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Raj Kandpal, PhD

Raj Kandpal, PhD

Professor of BiochemistryAssistant Chair of BMS

College of Osteopathic Medicine of the Pacific

rkandpal@westernu.edu

Phone: 909-706-3520

Join year: August 2007

  • Education

    Ph.D., Biochemistry, Indian Institute of Science, Bangalore, India, 1985
    M.Sc., Biochemistry, G.B. Pant University, Pantnagar, India, 1977
    B.Sc., Physics/Chem/Math, Kumaon University, Nainital, India, 1974

  • Education Experience

    Associate Research Scientist, Department of Genetics, Yale University School of Medicine, New Haven, CT, 1987

    Postdoctoral Research Fellow, Molecular Biology Institute, UCLA, Los Angeles, CA, 1985

  • Teaching Experience

    Associate Professor, College of Osteopathic Medicine of the Pacific, Pomona, CA, 2007-Present
    Associate Professor, Department of Biological Sciences, Fordham University, Bronx, NY, 2000-2007
    Assistant Professor, Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, 1993-2000

  • Courses

    Molecular and Cellular Basis of Medicine (Molecular Biology, Cell Biology and Genetics): 2007-2019

    Molecular and Cellular Basis of Life (Molecular Biology, Cell Biology and Genetics): 2010-2020

    Endocrine System (Cholesterol Metabolism, Bile Acids and Salts, Vitamin D and Steroid Hormones): 2007-2019

    Cardiovascular System (Cardiac Metabolism; Atherosclerosis and Genetics of Cardiovascular Diseases): 2007-2019

    Integrated Study of Osteopathic Medicine (ISOM): 2019- present

    Advanced Study of Osteopathic Medicine (ASOM): 2019- present

    Foundation of Osteopathic Medicine-I (FOM1): 2019-present

    Foundation of Osteopathic Medicine-III (FOM3): 2019-present

    Foundation of Osteopathic Medicine-IV (FOM4): 2019-present

    Foundation of Osteopathic Medicine-V(FOM5): 2019-present

    Foundation of Osteopathic Medicine-VII (FOM7): 2019-present

    Course Director-Molecular and Cellular Basis of Life: 2016-2020

    Course Director-Cardiovascular System: 2018

    Co-Block Lead- Foundation of Osteopathic Medicine-III (FOM3): 2019- present

  • Research Interest

    We have been using cell biological, molecular biological and genetic approaches to understand mechanisms underlying disease processes and to identify gene targets for therapeutic interventions. We have applied these approaches toward investigating breast, prostate and ovarian cancer, diabetic retinopathy, and genetic deafness. The following is a brief description of some of our current research topics and past projects.

    1. Epigenetic mechanisms of breast cancer invasiveness: We have profiled the expression of Eph receptors, the largest family of receptor tyrosine kinases, and their ephrin ligands in breast carcinoma cells. We are exploring epigenetic mechanisms responsible for transcriptional regulation of specific receptors/ligands receptor in invasive breast carcinoma cells, and characterizing interactions among Eph receptors, and between Eph receptors and cadherins. In addition, we are developing methylation sensitive PCR (MSP) assays of gene promoters as diagnostic tools to determine estrogen-positive and estrogen-negative cells in breast tumors.
    2. Breast cancer stem cells: We have characterized stem cells from cell lines representing normal breast cell line, and noninvasive breast cancer and invasive breast carcinoma cell lines. We are investigating interactions of Eph receptors and ephrin ligands of stem cells with bulk tumor cells and stroma to determine/predict potential phenotype and progression. The effects of known therapeutic agents on stem cells is also being investigated.
    3. Inactivation of senescence causing genes in human cancers: In a collaborative study, we have characterized transcriptional regulation of transcript variants of ionotropic glutamate receptor GluR6/GRIK2. We are exploring differential expression of this gene in neuronal and non-neuronal cells to determine biological significance of GluR6 transcriptional silencing and inhibition of the senescence program in cancer cell lines.
    4. Molecular basis of diabetic retinopathy: In collaboration with investigators at the National Eye Institute, we have characterized transcript profiles of normal and diabetic retina by RNA-seq strategy. Similar approach has been utilized for miRNA profiling.
    5. Human deafness: Genetic or acquired deafness is a major public health concern. Many nonsyndromic hearing loss phenotypes have been mapped to various human chromosomes. We have characterized cDNA libraries from human inner ear for applying cDNA selection strategies to map inner ear specific cDNAs to regions of human chromosomes harboring deafness loci.
  • Publications
    • Zhawar VK, Kandpal RP and Athwal RS (2019). Isoforms of ionotropic glutamate receptor GRIK2 induce senescence of carcinoma cells. Cancer Genomics Proteomics 16, 59-64.
    • Kuo CJ and Kandpal RP (2018). Differential expression patterns of Eph receptors and ephrin ligands in human cancers. BioMed Res Int 2018, https://doi.org/10.1155/2018/7390104
    • Zadeh T, Lucero M, Kandpal RP (2022) Artesunate Induced Cellular Effects are Mediated by Specific Eph Receptors and Ephrin Ligands in Breast Carcinoma Cells. Cancer Genomics Proteomics 19: 19-26.
    • Lucero M, Thind J, Sandoval J, Senaati S, Jimenez B, Kandpal RP (2020) Stem-like Cells from Invasive Breast Carcinoma Cell Line MDA-MB-231 Express a Distinct Set of Eph Receptors and Ephrin Ligands. Cancer Genomics Proteomics 17: 729-738.
    • Zhawar VK, Kandpal RP and Athwal RS (2020). Senescence of Normal Human Fibroblasts Relates to the Expression of Ionotropic Glutamate Receptor GluR6/Grik2. Cancer Genomics Proteomics 17: 707-714.
    • Kandpal RP, Sandhu AK, Kaur G, Kaur GP and Athwal RS (2017). Monochromosomal hybrids and chromosome transfer: A Funtional approach for gene identification. Cancer Genomics Proteomics 14, 93-102.
    • Johnson C, Segovia B, Kandpal RP. EPHA7 and EPHA10 Physically Interact and Differentially Co-localize in Normal Breast and Breast Carcinoma Cell Lines, and the Co-localization Pattern is Altered in EPHB6-expressing MDA-MB-231 Cells. Cancer Genomics Proteomics. 2016 09-10:13(5):359-68. PMID 27566654
    • Mishra B, Swaroop A and Kandpal RP. (2016) Genetic components in diabetic retinopathy. Indian J Ophtlmol. 64, 55-61. March 2016 doi: 10.4103/0301-4738.178153.
    • Bhushan L, Tavitian N, Dey D, Tumur Z, Parsa C, Kandpal RP (2014). Modulation of Liver-Intestine Cadherin (Cadherin 17) Expression, ERK Phosphorylation and WNT Signaling in EPHB6 Receptor-expressing MDA-MB-231 Cells. Cancer Genomics Proteomics. 09-10;11(5):239-249
    • Kandpal RP, Rajasimha HK, Brooks MJ, Nellissery J, Wan J, Qian J, Kern TS and Swaroop A (2012). Transcriptome analysis using next generation sequencing reveals molecular signatures of diabetic retinopathy and efficacy of candidate drugs. Mol Vis 18: 1123-1146.
    • Rane NS, Sandhu AK, Zhawar VS, Kaur G, Popescu NC, Kandpal RP*, Jhanwar-Uniyal M, Athwal RS*, (2011) Restoration of Senescence in Breast and Ovarian Cancer Cells Following the Transfer of the YAC Carrying SEN6A Gene Located at 6q16.3 Cancer Genomics Proteomics 8, 227-234. (*Co-corresponding authors)
    • Bhushan L and Kandpal RP (2012). EphB6 receptor. Atlas Genet Cytogenet Oncol Hematol.February 2012. http://AtlasGeneticsOncology.org/Genes/EPHB6ID40471ch7q34.html
    • Bhushan, L. and Kandpal, RP (2011), EphB6 Receptor Modulates Micro RNA Profile of Breast Carcinoma Cells. PLoS One, 6(7): e22484.doi:10.1371/journal.pone.0022484.
    • Fox, BP and Kandpal, RP. (2011), A Paradigm Shift in Eph Receptor Interaction: Biological Relevance of EphB6 Interaction with EphA2 and EphB2 in Breast Carcinoma Cell Lines. Cancer Genomics Proteomics, 8, 185-193.
    • Kandpal, RP. (2010), Tyrosine Kinase-Deficient EphB6 Receptor-Dependent Alterations in Proteomic Profiles of Invasive Breast Carcinoma Cells as Determined by Difference Gel Electrophoresis. Cancer Genomics Proteomics, 7, 253-260.
    • Zhawar, VK, Kaur, G, deRiel, JK, Kaur, GP, Kandpal, RP and Athwal, RS (2010), Novel spliced variants of ionotropic glutamate receptor GluR6 in normal human fibroblast and brain cells are transcribed by tissue specific promoters. Gene. 459, 1-10
    • Fox, BP and Kandpal RP. (2010) DNA-based assay for EPHB6 expression in breast carcinoma cells as potential diagnostic test for detecting tumor cells in circulation. Cancer Genomics Proteomics, 7, 9-16.
    • Liu J, Kaur G, Zhawar VK, Zimonjic DB, Popescu NC, Kandpal RP, Athwal RS. (2009) Role of SV40 integration site at chromosomal interval 1q21.1 in immortalized CRL2504 cells. Cancer Res. 69:7819-25.
    • Kandpal, R.P., Saviola, B. and Felton, J. (2009) The era of ’Omics unlimited. Biotechniques. 46, 351-355.
    • Liu, J., Kaur, G., Kaur, G.P., deRiel, J.K., Kandpal, R.P. and Athwal, R.S. (2009) Chromosome 6 encoded cytoplasmic RNaseT2 protein is a cell growth regulator. J. Cell. Mol. Med. 14, 1146-1155.
    • Fox, B.P. and Kandpal, R.P. (2009) EphB6 Receptor Significantly Alters Invasiveness and Other Phenotypic Characteristics of Human Breast Carcinoma Cells. Oncogene. 28, 1706–1713.
    • Fox, B.P. and Kandpal R.P. (2008) Yeast two-hybrid assay reveals several interactors of EphB6 receptor. The Open Proteomics J. 1, 79-86.

    For additional articles please click on the following link:

    http://www.ncbi.nlm.nih.gov/pubmed?term=Kandpal%20RP