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Channing Der

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  • Comment: Unquestionably notable as Fellow AAAS , one of the provisions of WP:PROF.
    The relevant standard is not whether there are third party sources to meet GNG. The relevant standard is WP:PROF., and that is normally met by showing the person to be influential in their subject as demonstrated by citations to their work. The previous review apparently used the wrong criterion DGG ( talk ) 06:08, 12 January 2022 (UTC)
  • Comment: Wikipedia articles require secondary sources that are independent of the subject and contain in-depth coverage of them. Interview-based items and the subjects own work are not independent secondary sources. Stuartyeates (talk) 02:44, 17 July 2021 (UTC)

This user has publicly declared that they have a conflict of interest regarding the Wikipedia article Channing Der.
Channing Der
CitizenshipUSA
OccupationProfessor
Board member ofNational Cancer Institute (NCI) Board of Scientific Counselors,

Council Delegate for the Medical Sciences division of American Association for the Advancement of Science (AAAS), Pancreatic Cancer Action Network (PanCAN)

(AACR)
AwardsSarah Graham Kenan Distinguished Professor
Academic background
Alma materUniversity of California, Los Angeles University of California, Irvine
Academic work
DisciplinePharmacology, Cancer Cell Biology, Molecular Therapeutics

Channing Joseph Der is an American scientist and educator, recognized for his work with the RAS oncoprotein RAS oncoprotein and its role in human oncogenesis.

Education

Der earned his B.S. in Biology from University of California, Los Angeles University of California, Los Angeles, and his Ph.D. in Microbiology from University of California, Irvine University of California, Irvine.

Work

After completing his postdoctoral training at Harvard Medical School Harvard Medical School and the Dana-Farber Cancer Institute Dana-Farber Cancer Institute, he became a staff scientist at the Sanford Burnham Prebys Medical Discovery Institute Sanford Burnham Prebys Medical Discovery Institute (formerly the La Jolla Cancer Research Foundation). He is currently Sarah Graham Kenan Distinguished Professor at University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center. Der has authored over 400 publications and mentored over 90 post-doctoral and pre-doctoral fellows in his career. DHe holds six patents and has worked as a consultant for many pharmaceutical companies as a consultant. Most recently, he has served on the scientific advisory boards for biotech companies that include Revolution Medicines and Mirati Therapeutics. He is also an Einstein Berlin Institute of Health Visiting Fellow at Charité Universitätsmedizin Charité Universitätsmedizin, Berlin, Germany

Research

Der has made contributions to the fields of molecular pharmacology pharmacology and cancer cell biology. One early discovery was presence of activated RAS oncogenes RAS oncogenes in human cancers in 1982, marking the identification of the very first cancer genes [1]. RAS genes comprise the most frequently mutated oncogene family in human cancers. The pursuit of anti-RAS therapeutic strategies has been a major focus of his research studies. A second was that RAS oncoproteingene function is dependent on modification by a farnesyl isoprenoid lipid group [2]. This discovery prompted intense pharmaceutical industry pursuit of inhibitors of the farnesyltransferase enzyme that catalyzes this lipid modification on RAS and other proteins [3]. This has led to a current Phase 2 clinical trial using farnesyltransferase inhibitors to inhibit HRAS-driven head and neck squamous cell carcinomas. In collaborative studies with Francis Collins, MD (Director, National Institutes of Health National Institutes of Health), he also demonstrated that these inhibitors corrected the protein defect that causes progeria progeria, a disease of “rapid aging” [4]. This discovery set the stage for the recent FDA approval of farnesyltransferase inhibitors for the only treatment for this rare childhood disease. A third finding is the discovery of a therapeutic approach that that ERK inhibition increases pancreatic cancer addiction to autophagy autophagy. Autophagy, derived from the Greek meaning “eating of self”, is a process whereby cancer cells acquire the energy needed to maintain their high growth capacity. This autophagy connection led Der to initiate, together with clinicians at the MD Anderson Cancer Center MD Anderson Cancer Center, to a new clinical trial evaluating the combination of the MEK inhibitor binimetinib binimetinib with the autophagy inhibitor hydroxychloroquine hydroxychloroquine in pancreatic cancer (NCT04132505).

Awards and Recognition

Der is a Fellow of the AAAS American Association for the Advancement of Science, a recipient of the NCI Outstanding Investigator Investigator Award, the University of North Carolina at Chapel Hill’s Mentor Award for Lifetime Achievement for mentoring, and the Hyman L. Battle Distinguished Cancer Research Award, and the University of California, Irvine Distinguished Alumni Award. He is also recipient of an Einstein BIH Visiting Fellow Award.

https://www.theguardian.com/science/2021/mar/06/the-long-war-on-cancer-death-star-gene-proteins-new-medicines?CMP=share_btn_link

https://www.einsteinfoundation.de/en/media/questionnaire/channing-der/

References

  1. ^ Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses. Der CJ, Krontiris TG, Cooper GM. Proc Natl Acad Sci U S A. 1982 Jun;79(11):3637-40. doi: 10.1073/pnas.79.11.3637. PMID: 6285355
  2. ^ p21ras is modified by a farnesyl isoprenoid. Casey PJ, Solski PA, Der CJ, Buss JE. Proc Natl Acad Sci U S A. 1989 Nov;86(21):8323-7. doi: 10.1073/pnas.86.21.8323. PMID: 2682646
  3. ^ Isoprenoid addition to Ras protein is the critical modification for its membrane association and transforming activity. Kato K, Cox AD, Hisaka MM, Graham SM, Buss JE, Der CJ. Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6403-7. doi: 10.1073/pnas.89.14.6403. PMID: 1631135
  4. ^ Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. Capell BC, Erdos MR, Madigan JP, Fiordalisi JJ, Varga R, Conneely KN, Gordon LB, Der CJ, Cox AD, Collins FS. Proc Natl Acad Sci U S A. 2005 Sep 6;102(36):12879-84. doi: 10.1073/pnas.0506001102. Epub 2005 Aug 29. PMID: 16129833