Postbac, Ph.D., and Postdoctoral Programs

Exceptional opportunities for research and training in a unique scientific environment

POSTBAC @ JAX

This two-year scientific training program allows you to undertake an independent research project and strengthen your professional and laboratory skills before pursing an MD-PhD or Ph.D.

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COOPERATIVE PHD PROGRAM

The Jackson Laboratory’s Cooperative PhD Program provides training in mammalian genetics and genomic medicine through partnerships with degree-granting academic institutions.

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POSTDOCTORAL ASSOCIATES

As a Postdoctoral Associate at The Jackson Laboratory, you can conduct cutting-edge research on the complex diseases impacting human health.

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Trends Cancer. 2024 Jan; 10(1):38-51

Non-genetic mechanisms of drug resistance in acute leukemias

Calderon A, Han C, Karma S, Wang E

Acute leukemia is characterized by clonal heterogeneity that contributes to poor drug responses in patients. Despite treatment advances, the occurrence of relapse remains a major barrier to achieving cures as current therapeutic approaches are inadequate to effectively prevent or overcome resistance. Given that only a few genetic mutations are associated with relapse in acute leukemia patients, there is a growing focus on 'non-genetic' mechanisms that affect the hallmarks of cancer to allow leukemic cells to survive post therapy. In this …
Copyright © 2023 Elsevier Inc. All rights reserved.
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Genome Med. 2023 May 10; 15(1):35

High level of complexity and global diversity of the 3q29 locus revealed by optical mapping and long-read sequencing

Yilmaz F, Gurusamy U, Mosley TJ, Hallast P, Kim K, Mostovoy Y, et al.

High sequence identity between segmental duplications (SDs) can facilitate copy number variants (CNVs) via non-allelic homologous recombination (NAHR). These CNVs are one of the fundamental causes of genomic disorders such as the 3q29 deletion syndrome (del3q29S). There are 21 protein-coding genes lost or gained as a result of such recurrent 1.6-Mbp deletions or duplications, respectively, in the 3q29 …
© 2023. The Author(s).
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Cell Genom. 2023 May 10; 3(5):100291

Resolution of structural variation in diverse mouse genomes reveals chromatin remodeling due to transposable elements

Ferraj A, Audano PA, Balachandran P, Czechanski A, Flores JI, Radecki AA, et al.

Diverse inbred mouse strains are important biomedical research models, yet genome characterization of many strains is fundamentally lacking in comparison with humans. In particular, catalogs of structural variants (SVs) (variants ≥ 50 bp) are incomplete, limiting the discovery of causative alleles for phenotypic variation. Here, we resolve genome-wide SVs in 20…
© 2023 The Author(s).
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Cell Genom. 2023 Apr 12; 3(4):100283

Genetic dissection of the pluripotent proteome through multi-omics data integration

Aydin S, Pham DT, Zhang T, Keele GR, Skelly DA, Paulo JA, et al.

Genetic background drives phenotypic variability in pluripotent stem cells (PSCs). Most studies to date have used transcript abundance as the primary molecular readout of cell state in PSCs. We performed a comprehensive proteogenomics analysis of 190 genetically diverse mouse embryonic stem cell (mESC) lines. The quantitative proteome is highly variable across lines, and we identified pluripotency-associated pathways …
© 2023 The Author(s).
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Sci Immunol. 2023 Feb 24; 8(80):eadd5204

Immunosuppressive reprogramming of neutrophils by lung mesenchymal cells promotes breast cancer metastasis

Gong Z, Li Q, Shi J, Li P, Hua L, Shultz LD, et al.

Neutrophils, the most abundant innate immune cells, function as crucial regulators of the adaptive immune system in diverse pathological conditions, including metastatic cancer. However, it remains largely unknown whether their immunomodulatory functions are intrinsic or acquired within the pathological tissue environment. Here, using mouse models of metastatic breast cancer in the lungs, we show that, although neutrophils isolated from bone marrow (BM) or blood are…
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