Damon Runyon News

Dr. Tasker is synthesizing a new set of small molecules based on natural products, designed to have structural features to allow them to cross the blood-brain barrier. The blood-brain barrier protects the brain, but it also prevents most chemotherapeutic agents from reaching tumor cells in brain cancers, meaning prognoses for cancers such as glioblastoma multiforme and brain metastases are often poor. She will test these new compounds for anticancer activity, and will study whether active compounds cross the blood-brain barrier.

Dr. Ordovas-Montanes studies how inflammation in the gut influences individual epithelial and immune cells. Inflammation is one of the largest risk factors for developing colon cancer. A better understanding of the cellular factors involved in precipitating malignancy may lead to novel approaches for blocking the initiation of cancer and restoring the gut to a healthy balanced state.

Dr. Jeffery studies “stromal cells” that support the function of blood stem cells in the bone marrow. Cancer treatments such as irradiation and chemotherapy damage the bone marrow, and the repair of this tissue is crucial for the recovery of the blood system. She is characterizing the role of a newly identified factor produced by stromal cells in this rebuilding process. These studies have the potential to enhance our understanding of bone marrow repair, and to identify new methods for improving the recovery of the blood system in cancer patients following irradiation or chemotherapy.

Dr. Jaeger is investigating how a protein called the Heat Shock Transcription Factor 1 (HSF1), a potent pro-survival transcription factor, orchestrates changes in the three-dimensional architecture of chromosomes to activate tumor supportive gene expression programs in diverse cancer types. Increasing evidence suggests that the three dimensional architecture of chromosomes can influence the unique gene expression programs that support tumor growth. He aims to determine how gene expression is significantly altered in cancer cells when compared to normal cells.

Dr. Hussmann is studying how translation is regulated in healthy cells and how this regulation goes awry in disease. Cells control protein abundance by modulating how frequently messenger RNAs are translated by ribosomes, but the mechanisms that determine how densely ribosomes are packed onto each individual transcript are poorly understood. He is developing experimental approaches to produce transcriptome‐wide single‐molecule measurements of ribosome density in order to advance this understanding.

Dr. Goldman is using single-molecule imaging to monitor the quality control process for messenger RNA (mRNA) in real time in living cells. The ribosome decodes genetic information encoded in mRNA and synthesizes protein. In some cases, faulty mRNAs are produced—caused either by genetic mutations, errors in transcription or pathological states such as cancer. When the ribosome encounters a problematic mRNA, quality control pathways in the cell intervene to remove the ribosome from the mRNA, aborting translation.

Dr. Gasic [CRIS Cancer Foundation Breakthrough Scientist] aims to elucidate the “microtubule integrity response,” mechanisms that monitor the health of microtubules in cell division under normal physiological conditions and in cancer. Microtubules are frequent chemotherapy targets in treatment of various cancers, such as leukemia, lymphomas, melanoma, lung, ovarian, and breast cancer. Microtubule-targeting chemotherapeutics are believed to kill cancer cells through mitotic arrest.

Dr. Daniels aims to improve the ability of engineered T cells to kill cancer. Specifically, his goal is to understand how signaling events during T cell activation determine the therapeutic properties of activated T cells. He uses synthetic immunology techniques and computational methods to search for synthetic receptors that confer desired functions upon T cells. Ultimately, he hopes to design and create receptors that improve the ability of T cells to proliferate, persist, recruit other immune cells, and kill cancer cells.

Dr. Rabik is examining how mutations in the WT1 gene result in methylation changes in acute myeloid leukemia (AML). WT1 recruits the machinery necessary for demethylation to its target genes, ultimately regulating gene expression. When WT1 is mutated, these genes remain methylated and inactive, preventing normal hematopoiesis. She is identifying WT1 target genes and mapping their methylation landscape both in leukemic and normal settings. She will also test drugs designed to cause demethylation to evaluate if these drugs can treat the leukemia caused by mutations in WT1.

Dr. Miller focuses on improving how the side effects of leukemia treatment are reported. Currently toxicities of cancer treatment for patients enrolled on clinical trials are identified through manual review of the medical record, but prior work has shown that this method of identification leads to under-reporting of side effects. She aims to develop a new method that uses electronic medical record data to identify and report toxicities during treatment for leukemia.