frequent bone neoplasm in children and often present with a high number of chromosomal amplifications and deletions, suggesting that genomic instability is linked to tumor development.
Recently, we identified CDC5L, a cell cycle regulator gene as target for 6p12-p21 amplicon found in osteosarcoma. Our recent in vivo studies suggest that CDC5L was a potential oncogene.
The goal of the laboratory is to investigate the role of CDC5L in the development of genomic instability and progression of osteosarcoma by overexpressing CDC5L cDNA and down-regulating by SiRNA in normal osteoblasts. A wide range of functional, comparative and cytogenetic techniques will be utilized in these studies, including: conventional and molecular cytogenetics- FISH, comparative genomic hybridization (CGH), multicolor spectral karyotyping (SKY), and array CGH.
Overholtzer M, Rao PH, Favis R, Lu XY, Elowitz MB, Barany F, Ladanyi M, Gorlick R, Levine AJ. The presence of p53 mutations in human osteosarcomas correlates with high levels of genomic instability. Proc Natl Acad Sci USA. 2003;100(20):11547-52.
Man TK, Lu XY, Jaeweon K, Perlaky L, Harris CP, Shah S, Ladanyi M, Gorlick R, Lau CC, Rao PH. Genome-wide array comparative genomic hybridization analysis reveals distinct amplifications in osteosarcoma. BMC Cancer, 2004, 4(1): 45.
Lau CC, Harris CP, Lu XY, PerlakyL, Gogineni S, Chintagumpala M, Hicks J, Johnson ME, Davino NA, HuvosAG, Meyers PA, Healy JH, Gorlick R, Rao PH. Frequent amplification and rearrangement of chromosomal bands 6p12-p21 and 17p11.2 in osteosarcoma. Genes Chromosomes Cancer 2004; 39:11–21.
Lu XY, Lu Y, Zhao YJ, Jaeweon K , Kang J, Li X, Ge G, Meyer R, PerlakyL, Hicks J, Chintagumpala M, Cai WW, Ladanyi M, Gorlick R, Lau CC, Pati D, Sheldon M, Rao PH. Cell Cycle Regulator Gene CDC5L, a Potential Target for 6p12-p21 Amplicon in Osteosarcoma. Mol Cancer Res 2008;6(6): 937–4.
Tao J, Jiang MM, Jiang L, Salvo JS, Zeng HC, Dawson B, Bertin TK, Rao PH, Chen R, Donehower LA, Gannon F, Lee BH. Notch activation as a driver of osteogenic sarcoma. Cancer Cell. 2014;26(3):390-401. doi: 10.1016/j.ccr.2014.07.023.
Zhao S, Kurenbekova L, Gao Y, Roos A, Creighton CJ, Rao P, Hicks J, Man TK, Lau C, Brown AM, Jones SN, Lazar AJ, Ingram D, Lev D, Donehower LA, Yustein JT. NKD2, a negative regulator of Wnt signaling, suppresses tumor growth and metastasis in osteosarcoma. Oncogene. 2015 Sep 24;34(39):5069-79.
Rao PH, Zhao S, Zhao YJ, Yu A, Rainusso N, Trucco M, Allen-Rhoades W, Satterfield L, Fuja D, Borra VJ, Man TK, Donehower LA, Yustein JT. Coamplification of Myc/Pvt1 and homozygous deletion of Nlrp1 locus are frequent genetics changes in mouse osteosarcoma. Genes Chromosomes Cancer. 2015;54(12):796-808.