Craig B. Thompson

Last updated
Craig B. Thompson
Craig B. Thompson by Rick DeWitt.jpg
Born1953 (age 70–71)
Alma mater
SpouseTullia Lindsten [1]
Scientific career
Institutions
Website The Craig Thompson Lab

Craig B. Thompson (born 1953) is an American cell biologist and a former president of the Memorial Sloan Kettering Cancer Center. [1]

Contents

Education and career

Thompson received his bachelor's degree from Dartmouth College and went on to earn his medical degree in 1977 from the University of Pennsylvania Medical School. He received clinical training in internal medicine at Harvard Medical School and in medical oncology at the Fred Hutchinson Cancer Research Center at the University of Washington. After completing his training, Thompson became a physician at the National Naval Medical Center in Bethesda, Maryland, and an assistant professor of medicine at the Uniformed Services University of the Health Sciences. In 1987, he joined the faculty of the University of Michigan as an assistant professor of medicine and an assistant investigator in the Howard Hughes Medical Institute. From 1993 until he joined the University of Pennsylvania, he was affiliated with the University of Chicago, where he was professor of medicine, a Howard Hughes investigator, and director of the Gwen Knapp Center for Lupus and Immunology Research.

Thompson joined the University of Pennsylvania in 1999 as a professor of medicine, the scientific director of The Leonard and Madlyn Abramson Family Cancer Research Institute, and the first chairman of the Department of Cancer Biology. In 2006 he was named director of the Abramson Cancer Center of the University of Pennsylvania and associate vice president for cancer services of the University of Pennsylvania Health System.

Thompson became president and chief executive officer of Memorial Sloan Kettering Cancer Center in November 2010.

He is married to Tullia Lindsten, also a cancer researcher. [1]

Research

Thompson's laboratory undertakes basic research in the fields of cancer biology and immunology. This research has helped advance the understanding and deployment of immunotherapy to treat cancer. Thompson has studied how genes regulate apoptosis and metabolism, and investigated their application in treating cancer. [2]

In his earlier work, Thompson was among the first to describe the unique co-stimulatory properties of CD28 in augmenting lymphoid effector function, proliferation, and survival. Thompson identified the evolutionary duplication of CD28 into CD28 and CTLA-4 and demonstrated that CTLA4 had an inhibitory effect on immune activation. [3] [4] [5] [6]

Thompson elucidated processes on the genes that control programmed cell death or apoptosis. [7] These processes shape lymphocyte development and immune system homeostasis. His group discovered the first Bcl-2 homolog to be identified, Bcl-Xl, and described the first BH3-only containing regulatory family member, Bcl-xS. [8] He published this work alongside Stanley Korsmeyer's report of the first pro-apoptotic family member, Bax, and together established the three classes of this gene family and defined their pro-apoptotic and anti-apoptotic roles. [9] [10] [11]

Thompson's recent research has focused on cellular metabolism. His discoveries in growth factor regulation of nutrient uptake and metabolism have provided direct mechanistic links between cellular metabolism and cell growth and survival. [12] [13] [14] [15] His work has also led to new insights into how intracellular metabolite levels can contribute to the regulation of gene expression, cellular differentiation and oncogenic transformation. This work has contributed to the resurgent interest in cancer cell metabolism and may form the basis for translational therapies to exploit the metabolic addictions exhibited by cancer cells. [16] [17] [18] [19]

Scientific contributions and patents

Thompson holds more than 30 patents related to immunotherapy and apoptosis, and is a founder of three biotechnology companies. [2]

Patents arising from Thompson's research describing the co-stimulatory/inhibitory properties of CD28/CTLA-4, in collaboration with Carl June and Jeffrey Bluestone, were licensed for the development of Abatacept (Orencia) for autoimmune diseases and for use in T cell cloning and CAR T cell production. [20] [21] [22]

Thompson's work with Stanley Korsmeyer establishing the existence of three classes of Bcl-2-related proteins and defining their role in apoptosis led to the development of ABT-263 (navitoclax) and ABT-199 (venetoclax), recently FDA-approved for certain patients with chronic lymphocytic leukemia (CLL).[ citation needed ]

Thompson's discovery of oncogenic metabolites (succinate, fumarate, and 2-hydroxyglutarate) that can inhibit tumor suppressor function and/or impair cellular differentiation has helped lead to the development of new treatments for leukemia, gliomas, sarcomas, and bladder cancer, currently in clinical trials. [23]

Criticism

In December 2011, The University and its Abramson Family Cancer Research Institute sued Thompson after his move to Memorial Sloan Kettering, charging that he had made use of research conducted at the University of Pennsylvania to start a biotechnology company, Agios Pharmaceuticals that Thompson had co-founded in 2007 while still at the University. [24]

While most of the details were not announced, the suit was settled with an agreement wherein Agios entered into a licensing agreement with the University of Pennsylvania regarding specific intellectual property. [25] [26]

Other roles

Past roles

Awards and honors

Related Research Articles

<span class="mw-page-title-main">Apoptosis</span> Programmed cell death in multicellular organisms

Apoptosis is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast. Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation, and mRNA decay. The average adult human loses 50 to 70 billion cells each day due to apoptosis. For the average human child between 8 and 14 years old, each day the approximate loss is 20 to 30 billion cells.

<span class="mw-page-title-main">Bcl-2</span> Protein found in humans

Bcl-2, encoded in humans by the BCL2 gene, is the founding member of the Bcl-2 family of regulator proteins that regulate cell death (apoptosis), by either inhibiting (anti-apoptotic) or inducing (pro-apoptotic) apoptosis. It was the first apoptosis regulator identified in any organism.

In oncology, the Warburg effect is the observation that most cancer cells release energy predominantly not through the 'usual' citric acid cycle and oxidative phosphorylation in the mitochondria as observed in normal cells, but through a less efficient process of 'anaerobic glycolysis' consisting of a high level of glucose uptake and glycolysis followed by lactic acid fermentation taking place in the cytosol, not the mitochondria, even in the presence of abundant oxygen. This observation was first published by Otto Heinrich Warburg, who was awarded the 1931 Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme". The precise mechanism and therapeutic implications of the Warburg effect, however, remain unclear.

<span class="mw-page-title-main">Stanley J. Korsmeyer</span> American oncologist (1950–2005)

Stanley Joel Korsmeyer was an American research scientist known for his work on B cell lymphomas and apoptosis. Born and educated in the US state of Illinois, Korsmeyer spent most of his career as a professor at Washington University School of Medicine and later the Dana–Farber Cancer Institute. He rose to prominence in the early 1980s as a research fellow at the National Cancer Institute. There he co-discovered the genetic cause of most cases of the cancer follicular lymphoma – the misregulation of the gene Bcl-2. Korsmeyer went on to start his own laboratory at Washington University in St. Louis, further studying the role of Bcl-2 in cell biology. His group's work expanded the paradigm of cancer-causing genes, providing the first example of how interfering with programmed cell death could lead to cancer development. Korsmeyer authored over 250 scientific papers over the course of his career. He was elected to the U.S. National Academy of Sciences at the age of 45. Korsmeyer died of lung cancer in 2005, at the age of 54.

Tak Wah Mak, is a Canadian medical researcher, geneticist, oncologist, and biochemist. He first became widely known for his discovery of the T-cell receptor in 1983 and pioneering work in the genetics of immunology. In 1995, Mak published a landmark paper on the discovery of the function of the immune checkpoint protein CTLA-4, thus opening the path for immunotherapy/checkpoint inhibitors as a means of cancer treatment. Mak is also the founder of Agios Pharmaceuticals, whose lead compound, IDHIFA®, was approved by the FDA for acute myeloid leukemia in August 2017, becoming the first drug specifically targeting cancer metabolism to be used for cancer treatment. He has worked in a variety of areas including biochemistry, immunology, and cancer genetics.

<span class="mw-page-title-main">Cytotoxic T-lymphocyte associated protein 4</span> Mammalian protein found in humans

Cytotoxic T-lymphocyte associated protein 4, (CTLA-4) also known as CD152, is a protein receptor that functions as an immune checkpoint and downregulates immune responses. CTLA-4 is constitutively expressed in regulatory T cells but only upregulated in conventional T cells after activation – a phenomenon which is particularly notable in cancers. It acts as an "off" switch when bound to CD80 or CD86 on the surface of antigen-presenting cells. It is encoded by the gene CTLA4 in humans.

<span class="mw-page-title-main">Apoptosis regulator BAX</span> Mammalian protein found in Homo sapiens

Apoptosis regulator BAX, also known as bcl-2-like protein 4, is a protein that in humans is encoded by the BAX gene. BAX is a member of the Bcl-2 gene family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis.

<span class="mw-page-title-main">CD80</span> Mammalian protein found in Homo sapiens

The Cluster of differentiation 80 is a B7, type I membrane protein in the immunoglobulin superfamily, with an extracellular immunoglobulin constant-like domain and a variable-like domain required for receptor binding. It is closely related to CD86, another B7 protein (B7-2), and often works in tandem. Both CD80 and CD86 interact with costimulatory receptors CD28, CTLA-4 (CD152) and the p75 neurotrophin receptor.

<span class="mw-page-title-main">CD86</span> Mammalian protein found in Homo sapiens

Cluster of Differentiation 86 is a protein constitutively expressed on dendritic cells, Langerhans cells, macrophages, B-cells, and on other antigen-presenting cells. Along with CD80, CD86 provides costimulatory signals necessary for T cell activation and survival. Depending on the ligand bound, CD86 can signal for self-regulation and cell-cell association, or for attenuation of regulation and cell-cell disassociation.

<span class="mw-page-title-main">CD134</span> Protein-coding gene in humans

Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor, is a member of the TNFR-superfamily of receptors which is not constitutively expressed on resting naïve T cells, unlike CD28. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. Expression of OX40 is dependent on full activation of the T cell; without CD28, expression of OX40 is delayed and of fourfold lower levels.

<span class="mw-page-title-main">Bcl-2 homologous antagonist killer</span> Protein-coding gene in the species Homo sapiens

Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein localizes to mitochondria, and functions to induce apoptosis. It interacts with and accelerates the opening of the mitochondrial voltage-dependent anion channel, which leads to a loss in membrane potential and the release of cytochrome c. This protein also interacts with the tumor suppressor P53 after exposure to cell stress.

<span class="mw-page-title-main">Bcl-2-associated death promoter</span> Mammalian protein found in Homo sapiens

The BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family which is involved in initiating apoptosis. BAD is a member of the BH3-only family, a subfamily of the Bcl-2 family. It does not contain a C-terminal transmembrane domain for outer mitochondrial membrane and nuclear envelope targeting, unlike most other members of the Bcl-2 family. After activation, it is able to form a heterodimer with anti-apoptotic proteins and prevent them from stopping apoptosis.

<span class="mw-page-title-main">Ipilimumab</span> Pharmaceutical drug

Ipilimumab, sold under the brand name Yervoy, is a monoclonal antibody medication that works to activate the immune system by targeting CTLA-4, a protein receptor that downregulates the immune system.

<span class="mw-page-title-main">Bcl-xL</span> Transmembrane molecule in the mitochondria

B-cell lymphoma-extra large (Bcl-xL), encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria. It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death.

<span class="mw-page-title-main">Cancer immunology</span> Study of the role of the immune system in cancer

Cancer immunology (immuno-oncology) is an interdisciplinary branch of biology and a sub-discipline of immunology that is concerned with understanding the role of the immune system in the progression and development of cancer; the most well known application is cancer immunotherapy, which utilises the immune system as a treatment for cancer. Cancer immunosurveillance and immunoediting are based on protection against development of tumors in animal systems and (ii) identification of targets for immune recognition of human cancer.

<span class="mw-page-title-main">Bcl-2-like protein 1</span> Protein-coding gene in the species Homo sapiens

Bcl-2-like protein 1 is a protein encoded in humans by the BCL2L1 gene. Through alternative splicing, the gene encodes both of the human proteins Bcl-xL and Bcl-xS.

<span class="mw-page-title-main">ADP/ATP translocase 4</span> Protein-coding gene in the species Homo sapiens

ADP/ATP translocase 4 (ANT4) is an enzyme that in humans is encoded by the SLC25A31 gene on chromosome 4. This enzyme inhibits apoptosis by catalyzing ADP/ATP exchange across the mitochondrial membranes and regulating membrane potential. In particular, ANT4 is essential to spermatogenesis, as it imports ATP into sperm mitochondria to support their development and survival. Outside this role, the SLC25AC31 gene has not been implicated in any human disease.

<span class="mw-page-title-main">Scott W. Lowe</span> American geneticist

Scott William Lowe is Chair of the Cancer Biology and Genetics Program in the Sloan Kettering Institute at Memorial Sloan Kettering Cancer Center. He is recognized for his research on the tumor suppressor gene, p53, which is mutated in nearly half of cancers.

Lydia W. S. Finley is an American scientist and an assistant member at the Cell Biology Program at Memorial Sloan Kettering Cancer Center and an assistant professor at Weill Cornell Medical College. Finley is known for her contributions to understanding the metabolic underpinnings of stem cell fate.

Ralph J. DeBerardinis is an American physician-scientist, the chief of the Division of Pediatric Genetics and Metabolism at the Children’s Medical Center Research Institute at UT Southwestern and a professor at the University of Texas Southwestern Medical Center. DeBerardinis became a Howard Hughes Medical Institute Investigator in 2018. DeBerardinis was elected to the National Academy of Medicine in 2020. DeBerardinis is known for his contributions to research on cancer and pediatric inborn errors of metabolism.

References

  1. 1 2 3 "Craig Thompson Named President of Memorial Sloan-Kettering". mskcc.org. 1 October 2010. Retrieved 6 September 2012.
  2. 1 2 "Leadership | Board or Directors, Founders, Scientific Advisors | Agios". www.agios.com. Retrieved 26 July 2017.
  3. ↑ June, CH; Ledbetter, JA; Gillespie, MM; Lindsten, T; Thompson, CB (December 1987). "T-cell proliferation involving the CD28 pathway is associated with cyclosporine-resistant interleukin 2 gene expression". Molecular and Cellular Biology. 7 (12): 4472–81. doi:10.1128/MCB.7.12.4472. PMC   368131 . PMID   2830495.
  4. ↑ Thompson, CB; Lindsten, T; Ledbetter, JA; Kunkel, SL; Young, HA; Emerson, SG; Leiden, JM; June, CH (February 1989). "CD28 activation pathway regulates the production of multiple T-cell-derived lymphokines/cytokines". Proceedings of the National Academy of Sciences of the United States of America. 86 (4): 1333–7. Bibcode:1989PNAS...86.1333T. doi: 10.1073/pnas.86.4.1333 . PMC   286684 . PMID   2465550.
  5. ↑ Walunas, TL; Lenschow, DJ; Bakker, CY; Linsley, PS; Freeman, GJ; Green, JM; Thompson, CB; Bluestone, JA (August 1994). "CTLA-4 can function as a negative regulator of T cell activation". Immunity. 1 (5): 405–13. doi:10.1016/1074-7613(94)90071-X. PMID   7882171.
  6. ↑ Boise, LH; Minn, AJ; Noel, PJ; June, CH; Accavitti, MA; Lindsten, T; Thompson, CB (July 1995). "CD28 costimulation can promote T cell survival by enhancing the expression of Bcl-XL". Immunity. 3 (1): 87–98. doi: 10.1016/1074-7613(95)90161-2 . PMID   7621080.
  7. ↑ Boise, LH; González-García, M; Postema, CE; Ding, L; Lindsten, T; Turka, LA; Mao, X; Nuñez, G; Thompson, CB (27 August 1993). "bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death" (PDF). Cell. 74 (4): 597–608. doi:10.1016/0092-8674(93)90508-N. hdl: 2027.42/30629 . PMID   8358789. S2CID   13542617.
  8. ↑ Sattler, M; Liang, H; Nettesheim, D; Meadows, RP; Harlan, JE; Eberstadt, M; Yoon, HS; Shuker, SB; Chang, BS; Minn, AJ; Thompson, CB; Fesik, SW (14 February 1997). "Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis". Science. 275 (5302): 983–6. doi:10.1126/science.275.5302.983. PMID   9020082. S2CID   22667419.
  9. ↑ "National Academy of Science". nas.nasonline.org.
  10. ↑ Lindsten, T; Ross, AJ; King, A; Zong, WX; Rathmell, JC; Shiels, HA; Ulrich, E; Waymire, KG; Mahar, P; Frauwirth, K; Chen, Y; Wei, M; Eng, VM; Adelman, DM; Simon, MC; Ma, A; Golden, JA; Evan, G; Korsmeyer, SJ; MacGregor, GR; Thompson, CB (December 2000). "The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues". Molecular Cell. 6 (6): 1389–99. doi:10.1016/S1097-2765(00)00136-2. PMC   3057227 . PMID   11163212.
  11. ↑ Wei, MC; Zong, WX; Cheng, EH; Lindsten, T; Panoutsakopoulou, V; Ross, AJ; Roth, KA; MacGregor, GR; Thompson, CB; Korsmeyer, SJ (27 April 2001). "Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death". Science. 292 (5517): 727–30. Bibcode:2001Sci...292..727W. doi:10.1126/science.1059108. PMC   3049805 . PMID   11326099.
  12. ↑ Rathmell, JC; Vander Heiden, MG; Harris, MH; Frauwirth, KA; Thompson, CB (September 2000). "In the absence of extrinsic signals, nutrient utilization by lymphocytes is insufficient to maintain either cell size or viability". Molecular Cell. 6 (3): 683–92. doi: 10.1016/S1097-2765(00)00066-6 . PMID   11030347.
  13. ↑ Vander Heiden, MG; Plas, DR; Rathmell, JC; Fox, CJ; Harris, MH; Thompson, CB (September 2001). "Growth factors can influence cell growth and survival through effects on glucose metabolism". Molecular and Cellular Biology. 21 (17): 5899–912. doi:10.1128/MCB.21.17.5899-5912.2001. PMC   87309 . PMID   11486029.
  14. ↑ Lum, JJ; Bauer, DE; Kong, M; Harris, MH; Li, C; Lindsten, T; Thompson, CB (28 January 2005). "Growth factor regulation of autophagy and cell survival in the absence of apoptosis". Cell. 120 (2): 237–48. doi: 10.1016/j.cell.2004.11.046 . PMID   15680329.
  15. ↑ Wise, DR; DeBerardinis, RJ; Mancuso, A; Sayed, N; Zhang, XY; Pfeiffer, HK; Nissim, I; Daikhin, E; Yudkoff, M; McMahon, SB; Thompson, CB (2 December 2008). "Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction". Proceedings of the National Academy of Sciences of the United States of America. 105 (48): 18782–7. Bibcode:2008PNAS..10518782W. doi: 10.1073/pnas.0810199105 . PMC   2596212 . PMID   19033189.
  16. ↑ Selak, MA; Armour, SM; MacKenzie, ED; Boulahbel, H; Watson, DG; Mansfield, KD; Pan, Y; Simon, MC; Thompson, CB; Gottlieb, E (January 2005). "Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase". Cancer Cell. 7 (1): 77–85. doi: 10.1016/j.ccr.2004.11.022 . PMID   15652751.
  17. ↑ Ward, PS; Patel, J; Wise, DR; Abdel-Wahab, O; Bennett, BD; Coller, HA; Cross, JR; Fantin, VR; Hedvat, CV; Perl, AE; Rabinowitz, JD; Carroll, M; Su, SM; Sharp, KA; Levine, RL; Thompson, CB (16 March 2010). "The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate". Cancer Cell. 17 (3): 225–34. doi:10.1016/j.ccr.2010.01.020. PMC   2849316 . PMID   20171147.
  18. ↑ Figueroa, ME; Abdel-Wahab, O; Lu, C; Ward, PS; Patel, J; Shih, A; Li, Y; Bhagwat, N; Vasanthakumar, A; Fernandez, HF; Tallman, MS; Sun, Z; Wolniak, K; Peeters, JK; Liu, W; Choe, SE; Fantin, VR; Paietta, E; Löwenberg, B; Licht, JD; Godley, LA; Delwel, R; Valk, PJ; Thompson, CB; Levine, RL; Melnick, A (14 December 2010). "Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation". Cancer Cell. 18 (6): 553–67. doi:10.1016/j.ccr.2010.11.015. PMC   4105845 . PMID   21130701.
  19. ↑ Lu, C; Ward, PS; Kapoor, GS; Rohle, D; Turcan, S; Abdel-Wahab, O; Edwards, CR; Khanin, R; Figueroa, ME; Melnick, A; Wellen, KE; O'Rourke, DM; Berger, SL; Chan, TA; Levine, RL; Mellinghoff, IK; Thompson, CB (15 February 2012). "IDH mutation impairs histone demethylation and results in a block to cell differentiation". Nature. 483 (7390): 474–8. Bibcode:2012Natur.483..474L. doi:10.1038/nature10860. PMC   3478770 . PMID   22343901.
  20. ↑ Thompson, Craig B.; June, Carl H. (2004). "Methods of treating autoimmune disease via CTLA-4Ig" . Retrieved 27 July 2017.
  21. ↑ June, Carl H.; Thompson, Craig B.; Nabel, Gary J.; Gray, Gary S.; Rennert, Paul D.; Freeman, Gordon J. (1999). "Methods for selectively stimulating proliferation of T cells" . Retrieved 27 July 2017.
  22. ↑ Davis, Ryan. "Bristol-Myers Shells Out $21M To Settle Orencia Suit - Law360". www.law360.com. Retrieved 27 July 2017.
  23. ↑ Apple, Sam (12 May 2016). "An Old Idea, Revived: Starve Cancer to Death". The New York Times. Retrieved 26 July 2017.
  24. ↑ "Pollack, Andrew (5 February 2012). "Sloan-Kettering Chief Is Accused of Taking Research". The New York Times . Retrieved 6 September 2012.
  25. ↑ Pollack, Andrew (31 August 2012). "Suits That Accused Sloan-Kettering Chief of Stealing Research Are Settled". nytimes.com. Retrieved 6 September 2012.
  26. ↑ Mytelka, Andrew (1 September 2012). "Penn and Cancer Institute Settle Lawsuits Accusing Scientist of Stealing Research". The Chronicle of Higher Education . Retrieved 6 September 2012.
  27. ↑ "Medical Advisory Board". HHMI.org. Retrieved 17 May 2017.
  28. ↑ Foundation, Lasker. "2016 Lasker Awards | The Lasker Foundation". The Lasker Foundation. Retrieved 17 May 2017.
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  31. ↑ "Editorial Board: Cancer Cell". www.cell.com. Retrieved 17 May 2017.
  32. ↑ "Editors | Cancer Discovery". cancerdiscovery.aacrjournals.org. Retrieved 17 May 2017.
  33. 1 2 "Craig B. Thompson, MD". AACR.org. Retrieved 26 May 2017.
  34. ↑ "09/19/06, Abramson Cancer Center Director: Craig Thompson - Almanac, Vol. 53, No. 4". www.upenn.edu. Retrieved 26 May 2017.
  35. ↑ "Medical Advisory Board". HHMI.org. Retrieved 26 May 2017.
  36. ↑ "Symposia on Cancer Research 2017" (PDF). mdanderson.org. Retrieved 26 May 2017.
  37. ↑ "Symposium to Address Treatment and Prevention of Infectious Inflammatory and Oncogenic Disease - College of Medicine". College of Medicine. 5 June 2014. Retrieved 26 May 2017.
  38. ↑ "ACP National Award Recipients" (PDF). American College Of Physicians. Archived from the original (PDF) on 5 August 2017. Retrieved 13 June 2017.
  39. ↑ "Steven C. Beering Award | Office of Faculty Affairs and Professional Development". faculty.medicine.iu.edu. Archived from the original on 11 July 2018. Retrieved 26 May 2017.
  40. ↑ "Award & PhD Recipients | Memorial Sloan Kettering Cancer Center". www.mskcc.org. Retrieved 26 May 2017.
  41. ↑ "Craig Thompson". www.nasonline.org. Retrieved 26 May 2017.
  42. ↑ "Recipients of Research Awards" (PDF). med.upenn.edu. Retrieved 26 May 2017.
  43. 1 2 "The American Society for Clinical Investigation". www.the-asci.org. Retrieved 26 May 2017.
  44. ↑ "Craig B. Thompson, M.D." nam.edu. Retrieved 26 May 2017.
  45. ↑ "Academy Member Connection". www.amacad.org. Archived from the original on 3 March 2018. Retrieved 26 May 2017.
  46. ↑ "Association of American Physicians". aap-online.org. Retrieved 13 June 2017.
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