Isabella [National Mah Jongg League Scholar] was born and raised in Puyallup, Washington. She graduated from Pacific Lutheran University, Tacoma, with a BS in Biological Sciences with minors in Chemistry and Business Administration. Her motivation to pursue cancer research stems from her own health struggles, which sparked a strong interest in human health and biology from an early age. Over time, that interest has evolved into a deep intellectual curiosity about the molecular mechanisms of cancer. During her undergraduate studies, she had the opportunity to work as a summer intern in the laboratory of Christina M. Termini, PhD, where she investigated how inhibiting isoprenoid production impacts hematopoietic stem cell (HSC) maintenance, expansion, and survival. Her ultimate goal is to contribute meaningfully to improving patient outcomes by developing safe, accessible, and effective cancer treatments. Outside the lab, she enjoys being outdoors, cooking, dancing, and spending quality time with her family. 

Dr. Ardy [Robert Black Fellow] is investigating the genetic determinants that govern the behavior of fibroblasts, a type of connective tissue cell that has been implicated in arthritis, heart disease, and cancer. Activated fibroblasts can exacerbate disease through various mechanisms, including remodeling tissue architecture and modulating the immune system. Dr. Ardy plans on using state-of-the-art genetic tools, including CRISPR inhibition and activation coupled with single-cell RNA sequencing technology, to uncover the proteins and pathways that regulate fibroblast behavior and thereby inform the development of new targeted cancer treatments. Dr. Ardy received his PhD from the Medical University of Vienna and his BS from the University of California, Los Angeles.

Attaching a small molecule known as ubiquitin to a protein, in a process called ubiquitylation, targets that protein for degradation. By utilizing the ubiquitylation machinery, scientists are now able to target cancer-causing proteins for degradation, a strategy that has proven effective with drugs such as Lenalidomide/Revlimid to treat multiple myeloma. One way to bring proteins in proximity to ubiquitin ligases (attachers) is with synthetic adhesion molecules, or “molecular glue.” This may provide a means of targeting proteins previously deemed undruggable, including those that lack a binding site for inhibitors. Dr. Baek [Meghan E. Raveis Fellow] aims to expand the degradable proteome by establishing a formula for the design of molecular glues to target cancer-causing proteins as a therapeutic modality. Dr. Baek received his PhD from Technical University of Munich and Max Planck Institute of Biochemistry, Munich, his MS from University of Tennessee Health Science Center, Memphis, and his BA from Rutgers University, New Brunswick.

Peptide drugs, which mimic the function of natural peptides such as hormones or growth factors, have emerged as a promising strategy for the treatment of cancer. Despite their potential, however, very few have reached the clinic in the past decade, primarily due to their off-target toxicity. The design of a suitable system to deliver peptides in a site-specific manner would address a major challenge in the development of anticancer peptide drugs. De novo protein design, or building proteins “from scratch,” has allowed for the engineering of functional proteins for a broad range of applications, from catalysis to pharmaceuticals. Dr. Bhattacharya [Connie and Bob Lurie Fellow] aims to design proteins from scratch that can “mask” a peptide of interest for systemic delivery to the desired location. This project will initially target pediatric sarcomas, but eventually extend to other cancers like glioblastoma and breast cancer. Dr. Bhattacharya received his PhD from Syracuse University, Syracuse and his MS and BS from University of Calcutta, Kolkata.

Evidence that aging is driven by defined, regulated processes (rather than simple “wear and tear”) has sparked hope that we might target these processes to fight age-related diseases. A particularly exciting example is the regulation of protein homeostasis, or the balance between protein synthesis, folding, and degradation. Protein homeostasis is deregulated in both cancer and normal aging, but the underlying mechanisms remain elusive. Dr. Boos will use the short-lived African turquoise killifish as a new model organism to study how different cells and tissues respond to protein misfolding, how they coordinate their responses, and how aging influences these pathways. This research will not only unravel fundamental mechanisms of aging, but also inform new strategies to fight multiple types of cancer. Dr. Boos received his PhD and his B.Ed. from the University of Kaiserslautern.

B cells, especially those that target cancer antigens, are crucial for fighting tumors; however, not everyone develops them. Our gut bacteria play a vital role in training B cells to recognize a wider range of threats. Dr. Brewer’s [HHMI Fellow] research explores how these gut bacteria influence the specificity of B cells, and thus our body’s ability to combat tumors. Dr. Brewer’s research aims to determine if the “training” of B cells by gut bacteria early in life influences their later responses to vaccines and cancer. This investigation may not only improve our understanding of how gut bacteria shape our immune system, but also pave the way for novel cancer treatments utilizing gut bacteria. Dr. Brewer received her PhD from Stanford University, Stanford and her BS from Massachusetts Institute of Technology, Cambridge.

Proper cell division, including equal partitioning of DNA into two “daughter” cells, is critical for cell viability. However, many cancers continue to divide despite having atypical numbers of chromosomes and can even contain additional copies of the entire genome (polyploidy). Understanding how large increases in chromosome number affect cell division machinery has been limited by the methods used to generate polyploid cells. Serendipitously, stable polyploidy has arisen in multiple organisms, such as plants, fish, and amphibians. By utilizing the natural polyploidy found in Xenopus clawed frogs (ranging from two copies to twelve copies of the genome), Dr. Cavin-Meza [Merck Fellow] will explore the mechanisms that lead to increased but stable genome size. He will also analyze the proteome across Xenopus species to reveal how proteins have adapted to promote stable polyploidy over time, giving valuable insight into how stable polyploidy could arise in cancers. Dr. Cavin-Meza received his PhD from Northwestern University, Evanston and received his BS from the University of California, San Diego.

Dr. Chan’s [Sijbrandij Foundation Fellow] research focuses on gamma delta T cells, an unusual and understudied population of immune cells. While gamma delta T cells have strong antitumor activity, they are most highly stimulated not by cancer cells but by signals produced by microorganisms. Dr. Chan’s work examines the mechanisms by which gamma delta T cells detect and respond to leukemia versus pathogenic microorganisms, and how infection with these microorganisms subsequently impacts the trajectory of leukemia. This is particularly relevant to patients undergoing conventional cancer treatments (e.g., chemotherapy) that suppress the immune system, rendering them susceptible to infection. Furthermore, gamma delta T cells are capable of both rapid and long-term responses against their targets, which positions them as a tool to treat initial cancer as well as prevent disease recurrence. Dr. Chan received her PhD from Yale University, New Haven, and her BS from the University of California, Los Angeles.

Dr. Chappleboim studies how cells communicate during a developmental process called somitogenesis, which drives the formation of repeated structures such as the spinal vertebrae. The signals that guide cell communication during this process can get misinterpreted by cancer cells, resulting in uncontrolled growth. These pathways are implicated in numerous cancer types but are notably associated with colorectal, ovarian, and breast cancer. Using cutting-edge techniques in human stem cells and 3D-models called organoids, along with the tools of computational biology, Dr. Chappleboim aims to deliberately perturb and examine these signaling pathways to gain a comprehensive understanding of how they function. Dr. Chappleboim received his PhD, MS, and BS from Hebrew University of Jerusalem, Jerusalem.

Dr. Chen is genetically re-engineering cancer-infecting viruses so that, once inside a tumor cell, they flip on a built-in “self-destruct” circuit called pyroptosis. This explosive form of cell death not only wipes out the infected cell but also broadcasts an alarm that rallies the immune system against the whole tumor. By pairing this viral upgrade with an ultrasound trigger, Dr. Chen aims to turn treatment-resistant pancreatic cancer—and, ultimately, other solid tumors—into diseases the immune system can eradicate. Dr. Chen received his PhD and MS from Zhejiang University, Hangzhou, and his BS from Southwest Jiaotong University, Chengdu.