Emerald Foundation Inc

To study how ferroptosis-based strategies can enhance the efficacy of immunotherapies in breast cancer.

To investigate the regulation of treg lymphatic tumor migration and the interaction among tregs, lymphatic endothelial cells, and tumors to develop strategies of delivering targeted therapies locally instead of systemically.

To enhance nanoparticle accumulation in desired cell types to develop more effective and safer targeted nanotherapies.

To investigate the regulation of Treg lymphatic tumor migration and the interaction among Tregs, lymphatic endothelial cells, and tumors to develop strategies of delivering targeted therapies locally instead of systemically.

To examine the cellular mechanisms through which dendrite-centric Alzheimer's disease pathologies result in cognitive dysfunction and hyper-excitability.

To identify regulators of lineage reversion that impact resistance to WNT-targeted therapies in colorectal cancer.

To map the transcriptional and protein changes induced by lactate and identify the mechanisms that cause NK suppression, on both NK and tumor cells, using high-throughput and unbiased approaches.

To uncover the set of cell-surface proteins that mediate essential interactions between PDAC cells and their microenvironment.

To investigate how the colon microbiota and host genetics intersect to alter responsiveness to immunotherapy in colorectal cancer.

To use innovative cell biology techniques coupled with genomics to investigate the role of mitochondrial-derived vesicles in cancer cell metabolism.

To understand how maladaptive changes to the integrated stress response pathway alter the force generating ability of human heart cells and determine if pharmacological manipulation can rescue cardiomyocyte function.

To use innovative cell biology techniques coupled with genomics to investigate the role of mitochondrial-derived vesicles in cancer cell metabolism.

To identify molecular mechanisms that help anaerobes cope with oxygen exposure and/or oxidative stress.

To identify molecular mechanisms that help anaerobes cope with oxygen exposure and/or oxidative stress.

To determine the mechanism through which breast cancer cell clusters dissociate into single cells and proliferate at distant sites and to determine the impact of the new environment on metastasis formation.

To understand the molecular mechanism underlying immunosuppression and immunoactivation and develop new treatment strategies for hepatic malignancies.

To map the transcriptional and protein changes induced by lactate and identify the mechanisms that cause NK suppression, on both NK and tumor cells, using high-throughput and unbiased approaches.

To understand the molecular mechanism underlying immunosuppression and immunoactivation and develop new treatment strategies for hepatic malignancies.

To understand how maladaptive changes to the integrated stress response pathway alter the force generating ability of human heart cells and determine if pharmacological manipulation can rescue cardiomyocyte function.

To use tumor organoid and mouse models to determine how loss of Claudin proteins impacts tumor invasion and metastasis.

To develop interpretable machine learning methods that link spatial phenotypes in imaging data of solid tumors with patient outcomes.

To use tumor organoid and mouse models to determine how loss of claudin proteins impacts tumor invasion and metastasis.

To characterize exosomes from nave and tumor-educated platelets and determine their contribution to metastatic dormancy and recurrence.

To investigate the role of Brg1-dependent epigenetic regulation on PDAC fibroblast pro-tumorigenic functions.

To develop interpretable machine learning methods that link spatial phenotypes in imaging data of solid tumors with patient outcomes.

To screen young students for previously undiagnosed heart ailments and generate data that can be used to train AI programs to better evaluate electrocardiograms.

To study how SLC7A5 regulates metabolic reprogramming and signaling pathways that enable cancer cells to survive CDK4/6i treatment.

To study how SLC7A5 regulates metabolic reprogramming and signaling pathways that enable cancer cells to survive CDK4/6i treatment.

To characterize interactions between proteins that associate only with the KRAS4A isoform to identifying pathways that can be rationally targeted to achieve a more comprehensive interruption of KRAS stimulation.

To characterize exosomes from nave and tumor-educated platelets and determine their contribution to metastatic dormancy and recurrence.

Sponsorship of [individual] conferences Sponsorship fee - Travel Bursaries for those attending the Black in [individual] Conference (2022).