My name is Steven Yang and I’m a rising junior at Cornell University, and I’m originally from Rochester, Minnesota. At Cornell, I am majoring in Biology and potentially minoring in Anthropology, and currently work in a lab where I study the interactions between the immune system and cancer. After undergrad, I hope to pursue a MD-PhD program and eventually lead my own lab in a hopstial in oncology.
This summer, I’m working in Dr. Matt Walter’s lab where I study myelodysplastic syndromes (MDS), a type of leukemia characterized by hematopoietic stem cells failing to properly mature, leading to abnormally low blood counts. MDS is part of a “chain” of diseases, in which an accumulation of mutations and symptoms may cause a patient to develop MDS from clonal hematopoiesis and clonal cytopenia of undetermined significance, and may further cause MDS to evolve into secondary acute myeloid leukemia. About 50% of all MDS arise from spliceosome mutations, and my main focus is on U2AF1, one of the most common spliceosomes that are mutated in this disease. Cells with this mutation often accumulate DNA damage such as R-loops (DNA-RNA hybrids) that is sensed and repaired by proteins such as PARP and ATR, allowing for the mutant cell to survive. Our lab is developing treatments against this disease by targeting and inhibiting these proteins involved in the DNA damage response. By doing this, we hope to target these mutant cells and kill them as they accumulate too much damage to their DNA.