KALADHAR REDDY

Summary

Affiliation: Wayne State University
Country: USA

Publications

  1. ncbi MAP kinase/estrogen receptor cross-talk enhances estrogen-mediated signaling and tumor growth but does not confer tamoxifen resistance
    Natasha Atanaskova
    Department of Pathology, Wayne State University School of Medicine, 540 E. Canfield, Detroit, Michigan 48201, USA
    Oncogene 21:4000-8. 2002
  2. ncbi Tumor-Initiating Cells and FZD8 Play a Major Role in Drug Resistance in Triple-Negative Breast Cancer
    Shuping Yin
    Corresponding Author Kaladhar B Reddy, Department of Pathology, Wayne State University, 540 E Canfield Avenue, Detroit, MI 48201
    Mol Cancer Ther 12:491-8. 2013
  3. ncbi Inhibition of the MAP kinase activity suppresses estrogen-induced breast tumor growth both in vitro and in vivo
    Kaladhar B Reddy
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Int J Oncol 30:971-5. 2007
  4. ncbi Mitogen-activated protein kinase (MAPK) regulates the expression of progelatinase B (MMP-9) in breast epithelial cells
    K B Reddy
    Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
    Int J Cancer 82:268-73. 1999
  5. ncbi Role of MAP kinase in tumor progression and invasion
    Kaladhar B Reddy
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Cancer Metastasis Rev 22:395-403. 2003
  6. ncbi Distinct mechanisms mediate the initial and sustained phases of cell migration in epidermal growth factor receptor-overexpressing cells
    Joseph S Kruger
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mol Cancer Res 1:801-9. 2003
  7. ncbi Upregulation of PKC-delta contributes to antiestrogen resistance in mammary tumor cells
    Sanaa M Nabha
    Department of Pathology, Wayne State University School of Medicine, 540 E Canfield, Detroit, MI 48201, USA
    Oncogene 24:3166-76. 2005
  8. ncbi Activation function-1 domain of estrogen receptor regulates the agonistic and antagonistic actions of tamoxifen
    Selina Glaros
    Department of Pathology, Wayne State University School of Medicine, 540 East Canfield Avenue, and the Barbara Ann Karmanos Cancer Institute, Detroit, Michigan 48201, USA
    Mol Endocrinol 20:996-1008. 2006
  9. ncbi Mechanism of 17-beta-estradiol-induced Erk1/2 activation in breast cancer cells. A role for HER2 AND PKC-delta
    Venkateshwar G Keshamouni
    Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
    J Biol Chem 277:22558-65. 2002
  10. ncbi Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activities
    Lulu Farhana
    John D Dingell VA Medical Center, Karmanos Cancer Institute, Department of Internal Medicine, Wayne State University, Detroit, MI 48201, USA
    Oncogene 23:1874-84. 2004

Research Grants

  1. Protein Kinase C Signaling and Breast Cancer
    Kaladhar B Reddy; Fiscal Year: 2010
  2. MITOGEN ACTIVATED PROTEIN KINASES AND BREAST CANCER
    KALADHAR REDDY; Fiscal Year: 2003
  3. Protein Kinase C Signaling and Breast Cancer
    KALADHAR REDDY; Fiscal Year: 2007

Collaborators

Detail Information

Publications11

  1. ncbi MAP kinase/estrogen receptor cross-talk enhances estrogen-mediated signaling and tumor growth but does not confer tamoxifen resistance
    Natasha Atanaskova
    Department of Pathology, Wayne State University School of Medicine, 540 E. Canfield, Detroit, Michigan 48201, USA
    Oncogene 21:4000-8. 2002
    ..Taken together, these data suggest that MAPK/ER cross-talk enhances ERalpha-mediated signaling and accelerates E(2)-dependent tumor growth without diminishing sensitivity to the inhibitory effects of anti-estrogens...
  2. ncbi Tumor-Initiating Cells and FZD8 Play a Major Role in Drug Resistance in Triple-Negative Breast Cancer
    Shuping Yin
    Corresponding Author Kaladhar B Reddy, Department of Pathology, Wayne State University, 540 E Canfield Avenue, Detroit, MI 48201
    Mol Cancer Ther 12:491-8. 2013
    ..Mol Cancer Ther; 12(4); 491-8. ©2013 AACR...
  3. ncbi Inhibition of the MAP kinase activity suppresses estrogen-induced breast tumor growth both in vitro and in vivo
    Kaladhar B Reddy
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Int J Oncol 30:971-5. 2007
    ..However, these findings also indicate that MAPK plays a critical role in E2-induced tumor growth, and that this could be a potential therapeutic target to combat hormonally regulated growth in ER-positive tumors...
  4. ncbi Mitogen-activated protein kinase (MAPK) regulates the expression of progelatinase B (MMP-9) in breast epithelial cells
    K B Reddy
    Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
    Int J Cancer 82:268-73. 1999
    ..Our results suggest that interfering with MAPK activity may provide a novel means of controlling growth and invasiveness of tumors in which the signalling cascade is activated...
  5. ncbi Role of MAP kinase in tumor progression and invasion
    Kaladhar B Reddy
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Cancer Metastasis Rev 22:395-403. 2003
    ..In this review, we discuss the potential role that MAPKs play in metastasis by regulating cell migration, proteinase-induction and apoptosis...
  6. ncbi Distinct mechanisms mediate the initial and sustained phases of cell migration in epidermal growth factor receptor-overexpressing cells
    Joseph S Kruger
    Department of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA
    Mol Cancer Res 1:801-9. 2003
    ..In addition, data suggest that inhibition of MAPK and PKC-delta signaling pathways should abrogate cell migration and invasion in EGFR-overexpressing human breast cancer cells...
  7. ncbi Upregulation of PKC-delta contributes to antiestrogen resistance in mammary tumor cells
    Sanaa M Nabha
    Department of Pathology, Wayne State University School of Medicine, 540 E Canfield, Detroit, MI 48201, USA
    Oncogene 24:3166-76. 2005
    ..05). Taken together, these data suggest that PKC-delta plays a major role in antiestrogen resistance in breast tumor cells and thus provides a new target for treatment...
  8. ncbi Activation function-1 domain of estrogen receptor regulates the agonistic and antagonistic actions of tamoxifen
    Selina Glaros
    Department of Pathology, Wayne State University School of Medicine, 540 East Canfield Avenue, and the Barbara Ann Karmanos Cancer Institute, Detroit, Michigan 48201, USA
    Mol Endocrinol 20:996-1008. 2006
    ..Taken together, these data demonstrate that different phosphorylation sites in the AF-1 domain of ERalpha regulate the agonistic and antagonistic actions of tamoxifen in human breast cancer cells...
  9. ncbi Mechanism of 17-beta-estradiol-induced Erk1/2 activation in breast cancer cells. A role for HER2 AND PKC-delta
    Venkateshwar G Keshamouni
    Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
    J Biol Chem 277:22558-65. 2002
    ..This evaluation of downstream signaling revealed that E(2)-induced Erk activation is mediated by a HRG/HER-2/PKC-delta/Ras pathway that could be crucial for E(2)-dependent growth-promoting effects in early stages of tumor progression...
  10. ncbi Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activities
    Lulu Farhana
    John D Dingell VA Medical Center, Karmanos Cancer Institute, Department of Internal Medicine, Wayne State University, Detroit, MI 48201, USA
    Oncogene 23:1874-84. 2004
    ..Inhibition of AKT activity by this compound results in the inability of AKT to phosphorylate and inactivate the proapoptotic forkhead transcription factor...
  11. ncbi Enhanced anticancer effect of the combination of cisplatin and TRAIL in triple-negative breast tumor cells
    Liping Xu
    Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
    Mol Cancer Ther 10:550-7. 2011
    ..Taken together the data suggest that cisplatin plus TRAIL treatment have the potential of providing a new strategy for improving the therapeutic outcome in TNBC patients...

Research Grants8

  1. Protein Kinase C Signaling and Breast Cancer
    Kaladhar B Reddy; Fiscal Year: 2010
    ..abstract_text> ..
  2. MITOGEN ACTIVATED PROTEIN KINASES AND BREAST CANCER
    KALADHAR REDDY; Fiscal Year: 2003
    ..The long term goal is the identification of molecular events underlying tumor progression that are potential targets for the development of rational therapeutic agents. ..
  3. Protein Kinase C Signaling and Breast Cancer
    KALADHAR REDDY; Fiscal Year: 2007
    ....