Skip to main content

Renee M. Demarest, Ph.D.

Assistant Professor

Science Center 276
856 566-6402


Temple University School of Medicine
Ph.D. (Molecular Biology and Genetics), 2005

Research Interests

Acute lymphoblastic leukemia (ALL) is a neoplastic disorder of lymphoblasts that are committed to the B-cell lineage (B-ALL) or the T-cell lineage (T-ALL).  Five-year survival rates (FSR) for children and adolescents with this disease are 75–85%, whereas, adult T-ALL patients have a 35–40% FSR.  T-ALL patients have essentially the same FSR of patients with B-ALL.  However, certain aspects about T-ALL make it a more aggressive disease with a poorer clinical outcome than B-ALL.  T-ALL patients have a higher percentage of induction failure and rate of relapse and invasion into the central nervous system than B-ALL.  The challenge to acquiring 100% remission in T-ALL treatment is the subset of patients (20–25%) whose disease is refractory to initial treatments or relapses after a short remission period due to drug resistance.  Therefore, it is imperative to delineate the molecular blueprint that collectively accounts for the variety of subtypes in T-ALL. The intracellular portion of Notch (Nic) is rendered constitutively active in more than half of all human T-ALL cases examined, by alternative mutations in the Notch1 gene.  Furthermore, the expression of Ikaros (Ik) isoforms that are capable of inhibiting Notch-mediated gene transcription are lost in 100% of childhood and adolescent T-ALL cases examined.  

The primary goal of my lab is to delineate the molecular pathways required for the formation, maintenance, and relapse of the various subsets of T-ALL. We utilize bone marrow reconstitution and genetically engineered murine models in order to generate T-ALL in various genetic backgrounds and modulate the expression of endogenous and exogenous genes in order to identify critical therapeutic targets.

In addition, we are developing novel methods to treat various murine models of cancer with human equivalent chemotherapeutic regimens in order to increase the translational success of new therapeutics to the clinic.

Recent Publications

  1. Weaver KL, Alves-Guerra MC, Jin K, Wang Z, Han X, Ranganathan P, Zhu X, DaSilva T, Liu W, Ratti F, Demarest RM, Tzimas C, Rice M, Vasquez-Del Carpio R, Dahmane N, Robbins DJ, Capobianco AJ. (2013) NACK is an integral component of the Notch transcriptional activation complex and is critical for development and tumorigenesis. Cancer Research, Aug 1;73(15):4960-1.
  2. Demarest, RM; Dahmane N; Capobiano, AJ. Notch is oncogenic dominant in T-ALL tumors. (2011) Blood, Mar 10;117(10):2901-9.
  3. Arthur LM; Demarest RM; Clark L; Gourevitch D; Bedelbaeva K; Anderson R; Snyder A; Capobianco AJ; Lieberman P; Feigenbaum L; Heber-Katz E. (2010) Epimorphic regeneration in mice is p53-independent. Cell Cycle Sep;9(18):3667-73
  4. Hanlon, L; Avila, JL; Demarest, RM; Troutman, S; Allen, M; Ratti F; Rustigi, AK; Stanger, BZ; Radtke, F; Adsay, V; Long, F; Capobianco, AJ; Kissil, JL. (2010) Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma. Cancer Research—Priority Report. Jun 1;70(11): 4280-6.
  5. Joshi I; Minter LM; Telfer J; Demarest RM; Capobianco AJ; Aster JC; Sicinski P; Fauq A; Golde TE; Osborne BA. (2009) Notch signaling mediates G1/S cell-cycle progression in T cells via cyclin D3 and its dependent kinases. Blood 113(8):1689-1698.
  6. Marie-Clotilde Alves-Guerra*, Renée M. Demarest* and Anthony J. Capobianco, Notch/Jagged Signaling, Encyclopedia of Cancer, 2009, Part 14, 2110-2116; *authors contributed equally
  7. Demarest, RM; Ratti, F; Capobianco, AJ. (2008). Invited Review: It’s T-ALL about Notch. Oncogene 38): 5082-5091.
  8. Salerno, D; Hasham, MG; Marshall, RM; Garriga, J.; Tsygankov, AY; and Grana, X. (2007). Direct inhibition of CDK9 blocks HIV-1 replication without preventing T-cell activation in primary human peripheral blood lymphocytes. Gene 405 (1-2): 65-78.
  9. Marshall, RM and Graña, X. (2006) Invited Review: Mechanisms controlling CDK9 activity. Frontiers in Bioscience (11): 2598-2613.
  10. Marshall RM; Salerno, D; Garriga, J.; Graña, X. (2005) Multiple signaling pathways regulate cyclin T1 expression by two distinct mechanisms during activation of human peripheral blood lymphocytes. Journal of Immunology (175): 6402-6411.
  11. Garriga, J; Bhattacharya, S; Calbo, J; Marshall, RM; Truongcao, M; Haines, DS; Graña, X. (2003) CDK9 is constitutively expressed throughout the cell cycle and its steady-state expression is independent of SKP2. Molecular and Cellular Biology (15): 5165-5173.
  12. Strauss, KI; Barbe, MF; Marshall, RM; Raghupathi, R; Mehta, S; Narayan, RJ. (2000) Prolonged cyclooxygenase-2 induction in neurons and glia following traumatic brain injury in the rat. Journal of Neurotrauma 17, 8, 695-711.