James Jackson
Tulane University of Louisiana, LA·Genetics
Damaged cells face a choice: repair, stop dividing, or die. These choices decide whether a tumor survives chemotherapy and whether normal tissues gather harmful mutations.
- Fields
Genetics
Medicine & Clinical Research
Microbiology & Immunology
- Topics
breast cancer
chemotherapy resistance
cellular senescence
- Grants
- 2 known grants, through Feb 2027
What they work on
- Test whether PD-L1-expressing senescent tumor cells have greater relapse potential than PD-L1-negative cells in chemotherapy-treated mouse mammary tumors, and compare their gene expression.
- Identify factors that drive PD-L1 on senescent tumor cells, including stromal interferon gamma, by treating tumors transplanted into mice lacking immune components such as T cells.
- Test whether BH3 mimetic drugs that kill senescent cells improve breast tumor responses to anti-PD-L1 immune checkpoint therapy after chemotherapy, and check PD-L1 induction in human specimens using multiplex staining.
- Determine how Brca1-dependent homology directed repair preserves viability after DNA damage in adult mice with inducible Brca1 deletion, measuring cell fate, gene expression and tissue pathology.
- Use deep sequencing and mutation-signature analysis to find which tissues rely on homology directed repair, and test survival when both Brca1 and the NHEJ gene Lig4 are deleted.
More about the research
James Jackson's grants study how cells respond to DNA damage, particularly through p53, a protein that stops the cell cycle or triggers cell death. One project examines breast tumors that survive chemotherapy. The other examines how normal adult tissues cope with DNA damage when a key repair system is turned off.
Why it matters
Breast cancer patients often relapse after chemotherapy. Combining drugs that kill senescent tumor cells with immune checkpoint inhibitors could help clear leftover disease and improve survival. Learning how adult tissues depend on Brca1-based repair after environmental DNA damage could clarify how mutations build up and cause disease, which matters for people carrying BRCA1 defects.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sandeep Burma
University of Texas Health Science Center at San Antonio, TX·Biochemistry
Determine the biological role of the newly found ability of 53BP1, a chromatin-reading DNA repair protein, to bind double-stranded DNA, and how this binding recruits partner proteins and sets which repair pathway a break uses.
Ramesh Ganju
Ohio State University, OH·Microbiology & Immunology
Determine how S100A7 signaling controls genes that respond to interferon-gamma, especially PD-L1 and Fas, in African American TNBC cells and in engineered mice that overproduce mouse S100a7.
Dale A Ramsden
University of North Carolina at Chapel Hill, NC·Biochemistry
Determine how Pol θ's interactions with the DNA-copying machinery, including the polymerase Pol δ and the DNA clamp PCNA, affect cells' need for Pol θ-mediated end joining.
The school
Tulane University of Louisiana: 17 labs on PI Pages, $276M a year on research, 187 research doctorates a year.
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