Carlos L Arteaga

Summary

Affiliation: Vanderbilt University
Country: USA

Publications

  1. ncbi request reprint HER2 kinase domain mutation results in constitutive phosphorylation and activation of HER2 and EGFR and resistance to EGFR tyrosine kinase inhibitors
    Shizhen Emily Wang
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Cell 10:25-38. 2006
  2. ncbi request reprint Inhibiting tyrosine kinases: successes and limitations
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Cancer Center, Varderbilt University School of Medicine, Nashville, TN 37232 6307, US
    Cancer Biol Ther 2:S79-83. 2003
  3. ncbi request reprint Overexpression of HER2 (erbB2) in human breast epithelial cells unmasks transforming growth factor beta-induced cell motility
    Yukiko Ueda
    Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Nashville, Tennessee 37232, USA
    J Biol Chem 279:24505-13. 2004
  4. ncbi request reprint HER2/Neu (ErbB2) signaling to Rac1-Pak1 is temporally and spatially modulated by transforming growth factor beta
    Shizhen Emily Wang
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Cancer Res 66:9591-600. 2006
  5. pmc Inhibition of mammalian target of rapamycin is required for optimal antitumor effect of HER2 inhibitors against HER2-overexpressing cancer cells
    Todd W Miller
    Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA
    Clin Cancer Res 15:7266-76. 2009
  6. pmc Transforming growth factor {beta} (TGF-{beta})-Smad target gene protein tyrosine phosphatase receptor type kappa is required for TGF-{beta} function
    Shizhen Emily Wang
    Division of Oncology, Department of Cancer Biology, Vanderbilt University School of Medicine, 2220 Pierce Ave, 777 PRB, Nashville, TN 37232 6307, USA
    Mol Cell Biol 25:4703-15. 2005
  7. pmc Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins
    Marta Guix
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    J Clin Invest 118:2609-19. 2008
  8. ncbi request reprint Loss of PTEN/MMAC1/TEP in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors
    Roberto Bianco
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    Oncogene 22:2812-22. 2003
  9. pmc TGF-β inhibition enhances chemotherapy action against triple-negative breast cancer
    Neil E Bhola
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA
    J Clin Invest 123:1348-58. 2013
  10. pmc A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer
    Emily M Fox
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA
    Cancer Res 71:6773-84. 2011

Collaborators

Detail Information

Publications107 found, 100 shown here

  1. ncbi request reprint HER2 kinase domain mutation results in constitutive phosphorylation and activation of HER2 and EGFR and resistance to EGFR tyrosine kinase inhibitors
    Shizhen Emily Wang
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Cell 10:25-38. 2006
    ..These data suggest that (1) HER2(YVMA) activates cellular substrates more potently than HER2(WT); and (2) cancer cells expressing this mutation remain sensitive to HER2-targeted therapies but insensitive to EGFR TKIs...
  2. ncbi request reprint Inhibiting tyrosine kinases: successes and limitations
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Cancer Center, Varderbilt University School of Medicine, Nashville, TN 37232 6307, US
    Cancer Biol Ther 2:S79-83. 2003
    ....
  3. ncbi request reprint Overexpression of HER2 (erbB2) in human breast epithelial cells unmasks transforming growth factor beta-induced cell motility
    Yukiko Ueda
    Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Nashville, Tennessee 37232, USA
    J Biol Chem 279:24505-13. 2004
    ....
  4. ncbi request reprint HER2/Neu (ErbB2) signaling to Rac1-Pak1 is temporally and spatially modulated by transforming growth factor beta
    Shizhen Emily Wang
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Cancer Res 66:9591-600. 2006
    ..Thus, by recruiting the actin skeleton, TGF-beta "cross-links" this signaling complex at cell lamellipodia; this prolongs Rac1 activation and increases metastatic properties and survival of HER2-overexpressing cells...
  5. pmc Inhibition of mammalian target of rapamycin is required for optimal antitumor effect of HER2 inhibitors against HER2-overexpressing cancer cells
    Todd W Miller
    Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA
    Clin Cancer Res 15:7266-76. 2009
    ..Therefore, we examined whether mTOR inhibitors synergize with trastuzumab...
  6. pmc Transforming growth factor {beta} (TGF-{beta})-Smad target gene protein tyrosine phosphatase receptor type kappa is required for TGF-{beta} function
    Shizhen Emily Wang
    Division of Oncology, Department of Cancer Biology, Vanderbilt University School of Medicine, 2220 Pierce Ave, 777 PRB, Nashville, TN 37232 6307, USA
    Mol Cell Biol 25:4703-15. 2005
    ....
  7. pmc Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins
    Marta Guix
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    J Clin Invest 118:2609-19. 2008
    ..Moreover, combined therapeutic inhibition of EGFR and IGFIR may abrogate this acquired mechanism of drug resistance and is thus worthy of prospective clinical investigation...
  8. ncbi request reprint Loss of PTEN/MMAC1/TEP in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors
    Roberto Bianco
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    Oncogene 22:2812-22. 2003
    ..Thus, in EGFR-expressing tumor cells with concomitant amplification(s) of PI3K-Akt signaling, combined blockade of the EGFR tyrosine kinase and Akt should be considered as a therapeutic approach...
  9. pmc TGF-β inhibition enhances chemotherapy action against triple-negative breast cancer
    Neil E Bhola
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA
    J Clin Invest 123:1348-58. 2013
    ..These findings support testing a combination of TGF-β inhibitors and anticancer chemotherapy in patients with TNBC...
  10. pmc A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer
    Emily M Fox
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA
    Cancer Res 71:6773-84. 2011
    ..We conclude that therapeutic targeting of both InsR and IGF-IR should be more effective than targeting IGF-IR alone in abrogating resistance to endocrine therapy in breast cancer...
  11. ncbi request reprint Reduction of cytosolic p27(Kip1) inhibits cancer cell motility, survival, and tumorigenicity
    Frederick Y Wu
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Cancer Res 66:2162-72. 2006
    ..These data suggest that cytoplasmic p27 can exert oncogenic functions by modulating Akt stability, cell survival, and tumorigenicity...
  12. ncbi request reprint Tyrosine kinase inhibitors: why does the current process of clinical development not apply to them?
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Cell 5:525-31. 2004
    ....
  13. ncbi request reprint Association with HSP90 inhibits Cbl-mediated down-regulation of mutant epidermal growth factor receptors
    Seungchan Yang
    Department of Medicine, Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Cancer Res 66:6990-7. 2006
    ..These results suggest that EGFR mutants form defective endocytic complexes. In addition, HSP90 plays a role in maintaining the functional conformation of EGFR mutants and protecting activated receptors from LIRD...
  14. pmc Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance
    Justin M Balko
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University, Nashville, Tennessee, USA
    Nat Med 18:1052-9. 2012
    ..Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy...
  15. pmc Loss of Phosphatase and Tensin homologue deleted on chromosome 10 engages ErbB3 and insulin-like growth factor-I receptor signaling to promote antiestrogen resistance in breast cancer
    Todd W Miller
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University, Nashville, TN 37232 6307, USA
    Cancer Res 69:4192-201. 2009
    ....
  16. pmc Discordant cellular response to presurgical letrozole in bilateral synchronous ER+ breast cancers with a KRAS mutation or FGFR1 gene amplification
    Justin M Balko
    Vanderbilt University Medical Center, 2200 Pierce Ave, 777 PRB, Nashville, TN 37232 6307, USA
    Mol Cancer Ther 11:2301-5. 2012
    ..Second, they suggest that the role of activating mutations in RAS, although rare in breast cancer, may need to be explored in the context of ER+ breast tumors...
  17. ncbi request reprint Modulation of NFkappaB activity and E-cadherin by the type III transforming growth factor beta receptor regulates cell growth and motility
    Tracy L Criswell
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    J Biol Chem 282:32491-500. 2007
    ..These data indicate that TbetaRIII acts as a tumor suppressor in nontumorigenic mammary epithelial cells at least in part by inhibiting NFkappaB-mediated repression of E-cadherin...
  18. doi request reprint Inhibition of PI3K and MEK: it is all about combinations and biomarkers
    Brent N Rexer
    Department of Medicine, Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 15:4518-20. 2009
    ..Therefore, MEK inhibitors should preferably be investigated in combination with PI3K inhibitors in basal-like breast cancers...
  19. pmc Trastuzumab has preferential activity against breast cancers driven by HER2 homodimers
    Ritwik Ghosh
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee 37232, USA
    Cancer Res 71:1871-82. 2011
    ..A clinical implication of our results is that high levels of HER2 homodimers may predict a positive response to trastuzumab...
  20. pmc Activation of MAPK pathways due to DUSP4 loss promotes cancer stem cell-like phenotypes in basal-like breast cancer
    Justin M Balko
    Authors Affiliations Departments of Medicine and Cancer Biology Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee Instituto Nacional de Enfermedades Neoplásicas, Lima, Perú and Department of Pharmacology and Toxicology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire
    Cancer Res 73:6346-58. 2013
    ..Our findings support the evaluation of MEK and JNK pathway inhibitors as therapeutic agents in BLBC to eliminate the CSC population...
  21. pmc Dual blockade of HER2 in HER2-overexpressing tumor cells does not completely eliminate HER3 function
    Joan T Garrett
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Clin Cancer Res 19:610-9. 2013
    ..We hypothesized that suppression of HER3 would synergize with dual blockade of HER2 in breast cancer cells sensitive and refractory to HER2 antagonists...
  22. pmc The receptor tyrosine kinase ErbB3 maintains the balance between luminal and basal breast epithelium
    Justin M Balko
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 109:221-6. 2012
    ..Taken together, these results suggest that ErbB3 regulates the balance of differentiated breast epithelial cell types by regulating their growth and survival through autocrine- and paracrine-signaling mechanisms...
  23. doi request reprint Short preoperative treatment with erlotinib inhibits tumor cell proliferation in hormone receptor-positive breast cancers
    Marta Guix
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    J Clin Oncol 26:897-906. 2008
    ....
  24. ncbi request reprint PKB/Akt mediates cell-cycle progression by phosphorylation of p27(Kip1) at threonine 157 and modulation of its cellular localization
    Incheol Shin
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Nat Med 8:1145-52. 2002
    ..These data indicate that Akt may contribute to tumor-cell proliferation by phosphorylation and cytosolic retention of p27, thus relieving CDK2 from p27-induced inhibition...
  25. ncbi request reprint A kinase-inactive type II TGFbeta receptor impairs BMP signaling in human breast cancer cells
    Nancy Dumont
    Department of Cancer Biology, Vanderbilt University School of Medicine, 2220 Pierce Avenue, 777 Preston Research Building, Nashville, TN 37232 6307, USA
    Biochem Biophys Res Commun 301:108-12. 2003
    ..The fact that dnTbetaRII not only abrogates TGFbeta signaling but BMP signaling as well has important implications for the interpretation of data in which dominant negative mutants are utilized...
  26. pmc Transforming growth factor-beta induces Cdk2 relocalization to the cytoplasm coincident with dephosphorylation of retinoblastoma tumor suppressor protein
    Kimberly A Brown
    Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA
    Breast Cancer Res 6:R130-9. 2004
    ..Growth arrest correlated with increased binding of p21 and p27 to cyclin-dependent kinase-2 (Cdk2), and inhibition of Cdk2 kinase activity. However, it was unclear how TGF-beta caused increased binding of p21 and p27 to Cdk2...
  27. ncbi request reprint Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer
    Li Yang
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Res 67:5587-93. 2007
    ..This effect is reversible in a subset of NSCLC upon treatment with an EGFR TKI...
  28. pmc HER3 is required for HER2-induced preneoplastic changes to the breast epithelium and tumor formation
    David B Vaught
    Department of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN 37232, USA
    Cancer Res 72:2672-82. 2012
    ..These results may have important translational implications for the treatment and prevention of HER2-amplified breast tumors through ErbB3 inhibition...
  29. pmc Feedback upregulation of HER3 (ErbB3) expression and activity attenuates antitumor effect of PI3K inhibitors
    Anindita Chakrabarty
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 109:2718-23. 2012
    ..As a result, PI3K pathway inhibitors may have limited clinical activity overall if used as single agents. In patients with HER2-overexpressing breast cancer, PI3K inhibitors should be used in combination with HER2/HER3 antagonists...
  30. ncbi request reprint ErbB-targeted therapeutic approaches in human cancer
    Carlos L Arteaga
    Department of Medicine, Vanderbilt University School of Medicine, and Breast Cancer Program, Vanderbilt Ingram Comprehensive Cancer Center, Nashville, TN 37232, USA
    Exp Cell Res 284:122-30. 2003
    ....
  31. pmc Inhibition of TGF-beta with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression
    Swati Biswas
    Department of Cancer Biology, Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, TN 37232, USA
    J Clin Invest 117:1305-13. 2007
    ..These data implicate TGF-beta induced by anticancer therapy as a pro-metastatic signal in tumor cells and provide a rationale for the simultaneous use of these therapies in combination with TGF-beta inhibitors...
  32. pmc Molecular profiling of the residual disease of triple-negative breast cancers after neoadjuvant chemotherapy identifies actionable therapeutic targets
    Justin M Balko
    Departments of 1Medicine, 2Pathology, Microbiology and Immunology, 3Cancer Biology, and 4Biochemistry 5Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee Departments of 6Cell and Tissue Biology and 7Medicine, University of California, San Francisco, San Francisco, California 8Foundation Medicine, Cambridge, Massachusetts 9Oncosalud and 10Instituto Nacional de Enfermedades Neoplásicas INEN, Lima, Peru
    Cancer Discov 4:232-45. 2014
    ..These data can guide biomarker-driven adjuvant studies targeting these micrometastases to improve the outcome of patients with TNBC who do not respond completely to NAC...
  33. ncbi request reprint The epidermal growth factor receptor-tyrosine kinase: a promising therapeutic target in solid tumors
    Christoph A Ritter
    Department of Medicine and Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Semin Oncol 30:3-11. 2003
    ..ZD1839 (Iressa; AstraZeneca Pharmaceuticals LP, Wilmington, DE) is the EGFR-TK inhibitor furthest along in clinical development, and it is currently being investigated in a variety of solid tumors, including non-small-cell lung cancer...
  34. ncbi request reprint Overview of epidermal growth factor receptor biology and its role as a therapeutic target in human neoplasia
    Carlos L Arteaga
    Departments of Medicine and Cancer Biology and the Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Semin Oncol 29:3-9. 2002
    ..Early clinical studies already suggest that both of these approaches, either alone or in combination with standard anticancer therapies, alter the natural history of EGFR-expressing cancers with little toxicity to the tumor-bearing host...
  35. pmc An antibody that locks HER3 in the inactive conformation inhibits tumor growth driven by HER2 or neuregulin
    Andrew P Garner
    Authors Affiliations Novartis Institutes for BioMedical Research, Cambridge, Massachusetts Departments of Medicine and Cancer Biology Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee MorphoSys AG, Martinsried, Germany and Genomics Institute of the Novartis Research Foundation, San Diego, California
    Cancer Res 73:6024-35. 2013
    ..Taken together, our findings establish that LJM716 possesses a novel mechanism of action that, in combination with HER2- or EGFR-targeted agents, may leverage their clinical efficacy in ErbB-driven cancers...
  36. pmc ERα-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer
    Todd W Miller
    Department of Cancer Biology, Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee 37232 6307, USA
    Cancer Discov 1:338-51. 2011
    ..These data support further development of ER downregulators and CDK4 inhibitors, and their combination with PI3K inhibitors for treatment of antiestrogen-resistant breast cancers...
  37. pmc Intrinsic and acquired resistance to HER2-targeted therapies in HER2 gene-amplified breast cancer: mechanisms and clinical implications
    Brent N Rexer
    Departments of Medicine and Cancer Biology, Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37212, USA
    Crit Rev Oncog 17:1-16. 2012
    ..Emerging clinical evidence already suggests that combinations of therapies targeting HER2 as well as these resistance pathways will be effective in overcoming or preventing resistance...
  38. pmc Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer
    Todd W Miller
    Department of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN 37232, USA
    Breast Cancer Res 13:224. 2011
    ..Here, we review alterations in the PI3K pathway in breast cancer, their association with therapeutic resistance, and the state of clinical development of PI3K pathway inhibitors...
  39. pmc Transcriptional and posttranslational up-regulation of HER3 (ErbB3) compensates for inhibition of the HER2 tyrosine kinase
    Joan T Garrett
    Department of Medicine, Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, and Vanderbilt University Institute of Imaging Sciences, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 108:5021-6. 2011
    ..They also suggest that therapeutic inhibitors of HER3 should be used in combination with HER2 inhibitors and PI3K pathway inhibitors in patients with HER2- and PI3K-dependent cancers...
  40. pmc Mutant PIK3CA accelerates HER2-driven transgenic mammary tumors and induces resistance to combinations of anti-HER2 therapies
    Ariella B Hanker
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 110:14372-7. 2013
    ....
  41. ncbi request reprint EGF receptor mutations in lung cancer: from humans to mice and maybe back to humans
    Carlos L Arteaga
    Department of Medicine, Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Cell 9:421-3. 2006
    ..These mouse models provide important opportunities for studying the biology of NSCLC and the refinement of anti-EGFR therapies...
  42. pmc Erlotinib attenuates homologous recombinational repair of chromosomal breaks in human breast cancer cells
    Liping Li
    Department of Radiation Oncology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Cancer Res 68:9141-6. 2008
    ..These findings suggest a novel mechanism of action of erlotinib through its effects on the BRCA1/HDR pathway. Furthermore, BRCA1/HDR status may be an innovative avenue to enhance the sensitivity of cancer cells to erlotinib...
  43. ncbi request reprint EGF receptor as a therapeutic target: patient selection and mechanisms of resistance to receptor-targeted drugs
    Carlos L Arteaga
    Department of Medicine and Cancer Biology and Breat Cancer Program, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    J Clin Oncol 21:289s-291s. 2003
    ..This approach would also exclude patients for whom these drugs will not induce any clinical benefit...
  44. ncbi request reprint Inhibition of transforming growth factor-beta signaling in human cancer: targeting a tumor suppressor network as a therapeutic strategy
    Swati Biswas
    Department of Medicine, Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 12:4142-6. 2006
  45. pmc Ligand-independent phosphorylation of Y869 (Y845) links mutant EGFR signaling to stat-mediated gene expression
    Seungchan Yang
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
    Exp Cell Res 314:413-9. 2008
    ..Our results suggest that ligand-independent and Src activity-independent phosphorylation of Y869 in mutant EGFR regulates STAT5 activation and c-myc expression...
  46. pmc Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence
    Justin M Balko
    Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA Department of Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN 37232, USA
    Sci Transl Med 8:334ra53. 2016
    ..Furthermore, JAK2 amplification is a potential biomarker for JAK2 dependence, which, in turn, can be used to select patients for clinical trials with JAK2 inhibitors...
  47. pmc Kinome-wide functional screen identifies role of PLK1 in hormone-independent, ER-positive breast cancer
    Neil E Bhola
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee
    Cancer Res 75:405-14. 2015
    ..These data support a critical role of PLK1 in acquired hormone-independent growth of ER(+) human breast cancer and is therefore a promising target in tumors that have escaped estrogen deprivation therapy...
  48. doi request reprint Progress in breast cancer: overview
    Carlos L Arteaga
    Author s Affiliation Departments of Medicine and Cancer Biology Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee
    Clin Cancer Res 19:6353-9. 2013
    ..The papers in this CCR Focus section are contributed by experts in the respective areas of investigation. Herein, key aspects of these contributions and the research directions they propose are reviewed...
  49. ncbi request reprint HER (erbB) tyrosine kinase inhibitors in the treatment of breast cancer
    Carlos L Arteaga
    Departments of Medicine and Cancer Biology and the Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Semin Oncol 29:4-10. 2002
    ..A rational therapeutic approach that builds on these results with trastuzumab and expands the targeting of the HER network will be presented...
  50. pmc Trastuzumab-resistant cells rely on a HER2-PI3K-FoxO-survivin axis and are sensitive to PI3K inhibitors
    Anindita Chakrabarty
    Departments of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
    Cancer Res 73:1190-200. 2013
    ....
  51. pmc Will PI3K pathway inhibitors be effective as single agents in patients with cancer?
    Joan T Garrett
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA
    Oncotarget 2:1314-21. 2011
    ..Thus, combination therapies that target RTKs, PI3K, and mTOR activities may be required to maximize the clinical benefit derived from treatment with these inhibitors...
  52. ncbi request reprint Challenges in the development of anti-epidermal growth factor receptor therapies in breast cancer
    Carlos L Arteaga
    Department of Medicine, Breast Cancer Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
    Semin Oncol 31:3-8. 2004
    ..A point of view regarding challenges in the development of anti-EGFR therapies for patients with breast cancer and possible approaches to overcome them is presented in this article...
  53. pmc RNA interference (RNAi) screening approach identifies agents that enhance paclitaxel activity in breast cancer cells
    Joshua A Bauer
    Department of Biochemistry, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, 2200 Pierce Avenue, Nashville, TN 37232, USA
    Breast Cancer Res 12:R41. 2010
    ..Strategies that increase sensitivity and limit resistance to paclitaxel would be of clinical use, especially for patients with triple-negative breast cancer (TNBC)...
  54. ncbi request reprint Clinical trial design and end points for epidermal growth factor receptor-targeted therapies: implications for drug development and practice
    Carlos L Arteaga
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 9:1579-89. 2003
  55. ncbi request reprint Herceptin-induced inhibition of phosphatidylinositol-3 kinase and Akt Is required for antibody-mediated effects on p27, cyclin D1, and antitumor action
    F Michael Yakes
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Res 62:4132-41. 2002
    ....
  56. pmc ErbB3 ablation impairs PI3K/Akt-dependent mammary tumorigenesis
    Rebecca S Cook
    Department of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Cancer Res 71:3941-51. 2011
    ..Our findings offer further preclinical evidence that ErbB3 ablation may be therapeutically effective in tumors where ErbB3 engages PI3K/Akt signaling...
  57. pmc ErbB2/Neu-induced, cyclin D1-dependent transformation is accelerated in p27-haploinsufficient mammary epithelial cells but impaired in p27-null cells
    Rebecca S Muraoka
    Department of Cancer Biology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Mol Cell Biol 22:2204-19. 2002
    ..These results suggest that p27(+/-) mammary epithelium may be more susceptible to oncogene-induced tumorigenesis, whereas p27-null glands, due to severely impaired cyclin D1/Cdk4 function, are more resistant to transformation...
  58. pmc Clinical development of phosphatidylinositol-3 kinase pathway inhibitors
    Carlos L Arteaga
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    Curr Top Microbiol Immunol 347:189-208. 2010
    ..These inhibitors are likely to be more effective in combination with established and other novel molecular therapies...
  59. ncbi request reprint Epidermal growth factor receptor dependence in human tumors: more than just expression?
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Oncologist 7:31-9. 2002
    ....
  60. pmc ERBB receptors in cancer: signaling from the inside
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Division of Hematology Oncology, VUMC, 2220 Pierce Avenue, 777 PRB, Nashville, TN 37232 6307, USA
    Breast Cancer Res 13:304. 2011
    ..These data highlight a novel mechanism of amplification of ERBB receptor signaling output that may contribute to embryogenesis and cancer progression...
  61. pmc Phosphatidylinositol 3-kinase and antiestrogen resistance in breast cancer
    Todd W Miller
    Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA
    J Clin Oncol 29:4452-61. 2011
    ....
  62. pmc Aromatase is phosphorylated in situ at serine-118
    Todd W Miller
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    J Steroid Biochem Mol Biol 112:95-101. 2008
    ..Our findings suggest that phosphorylation of S118 may decrease aromatase activity, presenting a mechanism whereby kinase signaling may modulate estrogen production and hormone balance...
  63. pmc A phase I-II study of combined blockade of the ErbB receptor network with trastuzumab and gefitinib in patients with HER2 (ErbB2)-overexpressing metastatic breast cancer
    Carlos L Arteaga
    Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University, 2200 Pierce Avenue, Nashville, TN 37232, USA
    Clin Cancer Res 14:6277-83. 2008
    ..To determine the safety, and efficacy of the epidermal growth factor receptor tyrosine kinase inhibitor gefitinib in combination with trastuzumab in patients with metastatic HER2-positive metastatic breast cancer...
  64. ncbi request reprint Multivariable difference gel electrophoresis and mass spectrometry: a case study on transforming growth factor-beta and ERBB2 signaling
    David B Friedman
    Mass Spectrometry Research Center, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Mol Cell Proteomics 6:150-69. 2007
    ..Several proteins with a potential role in breast cancer, such as maspin and cathepsin D, were identified as novel molecules associated with TGF-beta signaling...
  65. pmc relocating job wise? A mathematical model separates quantitatively the cytostatic and cytotoxic effects of a HER2 tyrosine kinase inhibitor
    Peter Hinow
    Department of Mathematics, Vanderbilt University, Nashville, TN 37240, USA
    Theor Biol Med Model 4:14. 2007
    ..A mathematical model was used to interpret the experimental data...
  66. pmc Transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab
    Shizhen Emily Wang
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Mol Cell Biol 28:5605-20. 2008
    ....
  67. ncbi request reprint Gene targeting of ErbB3 using a Cre-mediated unidirectional DNA inversion strategy
    Shimian Qu
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6838, USA
    Genesis 44:477-86. 2006
    ..Unidirectional DNA inversion by in vivo recombination is an effective strategy for targeted or ubiquitous gene knockout...
  68. pmc Differentiating proteomic biomarkers in breast cancer by laser capture microdissection and MALDI MS
    Melinda E Sanders
    Department of Pathology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Proteome Res 7:1500-7. 2008
    ..Several of the m/ z features used in the classifiers were identified by LC-MS/MS and two were confirmed by immunohistochemistry...
  69. pmc Dual inhibition of Type I and Type III PI3 kinases increases tumor cell apoptosis in HER2+ breast cancers
    Christian D Young
    Department of Medicine, Vanderbilt University, 2220 Pierce Avenue, Nashville, TN, 37232, USA
    Breast Cancer Res 17:148. 2015
    ..However, the impact of type III PI3K inhibition, particularly in combination with HER2 blockade or type I PI3K inhibition, remains less clear...
  70. pmc Optimal targeting of HER2-PI3K signaling in breast cancer: mechanistic insights and clinical implications
    Brent N Rexer
    Department of Medicine, Cancer Biology and Biostatistics, Breast Cancer Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Cancer Res 73:3817-20. 2013
    ..In this review the potential clinical implications of these findings are discussed...
  71. doi request reprint Impact of genomics on personalized cancer medicine
    Carlos L Arteaga
    Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 18:612-8. 2012
    ..However, for the majority of targeted therapies in development, there are still no clinical tools to determine which patients are most likely to benefit or, alternatively, be resistant de novo to these novel agents or drug combinations...
  72. doi request reprint Molecular signatures of lung cancer: defining new diagnostic and therapeutic paradigms
    Justin M Balko
    Department of Medicine, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University, Nashville, TN 37232 6307, USA
    Mol Diagn Ther 16:1-6. 2012
    ..Here, we present our opinion on the current state of the field of molecular signatures in lung cancer...
  73. pmc Trastuzumab, an appropriate first-line single-agent therapy for HER2-overexpressing metastatic breast cancer
    Carlos L Arteaga
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Breast Cancer Res 5:96-100. 2003
    ....
  74. pmc Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: mechanisms and clinical implications
    Joan T Garrett
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    Cancer Biol Ther 11:793-800. 2011
    ..In this review, we discuss how these models and mechanisms enhance our understanding of the clinical resistance to HER2-directed therapies...
  75. pmc New strategies in HER2-overexpressing breast cancer: many combinations of targeted drugs available
    Vandana Abramson
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 17:952-8. 2011
    ....
  76. ncbi request reprint Cdk inhibitor p27Kip1 and hormone dependence in breast cancer
    Carlos L Arteaga
    Departments of Medicine and Cancer Biology and Breast Cancer Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Clin Cancer Res 10:368S-71S. 2004
    ..These results imply that hormone receptor-positive tumors with low and/or cytosolic p27 respond poorly to antiestrogens and should be considered for alternative therapeutic strategies...
  77. ncbi request reprint Dual role of transforming growth factor beta in mammary tumorigenesis and metastatic progression
    Rebecca S Muraoka-Cook
    Department of Medicine, Vanderbilt University School of Medicine, and Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center, Nashville, Tennessee 37232 6307, USA
    Clin Cancer Res 11:937s-43s. 2005
    ....
  78. pmc Abrogating endocrine resistance by targeting ERα and PI3K in breast cancer
    Emily M Fox
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University Nashville, TN, USA
    Front Oncol 2:145. 2012
    ..We also discuss the need for clinical investigation of ER downregulators in combination with PI3K inhibitors...
  79. ncbi request reprint Inhibition of TGFbeta signaling in cancer therapy
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
    Curr Opin Genet Dev 16:30-7. 2006
    ..This suggests opportunities for dissecting molecular mechanisms of cross-talk as well as providing insights into possible combinatorial molecular anticancer therapies that will include TGFbeta inhibitors...
  80. pmc Why is this effective HSP90 inhibitor not being developed in HER2+ breast cancer?
    Carlos L Arteaga
    Departments of Medicine and Cancer Biology, Breast Cancer Research Program, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Clin Cancer Res 17:4919-21. 2011
    ..This combination is one of several HER2-targeted therapies that will significantly improve the outcome of patients with this subtype of breast cancer...
  81. ncbi request reprint p38 mitogen-activated protein kinase is required for TGFbeta-mediated fibroblastic transdifferentiation and cell migration
    Andrei V Bakin
    Department of Medicine, Vanderbilt University School of Medicine, 777 Preston Research Building, Nashville, TN 37232, USA
    J Cell Sci 115:3193-206. 2002
    ..These studies suggest that the p38MAPK pathway is required for TGFbeta-mediated EMT and cell migration...
  82. ncbi request reprint Overview of rationale and clinical trials with signal transduction inhibitors in lung cancer
    Carlos L Arteaga
    Department of Medicine, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232 6307, USA
    Semin Oncol 29:15-26. 2002
    ..We will review some of the more recent treatment strategies in non-small cell and small cell lung cancer targeted to dysregulated signaling pathways that are causally associated with tumor maintenance and progression...
  83. pmc Convergence of p53 and transforming growth factor beta (TGFbeta) signaling on activating expression of the tumor suppressor gene maspin in mammary epithelial cells
    Shizhen Emily Wang
    Department of Cancer Biology, Mass Spectrometry Research Center, Breast Cancer Research Program, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 282:5661-9. 2007
    ..Taken together, these data support cooperation between the p53 and TGFbeta tumor suppressor pathways in the induction of Maspin expression, thus leading to inhibition of cell migration...
  84. pmc Epidermal growth factor receptor plays a significant role in hepatocyte growth factor mediated biological responses in mammary epithelial cells
    Alyssa R Bonine-Summers
    Department of Cancer Biology, Vanderbilt lngram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6838, USA
    Cancer Biol Ther 6:561-70. 2007
    ..These results provide a novel mechanism of action for EGFR as a mediator of HGF signaling thereby linking EGFR to the oncogenic potential of c-Met in mammary carcinomas cells...
  85. ncbi request reprint Autocrine transforming growth factor-beta signaling mediates Smad-independent motility in human cancer cells
    Nancy Dumont
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 278:3275-85. 2003
    ....
  86. pmc Blockade of TGF-beta inhibits mammary tumor cell viability, migration, and metastases
    Rebecca S Muraoka
    Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 27232, USA
    J Clin Invest 109:1551-9. 2002
    ..Therefore, blockade of TGF-beta signaling may reduce tumor cell viability and migratory potential and represents a testable therapeutic approach against metastatic carcinomas...
  87. ncbi request reprint HER3 and mutant EGFR meet MET
    Carlos L Arteaga
    Nat Med 13:675-7. 2007
  88. ncbi request reprint Epidermal growth factor receptor (EGFR) antibody down-regulates mutant receptors and inhibits tumors expressing EGFR mutations
    Marianela Perez-Torres
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 281:40183-92. 2006
    ..These data suggest that cetuximab is an effective therapy against mutant EGFR-expressing cancer cells and thus can be considered in combination with other anti-EGFR molecules...
  89. ncbi request reprint Will single-time tumor profiling and a "guilt by association" approach allow us to outsmart HER2-positive breast cancer?
    Carlos L Arteaga
    Clin Cancer Res 13:1071-3. 2007
  90. ncbi request reprint TGFbeta1 -mediated epithelial to mesenchymal transition is accompanied by invasion in the SiHa cell line
    Jae Youn Yi
    Laboratory of Tissue Engineering, Korea Cancer Center Hospital, Seoul
    Eur J Cell Biol 81:457-68. 2002
    ..In conclusion, TGFbeta1 stimulated epithelial-mesenchymal transition of SiHa cells, indicating a positive role in the invasive transition of tumors...
  91. ncbi request reprint Conditional overexpression of active transforming growth factor beta1 in vivo accelerates metastases of transgenic mammary tumors
    Rebecca S Muraoka-Cook
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Cancer Res 64:9002-11. 2004
    ..Therefore, induction and/or activation of TGF-beta in hosts with established TGF-beta-responsive cancers can rapidly accelerate metastatic progression...
  92. ncbi request reprint Type I transforming growth factor beta receptor binds to and activates phosphatidylinositol 3-kinase
    Jae Youn Yi
    Department of Medicine and Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 280:10870-6. 2005
    ....
  93. pmc Expression of t-DARPP mediates trastuzumab resistance in breast cancer cells
    Abbes Belkhiri
    Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
    Clin Cancer Res 14:4564-71. 2008
    ..We have investigated the role of t-DARPP in trastuzumab resistance in ERBB2-amplified and overexpressed breast cancer cell lines...
  94. ncbi request reprint Early changes in protein expression detected by mass spectrometry predict tumor response to molecular therapeutics
    Michelle L Reyzer
    Mass Spectrometry Research Center, Department of Biochemistry, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
    Cancer Res 64:9093-100. 2004
    ..These results suggest that drug-induced early proteomic changes as measured by MALDI-MS can be used to predict the therapeutic response to established and novel therapies...
  95. pmc Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel
    Ayana Sawai
    Department of Molecular Pharmacology and Chemistry, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Cancer Res 68:589-96. 2008
    ....
  96. ncbi request reprint Selecting the right patient for tumor therapy
    Carlos L Arteaga
    Nat Med 10:577-8. 2004
  97. ncbi request reprint Critical update and emerging trends in epidermal growth factor receptor targeting in cancer
    Jose Baselga
    Medical Oncology Service, Vall d Hebron Research Institute and Vall d Hebron University Hospital, Paseo Vall d Hebron 119 129, Barcelona 08035, Spain
    J Clin Oncol 23:2445-59. 2005
    ....
  98. ncbi request reprint Human breast cancer cells selected for resistance to trastuzumab in vivo overexpress epidermal growth factor receptor and ErbB ligands and remain dependent on the ErbB receptor network
    Christoph A Ritter
    Institute of Pharmacology, University of Greifswald, Greifswald, Germany
    Clin Cancer Res 13:4909-19. 2007
    ..We have investigated mechanisms of acquired resistance to the HER2 antibody trastuzumab in BT-474 human breast cancer cells...
  99. ncbi request reprint Modeling the cancer patient with genetically engineered mice: prediction of toxicity from molecule-targeted therapies
    Reade B Roberts
    Department of Genetics, University of North Carolina, Chapel Hill, NC 27599, USA
    Cancer Cell 5:115-20. 2004
    ..Here we review and propose how genetically engineered mouse models can serve as valuable tools to predict targeted therapy toxicity, as well as to identify allelic variants that predispose individuals to side effects...
  100. ncbi request reprint ErbB receptor signaling and therapeutic resistance to aromatase inhibitors
    Incheol Shin
    Department of Cancer Biology, Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, University Medical Center, 2220 Pierce Avenue, Nashville, TN 37232, USA
    Clin Cancer Res 12:1008s-1012s. 2006
    ..These results suggest that ligand-independent recruitment of coactivator complexes to estrogen-responsive promoters as a result of HER-2 overexpression may play a role in the development of letrozole resistance...
  101. ncbi request reprint A Phase I/II Trial of trastuzumab and gefitinib in patients with Metastatic Breast Cancer that overexpresses HER2/neu (ErbB-2)
    Stacy L Moulder
    Comprehensive Breast Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA
    Clin Breast Cancer 4:142-5. 2003