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Ching C. Lau Baylor College of Medicine Department: Dept. of Pediatrics, Texas Children's Cancer Center Address: 6621 Fannin St., MC3-3320 Houston, TX 77030-4038 Phone: 832-824-4543 Fax: 832-825-4038 Email: clau@txccc.org Web: public2.bcm.tmc.edu/pediatrics/index.cfm?This_Template=pedi_bio_lau.cfm&Realm=99992434

Education

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)

Honors

Research Topic

Genomics and proteomics of cancer, bioinformatics, and development of targeted therapy.

Research Description

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% 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.

Selected Publications

• Lau CC, Harris CP, Lu X-Y, Perlaky L, Gogineni S, Chintagumpala M, Hicks J, Johnson M, Davino N, Huvos AG, Meyers PA, Healy JH, Gorlick R, and Rao PH. (2004). Frequent amplification and rearrangement of chromosomal bands 6p12-p21 and 17p11.2 in osteosarcoma. Genes Chromosomes Cancer 39: 11-21.
• Li XN, Parikh S, Shu Q, Jung H-L, Chow C-W, Perlaky L, Eastwood Leung H-C, Su J, Blaney S, and Lau CC. (2004). Phenylbutyrate and phenylacetate induce differentiation and inhibit proliferation of human medulloblastoma cells. Clin. Can. Res. 10: 1150-1159.
• Su JM, Perlaky L, Li X-N, E. Leung H-C, Antaffy BA, Armstrong DD and Lau CC. (2004). Comparison of ethanol versus formalin fixation on preservation of histology and RNA in laser capture microdissected brain tissues. Brain Pathol. 14: 175-182.
• Wong KK, Tsang YTM, Shen J, Cheng RS, Chang YM, Man TK and Lau CC. (2004). Allelic imbalance analysis by High-Density Single Nucleotide Polymorphic Allele (SNP) Array with Whole Genome Amplified DNA. Nucleic Acids Res. 32(9): e69.
• Wong KK, Chang Y-M, Tsang YTM, Perlaky L, Su J, Adesina A, Armstrong DL, Bhattacharjee M, Dauser R, Blaney SM, Chintagumpala M, and Lau CC. (2005). Expression analysis of juvenile pilocytic astrocytomas by oligonucleotide microarray reveals two potential subgroups. Cancer Res. 65: 76-84.
• Man TK, Chintagumpala M, Visvanathan J, Shen J, Perlaky L, Hicks J, Johnson M, Davino N, Murray J, Helman L, Meyer W, Triche T, Wong KK and Lau CC. (2005). Expression profiles of osteosarcoma that can predict response to chemotherapy. Cancer Res. In press.

Lab Members

Lab Photos

Last edited on: August 20, 2009