These lectures were presented at the 2025 Annual Meeting of the American Society for Biochemistry and Molecular Biology in Chicago. In 2026, the ASBMB's annual meeting will be held March 7–10 at National Harbor, just outside Washington, D.C. Learn more and sign up for email updates: https://www.asbmb.org/annual-meeting/sign-up.

2025 ASBMB Annual Meeting lectures

Success in poker requires taking risks based on incomplete information, reassessing as new information emerges, perseverance in the face of adversity, and a healthy dose of luck.  The same is true in scientific research.  I will speak to how persistence and serendipity helped define my career and why understanding poker fundamentals can up your scientific game.

Melissa Moore | Persistence and serendipity in science: A poker analogy

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the fastest-growing etiology of hepatocellular carcinoma (HCC). This work identifies novel gene and lipid associations in human MASLD-driven HCC that may be exploited for therapeutic benefit. Methods: Human HCC tumor (n=8) and adjacent non-tumor samples (n=8) were obtained from the Biospecimen Procurement and Translational Pathology Shared Resource Facility at the University of Kentucky Markey Cancer Center. All patients met cardiometabolic MASLD criteria and were negative for viral hepatitis. Hematoxylin and eosin (H&E) staining was used for pathological determination of tumor and adjacent nontumor tissue. Lipids were extracted using a methyl-tert-butyl ether extraction method and subjected to lipidomics by the West Coast Metabolomics Center. RNA was isolated and used for bulk sequencing. Data were analyzed using paired nonparametric analyses via a Wilcoxon or Mann-Whitney test, as appropriate. Results: Histological analysis by H&E showed significant lipid vacuole accumulation in HCC tumors relative to nontumor tissue. Lipidomic analysis revealed significant increases in long-chain nonesterified monounsaturated fatty acids (MUFAs; C16:1, C18:1, C20:1) and MUFA-enriched phospholipids (PC30:1, PC32:1, PE32:1, and PC36:1) in tumors relative to nontumor tissue. No significant differences were observed in nonesterified polyunsaturated fatty acids (PUFAs; C18:2, C20:4, and C22:6), PUFA-enriched phospholipids (C36:4, C38:4, C38:6, C40:6), or in fatty acid esters of hydroxy fatty acids (FAHFAs; C38:2, C38:4, C38:6). However, both MUFA- (C14:1, C18:1) and PUFA-enriched acylcarnitines (C18:2, C18:3) were collectively reduced in human tumors. Differential analysis of RNA sequencing revealed fatty acid oxidation genes (CPT1A, CPT2, ACADL, ACADM, ACADS, HADHA) were significantly reduced in tumor versus nontumor tissue. Further, genes involved in de novo lipogenesis were largely dysregulated (e.g. no differences in SREBF1 or FASN; increases in ACLY, ACACA, and SCD1; decreases in ACSL1) in tumor versus nontumor tissue. Conclusions: These results suggest human HCC tumors exhibit a reduced capacity to undergo mitochondrial β-oxidation resulting in accumulation of free and esterified MUFAs with concomitant reductions in MUFA-carnitines. Current studies are underway to determine the mechanisms by which impairment of hepatic MUFA catabolism via FAO promotes the development of HCC in mice.

Robert “Nate” Helsley  | Gene Expression and Lipid Profiling of Metabolically-driven Human Hepatocellular Carcinoma

Science is not performed in a vacuum, and scientists do not make strides without other who have helped them along the way. Throughout my career, I have been fortunate to have had many mentors who have been instrumental in my scientific journey. Now with a career in academia, I have worked hard to improve academia for scientists at all levels, especially those that have been historically marginalized. I will discuss my scientific career path through the lens of all the people that have supported, encouraged and inspired me throughout the years.

Benjamin Garcia | An unlikely career in science and academia

The study of DNA damage has broad relevance to human pathophysiology with its involvement in birth defects, cancer, premature aging syndromes, and certain neurologic disorders. Single strand breaks (SSBs) are among the most common form of endogenous DNA damage. Here we will describe mechanisms by which SSBs threaten genome integrity in mitotic and post-mitotic cells. If they are not resolved in a timely manner, SSBs can derail passing replication forks converting them to toxic double strand breaks (DSBs). These so called “collapsed forks” arise spontaneously in every S phase and are believed to be the primary physiological trigger of homologous recombination. We will describe a recent study using the CRISPR/Cas9 nicking enzymes to examine the interaction of the human replication machinery with SSBs. We combine direct analyses of DNA end structures at sites of DNA nick-induced fork collapse with detailed mapping of repair factor binding to establish a comprehensive high-resolution view of how replication-coupled DSBs are generated, processed, and repaired.  Our recent studies have also identified unexpected high levels of single strand breakage in neurons, which arise during metabolic processes intrinsic to neuronal development, differentiation, and maintenance. The source of this “programmed” DNA breakage in neurons will be described, and how this physiological process can be corrupted to drive neurodegenerative diseases and neurotoxicity after chemotherapy. Through these basic research efforts, we hope to identify vulnerabilities specific to cancer cells and to discover mechanisms underpinning chemotherapy-induced neurotoxities, which may contribute to new preventive and treatment strategies.

Andre Nussenzweig | Maintaining genome stability in mitotic and post-mitotic cells

The joy of teaching lies not only in helping students surpass their own expectations but in the collaborative process that makes learning a shared journey. In my approach, fostering a love for science and learning happens through meaningful collaboration—with students, colleagues, and the broader academic community. I believe that when we embrace collaboration, we empower students to actively engage with material, rediscover their scientific curiosity, and take ownership of their learning. By creating discussion-based classrooms and utilizing evidence-based pedagogies, I work alongside students to foster inquiry and critical thinking, helping them develop the skills to ask insightful questions and seek meaningful answers. Incorporating my own research into the classroom enriches this process, bringing real-world insights and cutting-edge developments into our discussions. This not only keeps students connected to the latest in the field but also demonstrates the dynamic relationship between teaching and research. Collaboration with peers further enhances my teaching by enabling me to share ideas, refine methods, and experiment with new approaches. While challenges such as administrative pressures and discipline-specific cultures can pose obstacles, our commitment to supporting one another’s growth—through both successes and setbacks—strengthens the teaching community as a whole. This collaborative mindset not only enhances student engagement and critical thinking but also fosters a deeper love for the work we do and a shared passion for teaching and learning that transforms the classroom experience. A good teacher, by necessity, is also a good researcher—constantly questioning, experimenting, and refining their approach to foster an environment of collaborative inquiry and growth.

Neena Grover | Embracing collaborations: Loving what we do and doing what we love

The first growth factors identified and studied during the early 1970s were Epidermal Growth Factor (EGF) and Nerve Growth Factor (NGF). It was soon demonstrated that EGF and NGF mediate their cellular and physiological effects by binding to specific cell membrane receptors: the EGF receptor (EGFR) and the NGF receptor (NGFR), respectively. The mechanisms of activation and signaling of these receptors were compared to those of insulin and IGF1, which bind and activate the Insulin Receptor (IR) and IGF1 Receptor (IGF1R). These comparisons gained further significance with the discovery that EGFR, NGFR, IR, IGF1R, and many other membrane receptors belong to the receptor tyrosine kinase (RTK) family of cell signaling molecules. Early insights into the activation and signaling mechanisms of EGFR revealed that ligand binding to its extracellular domain induces and stabilizes the formation of EGFR dimers. This dimerization plays a critical role in activating the receptor's intrinsic tyrosine kinase activity. Through an intermolecular process, this activation leads to the autophosphorylation of multiple tyrosine residues in the C-terminal tail of EGFR. The cytoplasmic domain of EGFR serves not only as an enzyme that phosphorylates various substrates but also as a scaffold that recruits and regulates multiple signaling proteins through complex formation. While different ligands induce RTK dimerization and activation through variations on a shared theme, this paradigm is universal among all RTKs and is similarly observed in the activation of other surface receptors. Further important discoveries regarding the mode of action of EGFR and other RTKs made during the 1970s and 1980s include the following: Signaling Modules: Molecules containing SH2, SH3, and other small protein modules were found to play key roles in mediating cellular activities downstream of RTKs and many other signaling molecules. Ligand-Dependent Endocytosis: Ligand binding to the extracellular domain of RTKs stimulates receptor-mediated endocytosis and intracellular trafficking ,which are essential for proper signal transduction. Oncogenic Mutations: A variety of gain-of-function oncogenic mutations were identified in EGFR and other RTKs. These mutations were shown to be critical drivers of many human cancers. These early discoveries, along with others made during the 1980s, laid the conceptual groundwork for the development of targeted therapies. They paved the way for the discovery and clinical application of more than 50 targeted small-molecule cancer drugs and therapeutic antibodies, which have significantly improved patient outcomes in oncology.

Joseph Schlessinger | Discovering how receptor tyrosine kinases are activated and signals

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