Meena Jhanwar-Uniyal

Summary

Affiliation: New York Medical College
Country: USA

Publications

  1. doi request reprint Distinct signaling mechanisms of mTORC1 and mTORC2 in glioblastoma multiforme: a tale of two complexes
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA Electronic address
    Adv Biol Regul 57:64-74. 2015
  2. doi request reprint Deconstructing mTOR complexes in regulation of Glioblastoma Multiforme and its stem cells
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Adv Biol Regul 53:202-10. 2013
  3. doi request reprint Deciphering the signaling pathways of cancer stem cells of glioblastoma multiforme: role of Akt/mTOR and MAPK pathways
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Adv Enzyme Regul 51:164-70. 2011
  4. doi request reprint Targeting cancer stem cells in glioblastoma multiforme using mTOR inhibitors and the differentiating agent all-trans retinoic acid
    Marissa D Friedman
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Oncol Rep 30:1645-50. 2013
  5. pmc Cell cycle arrest and apoptosis induced by human Polo-like kinase 3 is mediated through perturbation of microtubule integrity
    Qi Wang
    Department of Medicine and Brander Cancer Research Institute, New York Medical College, Hwathorne, 10532, USA
    Mol Cell Biol 22:3450-9. 2002
  6. ncbi request reprint Rho/ROCK and MAPK signaling pathways are involved in glioblastoma cell migration and proliferation
    Vahe Michael Zohrabian
    Department of Neurosurgery, New York Medical College, Valhalla, New York 10595, USA
    Anticancer Res 29:119-23. 2009
  7. ncbi request reprint Inhibition of mTOR Activates the MAPK Pathway in Glioblastoma Multiforme
    Ladislau Albert
    Departments of Neurosurgery and Experimental Pathology, New York Medical College, Valhalla, NY 10595, U S A
    Cancer Genomics Proteomics 6:255-61. 2009
  8. doi request reprint The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma
    Michael Karsy
    Department of Neurosurgery, University of Utah, 175 North Medical Dr East, Salt Lake City, UT, 84132, USA
    Tumour Biol 35:4567-80. 2014
  9. ncbi request reprint Involvement of mTORC1 and mTORC2 in regulation of glioblastoma multiforme growth and motility
    Nicholas Gulati
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 35:731-40. 2009
  10. ncbi request reprint Proteasome-dependent downregulation of p21(Waf1/Cip1) induced by reactive oxygen species
    Suqing Xie
    Department of Medicine, New York Medical College, Valhalla, NY 10595, USA
    J Interferon Cytokine Res 22:957-63. 2002

Collaborators

Detail Information

Publications26

  1. doi request reprint Distinct signaling mechanisms of mTORC1 and mTORC2 in glioblastoma multiforme: a tale of two complexes
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA Electronic address
    Adv Biol Regul 57:64-74. 2015
    ..This investigation describes the mechanism of action of pharmacological agents that effectively target mTORC1 and mTORC2 resulting in suppression of growth, proliferation, and migration of tumor and cancer stem cells. ..
  2. doi request reprint Deconstructing mTOR complexes in regulation of Glioblastoma Multiforme and its stem cells
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Adv Biol Regul 53:202-10. 2013
    ..mTORC2 has been linked to cytoskeletal reorganization and cell survival through Akt, and is crucial to many divergent physiological functions, which may include stem cell regulation...
  3. doi request reprint Deciphering the signaling pathways of cancer stem cells of glioblastoma multiforme: role of Akt/mTOR and MAPK pathways
    Meena Jhanwar-Uniyal
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Adv Enzyme Regul 51:164-70. 2011
    ..Future research should focus on further defining the PI3K/Akt/mTOR molecular network in the regulation of stem cell quiescence and provide rationale for targeting the cancer-initiating cells of GBM...
  4. doi request reprint Targeting cancer stem cells in glioblastoma multiforme using mTOR inhibitors and the differentiating agent all-trans retinoic acid
    Marissa D Friedman
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Oncol Rep 30:1645-50. 2013
    ..These findings indicate that ATRA-induced differentiation is mediated via the ERK1/2 pathway, and underscores the significance of including differentiating agents along with inhibitors of mTOR pathways in the treatment of GBM...
  5. pmc Cell cycle arrest and apoptosis induced by human Polo-like kinase 3 is mediated through perturbation of microtubule integrity
    Qi Wang
    Department of Medicine and Brander Cancer Research Institute, New York Medical College, Hwathorne, 10532, USA
    Mol Cell Biol 22:3450-9. 2002
    ....
  6. ncbi request reprint Rho/ROCK and MAPK signaling pathways are involved in glioblastoma cell migration and proliferation
    Vahe Michael Zohrabian
    Department of Neurosurgery, New York Medical College, Valhalla, New York 10595, USA
    Anticancer Res 29:119-23. 2009
    ..Here, the involvement of the Rho and Rho-associated protein kinase (ROCK) pathway, along with MAPK, was investigated to determine their roles in GBM cell migration and proliferation...
  7. ncbi request reprint Inhibition of mTOR Activates the MAPK Pathway in Glioblastoma Multiforme
    Ladislau Albert
    Departments of Neurosurgery and Experimental Pathology, New York Medical College, Valhalla, NY 10595, U S A
    Cancer Genomics Proteomics 6:255-61. 2009
    ..These results demonstrate activation of a mitogenic pathway involving a feedback mechanism between mTOR and PI3K/ERK1/2 and support the basis for combined inhibitors in GBM treatment...
  8. doi request reprint The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma
    Michael Karsy
    Department of Neurosurgery, University of Utah, 175 North Medical Dr East, Salt Lake City, UT, 84132, USA
    Tumour Biol 35:4567-80. 2014
    ..In conclusion, codon-specific mutant p53 conferred a more aggressive phenotype to our CSC model. However, ATO and ATRA could potently suppress CSC properties in vitro and may support further clinical investigation of these agents. ..
  9. ncbi request reprint Involvement of mTORC1 and mTORC2 in regulation of glioblastoma multiforme growth and motility
    Nicholas Gulati
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 35:731-40. 2009
    ..The results demonstrated that an activation of mTORC2 occurs when mTORC1 is inhibited by RAPA. Therefore, simultaneous suppression of mTORC1 and mTORC2 may provide novel therapy for GBM...
  10. ncbi request reprint Proteasome-dependent downregulation of p21(Waf1/Cip1) induced by reactive oxygen species
    Suqing Xie
    Department of Medicine, New York Medical College, Valhalla, NY 10595, USA
    J Interferon Cytokine Res 22:957-63. 2002
    ..Taken together, our studies indicate that oxidative stress induces rapid, but reversible, downregulation of functional p21 by accelerating its protein turnover...
  11. ncbi request reprint All-trans retinoic acid modulates cancer stem cells of glioblastoma multiforme in an MAPK-dependent manner
    Michael Karsy
    Departments of Neurosurgery and Experimental Pathology, New York Medical College, Valhalla, NY 10595, USA
    Anticancer Res 30:4915-20. 2010
    ..These results emphasize that low doses of ATRA may have therapeutic potential by differentiating GBM CSCs and rendering them sensitive to targeted therapy...
  12. ncbi request reprint Gene expression profiling of metastatic brain cancer
    Vahe Michael Zohrabian
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Oncol Rep 18:321-8. 2007
    ....
  13. pmc Stem cell therapy and curcumin synergistically enhance recovery from spinal cord injury
    D Ryan Ormond
    Department of Neurosurgery, New York Medical College, Valhalla, New York, United States of America
    PLoS ONE 9:e88916. 2014
    ..Furthermore, our results indicate that the effect of curcumin extends beyond its known anti-inflammatory properties to the regulation of stem cell proliferation. ..
  14. ncbi request reprint N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells
    Yang Ming Yang
    Division of Carcinogenesis, American Health Foundation Cancer Center, Institute for Cancer Prevention, Valhalla, New York, USA
    Cancer Res 65:8538-47. 2005
    ..The observation that PEITC-NAC induces apoptosis predominantly in growth-promoted cells, such as neoplastic cells, suggests a selective mechanism by which PEITC-NAC inhibits lung carcinogenesis...
  15. doi request reprint ATP-site binding inhibitor effectively targets mTORC1 and mTORC2 complexes in glioblastoma
    Jayson Neil
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 48:1045-52. 2016
    ..In conclusion, these results underscore the potential therapeutic use of the PP242, a novel ATP-competitive binding inhibitor of mTORC1/2 kinase, in suppression of GBM growth and dissemination. ..
  16. ncbi request reprint PI3K/mTOR signaling pathways in medulloblastoma
    Avinash L Mohan
    Department of Neurosurgery, New York Medical College, Valhalla, NY, USA
    Anticancer Res 32:3141-6. 2012
    ..These results indicate that the mTOR pathway is involved in the pathogenesis of medulloblastoma, and that targeting this pathway may provide a strategy for therapy of medulloblastoma...
  17. ncbi request reprint MEK1-induced Golgi dynamics during cell cycle progression is partly mediated by Polo-like kinase-3
    Suqing Xie
    Department of Medicine, New York Medical College, Valhalla, NY 10595, USA
    Oncogene 23:3822-9. 2004
    ..Thus, our studies strongly suggest that Plk3 may be a key protein kinase mediating MEK1 function in the Golgi fragmentation pathway during cell division...
  18. ncbi request reprint Mutant human tumor suppressor p53 modulates the activation of mitogen-activated protein kinase and nuclear factor-kappaB, but not c-Jun N-terminal kinase and activated protein-1
    Anthony P Gulati
    Department of Neurosurgery, New York Medical College, Valhalla, New York 10595, USA
    Mol Carcinog 45:26-37. 2006
    ..These differences may influence cellular processes such as proliferation, differentiation, and apoptosis...
  19. ncbi request reprint Molecular Pathways Mediating Metastases to the Brain via Epithelial-to-Mesenchymal Transition: Genes, Proteins, and Functional Analysis
    Dhruve S Jeevan
    Department of Neurosurgery, New York Medical College, Valhalla, NY, U S A
    Anticancer Res 36:523-32. 2016
    ..Here, we examined the expression of markers of EMT, MET, and stem cells in metastatic brain tumor samples...
  20. ncbi request reprint Involvement of mTOR signaling pathways in regulating growth and dissemination of metastatic brain tumors via EMT
    Amanda Kwasnicki
    Department of Neurosurgery, New York Medical College, Valhalla, NY, U S A
    Anticancer Res 35:689-96. 2015
    ..However, the role of mTOR in brain metastases remains elusive. We hypothesize that mTOR plays a crucial role in the process of EMT in brain metastasis and therefore serves as a target of therapy...
  21. doi request reprint Recovery from spinal cord injury using naturally occurring antiinflammatory compound curcumin: laboratory investigation
    D Ryan Ormond
    Department of Neurosurgery, New York Medical College, Valhalla, New York 10595, USA
    J Neurosurg Spine 16:497-503. 2012
    ..Curcumin longa is an active compound found in turmeric, which acts as an antiinflammatory agent primarily by inhibiting nuclear factor-κB. Here, the authors study the effect of curcumin on SCI recovery...
  22. ncbi request reprint Polo box domain of Plk3 functions as a centrosome localization signal, overexpression of which causes mitotic arrest, cytokinesis defects, and apoptosis
    Ning Jiang
    Division of Molecular Carcinogenesis, Department of Medicine, New York Medical College, Basic Science Building, Valhalla, NY 10595, USA
    J Biol Chem 281:10577-82. 2006
    ....
  23. ncbi request reprint Revisiting the role of p53 in primary and secondary glioblastomas
    Julie Nagpal
    Department of Neurosurgery, New York Medical College, Valhalla, New York 10595, USA
    Anticancer Res 26:4633-9. 2006
    ..Furthermore, cytoplasmic p53 may reflect an association of p53 with Cullin 7, PARC, or with the sequestering partner of p53, mortalin. These results underscore the significance of p53 in the tumorigenesis of de novo GBM...
  24. ncbi request reprint BRCA1 in cancer, cell cycle and genomic stability
    Meena Jhanwar-Uniyal
    Institute for Cancer Prevention, American Health Foundation Cancer Prevention Center, Valhalla, New York 10595, USA
    Front Biosci 8:s1107-17. 2003
    ..Thus, BRCA1 plays a significant role in maintaining genomic stability and serves as a tumor suppressor in breast cancer tumorigenesis...
  25. doi request reprint Prevention of cerebral vasospasm by local delivery of cromakalim with a biodegradable controlled-release system in a rat model of subarachnoid hemorrhage
    Ibrahim Omeis
    Departments of Neurosurgery, New York Medical College, Munger Pavilion, 3rd Floor, Valhalla, New York 10595, USA
    J Neurosurg 110:1015-20. 2009
    ..The authors tested the efficacy of locally delivered intrathecal cromakalim, a PCO, incorporated into a controlled-release system to prevent cerebral vasospasm in a rat model of SAH...
  26. ncbi request reprint The antiproliferative effect of Quercetin in cancer cells is mediated via inhibition of the PI3K-Akt/PKB pathway
    Nicholas Gulati
    Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA
    Anticancer Res 26:1177-81. 2006
    ..The naturally occurring bioflavonoid Quercetin (Qu) shares structural homology with the commercially available selective PI3K inhibitor, LY 294002 (LY). Here, the effects of Qu on the Akt/PKB pathway were evaluated...