Mentor Spotlight: Neil Ganem, PhD and Katrina Traber, MD/PhD – the New Co-Directors of the MD/PhD Program
For October, we would like to spotlight the newly appointed co-directors of the MD/PhD Program: Neil Ganem, PhD and Katrina Traber, MD/PhD. Drs. Ganem and Traber also joined the medical student research advisory committee.
Dr. Ganem is an associate Professor of Pharmacology, Physiology & Biophysics, and Medicine. Dr. Ganem’s lab seeks to define the tumor suppression mechanisms that limit the proliferation of highly abnormal aneuploid cells, as well as to identify the common genetic adaptations made by cancer cells to overcome these growth barriers. Dr. Ganem received his PhD in biochemistry from Dartmouth Medical School in 2007 studying the mechanisms underlying mitosis (cell division). After receiving my PhD at Dartmouth, he moved to the Dana-Farber Cancer Institute where his postdoctoral work was focused on understanding the causes of consequences of aneuploidy. Aneuploidy describes cells that have an abnormal number of chromosomes, and it’s important to understand aneuploidy because nearly all cancer cells are aneuploid, and aneuploidy is actually known to fuel tumor development and growth. In 2011, Dr. Ganem was promoted to instructor at Harvard Medical School before joining Boston University Medical School in 2013.
Dr. Ganem’s lab is highly focused on identifying “ploidy-specific lethal” proteins. These are proteins that are not essential for normal cells (which are not aneuploid and have a normal number of chromosomes) but are essential for aneuploid cancer cells (which have an abnormal number of chromosomes). They recently identified once such protein, called KIF18a. It is now known that drugs that inhibit KIF18A are able to kill aneuploid cancer cells while not harming normal, healthy cells. Phase I and II clinical trials for KIF18A inhibitors are now underway, and early data show tumor shrinkage with no harmful side effects to patients.
Dr. Ganem has graduated three MD/PhD students from his lab, all working on different cancer cell biology projects. All three are now in Physician Scientist Training Programs (Sanghee Lim at Mayo Clinic, Ryan Quinton at Stanford Medical School, and Marc Vittoria at Yale School of Medicine), as well as published fist-authors. He is currently mentoring another MD/PhD student, Rose Zhao, who is in her fourth year in the lab and who also wants to pursue a career in oncology.
Dr. Ganem on Mentorship: “Mentorship is the most important part of my job. I try to give my students the freedom to develop and pursue their own independent ideas and then support them in their endeavors as much as possible. The vast majority of experiments will end up giving unexpected data, or may fail to work altogether.” His advice to his mentees and students “is to learn to accept that failed experiments and rejected hypotheses are a big part of science, and it is critical to stay motivated, not get discouraged, and constantly think of new ideas to explain the unexpected data.”
Dr. Traber, MD, PhD, is a board-certified pulmonologist at Boston Medical Center (BMC) and an assistant professor of medicine at Boston University Chobanian & Avedisian School of Medicine. After receiving her medical degree from New York University, Dr. Traber completed a pulmonary disease and critical care medicine fellowship at BMC.
The long-term goal of the Traber Lab is to identify and develop new strategies to treat severe neutrophil-based sequelae of pneumonia such as ARDS and sepsis. To achieve this goal, we use in vivo and in vitro models of pneumonia to investigate mechanisms of neutrophil dysfunction in acute lung infections. Currently, we have been using two broad approaches to understand neutrophil biology. First, we are examining modulation of the neutrophil transcriptome during neutrophil migration from circulation to the alveolar space. Second, we are investigating how Oncostatin M (OSM), an IL-6 family cytokine produced by neutrophils in many acute and chronic inflammatory settings, including pneumonia, ARDS and sepsis potentiate neutrophil migration to the alveoli during pneumonia.