Bone Disease Program of Texas - BCM Participants
Collaboration seeks to turn research into treatment for bone disease
The Rolanette and Berdon Lawrence Bone Disease Program of Texas, a collaborative research, clinical and education program of Baylor College of Medicine and The University of Texas MD Anderson Cancer Center, was established to improve basic and translational research of bone diseases and to convert basic science findings to more effective treatment and prevention options. Read more about the bone program.
Latest News:
Bone Disease Program of Texas Receives National Recognition
Participants from Baylor College of Medicine:
Steven Abrams, M.D. Professor, Department of Pediatrics - Nutrition
E-mail:
Phone: 713-798-7124
Dr. Abrams is interested in studying the mineral metabolism of children using stable isotopes. His laboratory measures mineral absorption and bone calcium metabolism in healthy children and those with various bone related illnesses.
Carlos Bacino, M.D. Associate Professor, Department of Molecular and Human Genetics
E-mail:
Phone: 832-822-4291
Dr. Bacino's research interests include clinical studies in patients with imprinting disorders such as Angelman Syndrome, and anthropometric studies in craniofacial disorders.
Alan R. Davis, Ph.D. Associate Professor, Department of Pediatrics - Hematology-Oncology
E-mail:
Phone: 713-798-1237
My research interests are in the area of heterotopic ossification as it relates to endochondral bone formation. My laboratory has identified some of the earliest physiological cross talk between the immune system, vasculature, adipose and nervous systems that must occur in order for bone formation to proceed. Our goals are to develop both targeted inhibitors and imaging diagnostics against these early processes.
Elizabeth Olmsted-Davis, Ph.D. Associate Professor, Department of Pediatrics - Hematology-Oncology
E-mail:
Phone: 713-798-1237
My research interests are in the area of heterotopic ossification (HO) of bone formation at non-skeletal sites. Our laboratory extends this definition to include de novo bone formation which utilizes the processes of HO to form the bone. Thus we are attempting to harness this capacity to rapidly form bone at targeted locations for a variety of musculoskeletal problems including critical size defect, and spinal arthrodesis.
Lawrence A. Donehower, Ph.D. Professor, Department of Molecular Virology & Microbiology
E-mail:
Phone: 713-798-3594
Our laboratory studies p53 signaling, using genetically engineered mouse models. In particular, we are interested in the role of p53 and osteosarcoma formation and progression. We have developed and characterized a p53-deficient mouse osteosarcoma model to study genetic alterations and gene expression changes that might ultimately be exploited as therapeutic targets.
Kenneth Ellis, Ph.D. Professor, Department of Pediatrics - Nutrition
E-mail:
Phone: 713-798-7131
The Body Composition Laboratory at the CNRC provides measurements of bone mineral mass in pediatric populations from infancy through adolescence. DXA measurements in more than 1200 healthy children have been used to establish reference curves for bone, which provide a means of assessing the bone status of children with diseases that may affect bone growth.
Xin-Hua Feng, Ph.D. Professor, Departments of Molecular & Cellular Biology and Surgery
E-mail:
Phone: 713-798-4756
Our research is aimed at elucidating the underlying mechanisms and interplays among protein modifications, signaling networks and gene transcription. We are particularly interested in the BMP/TGFbeta signaling pathways and protein phosphatases involved in cell functions, tissue differentiation and pathogenesis of human diseases. One part of our recent research focuses on the in vivo functions of Smads and their phosphatases in skeletal development.
Kenneth Gabbay, M.D. Professor, Departments of Pediatrics - Molecular Diabetes and Metabolism
E-mail:
Phone: 832-824-3764
Dr. Gabbay's main research interests are the genetics of type I diabetes mellitus and its complications; the molecular mechanism of pathogenesis of diabetic complications and development of drugs to prevent such complications; and the genetic and molecular basis for beta cell growth, development, and maintenance. The goal is to cure and prevent type I diabetes mellitus and its complications. The current focus of his activities relates to the pathogenesis of osteoporosis and more specifically, the role of diabetes and oxidative stress in its development.
Frank Gannon, M.D. Associate Professor, Department of Pathology
E-mail:
Phone: 713-798-4340
My research involves the earliest stages of bone formation with particular emphasis on the events prior to actual bone and cartilage formation. I work in conjunction with Drs. Alan and Betsy Davis in the Center for Cell and Gene Therapy and Dr. Michael Heggeness in the Department of Orthopedic Surgery.
Andy Groves, Ph.D. Associate Professor, Department of Molecular and Human Genetics
E-mail:
Phone: 713-798-8743
We are interested in understanding the transcriptional control of craniofacial development, in particular the branchial arches. Current projects in our lab include an analysis of the Foxi3 transcription factor. Foxi3 mutant mice lack all pharyngeal arch structures.
Michael H., Heggeness, M.D., Ph.D. Chair and Professor, Department of Orthopedic Surgery
E-mail:
Phone: 713-986-5730
My research interests include the study of intraosseous nerves, and the biology of osteogenesis.
Brendan Lee, M.D., Ph.D. - Director Professor, Department of Molecular and Human Genetics
E-mail:
Phone: 713-798-8835
We are interested in studying rare disorders of skeletal development to elucidate the common mechanisms that cause osteoporosis, osteoarthritis, and bone cancer. Specifically, we have focused on transcription factors that regulate cell differentiation, growth factor signaling upstream of these factors, and downstream target matrix protein function.
Joel Morrisett, Ph.D. Professor, Departments of Medicine and Biochemistry & Molecular Biology
E-mail:
Phone: 713-798-4164
Dr. Morrisett's research interests focuses on the integrated investigation of the mechanism(s) of calcification and demineralization of the arterial wall using magnetic resonance imaging, cell culture, proteomics, and genomics.
Sandesh Sreenath Nagamani, M.B.B.S., M.D. Assistant Professor, Department of Molecular and Human Genetics
E-mail:
Phone: 713-798-7820
My laboratory research involves translational research in urea cycle disorders, and nitric oxide signaling in diabetes, metabolic syndrome and atherosclerosis. My clinical research involves trials related to Urea cycle disorders and Osteogenesis Imperfecta.
Philip Noble, Ph.D. Professor, Department of Orthopedic Surgery
E-mail:
Phone: 713-986-5460
Dr. Noble's diverse research interests include the biomechanics of human and artificial joints, the morphometry of human bones, the biology and biomechanics of cartilage, ligament fixation, computer graphics, virtual biomechanics, and the quantitative assessment of clinical outcomes.
Yuxiang Sun, Ph.D. Assistant Professor, Department of Pediatrics - Nutrition
E-mail:
Phone: 713-798-7167
Dr. Sun is investigating the role of ghrelin and ghrelin receptor in obesity and diabetes.
Vernon R. Sutton, M.D. Associate Professor, Department of Molecular and Human Genetics
E-mail:
Phone: 832-822-4296
Dr. Reid Sutton is a clinician with expertise in skeletal dysplasias and osteogenesis imperfecta. He is the Co-Director of the Osteogenesis Imperfecta Foundation's Linked Clinical Research Center and is a member of the International Skeletal Dysplasia Society.
Ming-Jer Tsai, Ph.D. Professor, Department of Molecular and Cellular Biology
E-mail:
Phone: 713-798-6253
My laboratory is studying the physiological function of COUP-TFs which are orphan members of the steroid/thyroid receptor superfamily. COUP-TFs are important for various diseases, such as congenital diaphragmatic hernia (CDH), congenital heart defects (CHD), coloboma, kidney diseases, diabetes and cancers. It also plays a role in organogenesis and cell fate determination of the mesenchymal stem cells, which can develop into bone, muscle, fat or chondrocyte. We are currently dissecting their underlying mechanisms.
Ignatia B. Van den Veyver, M.D. Associate Professor, Departments of Obstetrics & Gynecology and Molecular and Human Genetics
E-mail:
Phone: 713-798-4914
My laboratory discovered that Goltz syndrome, characterized by developmental abnormalities of limbs, skin and ectodermal appendages is caused by mutations in PORCN, a gene on the X chromosome that encodes the human homolog of Drosophila Porcupine. PORCN is important for secretion of WNT proteins from the endoplasmic reticulum, an important first step in Wnt signaling. We have generated a mouse model for conditional inactivation of the Porcn gene. Mice with Porcn mutations have skeletal abnormalities with missing digits and fusion of digits and shortening of limbs. We are using this mouse model to examine the how Porcn in co-regulates signaling of different Wnt proteins in the control of early limb development and patterning.
Lisa L. Wang, M.D. Assistant Professor, Department of Pediatrics - Hematology & Oncology
E-mail:
Phone: 832-824-4822
Our lab is studying the role of the RECQL4 gene pathway in bone development and cancer (osteosarcoma) through study of a rare genetic disorder called Rothmund-Thomson syndrome. We are generating conditional knockout and transgenic recql4 mouse models in order to investigate the effects of RECQL4 in the skeletal system.
Xiang (Shawn) Zhang, Ph.D. Assistant Professor, Lester and Sue Smith Breast Center
E-mail:
Phone: 713-798-1649
We aim to study how cancer cells evolve to acquire metastasis ability and how they colonize in different organs including bones, with an emphasis on cancer-stroma cross-talks at the stage of micro-metastasis.