Nicholas A Cacalano

Nicholas A Cacalano

Associate Professor, Radiation Oncology, University of California Los Angeles

(310) 267-2803

B3-109 CHS
Campus - 171415
CA

Affiliations

Member, JCCC Signal Transduction and Therapeutics Program Area, Molecular Pharmacology GPB Home Area, Molecular, Cellular & Integrative Physiology GPB Home Area, Physics & Biology in Medicine GPB Home Area
 

Publications

A selected list of publications:
  • Paranjpe, A, Cacalano, NA, Hume, W, Jewett, A   N-acetyl cysteine (NAC) mediates protection from 2-hydroxy methacrylate (HEMA) induced apoptosis via NF_B dependent and independent pathways: Potential involvement of JNK, Toxicological Sciences, 2009; 108: 356-366.
  • Kim, K, Brush, JM, Watson, PA, Cacalano, NA, Iwamoto, KS, McBride, WH   EGFRvIII expression in U87 glioboastoma cells alters their proteasome composition, function, and response to irradiation, Mol Cancer Res, 2008; 6: 426-434.
  • Paranjpe A, Cacalano NA, Hume WR, Jewett A   Mechanisms of N-acetyl cysteine-mediated protection from 2-hydroxyethyl methacrylate-induced apoptosis, J Endod, 2008; 34: 1191-1197.
  • Paranjpe, A, Sung, EC, Cacalano, NA, Hume, WR, Jewett, A   N-acetyl cysteine protects pulp cells from resin toxins in vivo, J. Dental Research , 2008; 87: 537-541.
  • Jewett, A. Teruel, A, Romero, M, Head, C, Cacalano, NA   Rapid and potent induction of cell death and loss of NK cell cytotoxicity by F(ab’)2 fragment of anti-CD16 antibody, Cancer Immunology and Immunotherapy, 2008; 57: 1053-1066.
  • Cacalano, NA, Wang, MY, Park, NH, Jewett, A   Regulation of IgFbp6 and induction of cell death in HEp2 tumor cells is mediated by inverse expression and function of c-jun N- terminal Kinase (JNK) and NFkB, Apoptosis, 2008; 13: 1439-1449.
  • Cacalano, NA, Wang, MY, Park, NH, Jewett, A.   Regulation of IgFbp6 and induction of cell death in HEp2 tumor cells is mediated by inverse expression and function of c-jun N- terminal Kinase (JNK) and NFkB, Apoptosis, 2008; 13: 1439-1449.
  • Sitko, J, Zhou, H, Takaesu, G, Yoshimura, A, McBride, WH, Jamieson, CAM, Jewett, A, Cacalano, NA   SOCS3 regulates p21 expression and cell cycle arrest in response to DNA damage, Cellular Signalling, 2008; 20: 221-2230.
  • Paranjpe, A, Cacalano, NA, Hume, WR, Jewett , A   N-acetylcysteine protects Dental Pulp Stromal Cells from HEMA-induced apoptosis by inducing differentiation of the cells, Free Radical Biology and Medicine , 2007; 43: 1394-1408.
  • Romero-Reyes, M, Head, C, Cacalano NA, Jewett A   Potent induction of TNF-_ during interaction of immune effectors with oral tumors is a potential mechanism for the loss of NK cell viability and function, Apoptosis, 2007; 12: 2063-2075.
  • Teruel, A, Romero-Reyes, M, Head, C, Cacalano, NA, Jewett, A   Potential contribution of naïve immune effectors to oral tumor resistance: role in synergistic induction of VEGF, IL-6, and IL-8 secretion, Cancer Immunology and Immunotherapy, 2007; 57: 359-366.
  • Zhou, H, Miki, R, Eeva, M, Fike, FM, Seligson, D, Yang, L, Yoshimura, A, Teitell, MA, Christina A.M. Jamieson, CAM, Cacalano, NA   Reciprocal regulation of SOCS1 and SOCS3 enhances resistance to ionizing radiation in glioblastoma multiforme Clin, Cancer Res, 2007; 13: 2344-2353.
  • Cui, X, Zhang, L, Luo, J, Rajasekaran, A, Hazra, S, Cacalano, NA, Dubinett, SM   Unphosphorylated STAT6 contributes to constitutive cyclooxygenase-2 expression in human non-small cell lung cancer, Oncogene, 2007; 26: 4253-4260.
  • Jewett A, Cacalano NA, Head C, Teruel A.   Coengagement of CD16 and CD94 receptors mediates secretion of chemokines and induces apoptotic death of naive natural killer cells, Clin Cancer Res, 2006; 12: 1994-2003.
  • Qasimi P, Ming-Lum A, Ghanipour A, Ong CJ, Cox ME, Ihle J, Cacalano N, Yoshimura A, Mui AL   Divergent mechanisms utilized by SOCS3 to mediate interleukin-10 inhibition of tumour necrosis factor alpha and nitric oxide production by macrophages, J Biol Chem, 2006; 281: 6316-6324.
  • Jewett A, Head C, Cacalano NA   Emerging mechanisms of immunosuppression in oral cancers, J Dent Res, 2006; 85: 1061-1073.
  • Wang CC, Liao YP, Mischel PS, Iwamoto KS, Cacalano NA, McBride WH   HDJ-2 as a target for radiosensitization of glioblastoma multiforme cells by the farnesyltransferase inhibitor R115777 and the role of the p53/p21 pathway, Cancer Res, 2006; 66(13): 6756-6762.
  • Jewett A, Cacalano NA, Teruel A, Romero M, Rashedi M, Wang M, Nakamura H   Inhibition of nuclear factor kappa B (NFkappaB) activity in oral tumor cells prevents depletion of NK cells and increases their functional activation, Cancer Immunol Immunother, 2006; 18: 1-12.
  • Dalwadi H, Krysan K, Heuze-Vourc’h N, Dohadwala M, Elashoff D, Sharma S, Cacalano N, Lichtenstein A, Dubinett S   Cyclooxygenase-2-dependent activation of signal transducer and activator of transcription 3 by interleukin-6 in non-small cell lung cancer, Clin Cancer Res, 2005; 11: 7674-7682.
  • Tannahill GM, Elliott J, Barry AC, Hibbert L, Cacalano NA, Johnston JA   SOCS2 can enhance interleukin-2 (IL-2) and IL-3 signaling by accelerating SOCS3 degradation, Mol Cell Biol, 2005; 25: 9115-9126.
  • Sitko JC, Guevara CI, Cacalano NA   Tyrosine-phosphorylated SOCS3 interacts with the Nck and Crk-L adapter proteins and regulates Nck activation The Journal of biological chemistry. , 2004; 279(36): 37662-9.
  • Sitko JC, Guevara CI and Cacalano NA   Tyrosine-phosphorylated SOCS3 interacts with NcK and Crk-L adapter proteins and regulates Nck activation, Journal of Biological Chemistry, 2004; 279: 37662-37669.
  • Haan S, Ferguson P, Sommer U, Hiremath M, McVicar DW, Heinrich PC, Johnston JA, Cacalano NA   Tyrosine phosphorylation disrupts elongin interaction and accelerates SOCS3 degradation The Journal of biological chemistry. , 2003; 278(34): 31972-9.
  • Seki Y, Inoue H, Nagata N, Hayashi K, Fukuyama S, Matsumoto K, Komine O, Hamano S, Himeno K, Inagaki-Ohara K, Cacalano N, O’Garra A, Oshida T, Saito H, Johnston JA, Yoshimura A, Kubo M   SOCS-3 regulates onset and maintenance of T(H)2-mediated allergic responses Nat Med, 2003; 9(8): 1047-54.
  • Seki, Y-I, Inoue, H, Nagata N, Hayashi K, Fukuyama S, Matsumoto K, Komine O, Hamano S, Himeno K, Inagaki-Ohara K, Cacalano NA, O’Garra A, Oshida T, Saito H, Johnston JA, Yoshimura A and Kubo M   SOCS-3 regulates onset and maintenance of TH2-mediated allergic responses, Nature Medicine, 2003; 9: 1047-1054.
  • Haan, S, Ferguson, P, Sommer, U, McVicar, D, Heinrich, PC, Johnston, JA, and Cacalano, NA   Tyrosine phosphorylation disrupts elongin interaction and accelerates SOCS3 degradation, Journal of Biological Chemistry, 2003; 278: 31972-31979.
  • Cacalano NA and Johnston JA   Jak3-dependent pathways in hematopoiesis and SCID. In: The JAK-Stat Pathway in Hematopoiesis and Disease, AC Ward, A. ed, Plenum Publishers, 2002; 10-50.
  • Cacalano, NA   Role of Jak3 in Hematopoiesis and SCID. In: JAK-STAT Signaling in Hematopoiesis, Ward, A. ed. Eureka Press, 2001; .
  • Cacalano, NA, Sanden, D, and Johnston, JA   Tyrosine-phosphorylated SOCS-3 inhibits STAT activation but binds to p120 RasGAP and activates Ras, Nature Cell Biology , 2001; 3: 460-465.
  • Cacalano, NA, Migone, TS, Bazan, F, Hanson, EP, Chen, M, Candotti, F, OíShea, JJ, and Johnston, JA   Autsosomal SCID caused by a point mutation in the N-terminus of Jak3: mapping of the Jak3- receptor interaction domain, EMBO J, 1999; 18(6): 1549-1558.
  • Cacalano, NA, and Johnston, JA   Interleukin-2 signaling and inherited immunodeficiency, Am. J. Hum. Genet, 1999; 65(2): 287-293.
  • Cohney, SJ, Sanden, D, Cacalano, NA, Yoshimura, A, Mui, A, Migone, TS, and Johnston, JA   SOCS-3 is tyrosine phosphorylated in response to interleukin-2 and suppresses STAT5 phosphorylation and lymphocyte proliferation, Mol. Cell. Biol, 1999; 19(7): 4980-4988.

Publications