Postdoctoral Training

Contact us

Carol Lange, Ph.D.
Director, Cancer Biology Training Grant
University of Minnesota Medical School
Mayo Mail Code 806
420 Delaware St. SE
Phone: 612-626-0621 Fax: 612-624-3913

The postdoctoral training program is designed to provide training in the conduct of scholarly investigation in one of the four scientific areas of expertise of the Cancer Biology Training Grant preceptors. The training is designed for biomedical scientists who have a Ph.D. in basic science (biochemistry, cell biology, genetics, microbiology, immunology, etc.) and for physicians who have basic research experience and interest in the areas studied by the preceptors. Support for postdoctoral trainees is typically for two years. However, all postdoctoral trainees are encouraged to apply for independent postdoctoral funding while they are being supported on the training grant.

Interested postdoctoral fellows currently training in a preceptor's laboratory may apply for support on the Cancer Biology Training Grant when a position becomes available. All positions are selected on a competitive basis by the Cancer Biology Training Grant Steering Committee. Contact the Cancer Biology Training Grant Director for information on how to apply.

If you are interested in postdoctoral training with one of our preceptors, you may contact them directly or direct an inquiry to Carol Lange, Ph.D. at

Heather Edgerton, PhD

Heather Edgerton, PhD

Clarke lab
Phone: 612-624-4966

The cell has numerous checkpoints to ensure that DNA is faithfully replicated and then divided equally between daughter cells. Failure or bypass of these checkpoints can lead to aneuploidy, which is a hallmark of cancer. By using the power of yeast genetics and its capability of live cell imaging, our lab is exploring the still incompletely understood mechanisms that are crucial for proper chromosome segregation.

One cellular checkpoint to prevent aneuploidy is error correction. Aurora B, an essential protein in error correction, is activated in the presence of syntelic kinetochore-microtubule attachments (where one kinetochore is attached to two microtubules emanating from the same pole of the mitotic spindle). If this improper attachment was left uncorrected, one daughter cell would get two copies of this chromosome while the other would be left without a copy at all.  Aurora B senses these syntelic attachments and destabilizes them, activating the Spindle Assembly Checkpoint (SAC). When activated, the SAC halts mitosis, preventing anaphase until all kinetochores are properly attached in a bipolar fashion to kinetochore microtubules. This allows time for any previous syntelic attachments to reattach properly. Misregulation of both error correction and the SAC are known to lead to chromosome mis-segregation and aneuploidy; however their complex mechanism and interrelationship is poorly understood.

Topoisomerase IIα (Topo II) is also required for proper chromosome segregation. It has a well-understood role in detangling sister chromatids prior to division. However, the C-terminal domain (CTD) of Topo II is not essential for this catalytic function, but it is required for proper SAC signaling. I recently published data clearly demonstrating that SUMOylation of the Topo II CTD is necessary for Aurora B recruitment to mitotic centromeres in budding yeast. My data, along with data from our collaborators, strongly suggest that SUMOylation of the Topo II CTD recruits Haspin kinase, which phosphorylates histone H3 at residue T3, which is responsible for recruitment of Aurora B, and this mechanism is evolutionarily conserved from yeast to higher organisms. I am currently investigating chromosome mis-segregation in mutants that are defective in this Aurora B recruitment pathway. I also aim to identify what proteins lie upstream of Topo II SUMOylation and Aurora B recruitment. 

Chelsea Lassiter, PhD

Chelsea Lassiter, PhD

Schwertfeger lab
Phone: 612-626-5059

Immunotherapy has shown promise in some solid tumors including breast cancers with high levels of tumor infiltrating lymphocytes (TILs). In other cancers, enhancing T cell infiltration into tumors that lack significant levels of TILs enhances responsiveness to immune based therapies (TILs). TIL infiltration is found in approximately 20% of triple negative breast cancers (TNBCs) and correlates with favorable patient outcome. Therefore, developing approaches to enhance T cell infiltration into primary and metastatic lesions could enhance the percentage of breast cancer patients that respond to immunotherapy.

The signal transducer and activator of transcription (STAT) protein family regulates gene expression changes related to proliferation, apoptosis, and immune response. Constitutively active STAT3 is found in 70% of human solid tumors and regulates immune response to tumor cells.  STAT3 is a potent oncogene and a promising target for immunotherapy. Our lab has shown that a loss of STAT3 leads to an increase in a potent tumor suppressor, STAT1, in multiple cell types. There is also an increase in immunomodulatory genes. In addition, we see a compensatory increase in an immune checkpoint protein, PD-L1, expressed by tumor cells and macrophages

We predict that STAT3 inhibition will enhance T cell infiltration into tumors through increased expression of T cell chemokines, although this will not be sufficient to elicit an anti-tumor response due to increased PD-L1 expression. Therefore, we hypothesize that selectively inhibiting STAT3 and PD-L1 will increase recruitment and enhance activation of T cells at the tumor site, and lead to an effective anti-tumor immune response. 


Milagros Silva Morales, PhD

Milagros Silva Morales, PhD

Mueller lab

Peripheral Immune Self-Tolerance Mechanisms: Anergy, Treg cells and Cancer
Peripheral tolerance is a necessary mechanism to control auto-reactive lymphocytes outside of the thymus. Anergy is a peripheral tolerance mechanism wherein self-reactive lymphocytes become unresponsive after antigen encounter but remain alive. Anergic CD4+ T cells lose their ability to produce growth factors such as IL-2 in response to antigen and develop poor proliferation. Recently, our laboratory reported on an anergic subset of naturally occurring Foxp3CD44hiCD73hiFR4hi polyclonal CD4+ T cells in healthy hosts. Responder CD4+ T cells with this phenotype could also be induced in response to recognition of fetal anti­gens during pregnancy. Interestingly, more than 80% of anergic T cells also specifically expressed the semaphorin receptor Nrp1 by day 18 of pregnancy. Foxp3+ Treg cells are also essential for peripheral immune tolerance and for anergy induction. Remarkably, polyclonal anergic CD4+ T cells can be induced to differentiate into Treg cells when they are adoptively transferred to a lymphopenic host. In particular, Nrp1+ anergic conventional CD4+ T cells displaying a partially de-methylated tTreg-me signature gave rise to functional Foxp3+Nrp1+ pTreg cells with a fully de-methylated Treg-me signature in vivo.

T cell anergy is proposed to be a cellular mechanism of immune evasion contributing to the failure of T cells to eradicate tumors. Tumor antigens can be taken up and presented by APCs in the absence of co-stimulatory signals promoting anergy in antigen-specific CD4+ T cell populations. In addition to anergy, regulatory T cells also have a principal role in promoting immune evasion by cancer cells. Foxp3+ Tregs are specifically recruited to the tumor sites and suppress tumor-specific T cell responses. Their abundant presence is one of the major obstacles to effective antitumor immunotherapy and it is often associated with poor clinical prognosis. In spite of these important discoveries the role of Treg in cancer is controversial. Finally, Nrp1 up-regulation appears to be associated with the tumor invasive behavior and metastatic potential. Increased levels of Nrp1 correlate with tumor aggressiveness, advanced disease stage, and poor prognosis.

Our hypothesis for why Treg cells arise in tumors is that Nrp1+ anergic CD4+ T cells are ideal progenitors for Foxp3+ Treg cells. The objective of my project is to specifically study the role of Nrp1 on the induction of CD4 T cell anergy and the trans-differentiation of anergic conventional T cells into the Foxp3+ Treg cell lineage.

Laura Marholz, PhD

Laura Marholz, PhD

Parker Lab
Phone: 720-485- 9638

Primary or acquired resistance to cancer therapy is a major problem for many commonly prescribed clinical treatments. The mechanisms of such resistance often depend on the cancer type and exact treatment, and can potentially involve modifications of the drug target through genetic mutation, changing the flux of cellular drug uptake, or even adapting and upregulating certain advantageous pathways which may help cancer cells survive and proliferate in stressful conditions. For example, cancerous cells have been observed to have a different metabolic profile from noncancerous cells, especially with increased uptake of nutrients and observed glycolysis under aerobic conditions. This altering of metabolic pathways enables a cancer cell to support enhanced growth and proliferation, and recent evidence suggests that increasing dependence on such advantages may provide answers into why some cancers become more resistant to certain therapies over time. Despite the body of research detailing observations of these metabolic differences in cancer, our understanding of the precise mechanisms involved in how these pathways are altered remains lacking. Elucidation of potential signaling pathways involved in cancer metabolism regulation could provide promising therapeutic targets.

The first-line treatment against chronic myeloid leukemia (CML) is the targeted Bcr-Abl kinase inhibitor imatinib, also known as Gleevec. Despite the incredible success of this drug, a subset of patients either do not respond to the treatment at all or their response degrades over time, and there remains a need to understand the cause of such resistance in order to identify therapeutic options that could reestablish patient sensitivity to therapy. Our laboratory has preliminary data that suggest metabolism may be altered in kinase inhibitor resistant CML cells.

Regulation of cellular metabolism is controlled by a complex network of pathways which determine how a cell produces its energy depending on need and environmental conditions. Cell signaling with protein kinases is one of the most common methods a cell uses to communicate, coordinate, and control many of its necessary activities, including metabolism. The goal of this project will be the development of novel biosensors to detect the intracellular signaling of a panel of metabolically relevant kinases (Akt, LKB1, mTOR and AMPK), and then to use these biosensors to screen for differential signaling in drug-sensitive and drug-resistant CML lines. Results from this research will provide quantitative information into metabolic kinase signaling activity which may provide mechanistic answers detailing how a cancer cell is able to manipulate its metabolic pathways for acquired advantages.

Kelly Makielski, PhD

Kelly Makielski, PhD

Modiano Lab

Osteosarcoma (OSA) is an uncommon but devastating bone cancer, typically diagnosed in children and adolescents. Despite aggressive treatment, many affected children develop metastatic disease for which there is no effective therapy. Despite advances in cancer therapy, the prognosis with OSA has remained stagnant for over thirty years, highlighting the need for novel treatment strategies. OSA is an immune responsive tumor, making immunotherapy a promising new treatment. One approach to activate the immune system is with oncolytic viruses, such as vesicular stomatitis virus (VSV). Oncolytic viruses selectively replicate in and destroy tumor cells, exposing viral antigens and tumor-associated antigens, triggering an anti-tumor immune response to potentially delay or prevent metastases.

Pediatric OSA research is hindered by its rarity, with fewer than 1,000 new cases diagnosed annually. In contrast, OSA occurs commonly in dogs, and its comparable clinical presentation makes the dog a useful model for translational OSA research. We have previously shown the existence of two molecular OSA phenotypes with distinct biological behavior and prognosis, characterized by both intrinsic tumor properties and host factors. This provides the opportunity to test experimental therapies on two disease phenotypes expected to have different prognoses with standard of care alone.

We are investigating the potential of oncolytic virotherapy with VSV to initiate anti-tumor immunity in canine OSA, with the intent to inform future clinical trials for human patients. Dogs with naturally-occurring OSA will be administered oncolytic VSV in addition to standard of care. We will characterize the anti-tumor immune response induced by VSV, and correlate it with the presence of resident or infiltrating immune cells in the tumor, as well as with clinical endpoints, including time to metastasis and survival time.

We hypothesize that VSV treatment will increase infiltration of immune cells into tumors, generating clonal populations with anti-tumor activity. We anticipate that this immune activation will be associated with improved survival compared to that expected with standard of care alone.Our results will provide valuable information regarding the mechanisms of immune activation by VSV and its potential translation to humans with OSA and other tumors. Determining prognostic factors will help guide treatment decisions, targeting VSV therapy primarily toward patients expected to respond favorably.

More postdoctoral fellowship opportunities

Numerous NIH fellowship opportunities are available in the Masonic Cancer Center and throughout the Academic Health Center for predoctoral and postdoctoral fellows currently training in laboratories of faculty at the University of Minnesota. Candidates not currently working at the U of M can contact training grant directors and faculty preceptors direcly by clicking on the links below to find out about available positions: