Paul Mischel

Last updated
Paul Salomon Mischel
20240203 PaulMischel-02793 reduced size.jpg
Born (1962-07-13) July 13, 1962 (age 62)
Syracuse, NY, USA.
Education
Known forExtrachromosomal DNA in cancer (ecDNA)
Relatives Doborah Kado, M.D. Walter Mischel
AwardsNational Academy of Medicine

Ernst W. Bertner Prize for Distinbuished Contributions to Cancer Research

Contents

American Society for Clinical Investigation (President, 2010/2011)

American Association of Physicians

Fellow, American Association for the Advancement of Science
Scientific career
FieldsCancer genetics and pathology
Institutions Stanford University, University of California, San Diego, University of California, Los Angeles
Website Group Website

PubMed

Stanford Profile

Google Scholar

Paul S. Mischel (born July 13, 1962) is a physician-scientist whose laboratory has made pioneering discoveries in the pathogenesis of human cancer. [1] He is the Fortinet Founders Professor, and Vice Chair for Research for the Department of Pathology, Stanford Medicine, an Institute Scholar in Sarafan ChEM-H. He is also a Faculty Advisor for Experimental Biology at the Innovative Medicines Accelerator at Stanford University. Mischel’s research published in a series of papers in Nature and Science, has catalyzed a paradigm shift in precision oncology that promises to transform the diagnosis and treatment of patients suffering from some of the most aggressive forms of cancer. [2]

Career

Mischel was born on July 13, 1962. After losing his father to cancer, he became committed to a career in cancer research. He attended the University of Pennsylvania and received his M.D. from Cornell University Medical College in 1991, graduating Alpha Omega Alpha. Mischel completed residency training in Anatomic Pathology and Neuropathology at UCLA, followed by post-doctoral research training with Louis Reichardt at HHMI-UCSF. Mischel joined the faculty of UCLA in 1998. In August 2012, he was recruited to the Ludwig Institute for Cancer Research, San Diego and UCSD. In 2021, he joined Stanford University School of Medicine, where he currently serves as a Professor and Vice Chair of Research for the Department of Pathology and Institute Scholar of ChEM-H. Mischel leads the team of eDyNAmiC project.

Research

Mischel’s research has demonstrated a central role for ecDNA in cancer. Studies he has led, published in a series of papers in Nature and Science, has provided a mechanistic understanding of the molecular basis of intratumoral genetic heterogeneity, accelerated evolution and treatment resistance driven by ecDNA oncogene amplification. His team’s research has shown that ecDNA occurs in close to 20% of all solid cancers, of women and men, children and adults, that it is associated with poor outcome for patients. This research has revealed clinical implications and underlying molecular mechanisms of ecDNA in cancer development and progression, suggesting the potential for future ecDNA-directed cancer treatments. [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]

Honors

Mischel is a member of the National Academy of Medicine [15] and recipient of the Ernst W. Bertner Memorial Award from MD Anderson for Distinguished Contributions to Cancer Research. Mischel is also an elected Fellow and Past-President of the American Society for Clinical Investigation, and an elected Fellow of the American Association of Physicians and The American Association for the Advancement of Science.

Personal life

Mischel is married to Professor Deborah Kado, Chief of Geriatrics Research, co-director of the Stanford Longevity Center, and Director of the Palo Alto VA Geriatrics Research, Education, and Clinical Center. They have two daughters, Dr. Anna Mischel and Dr. Sarah Mischel.  Paul is the son of the cognitive philosopher Theodore Mischel and the nephew of the famed psychologist, Walter Mischel.

Related Research Articles

Gene duplication is a major mechanism through which new genetic material is generated during molecular evolution. It can be defined as any duplication of a region of DNA that contains a gene. Gene duplications can arise as products of several types of errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements. Common sources of gene duplications include ectopic recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

Double minutes (DMs) are small fragments of extrachromosomal DNA, which have been observed in a large number of human tumors including breast, lung, ovary, colon, and most notably, neuroblastoma. They are a manifestation of gene amplification as a result of chromothripsis, during the development of tumors, which give the cells selective advantages for growth and survival. This selective advantage is as a result of double minutes frequently harboring amplified oncogenes and genes involved in drug resistance. DMs, like actual chromosomes, are composed of chromatin and replicate in the nucleus of the cell during cell division. Unlike typical chromosomes, they are composed of circular fragments of DNA, up to only a few million base pairs in size, and contain no centromere or telomere. Further to this, they often lack key regulatory elements, allowing genes to be constitutively expressed. The term ecDNA may be used to refer to DMs in a more general manner. The term Double Minute originates from the visualization of these features under microscope; double because the dots were found in pairs, and minute because they were minuscule.

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References

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