Baylor College of Medicine
Monday - Friday, 8 a.m. - 5 p.m.
Summary We are seeking a highly motivated Staff Scientist to join our team investigating the mechanisms of T-cell dysfunction and immune evasion following allogeneic hematopoietic cell transplantation (allo-HCT). Our laboratory integrates expertise in epigenetics, chromatin regulation, and immunology to understand how altered gene regulatory programs drive T-cell exhaustion, impaired graft-versus-leukemia (GVL) responses, and post-transplant relapse in acute myeloid leukemia. The Staff Scientist will play a central role in developing and leading mechanistic projects, applying chromatin profiling, CRISPR functional genomics, and single-cell multi-omics to dissect the regulatory networks underlying T-cell dysfunction and identify therapeutic strategies to restore immune surveillance.
What We Offer
A highly collaborative environment bridging epigenetics, immunology, and cancer therapy.
Access to state-of-the-art single-cell platforms, CRISPR libraries, and mouse models for allo-HCT and leukemia.
Opportunities for professional growth, including mentorship in grant writing.
Job Duties
Lead mechanistic studies of donor T-cell dysfunction post-allo-HCT, with a focus on chromatin regulators, histone modifications, and transcriptional/epigenetic drivers of exhaustion.
Apply single-cell transcriptomics, epigenomics (ATAC-seq, CUT&Tag), and CITE-seq to map dysfunctional T-cell states in murine models and patient samples.
Use CRISPR/Cas9 screening and perturbation approaches to identify novel regulators of T-cell persistence, effector function, and exhaustion.
Collaborate with wet-lab and computational teams to integrate multi-omics datasets with clinical outcomes.
Mentor trainees and contribute to team science efforts, including multi-PI grants and translational collaborations.
Contribute to manuscripts, conference presentations, and grant applications.
Perform other job related duties as assigned.
Minimum Qualifications
Doctoral Degree. Experience may not be substituted in lieu of degree.
Three years of post doctoral research experience.
Preferred Qualifications
Ph.D. in Immunology, Epigenetics, Computational Biology, or related fields.
Strong publication record with first-author papers in relevant areas.
Demonstrated expertise in epigenetic/chromatin biology and its role in immune regulation or cancer biology.
Hands-on experience with T-cell biology, single-cell approaches, or CRISPR screening.
Strong data analysis skills and ability to work collaboratively across experimental and computational projects.
Experience studying T-cell exhaustion, GVHD/GVL biology, or allo-HCT models.
Knowledge of checkpoint pathways, metabolic regulation, or cytokine signaling in T cells.
Background in integrating clinical datasets with mechanistic studies.
Familiarity with drug discovery approaches (e.g., PROTACs, epigenetic inhibitors) that may reverse T-cell dysfunction.
Baylor College of Medicine is an Equal Opportunity/Affirmative Action/Equal Access Employer.
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Summary We are seeking a highly motivated Staff Scientist to join our team investigating the mechanisms of T-cell dysfunction and immune evasion following allogeneic hematopoietic cell transplantation (allo-HCT). Our laboratory integrates expertise in epigenetics, chromatin regulation, and immunology to understand how altered gene regulatory programs drive T-cell exhaustion, impaired graft-versus-leukemia (GVL) responses, and post-transplant relapse in acute myeloid leukemia. The Staff Scientist will play a central role in developing and leading mechanistic projects, applying chromatin profiling, CRISPR functional genomics, and single-cell multi-omics to dissect the regulatory networks underlying T-cell dysfunction and identify therapeutic strategies to restore immune surveillance.
What We Offer
A highly collaborative environment bridging epigenetics, immunology, and cancer therapy.
Access to state-of-the-art single-cell platforms, CRISPR libraries, and mouse models for allo-HCT and leukemia.
Opportunities for professional growth, including mentorship in grant writing.
Job Duties
Lead mechanistic studies of donor T-cell dysfunction post-allo-HCT, with a focus on chromatin regulators, histone modifications, and transcriptional/epigenetic drivers of exhaustion.
Apply single-cell transcriptomics, epigenomics (ATAC-seq, CUT&Tag), and CITE-seq to map dysfunctional T-cell states in murine models and patient samples.
Use CRISPR/Cas9 screening and perturbation approaches to identify novel regulators of T-cell persistence, effector function, and exhaustion.
Collaborate with wet-lab and computational teams to integrate multi-omics datasets with clinical outcomes.
Mentor trainees and contribute to team science efforts, including multi-PI grants and translational collaborations.
Contribute to manuscripts, conference presentations, and grant applications.
Perform other job related duties as assigned.
Minimum Qualifications
Doctoral Degree. Experience may not be substituted in lieu of degree.
Three years of post doctoral research experience.
Preferred Qualifications
Ph.D. in Immunology, Epigenetics, Computational Biology, or related fields.
Strong publication record with first-author papers in relevant areas.
Demonstrated expertise in epigenetic/chromatin biology and its role in immune regulation or cancer biology.
Hands-on experience with T-cell biology, single-cell approaches, or CRISPR screening.
Strong data analysis skills and ability to work collaboratively across experimental and computational projects.
Experience studying T-cell exhaustion, GVHD/GVL biology, or allo-HCT models.
Knowledge of checkpoint pathways, metabolic regulation, or cytokine signaling in T cells.
Background in integrating clinical datasets with mechanistic studies.
Familiarity with drug discovery approaches (e.g., PROTACs, epigenetic inhibitors) that may reverse T-cell dysfunction.
Baylor College of Medicine is an Equal Opportunity/Affirmative Action/Equal Access Employer.
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