Josh Lauring

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations
    J Lauring
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Oncogene 29:2337-45. 2010
  2. pmc The multiple myeloma associated MMSET gene contributes to cellular adhesion, clonogenic growth, and tumorigenicity
    Josh Lauring
    Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Department of Chemical and Biomolecular Engineering, Baltimore, MD 21231, USA
    Blood 111:856-64. 2008
  3. pmc Knockin of mutant PIK3CA activates multiple oncogenic pathways
    John P Gustin
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 106:2835-40. 2009
  4. pmc The growth response to androgen receptor signaling in ERα-negative human breast cells is dependent on p21 and mediated by MAPK activation
    Joseph P Garay
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Breast Cancer Res 14:R27. 2012
  5. pmc PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system
    Julia A Beaver
    Authors Affiliation The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    Clin Cancer Res 19:5413-22. 2013
  6. pmc Single copies of mutant KRAS and mutant PIK3CA cooperate in immortalized human epithelial cells to induce tumor formation
    Grace M Wang
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of, The Johns Hopkins University, Baltimore, Maryland 21287, USA
    Cancer Res 73:3248-61. 2013
  7. pmc Tamoxifen-stimulated growth of breast cancer due to p21 loss
    Abde M Abukhdeir
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 105:288-93. 2008
  8. pmc ESR1 Mutations in Circulating Plasma Tumor DNA from Metastatic Breast Cancer Patients
    David Chu
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    Clin Cancer Res 22:993-9. 2016
  9. pmc TMSB4Y is a candidate tumor suppressor on the Y chromosome and is deleted in male breast cancer
    Hong Yuen Wong
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 6:44927-40. 2015
  10. pmc Functional isogenic modeling of BRCA1 alleles reveals distinct carrier phenotypes
    Rory L Cochran
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 6:25240-51. 2015

Collaborators

Detail Information

Publications25

  1. pmc Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations
    J Lauring
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Oncogene 29:2337-45. 2010
    ....
  2. pmc The multiple myeloma associated MMSET gene contributes to cellular adhesion, clonogenic growth, and tumorigenicity
    Josh Lauring
    Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Department of Chemical and Biomolecular Engineering, Baltimore, MD 21231, USA
    Blood 111:856-64. 2008
    ..These results provide the first direct evidence that MMSET plays a significant role in t(4;14) MM and suggest that therapies targeting this gene could impact this particular subset of poor-prognosis patients...
  3. pmc Knockin of mutant PIK3CA activates multiple oncogenic pathways
    John P Gustin
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 106:2835-40. 2009
    ..Our findings suggest GSK3beta is an important effector of mutant PIK3CA, and that lithium, an FDA-approved therapy for bipolar disorders, has selective antineoplastic properties against cancers that harbor these mutations...
  4. pmc The growth response to androgen receptor signaling in ERα-negative human breast cells is dependent on p21 and mediated by MAPK activation
    Joseph P Garay
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Breast Cancer Res 14:R27. 2012
    ..In addition, many breast cancers co-express other steroid hormone receptors that can affect AR signaling, further obfuscating the effects of androgens on breast cancer cells...
  5. pmc PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system
    Julia A Beaver
    Authors Affiliation The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    Clin Cancer Res 19:5413-22. 2013
    ..Pathway mutations have been proposed as predictive biomarkers for efficacy of PI3K-targeted therapies. However, the precise contribution of distinct PI3K pathway mutations to drug sensitivity is unknown...
  6. pmc Single copies of mutant KRAS and mutant PIK3CA cooperate in immortalized human epithelial cells to induce tumor formation
    Grace M Wang
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of, The Johns Hopkins University, Baltimore, Maryland 21287, USA
    Cancer Res 73:3248-61. 2013
    ..In addition, Pdk1 activation of the downstream effector p90RSK is also increased by the combined presence of mutant KRAS and PIK3CA. These results provide new insights into mutant KRAS function and its role in carcinogenesis...
  7. pmc Tamoxifen-stimulated growth of breast cancer due to p21 loss
    Abde M Abukhdeir
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 105:288-93. 2008
    ..These data reveal a previously uncharacterized molecular mechanism of tamoxifen resistance and have potential clinical implications for the management of tamoxifen-resistant breast cancers...
  8. pmc ESR1 Mutations in Circulating Plasma Tumor DNA from Metastatic Breast Cancer Patients
    David Chu
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    Clin Cancer Res 22:993-9. 2016
    ..Here, we show a high frequency of ESR1 mutations using circulating plasma tumor DNA (ptDNA) from patients with metastatic breast cancer...
  9. pmc TMSB4Y is a candidate tumor suppressor on the Y chromosome and is deleted in male breast cancer
    Hong Yuen Wong
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 6:44927-40. 2015
    ..Taken together, our results suggest that clonal loss of the Y chromosome may contribute to male breast carcinogenesis, and that the TMSB4Y gene has tumor suppressor properties. ..
  10. pmc Functional isogenic modeling of BRCA1 alleles reveals distinct carrier phenotypes
    Rory L Cochran
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 6:25240-51. 2015
    ..These results demonstrate that functional isogenic modeling of BRCA1 alleles could aid in classifying BRCA1 mutations and VUS, and determining BRCA allele cancer risk. ..
  11. ncbi request reprint A PCR-based high-throughput screen with multiround sample pooling: application to somatic cell gene targeting
    Hiroyuki Konishi
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, Maryland 21231, USA
    Nat Protoc 2:2865-74. 2007
    ..Single-cell cloning is subsequently performed to isolate gene-targeted clones. The entire protocol can be completed in 4-8 weeks depending on the proliferative capacity of the cell line...
  12. pmc Ki-67 is required for maintenance of cancer stem cells but not cell proliferation
    Justin Cidado
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 7:6281-93. 2016
    ..These results elucidate Ki-67's role in maintaining the cancer stem cell niche, which has potential diagnostic and therapeutic implications for human malignancies. ..
  13. pmc Comparison of cell stabilizing blood collection tubes for circulating plasma tumor DNA
    Patricia Valda Toro
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Clin Biochem 48:993-8. 2015
    ..However, the majority of cell stabilizing reagents have not been formally tested for their ability to preserve circulating plasma tumor DNA...
  14. ncbi request reprint Knock-in of mutant K-ras in nontumorigenic human epithelial cells as a new model for studying K-ras mediated transformation
    Hiroyuki Konishi
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 67:8460-7. 2007
    ..Thus, this system serves as a new model for elucidating the oncogenic contribution of mutant K-ras as expressed in a large fraction of human cancer cells...
  15. pmc Mutation of a single allele of the cancer susceptibility gene BRCA1 leads to genomic instability in human breast epithelial cells
    Hiroyuki Konishi
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 108:17773-8. 2011
    ..Thus, BRCA1 haploinsufficiency may accelerate hereditary breast carcinogenesis by facilitating additional genetic alterations...
  16. pmc HER2 missense mutations have distinct effects on oncogenic signaling and migration
    Daniel J Zabransky
    Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287
    Proc Natl Acad Sci U S A 112:E6205-14. 2015
    ....
  17. pmc NDRG1 links p53 with proliferation-mediated centrosome homeostasis and genome stability
    Sarah Croessmann
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287
    Proc Natl Acad Sci U S A 112:11583-8. 2015
    ..Our study elucidates a mechanism of how TP53 loss leads to abnormal centrosome numbers and genomic instability mediated by NDRG1. ..
  18. pmc Individualized Molecular Analyses Guide Efforts (IMAGE): A Prospective Study of Molecular Profiling of Tissue and Blood in Metastatic Triple-Negative Breast Cancer
    Heather A Parsons
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland
    Clin Cancer Res . 2016
    ..We hypothesized that we could perform NGS of a new biopsy from patients with metastatic triple-negative breast cancer (TNBC) in a clinically actionable timeframe...
  19. pmc MACROD2 overexpression mediates estrogen independent growth and tamoxifen resistance in breast cancers
    Morassa Mohseni
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287 and
    Proc Natl Acad Sci U S A 111:17606-11. 2014
    ..These studies establish MACROD2 as a key mediator of estrogen independent growth and tamoxifen resistance, as well as a potential novel target for diagnostics and therapy. ..
  20. pmc Functional analysis of non-hotspot AKT1 mutants found in human breast cancers identifies novel driver mutations: implications for personalized medicine
    Kyung H Yi
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Oncotarget 4:29-34. 2013
    ..The other three mutants were inactive in all assays. These findings validate novel driver mutations in AKT1, and extend the number and type of mutations that activate the PI3-kinase pathway in human breast cancers...
  21. ncbi request reprint A Polycythemia Vera JAK2 Mutation Masquerading as a Duodenal Cancer Mutation
    Justin Lee
    From the Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, and The Whiting School of Engineering, Department of Chemical and Biomolecular Engineering, The Johns Hopkins University, Baltimore, Maryland
    J Natl Compr Canc Netw 14:1495-1498. 2016
    ..This report highlights important nuances of NGS that can lead to misinterpretation of results with potential clinical implications...
  22. pmc The phosphoinositide-3-kinase-Akt-mTOR pathway as a therapeutic target in breast cancer
    Josh Lauring
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21287, USA
    J Natl Compr Canc Netw 11:670-8. 2013
    ..This article reviews the role of the PI3-kinase-Akt-mTOR pathway in breast cancer biology and the clinical trial evidence available to date...
  23. pmc Recurrent AKT mutations in human cancers: functional consequences and effects on drug sensitivity
    Kyung H Yi
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Oncotarget 7:4241-51. 2016
    ..The hypothesis that activating Akt mutations predict for Akt inhibitor sensitivity remains to be tested clinically, but is not yet supported by our preclinical data...
  24. pmc Engineering targeted chromosomal amplifications in human breast epithelial cells
    Simeon Springer
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, CRB 1 Room 146, 1650 Orleans Street, Baltimore, MD, 21287, USA
    Breast Cancer Res Treat 152:313-21. 2015
    ..This system will allow study of the cis- and trans-acting factors that are permissive for chromosomal amplification and provide a model to analyze oncogene cooperativity in amplifications harboring multiple candidate driver genes. ..
  25. pmc BEAMing sheds light on drug resistance
    Josh Lauring
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA
    Clin Cancer Res 17:7508-10. 2011
    ....