Perhaps reforming the executive pay would be a start to being able to charge real-world costs:
The president of MD Anderson is paid like someone running a prosperous business. Ronald DePinho’s total compensation last year was $1,845,000. That does not count outside earnings derived from a much publicized waiver he received from the university that, according to the Houston Chronicle, allows him to maintain unspecified “financial ties with his three principal pharmaceutical companies.”
DePinho’s salary is nearly two and a half times the $750,000 paid to Francisco Cigarroa, the chancellor of entire University of Texas system, of which MD Anderson is a part. This pay structure is emblematic of American medical economics and is reflected on campuses across the U.S., where the president of a hospital or hospital system associated with a university — whether it’s Texas, Stanford, Duke or Yale — is invariably paid much more than the person in charge of the university.
You have to be kidding me. You don't think one of the best oncologists in medicine is worth 2 million a year???
DePinho's laboratory has produced an array of discoveries leading to better methods of early cancer detection, improved cancer patient care and new cancer drug development. The range of his research includes cancer drug and biomarker development, cancer gene discovery, stem cell biology and development of genetically engineered mouse models to study cancer in humans.
DePinho was the first to show that the Myc family of oncogenes (cancer-causing genes) function through common cell signaling pathways to transform “normal” cells into malignant ones.
In a series of key experiments, DePinho established the concept of “tumor maintenance” to address the question of whether an original cancer-causing oncogene can remain active in maintaining a tumor despite the accumulation of many alterations in DNA during the malignant transformation process. This concept has contributed to cancer drug development by guiding identification of new therapeutic points of attack, as well as novel biomarkers that measure a patient’s response to a drug during a course of treatment.
His research also provided some of the first evidence that the p53 gene can suppress the development of some cancers by stimulating apoptosis, a process by which the majority of cancer cells die naturally. DePinho and Robert Eisenman discovered a co-repressor complex (known as mSin3/HDAC) that links a transcription factor and chromatin regulation in suppressing cancers. His lab also provided the first genetic evidence that a familial melanoma gene serves as a potent tumor suppressor in melanoma and many other cancer types.
With about 78% of all cancers diagnosed in people older than 55, perhaps DePinho’s most notable contributions concern the link between advancing age and increasing risk of cancer. He convincingly established that three factors — telomere dysfunction, an impaired ability of a cell to repair DNA damage and the continued renewal of the epithelial layer of tissue that covers organs — all unite to cause rearrangements in the DNA that drive the genesis of many common cancers.
Telomeres are sections of DNA at the ends of chromosomes. Each time a cell divides, telomeres lose a small amount of DNA and become shorter. In cancer cells, however, the telomeres are maintained by activation of a special enzyme, telomerase. Cancer cells usually have more telomerase than most normal cells, which contributes to their immortality and ability to spread.
Beyond cancer, DePinho’s work on telomeres has established the role of telomere dysfunction in acquired and inherited degenerative disorders, such as end-stage liver failure. His findings even suggest that there may be a “point of return” in which medicines might help severely aged organs recover a youthful state.
DePinho has created many faithful mouse models of human cancer. Most recently, he has developed the first metastatic prostate cancer model in mice, which he has used to identify tumor biomarkers that can stratify men into either high risk or low risk for spread of their disease. Using this approach, his laboratory has discovered prostate cancer markers that predict how lethal a cancer may be, which will better direct the course of therapy for men with this common cancer.
In addition to his presidential duties at MD Anderson, DePinho remains an active scientist in his laboratory and in the new Institute for Applied Cancer Science. His lab focuses mainly on basic-to-translational research programs for brain, colorectal, pancreas and prostate cancers, as well as aging and neuro-degeneration.
Honors
DePinho is a member of the National Academy of Sciences and the Institute of Medicine, a fellow of the American Academy of Arts and Sciences, and has received numerous other honors and awards including:
American Italian Cancer Foundation Prize for Scientific Excellence in Medicine, 2012
Albert Szent-Gyorgyi Prize for Progress in Cancer Research, 2009
Helsinki Medal, 2007
Albert Einstein College of Medicine Distinguished Alumnus Award, 2004
American Association for Cancer Research Clowes Memorial Award, 2003
American Society for Clinical Investigation Award, 2002