Mary Beckerle

Mary Beckerle PhD is an American cell biologist who studies cancer at the Huntsman Cancer Institute at the University of Utah Medical School. At Huntsman Cancer Institute, she serves as the CEO and Director, and also as Associate Vice President of Cancer Affairs at the University of Utah. Dr. Beckerle’s research helped to define a novel molecular pathway for cell motility, and more recently, she has begun research into Ewing’s sarcoma, a pediatric bone cancer. Dr. Beckerle’s lab has already made a ground breaking discover in regards to Ewing’s Sarcoma in relation to the EWS/FLI protein.[1] Her lab discovered EWS/FLI to disrupt the internal cellular skeleton, which decreases the ability of cells to adhere to their proper environment. This can help explain the metastasis of tumors in patients suffering from Ewing’s sarcoma.

Early life

Mary Catherine Beckerle was born in Rivers Edge, New Jersey to Martin and Mickey Beckerle. She is the oldest of three daughters, with sisters Bobby and Jeanne. Her father worked at the New York Telephone Co. and died suddenly at the age of 36 of emphysema.[2] Mary was twelve at the time. Her mother, a registered nurse, worked hard to keep the family together. Mary’s interest growing up included swimming and participation in Girl Scouts. As a teenager, she held jobs in a bakery, in a library, as a lifeguard, and at a Howard Johnson restaurant. Even with all these activities, school always remained Mary’s chief focus. After high school, she attended Wells College, a small all girls’ school in New York, where she earned a B. A. in Biology and Psychology.[2] She graduated magna cum laude and was a member of Phi Beta Kappa.[3] Before continuing her education, she took a year off and worked in a cellular biology research laboratory at University of Texas Southwest Medical Center. After this, she attended the University of Colorado Boulder where she earned a PhD. in Molecular Biology. Her education then continued at the University of North Carolina Chapel Hill where she was a postdoctoral fellow in Anatomy and Cell Biology.[1]

Personal life

While at the University of North Carolina Chapel Hill, Dr. Beckerle met David Murrell. She would go on to marry him. The couple shares one son, David, who Mary describes as “my greatest joy in life.” Since moving to Utah, Dr. Beckerle has taken interest in mountain biking and hiking over the areas rugged terrain.[3]

Career

After finishing her postdoctoral research, Dr. Beckerle joined the University of Utah faculty as an assistant professor of Biology. She continued teaching at the University of Utah as well research and was one of the first professors to move into the Huntsman Cancer Institute when it opened in 1999. Also in 1999, she was named a Ralph E. and Willa T. Main Presidential Professor at the University of Utah. Upon moving into the institute, she led a program specializing in cancer cell biology until 2003. In 2003, she was named the deputy director of the center. In 2006, she was named the CEO and the director over the entire Huntsman Cancer Institute. In 2009, she was also named the Associate Vice President of Cancer Affairs at the University of Utah. Throughout her career, Dr. Beckerle has served on many boards and committees, both within Huntsman Cancer Institute and nationally. In 1990, she served on the editorial board of Molecular Biology of the cell.[3] In 2006, Dr. Beckerle served as the president of the American Society of Cell Biology. Recently, she has been named to the American Association of Cancer Research Science Policy and Legislative Affairs Committee. She has served in many capacities for the National Institute of Health, both on tasks forces as well as n the NIH Advisory Committee to the Director from 2007-2010. She has also served as chair of the American Cancer Society Council for Extramural Grants. Currently, she serves on the Scientific Review Board of the Howard Hughes Medical Institute, the Board of Directors of the American Association for Cancer Research, the Coalition for Life Sciences Board of Directors. She serves on the Scientific Advisory Boards of the National Center for Biological Sciences at the Tata Institute of Fundamental Research in Bangalore, and the Mechanobiology Institute of the National University of Singapore. Beckerle serves on numerous National Cancer Institute-designated Cancer Center External Scientific Advisory Boards, including the Georgetown Lombardi Comprehensive Cancer Center, the Abramson Cancer Center of the University of Pennsylvania, and Dana-Farber/Harvard Cancer Center. In 2013, she was elected to the Board of Directors of the American Association for Cancer Research.[4]

Research and Ewing’s Sacroma

Dr. Beckerle’s research employs several different techniques to exam signaling problems and cell motility issues. Both of these problems could potentially play a role in the development of Ewing’s sarcoma. Her lab is currently focusing on projects involving: the physiological roles of the motility machinery in normal and transformed cells, cell adhesion events at the cell surface can affect processes that depend on the activity of the cell nucleus, how the cell integrates information from multiple receptors to achieve the appropriate response.

Ewing’s Sarcoma is a bone cancer affecting mainly children and adolescents.[5] Tumors of Ewing’ Sarcoma are typically found in the long bones of the legs and arms, or bones in the chest, trunk, pelvis, back, or head.[6] Dr. Beckerle’s research in this area focuses on a key pathway as believed to be a mechanism by which the cancer cells can spread. Ewing sarcoma occurs due to a chromosomal mutation that causes an atypical protein, known as EWS/FLI, to be present (also called expressed), and that when EWS/FLI is expressed, literally thousands of genes are misregulated, leading to abnormal behavior. Dr. Beckerle’s lab found that the EWS/FLI protein disrupted cell adhesion and limited the ability of cells to remain in their normal environment. The EWS/FLI protein is difficult to regulate so Dr. Beckerle’s team is focused on an essential regulating protein called ysine specific demethylase (LSD1). Preliminary research has aimed to halt the function of LSD1 to prevent the spread of Ewing Sarcoma cells.[1]

Selected publications

  1. Smith MA, Blankman E, Deakin NO, Hoffman LM, Jensen CC, Turner CE, Beckerle MC. (2013) LIM domains target actin regulators paxillin and zyxin to sites of stress fiber strain. PLoS One. 8(8):e69378.[7]
  2. Pronovost SM, Beckerle MC, Kadrmas JL. (2013) Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants. PLoS Genet 9(3):e1003406.[8]
  3. Chapin LM, Blankman E, Smith MA, Shiu YT, Beckerle MC. (2012) Lateral communication between stress fiber sarcomeres facilitates a local remodeling response. Biophys J. 103(10):2082-92.[9]
  4. Elias MC, Pronovost SM, Cahill KJ, Beckerle MC, Kadrmas JL. (2012) A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted. J Cell Sci. 125(Pt 13):3185-94.[10]
  5. Hoffman LM, Jensen CC, Chaturvedi A, Yoshigi M, Beckerle MC. (2012) Stretch-induced actin remodeling requires targeting of zyxin to stress fibers and recruitment of actin regulators. Mol Biol Cell. 23(10):1846-59.[11]
  6. Chaturvedi A, Hoffman LM, Welm AL, Lessnick SL, Beckerle MC. (2012) The EWS/FLI Oncogene Drives Changes in Cellular Morphology, Adhesion, and Migration in Ewing Sarcoma. Genes Cancer. 3(2):102-16.[12]
  7. Beckerle MC. (2010) How cell biologists can contribute to improving cancer outcomes. Mol Biol Cell. 21(22):3788-9.[13]

References

  1. 1 2 3 Neufield, Erica. “Huntsman Cancer Institute Awarded Grant for Children's Cancer Research” CureSearch for Children’s Cancer.
  2. 1 2 Benson, Lee, “They all want what Huntsman has — The woman in charge”. Deseret News. March 1, 2014. Accessed November 11, 2014.
  3. 1 2 3 “Mary Beckerle” American Society of Cell Biology. 1994
  4. ↑ Mary Beckerle. Huntsman Cancer Institute
  5. ↑ Ewing Sarcoma. St’ Jude’s Children’s Hospital
  6. ↑ Ewing’s Sarcoma. WebMD
  7. ↑ Smith MA, Blankman E, Deakin NO, Hoffman LM, Jensen CC, Turner CE, Beckerle MC. (2013) LIM domains target actin regulators paxillin and zyxin to sites of stress fiber strain. PLoS One. 8(8):e69378.
  8. ↑ Pronovost SM, Beckerle MC, Kadrmas JL. (2013) Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants. PLoS Genet 9(3):e1003406.[LIM domains target actin regulators paxillin and zyxin to sites of stress fiber strain.Smith MA, Blankman E, Deakin NO, Hoffman LM, Jensen CC, Turner CE, Beckerle MC (2013). LIM domains target actin regulators paxillin and zyxin to sites of stress fiber strain. PLoS One, 8(8), e69378]
  9. ↑ Chapin LM, Blankman E, Smith MA, Shiu YT, Beckerle MC. (2012) Lateral communication between stress fiber sarcomeres facilitates a local remodeling response. Biophys J. 103(10):2082-92.[Integrin-beta5 and zyxin mediate formation of ventral stress fibers in response to transforming growth factor beta.Bianchi-Smiraglia A, Kunnev D, Limoge M, Lee A, Beckerle MC, Bakin AV (2013). Integrin-beta5 and zyxin mediate formation of ventral stress fibers in response to transforming growth factor beta. Cell Cycle, 12(21), 3377-89.]
  10. ↑ Elias MC, Pronovost SM, Cahill KJ, Beckerle MC, Kadrmas JL. (2012) A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted. J Cell Sci. 125(Pt 13):3185-94.[A novel role for keratin 17 in coordinating oncogenic transformation and cellular adhesion in Ewing sarcoma.Sankar S, Tanner JM, Bell R, Chaturvedi A, Randall RL, Beckerle MC, Lessnick SL (2013). A novel role for keratin 17 in coordinating oncogenic transformation and cellular adhesion in Ewing sarcoma. Mol Cell Biol, 33(22), 4448-60.]
  11. ↑ Hoffman LM, Jensen CC, Chaturvedi A, Yoshigi M, Beckerle MC. (2012) Stretch-induced actin remodeling requires targeting of zyxin to stress fibers and recruitment of actin regulators. Mol Biol Cell. 23(10):1846-59.[ZEB2 Represses the Epithelial Phenotype and Facilitates Metastasis in Ewing Sarcoma.Wiles ET, Bell R, Thomas D, Beckerle M, Lessnick SL (2013). ZEB2 Represses the Epithelial Phenotype and Facilitates Metastasis in Ewing Sarcoma. Genes Cancer, 4(11-12), 486-500.]
  12. ↑ Chaturvedi A, Hoffman LM, Welm AL, Lessnick SL, Beckerle MC. (2012) The EWS/FLI Oncogene Drives Changes in Cellular Morphology, Adhesion, and Migration in Ewing Sarcoma. Genes Cancer. 3(2):102-16.[Stretch-induced actin remodeling requires targeting of zyxin to stress fibers and recruitment of actin regulators.Hoffman LM, Jensen CC, Chaturvedi A, Yoshigi M, Beckerle MC (2012). Stretch-induced actin remodeling requires targeting of zyxin to stress fibers and recruitment of actin regulators. Mol Biol Cell, 23(10), 1846-59.]
  13. ↑ Beckerle MC. (2010) How cell biologists can contribute to improving cancer outcomes. Mol Biol Cell. 21(22):3788-9.[A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted.Elias MC, Pronovost SM, Cahill KJ, Beckerle MC, Kadrmas JL (2012). A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted. J Cell Sci, 125(Pt 13), 3185-94.]
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