Many cancer treatments kill healthy cells along with cancer cells and tumors frequently adapt to treatment and build resistance. These challenges exist because the most important pathological cancer processes occur through complex interactions inside living cells, and the current models used to study cancer cannot fully mimic these complex living interactions. Dr. Zheng aims to combine large-scale genetic screening, advanced single-molecule imaging, and AI modeling to create detailed maps of how cancer-driving genes behave inside living human cells. These maps will show how networks of genes, as well as small DNA changes, alter the real-time behavior of powerful cancer drivers. This work will guide the development of treatments that cause less harm, stay effective longer, and act with far greater precision. Dr. Zheng received his PhD from Massachusetts Institute of Technology, Cambridge, and his BS from Peking University, Beijing.

CAR T cell therapy, which involves genetically engineering a patient’s own immune cells to seek and destroy cancer, has revolutionized the treatment of certain blood cancers. However, it frequently performs poorly against solid tumors because T cells become exhausted or cannot effectively detect the cancer cells. Dr. Banerjee aims to learn the fundamental molecular, genetic, and biophysical rules of internal signaling in T cells. By decoding these rules, he aims to design next-generation CAR T cells with enhanced sensitivity, persistence, and versatility. Taking an atypical approach, he will combine multiple cutting-edge technologies to dissect and engineer the “immunological synapse,” the connection that forms between a T-cell and a tumor cell, to ultimately tune the function of the T cells. This study aims to overcome current limitations in treating leukemias and extend the success of immunotherapy to solid tumors, specifically melanoma. Dr. Banerjee received his PhD from Johns Hopkins University, Baltimore, his MTech from the Indian Institute of Technology, Kanpur, and his BEng from Jadavpur University, Kolkata.

While much has been uncovered about the specific mutations that arise within a tumor, it is not fully understood how the DNA a person is born with (their inherited genetics) influences how those tumors grow. Dr. Mei’s research focuses on a specific, aggressive cancer gene called ERBB2, which is responsible for many breast, lung, and stomach cancers. Dr. Mei aims to discover if a patient’s inherited genetics makes them more likely to develop these specific tumor mutations or makes the cancer more dangerous. By understanding the interaction between a patient’s natural DNA and their tumor’s DNA, we can better predict cancer risks and find more effective, personalized treatments. Dr. Mei received his PhD from The Rockefeller University, New York, and his BS from Peking University, Beijing.

Cancer cells and certain immune cells inside tumors need a lot of energy to survive and function, creating a kind of “tug-of-war” for nutrients in the tumor’s environment. However, until recently, there has not been a good way to measure how these cells use nutrients for energy inside a living tumor. To tackle this challenge, Dr. Peace developed a new technology that can track which nutrients power a key energy pathway—the TCA cycle—in both cancer cells and immune cells, directly in vivo in tumors. By uncovering these details, his work aims to improve how we design cancer treatments, especially immunotherapies that help the immune system fight cancer more effectively. This work has the potential to be relevant for all cancers. Dr. Peace received his PhD and BA from Trinity College, Dublin.

Metastasis, the spread of cancer cells from primary tumors to healthy tissues, accounts for over 90% of cancer-related deaths. A protein called dynein is crucial for cell movement and research indicates that inhibiting dynein can reduce breast cancer cell spread. Typically, dynein moves toward the cell nucleus along microtubules from the plus-end (typically near the cell periphery) to the minus-end (usually near nucleus). However, during cell migration, dynein congregates at the microtubule’s plus-end by a process that is poorly understood. Dr. Mishra aims to establish the molecular mechanism underlying dynein’s localization at the plus-end of the microtubule. This understanding will help elucidate how dynein facilitates cell migration and metastasis, potentially leading to new cancer treatment strategies applicable to various cancer types. Dr. Mishra received his PhD from the Indian Institute of Science, Bengaluru, and his BS from Banaras Hindu University, Varanasi.

Our immune system uses many strategies to defend against viruses. Recent studies have uncovered a surprising bacterial antiviral strategy—instead of cutting DNA to destroy it, this system builds new DNA molecules to stop infections. Dr. He’s project will focus on understanding how this bacterial defense system works and explore whether this system can be repurposed to safely make DNA inside human cells. This could offer a new way to address a major challenge in the development of gene therapy and cancer immunotherapy more broadly: safely and efficiently delivering DNA into target cells without triggering harmful immune reactions. Dr. He received his PhD from the University of Wisconsin-Madison, Madison, and his BS from the University of Chinese Academy of Sciences, Beijing.

Asymmetric cell division is a mechanism by which adult stem cells generate one self-renewing stem cell and one differentiating daughter cell in order to maintain tissue homeostasis. A fundamental unsolved question is how two daughter cells adopt distinct cell fates (e.g., how one becomes a blood cell and one becomes a blood vessel cell) to prevent unchecked proliferation and tumorigenesis. Using fruit flies as a model system, Dr. Yu will investigate the selective inheritance of chromosomes for cell fate decision during asymmetric divisions of stem cells. This work will reveal a fundamental principle of how stem cells use chromatin-based mechanisms to determine cell fate and maintain homeostasis. Moreover, it will provide key insights into how cancer cells hijack these pathways to sustain their immortality and uncover novel vulnerabilities in cancer that could be targeted therapeutically. Dr. Yu received his PhD from Harvard University, Cambridge, and his BS from the University of Science and Technology of China, Hefei.

Cancer is fundamentally a disease of lost tissue integrity, in which cells fail to properly coordinate and regulate one another, leading to abnormal cell growth and invasion within tissues. Dr. Hung aims to uncover basic principles of how cells combine chemical and mechanical signals to maintain tissue integrity. Using flatworms that are capable of tissue regeneration as a model, he will employ live whole-worm imaging of tissue regeneration to study mechanical and chemical signaling at the cellular level. This project will provide key insights about the logic of multicellular signaling circuits for maintaining normal tissue integrity and clues about how these signaling circuits can be dysregulated in cancer. Dr. Hung received his PhD from Stanford University, Stanford, and his BS from the University of Washington, Seattle.

Many different kinds of mutations affect cancer genomes, but the most recurrent are copy number alterations, resulting in a cancer cell with more or fewer copies of a gene than a normal genome. Dr. Baslan is focused on developing novel therapies that target this class of mutations with an emphasis on deletion events. More specifically, using a combination of advanced algorithms and chemical biology tools, Dr. Baslan is investigating specific vulnerabilities that are associated with deletion events and developing strategies to target these sensitivities in pancreatic cancers. Ultimately, Dr. Baslan aims to explore the generalizability of these therapeutic strategies across cancers, as the majority of cancer genomes contain recurrent deletions.

Kinase pathways control how cells grow, divide, and survive. When they malfunction, they drive many forms of cancer. Abnormal kinase signaling also contributes to resistance against current therapies. Rather than blocking these pathways as traditional treatments do, Dr. Zhou’s research explores ways to change the outcome of aberrant kinase signaling. By redirecting these pathways toward anti-tumor responses, this approach has the potential to provide more durable treatments for cancers that evade existing therapies.