Ronald A. DePinho | |
---|---|
Born | 1955 (age 67–68) |
Nationality | American |
Citizenship | U.S |
Alma mater | |
Known for | Genetic and biological mechanisms governing the development of cancer and driving the aging process and age-associated degenerative diseases. |
Spouse | Lynda Chin |
Children | 3 |
Scientific career | |
Institutions |
Ronald A. DePinho (born 1955) is an American physician and research scientist. He served as president of MD Anderson Cancer Center from 2011 to 2017. [1] DePinho states that his concern for reducing the burden of cancer suffering became his life goal in 1998, when his father died of colon cancer. [2]
DePinho was born in the Bronx, New York City in 1955 to Celeste and Alvaro DePinho. He is the third of five children. He earned a bachelor's degree in biological sciences in 1977 from Fordham University. He received his medical degree with distinction in microbiology and immunology in 1981 from Albert Einstein College of Medicine.[ citation needed ]
He completed an internship and residency in internal medicine at Columbia-Presbyterian Medical Center, followed by postdoctoral fellowships in the Department of Cell Biology at Albert Einstein College of Medicine and in the Department of Biochemistry and Biophysics at Columbia-Presbyterian Medical Center.[ citation needed ] [3]
DePinho spent 14 years at Dana–Farber Cancer Institute. He served as founding director of the Belfer Institute for Applied Cancer Science and was an American Cancer Society Research Professor in the Department of Medicine (Genetics) at Harvard Medical School. Previously, he held several faculty positions during 10 years at Albert Einstein College of Medicine in New York, where he was the Betty and Sheldon Feinberg Senior Scholar in Cancer Research.[ citation needed ]
DePinho is Professor and former president in the Department of Cancer Biology at The University of Texas MD Anderson Cancer Center in Houston, Texas, and holds the Harry Graves Burkhart III Distinguished University Chair in Cancer Biology. [4] He assumed the presidency at MD Anderson on September 1, 2011. There, he founded the Institute for Applied Cancer Science to accelerate development of next-generation targeted immune- and cell-based cancer therapies. He launched MD Anderson's Cancer Moon Shots Program, which became a model for the White House Cancer Moonshot funded by President Barack Obama under the leadership of then-Vice President Joe Biden [5] [6] and administered by National Cancer Institute. [7]
DePinho publicly announced his resignation as MD Anderson president on March 8, 2017, after scrutiny over the administration of the organization had put him in the spotlight. "DePinho's five-and-a-half years at the helm of the world's largest cancer center were marked by unprecedented turbulence, questions of conflicts of interest, and unhappiness on the part of the faculty." [8]
DePinho is best known for his work on telomerase and telomere disfunction as it relates to cancer and aging. Specifically, in collaboration with Carol Greider, he generated the first telomerase knockout mouse. [9] This work led to a deeper understanding of telomerase and telomere dysfunction in cancer, aging and a range of degenerative diseases, including fibrosis.
DePinho's scientific program has made basic discoveries underlying cancer in the aged and factors governing acquired and inherited degenerative disorders. His laboratory established the concept of tumor maintenance, discovered a core pathway of aging and demonstrated that aging is a reversible process. [10] He has constructed and used refined mouse models of cancer to identify many new cancer targets and diagnostics.[ citation needed ]
He has published over 400 peer-reviewed research articles, review articles and book chapters (h-index 171). [11] He was inducted into the National Academy of Medicine in 2008, [12] the American Academy of Arts and Sciences in 2010, [13] the National Academy of Sciences in 2012, [14] and named an American Association for Cancer Research fellow in 2015. [15]
A telomere is a region of repetitive nucleotide sequences associated with specialized proteins at the ends of linear chromosomes. Telomeres are a widespread genetic feature most commonly found in eukaryotes. In most, if not all species possessing them, they protect the terminal regions of chromosomal DNA from progressive degradation and ensure the integrity of linear chromosomes by preventing DNA repair systems from mistaking the very ends of the DNA strand for a double-strand break.
Telomerase, also called terminal transferase, is a ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3' end of telomeres. A telomere is a region of repetitive sequences at each end of the chromosomes of most eukaryotes. Telomeres protect the end of the chromosome from DNA damage or from fusion with neighbouring chromosomes. The fruit fly Drosophila melanogaster lacks telomerase, but instead uses retrotransposons to maintain telomeres.
Embryonic stem cells (ESCs) are pluripotent stem cells derived from the inner cell mass of a blastocyst, an early-stage pre-implantation embryo. Human embryos reach the blastocyst stage 4–5 days post fertilization, at which time they consist of 50–150 cells. Isolating the inner cell mass (embryoblast) using immunosurgery results in destruction of the blastocyst, a process which raises ethical issues, including whether or not embryos at the pre-implantation stage have the same moral considerations as embryos in the post-implantation stage of development.
The Hayflick limit, or Hayflick phenomenon, is the number of times a normal somatic, differentiated human cell population will divide before cell division stops. However, this limit does not apply to stem cells.
Michael D. West is an American biogerontologist, and a pioneer in stem cells, cellular aging and telomerase. He is the founder and CEO of AgeX Therapeutics, a startup focused on the field of experimental gerontology.
Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc was the first gene to be discovered in this family, due to homology with the viral gene v-myc.
Carolyn Widney Greider is an American molecular biologist and Nobel laureate. She joined the University of California, Santa Cruz as a Distinguished Professor in the department of molecular, cell, and developmental biology in October 2020.
Induced pluripotent stem cells are a type of pluripotent stem cell that can be generated directly from a somatic cell. The iPSC technology was pioneered by Shinya Yamanaka and Kazutoshi Takahashi in Kyoto, Japan, who together showed in 2006 that the introduction of four specific genes, collectively known as Yamanaka factors, encoding transcription factors could convert somatic cells into pluripotent stem cells. Shinya Yamanaka was awarded the 2012 Nobel Prize along with Sir John Gurdon "for the discovery that mature cells can be reprogrammed to become pluripotent."
Telomerase reverse transcriptase is a catalytic subunit of the enzyme telomerase, which, together with the telomerase RNA component (TERC), comprises the most important unit of the telomerase complex.
Forkhead box O3, also known as FOXO3 or FOXO3a, is a human protein encoded by the FOXO3 gene.
Kruppel-like factor 4 is a member of the KLF family of zinc finger transcription factors, which belongs to the relatively large family of SP1-like transcription factors. KLF4 is involved in the regulation of proliferation, differentiation, apoptosis and somatic cell reprogramming. Evidence also suggests that KLF4 is a tumor suppressor in certain cancers, including colorectal cancer. It has three C2H2-zinc fingers at its carboxyl terminus that are closely related to another KLF, KLF2. It has two nuclear localization sequences that signals it to localize to the nucleus. In embryonic stem cells (ESCs), KLF4 has been demonstrated to be a good indicator of stem-like capacity. It is suggested that the same is true in mesenchymal stem cells (MSCs).
Telomerase protein component 1 is an enzyme that in humans is encoded by the TEP1 gene.
The stem cell theory of aging postulates that the aging process is the result of the inability of various types of stem cells to continue to replenish the tissues of an organism with functional differentiated cells capable of maintaining that tissue's original function. Damage and error accumulation in genetic material is always a problem for systems regardless of the age. The number of stem cells in young people is very much higher than older people and thus creates a better and more efficient replacement mechanism in the young contrary to the old. In other words, aging is not a matter of the increase in damage, but a matter of failure to replace it due to a decreased number of stem cells. Stem cells decrease in number and tend to lose the ability to differentiate into progenies or lymphoid lineages and myeloid lineages.
Neurogenin-3 (NGN3) is a protein that in humans is encoded by the Neurog3 gene.
Wafik El-Deiry is an American physician and cancer researcher who is the Associate Dean for Oncologic Sciences at the Warren Alpert Medical School, Brown University, Director of the Cancer Center at Brown University, and the Director of the Joint Program in Cancer Biology at Brown University and its affiliated hospitals. He was previously deputy director of Translational Research at Fox Chase Cancer Center, where he was also co-Leader of the Molecular Therapeutics Program.
María Antonia Blasco Marhuenda, known as María Blasco, is a Spanish molecular biologist. She is the current director of the Spanish National Cancer Research Centre.
Zinc finger and SCAN domain containing 4 is a protein that in humans is encoded by the ZSCAN4 gene.
Telomeres, the caps on the ends of eukaryotic chromosomes, play critical roles in cellular aging and cancer. An important facet to how telomeres function in these roles is their involvement in cell cycle regulation.
Zhimin (James) Lu is a Chinese-American biologist and oncologist. He is a professor, Kuancheng Wang Distinguished Chair, and Dean of Institute of Translational Medicine at Zhejiang University. Prior to joining Zhejiang University in 2019, he was the Ruby E. Rutherford Distinguished Professor and the director of Cancer Metabolism Program at the University of Texas MD Anderson Cancer Center.
Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. The hallmarks of aging are the types of biochemical changes that occur in all organisms that experience biological aging and lead to a progressive loss of physiological integrity, impaired function and, eventually, death. They were first listed in a landmark paper in 2013 to conceptualize the essence of biological aging and its underlying mechanisms.