Ching Ching Lau, M.D., Ph.D.
Associate Professor, Pediatrics - Hematology & Oncology
SCBMB Executive Committee Member
Baylor College of Medicine
B.A., Chemistry, Rice Univ (1977)
M.A., Ph.D., Pharmacology, Harvard Univ (1982)
M.D., Harvard Univ (1993)
Postdoc, Dana Farber Cancer Center (1982-84)
Pediatrics Residency, Baylor College of Medicine (1993-96)
Research interests include the molecular biology of pediatric brain and bone tumors and the clinical applications of genomic technologies.
Pediatric brain tumors are the most common solid tumor in children with an annual incidence of about 2,000 in the United States. Despite recent advances in multi-modality therapy involving surgery, radiation- and chemotherapy, many of the malignant brain tumors continue to have a poor prognosis especially among children less than three years of age. For example, the mortality rate for patients with metastatic or recurrent medulloblastoma, the most common malignant brain tumor in children, has remained greater than 50 percent in the last 15 years. Even its survivors are faced with long-term neuro-cognitive sequelae as a result of the therapies they received. Improving the clinical outcome of children with brain tumors such as medulloblastoma poses the single greatest challenge for pediatric oncologists today. The goal of current therapeutic strategies is to stratify patients to the most appropriate therapy based on prognosis such that survival will be optimized in the high-risk patients while toxicity will be minimized in low risk patients. However, such strategies are hampered by the lack of reliable markers that can accurately predict the clinical outcome of these tumors.
Because the biological and clinical behavior of a tumor is ultimately determined by its genetic make-up, Dr. Lau hypothesizes that comprehensive genetic profiling is a systematic and unbiased approach to recognize tumor subtypes. His laboratory seeks to identify new and reliable prognostic markers in pediatric brain tumors by using some of the most powerful genomic technologies currently available. These technologies, which have been optimized in our Cancer Genomics Program for analyzing clinical specimens, include comparative genomic hybridization, spectral karyotyping, whole genome allelotyping, expression profiling by cDNA microarrays, as well as proteomics. These techniques are carefully chosen for their exquisite sensitivity and their ability to complement each other in creating comprehensive genetic profiles of clinical specimens. Through NIH-funded projects, Dr. Lau’s laboratory is focusing on establishing the molecular classification of three major types of pediatric brain tumors: medulloblastoma, ependymoma, and low-grade glioma as well as that of the bone tumor osteosarcoma. These improved approaches to classification will be used in future trials to stratify patents more accurately to the most appropriate risk-based therapy. In addition, Dr. Lau’s laboratory is also studying the genetic regulation of normal brain development and its role in the pathogenesis of brain tumors. The laboratory is also active in experimental therapeutics, using molecular genetics in an attempt to dissect the molecular mechanisms of action of chemotherapeutic agents used in treating pediatric cancers.
- Liu Z, Zhao X, Mao H, Baxter PA, Huang Y, Yu L, Wadhwa L, Su JM, Adesina A, Perlaky L, Hurwitz M, Idamakanti N, Police SR, Hallenbeck PL, Hurwitz RL, Lau CC, Chintagumpala M, Blaney SM and Li XN. Intravenous injection of oncolytic picornavirus SVV-001 prolongs animal survival in a panel of primary tumor-based orthotopic xenograft mouse models of pediatric glioma. Neuro Oncol, [Epub ahead of print] (2013). PubMed
- Teo WY, Shen J, Su JM, Yu A, Wang J, Chow WY, Li X, Jones J, Dauser R, Whitehead W, Adesina AM, Chintagumpala M, Man TK and Lau CC. Implications of Tumor Location on Subtypes of Medulloblastoma. Pediatr Blood Cancer, [Epub ahead of print] (2013). PubMed
- Rednam S, Scheurer ME, Adesina A, Lau CC and Okcu MF. Glutathione S-transferase P1 single nucleotide polymorphism predicts permanent ototoxicity in children with medulloblastoma. Pediatr Blood Cancer, 60(4):593-8 (2013). PubMed
- Liu Y, Melin BS, Rajaraman P, Wang Z, Linet M, Shete S, Amos CI, Lau CC, Scheurer ME, Tsavachidis S, Armstrong GN, Houlston RS, Hosking FJ, Claus EB, Barnholtz-Sloan J, Lai R, Il'yasova D, Schildkraut J, Sadetzki S, Johansen C, Bernstein JL, Olson SH, Jenkins RB, Lachance D, Vick NA, Wrensch M, Davis F, McCarthy BJ, Andersson U, Thompson PA, Chanock S; The Gliogene Consortium and Bondy, M.L. Insight in glioma susceptibility through and analysis of 6p22.3, 12p13.33-12.1, 17q22-23.2 and 18q23 SNP genotypes in familial and non-familial glioma. Hum Genet, 131(9):1507-17 (2012). PubMed
- McGuire AL, Oliver JM, Slashinski MJ, Graves JL, Wang T, Kelly PA, Fisher W, Lau CC, Goss J, Okcu M, Treadwell-Deering D, Goldman AM, Noebels JL and Hilsenbeck SG. To share or not to share: a randomized trial of consent for data sharing in genome research. Genet Med, 13(11):948-55 (2011). PubMed
- Daves MH, Hilsenbeck SG, Lau CC and Man TK. Meta-analysis of multiple microarray datasets reveals a common gene signature of metastasis in solid tumors. BMC Med Genomics, 4:56 (2011). PubMed
- Li Y, Flores R, Yu A, Okcu MF, Murray J, Chintagumpala M, Hicks J, Lau CC and Man TK. Elevated expression of CXC chemokines in pediatric osteosarcoma patients. Cancer, 117(1):207-17 (2011).PubMed
For more publications, see listing on PubMed.
Department: Dept. of Pediatrics, Texas Children's Cancer and Hematology Centers
Address: 1102 Bates, Suite 1030.11
Houston, TX 77030-4038
Additional Links: Texas Childrens Cancer and Hematology Centers