Contact Information
Call us at: (614)722-5598
Fax us at: (614)722.5895
Center for Childhood CancerAbigail Wexner Research Institute700 Children’s DriveColumbus, Ohio 43205 (map)
Learn more about Dawn S. Chandler
Biography
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Academic and Clinical Areas
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
Research
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Contact Information
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Contact Information
Call us at: (614)722-5598
Fax us at: (614)722.5895
Center for Childhood CancerAbigail Wexner Research Institute700 Children’s DriveColumbus, Ohio 43205 (map)
Learn more about Dawn S. Chandler
Biography
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Academic and Clinical Areas
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
Research
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Contact Information
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Contact Information
Call us at: (614)722-5598
Fax us at: (614)722.5895
Center for Childhood CancerAbigail Wexner Research Institute700 Children’s DriveColumbus, Ohio 43205 (map)
Learn more about Dawn S. Chandler
Contact Information
- Call us at:
- (614)722-5598
- Fax us at:
- (614)722.5895
- Center for Childhood CancerAbigail Wexner Research Institute700 Children’s DriveColumbus, Ohio 43205 (map)
Learn more about Dawn S. Chandler
Biography
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Biography
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Biography
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Dawn S. Chandler, PhD, is a principal investigator in the Center for Childhood Cancer at The Research Institute at Nationwide Children’s Hospital and an associate professor in the Department of Pediatrics at The Ohio State University College of Medicine. She received her PhD from the University of Texas Graduate School of Biomedical Sciences at Houston. Dr. Chandler’s NIH funded research programs are focused on studying pre-mRNA splicing in the neurodegenerative disease, Spinal Muscular Atrophy (SMA), and in the pediatric cancer, rhabdomyosarcoma (RMS).
Academic and Clinical Areas
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
Academic and Clinical Areas
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
Academic and Clinical Areas
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
Hematology/Oncology & BMT
Principal Investigator
Dawn Chandler Lab
Principal Investigator
Center for Childhood Cancer
Principal Investigator
Hematology, Oncology and BMT Fellowship
Faculty
Primary Department
Center for Childhood Cancer
- Hematology/Oncology & BMT
- Principal Investigator
- Dawn Chandler Lab
- Principal Investigator
- Center for Childhood Cancer
- Principal Investigator
- Hematology, Oncology and BMT Fellowship
- Faculty
- Primary Department
- Center for Childhood Cancer
Research
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Research
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Research
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future. Publications
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
Lab(s)
Center for Childhood Cancer
Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease. Another pediatric disease Proximal Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality in humans, is in part due to a mutation that affects splicing of a duplicated gene that controls neuronal growth (SMN2). We are interested in generating viable mouse models for human SMA with the long-term goal of testing candidate therapies that target the human SMN2 gene. To do this, we are generating mouse lines that will be utilized to answer many questions pertaining the therapeutic possibilities of SMN replacement, splicing correction by drug or antisense treatment, and the correct timing of such therapies.Our research represents a novel perspective in pediatric research that highlights the role of perturbation of pre-mRNA processing in disease phenotypes. The increased awareness of regulated RNA processing and recent identification of several disease-causing mutations that affect splicing give rise to a new generation of potential therapeutic targets. Point mutations and the resultant splice variants may both be successfully targeted for therapeutic benefits in the future.
Lab(s)
Center for Childhood Cancer
Center for Childhood Cancer
Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890. Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256. Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1. Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
View More Publications
- Cripe TP, Hutzen B, Currier MA, Chen CY, Glaspell AM, Sullivan GC, Hurley JM, Deighen MR, Venkataramany AS, Mo X, Stanek JR, Miller AR, Wijeratne S, Magrini V, Mardis ER, Mendell JR, Chandler DS, Wang PY. Leveraging gene therapy to achieve long-term continuous or controllable expression of biotherapeutics. Sci Adv. 2022 Jul 15; 8: eabm1890.
- Dominguez CE, Cunningham D, Venkataramany AS, Chandler DS. Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA. Hum Genet. 2022 Feb; 141: 239-256.
- Khurshid S, Montes M, Comiskey DF Jr, Shane B, Matsa E, Jung F, Brown C, Bid HK, Wang R, Houghton PJ, Roberts R, Rigo F, Chandler D. Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma. NPJ Precis Oncol. 2022 Jan 11; 6: 1.
- Montes M, Sanford BL, Comiskey DF, Chandler DS. RNA Splicing and Disease: Animal Models to Therapies. Trends Genet. 2019 Jan; 35: 68-87.
Contact Information
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Contact Information
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Contact Information
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Center for Childhood Cancer
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
Call us at: (614)722-5598
Fax us at: (614)722.5895
Abigail Wexner Research Institute700 Children's DriveColumbus, Ohio 43205 (map)
- Call us at:
- (614)722-5598
- Fax us at:
- (614)722.5895
- Abigail Wexner Research Institute700 Children’s DriveColumbus, Ohio 43205 (map)
