Professor of Medicine, Vanderbilt University
Oncology
Dr. Carlos L. Arteaga, MD
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Carlos Arteaga practices Oncology. He received awards:"America's Top Doctors", "America's Top Doctors for Cancer", "Elected Member" and "Whos Who in Medicine and Healthcare". Carlos L. Arteaga is also a published physician. He has 99 paper published. The most recent paper is: Systematic Prioritization of Druggable Mutations in ∼5000 Genomes Across 16 Cancer Types Using a Structural Genomics-based Approach.
Publications
- Systematic Prioritization of Druggable Mutations in ∼5000 Genomes Across 16 Cancer Types Using a Structural Genomics-based Approach.
- Drug-Resistant Brain Metastases: A Role for Pharmacology, Tumor Evolution, and Too-Late Therapy.
- HER2 missense mutations have distinct effects on oncogenic signaling and migration.
- Pitfalls in RECIST Data Extraction for Clinical Trials: Beyond the Basics.
- Collagen density and alignment in responsive and resistant trastuzumab-treated breast cancer xenografts.
- Kinome-wide functional screen identifies role of PLK1 in hormone-independent, ER-positive breast cancer.
- PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers.
- P-REX1 creates a positive feedback loop to activate growth factor receptor, PI3K/AKT and MEK/ERK signaling in breast cancer.
- Cancer Progress Report 2014.
- Quantitative optical imaging of primary tumor organoid metabolism predicts drug response in breast cancer.
- Utility of [(18) F]FLT-PET to Assess Treatment Response in Trastuzumab-Resistant and Trastuzumab-Sensitive HER2-Overexpressing Human Breast Cancer Xenografts.
- Targeting tyrosine-kinases and estrogen receptor abrogates resistance to endocrine therapy in breast cancer.
- Enabling a Genetically Informed Approach to Cancer Medicine: A Retrospective Evaluation of the Impact of Comprehensive Tumor Profiling Using a Targeted Next-Generation...
- Characterization of breast cancers with PI3K mutations in an academic practice setting using SNaPshot profiling.
- Stand up to cancer phase ib study of pan-phosphoinositide-3-kinase inhibitor buparlisib with letrozole in estrogen receptor-positive/human epidermal growth factor rece...
- ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics.
- Molecular profiling of the residual disease of triple-negative breast cancers after neoadjuvant chemotherapy identifies actionable therapeutic targets.
- Evaluating HER2 amplification status and acquired drug resistance in breast cancer cells using Raman spectroscopy.
- Progress in breast cancer: overview.
- Mouse models and anti-HER2 therapies.
- Activation of MAPK pathways due to DUSP4 loss promotes cancer stem cell-like phenotypes in basal-like breast cancer.
- Combination of Antibody That Inhibits Ligand-Independent HER3 Dimerization and a p110α Inhibitor Potently Blocks PI3K Signaling and Growth of HER2+ Breast Cancers.
- Optical metabolic imaging identifies glycolytic levels, subtypes, and early-treatment response in breast cancer.
- Human Breast Cancer Cells Harboring a Gatekeeper T798M Mutation in HER2 Overexpress EGFR Ligands and Are Sensitive to Dual Inhibition of EGFR and HER2.
- An Antibody That Locks HER3 in the Inactive Conformation Inhibits Tumor Growth Driven by HER2 or Neuregulin.
- Role of inhibitors of mammalian target of rapamycin in the treatment of luminal breast cancer.
- Mutant PIK3CA accelerates HER2-driven transgenic mammary tumors and induces resistance to combinations of anti-HER2 therapies.
- Conditional Loss of ErbB3 Delays Mammary Gland Hyperplasia Induced by Mutant PIK3CA without Affecting Mammary Tumor Latency, Gene Expression, or Signaling.
- The genomic map of breast cancer: which roads lead to better targeted therapies?
- Autocrine IGF-I/insulin receptor axis compensates for inhibition of AKT in ER-positive breast cancer cells with resistance to estrogen deprivation.
- Optimal Targeting of HER2-PI3K Signaling in Breast Cancer: Mechanistic Insights and Clinical Implications.
- Lactate Dehydrogenase B: A Metabolic Marker of Response to Neoadjuvant Chemotherapy in Breast Cancer.
- Dual Blockade of HER2 in HER2-Overexpressing Tumor Cells Does Not Completely Eliminate HER3 Function.
- Trastuzumab-Resistant Cells Rely on a HER2-PI3K-FoxO-Survivin Axis and Are Sensitive to PI3K Inhibitors.
- Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance.
- The receptor tyrosine kinase ErbB3 maintains the balance between luminal and basal breast epithelium.
- Optical imaging of metabolism in HER2 overexpressing breast cancer cells.
- Will PI3K pathway inhibitors be effective as single agents in patients with cancer?
- Phosphatidylinositol 3-kinase and antiestrogen resistance in breast cancer.
- Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer.
- A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer.
- Using Tandem Mass Spectrometry in Targeted Mode to Identify Activators of Class IA PI3K in Cancer.
- ER?-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer.
- Optimizing chemotherapy-free survival for the ER/HER2-positive metastatic breast cancer patient.
- Why is this effective HSP90 inhibitor not being developed in HER2+ breast cancer?
- BIM expression in treatment-naive cancers predicts responsiveness to kinase inhibitors.
- When tumor suppressor TGF? meets the HER2 (ERBB2) oncogene.
- ErbB3 ablation impairs PI3K/Akt-dependent mammary tumorigenesis.
- Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: mechanisms and clinical implications.
- A gene expression signature from human breast cancer cells with acquired hormone independence identifies MYC as a mediator of antiestrogen resistance.
- Transcriptional and posttranslational up-regulation of HER3 (ErbB3) compensates for inhibition of the HER2 tyrosine kinase.
- Trastuzumab has preferential activity against breast cancers driven by HER2 homodimers.
- New strategies in HER2-overexpressing breast cancer: many combinations of targeted drugs available.
- Feedback upregulation of HER3 (ErbB3) expression and activity attenuates antitumor effect of PI3K inhibitors.
- Hyperactivation of phosphatidylinositol-3 kinase promotes escape from hormone dependence in estrogen receptor-positive human breast cancer.
- Does lapatinib work against HER2-negative breast cancers?
- Linking changes in epithelial morphogenesis to cancer mutations using computational modeling.
- Inhibition of mammalian target of rapamycin is required for optimal antitumor effect of HER2 inhibitors against HER2-overexpressing cancer cells.
- Microenvironmental independence associated with tumor progression.
- Brain metastasis: opportunities in basic and translational research.
- Inhibition of PI3K and MEK: it is all about combinations and biomarkers.
- Imaging biomarkers predict response to anti-HER2 (ErbB2) therapy in preclinical models of breast cancer.
- ERBB1 and ERBB2 have distinct functions in tumor cell invasion and intravasation.
- Loss of Phosphatase and Tensin homologue deleted on chromosome 10 engages ErbB3 and insulin-like growth factor-I receptor signaling to promote antiestrogen resistance ...
- A molecular imaging paradigm to rapidly profile response to angiogenesis-directed therapy in small animals.
- Design of isoform-selective phospholipase D inhibitors that modulate cancer cell invasiveness.
- Transforming growth factor beta induces clustering of HER2 and integrins by activating Src-focal adhesion kinase and receptor association to the cytoskeleton.
- Overcoming resistance to tyrosine kinase inhibitors: lessons learned from cancer cells treated with EGFR antagonists.
- Erlotinib attenuates homologous recombinational repair of chromosomal breaks in human breast cancer cells.
- 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.
- Knockdown of the transforming growth factor-beta type III receptor impairs motility and invasion of metastatic cancer cells.
- Transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to tr...
- Expression of t-DARPP mediates trastuzumab resistance in breast cancer cells.
- Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins.
- Does gefitinib shorten lung cancer survival? Chaos redux.
- Differentiating proteomic biomarkers in breast cancer by laser capture microdissection and MALDI MS.
- Short preoperative treatment with erlotinib inhibits tumor cell proliferation in hormone receptor-positive breast cancers.
- Ligand-independent phosphorylation of Y869 (Y845) links mutant EGFR signaling to stat-mediated gene expression.
- Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel.
- Modulation of NFkappaB activity and E-cadherin by the type III transforming growth factor beta receptor regulates cell growth and motility.
- 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...
- Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer.
- HER3 and mutant EGFR meet MET.
- Inhibition of TGF-beta with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression.
- Epidermal growth factor receptor plays a significant role in hepatocyte growth factor mediated biological responses in mammary epithelial cells.
- Convergence of p53 and transforming growth factor beta (TGFbeta) signaling on activating expression of the tumor suppressor gene maspin in mammary epithelial cells.
- Will single-time tumor profiling and a "guilt by association" approach allow us to outsmart HER2-positive breast cancer?
- Multivariable difference gel electrophoresis and mass spectrometry: a case study on transforming growth factor-beta and ERBB2 signaling.
- Epidermal growth factor receptor (EGFR) antibody down-regulates mutant receptors and inhibits tumors expressing EGFR mutations.
- HER2/Neu (ErbB2) signaling to Rac1-Pak1 is temporally and spatially modulated by transforming growth factor beta.
- Gene targeting of ErbB3 using a Cre-mediated unidirectional DNA inversion strategy.
- A novel histology-directed strategy for MALDI-MS tissue profiling that improves throughput and cellular specificity in human breast cancer.
- Can trastuzumab be effective against tumors with low HER2/Neu (ErbB2) receptors?
- Inhibition of transforming growth factor-beta signaling in human cancer: targeting a tumor suppressor network as a therapeutic strategy.
- Association with HSP90 inhibits Cbl-mediated down-regulation of mutant epidermal growth factor receptors.
- HER2 kinase domain mutation results in constitutive phosphorylation and activation of HER2 and EGFR and resistance to EGFR tyrosine kinase inhibitors.
- EGF receptor mutations in lung cancer: from humans to mice and maybe back to humans.
- Reduction of cytosolic p27(Kip1) inhibits cancer cell motility, survival, and tumorigenicity.
Schools
Universidad De Guayaquil Facultad De Ciencias Medicas
Grady Memorial Hospital
University Tex Health Science Center
Doctors Specialties
- Hematology
- Medical Oncology
- Oncology
Accepted Insurances
Awards
- America's Top Doctors
- America's Top Doctors for Cancer
- Elected Member
- Whos Who in Medicine and Healthcare
Education
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University of Texas Health Science Center -
Emory University
Hospital
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Vanderbilt Hospital and Clinics
Drug Facts
| NPI NUMBER | 1902980014 | |
| NPPES Provider LastName | ARTEAGA | |
| NPPES Provider FirstName | CARLOS | |
| NPPES Provider ZIPCode | 372326307 | |
| NPPES Provider State | TN | |
| Specialty Description | Medical Oncology | |
| Total Claim Count | 55.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1902980014 |
| Last Name Of The Provider | ARTEAGA |
| First Name Of The Provider | CARLOS |
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