Professor, Medicine, Uniformed Services Hebert SOM
Oncology
Dr. Stanley Lipkowitz, MD
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Stanley Lipkowitz, MD is an expert in the field of Oncology. He researched medicine at Weill Cornell Medical College of Cornell University. Weill Cornell Medical College of Cornell University is ranked 18 in research and 49 in primary care medicine Stanley Lipkowitz, MD is a published MD as well. He has 76 publications published. The latest was: Chemotherapy augments TRAIL-induced apoptosis in breast cell lines.
Publications
- New insights on PI3K/AKT pathway alterations and clinical outcomes in breast cancer.
- Balancing Protein Stability and Activity in Cancer: A New Approach for Identifying Driver Mutations Affecting CBL Ubiquitin Ligase Activation.
- E3Â Ubiquitin Ligase Cbl-b Suppresses Proallergic T Cell Development and Allergic Airway Inflammation.
- Enigma Prevents Cbl-c-Mediated Ubiquitination and Degradation of RETMEN2A.
- E3 Ubiquitin Ligase Cbl-b Regulates Pten via Nedd4 in T Cells Independently of Its Ubiquitin Ligase Activity.
- Cbl exposes its RING finger.
- WEE1 inhibition sensitizes basal breast cancer cells to TRAIL-induced apoptosis.
- RINGs of good and evil: RING finger ubiquitin ligases at the crossroads of tumour suppression and oncogenesis.
- Triple negative breast cancer cell lines: one tool in the search for better treatment of triple negative breast cancer.
- ARAP1 association with CIN85 affects epidermal growth factor receptor endocytic trafficking.
- The N terminus of Cbl-c regulates ubiquitin ligase activity by modulating affinity for the ubiquitin-conjugating enzyme.
- Identification of WEE1 as a potential molecular target in cancer cells by RNAi screening of the human tyrosine kinome.
- Cbl and human myeloid neoplasms: the Cbl oncogene comes of age.
- CBL is frequently altered in lung cancers: its relationship to mutations in MET and EGFR tyrosine kinases.
- The TRAIL to targeted therapy of breast cancer.
- Pümpfrage redivivus.
- TRAIL induces apoptosis in triple-negative breast cancer cells with a mesenchymal phenotype.
- 2-methoxyestradiol mediates apoptosis through caspase-dependent and independent mechanisms in ovarian cancer cells but not in normal counterparts.
- Structural basis for ubiquitin-mediated dimerization and activation of the ubiquitin protein ligase Cbl-b.
- PPARgamma agonists follow an unknown TRAIL in lung cancer.
- TRAIL mediates apoptosis in cancerous but not normal primary cultured cells of the human reproductive tract.
- EGFRvIII undergoes activation-dependent downregulation mediated by the Cbl proteins.
- Regulating the regulator: negative regulation of Cbl ubiquitin ligases.
- Gefitinib response of erlotinib-refractory lung cancer involving meninges--role of EGFR mutation.
- Epidermal growth factor receptor expression in breast cancer.
- Randomized comparison of group versus individual genetic education and counseling for familial breast and/or ovarian cancer.
- Apoptosis and the treatment of breast cancer.
- Regulation of stem cell factor receptor signaling by Cbl family proteins (Cbl-b/c-Cbl).
- Cbl-b interacts with ubiquitinated proteins; differential functions of the UBA domains of c-Cbl and Cbl-b.
- Evaluation of biologic end points and pharmacokinetics in patients with metastatic breast cancer after treatment with erlotinib, an epidermal growth factor receptor ty...
- A conserved DpYR motif in the juxtamembrane domain of the Met receptor family forms an atypical c-Cbl/Cbl-b tyrosine kinase binding domain binding site required for su...
- N-(4-hydroxyphenyl) retinamide (4HPR) enhances TRAIL-mediated apoptosis through enhancement of a mitochondrial-dependent amplification loop in ovarian cancer cell lines.
- Thymidylate synthase as an oncogene: a novel role for an essential DNA synthesis enzyme.
- Cbl-3-deficient mice exhibit normal epithelial development.
- WW domain HECT E3s target Cbl RING finger E3s for proteasomal degradation.
- Comparative genomic organization of the cbl genes.
- The role of the ubiquitination-proteasome pathway in breast cancer: ubiquitin mediated degradation of growth factor receptors in the pathogenesis and treatment of cancer.
- CIN85 participates in Cbl-b-mediated down-regulation of receptor tyrosine kinases.
- Cutting edge: regulation of T cell activation threshold by CD28 costimulation through targeting Cbl-b for ubiquitination.
- Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cells.
- Biomarker assays in nipple aspirate fluid.
- Cbl-b-dependent coordinated degradation of the epidermal growth factor receptor signaling complex.
- Down-regulation of the erbB-2 receptor by trastuzumab (herceptin) enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in breast and ova...
- Synergistic induction of apoptosis by the combination of trail and chemotherapy in chemoresistant ovarian cancer cells.
- SETA is a multifunctional adapter protein with three SH3 domains that binds Grb2, Cbl, and the novel SB1 proteins.
- Inhibition of NF-kappaB activity enhances TRAIL mediated apoptosis in breast cancer cell lines.
- The death domain kinase RIP is essential for TRAIL (Apo2L)-induced activation of IkappaB kinase and c-Jun N-terminal kinase.
- Negative regulation of lymphocyte activation and autoimmunity by the molecular adaptor Cbl-b.
- Ubiquitin ligase activity and tyrosine phosphorylation underlie suppression of growth factor signaling by c-Cbl/Sli-1.
- cbl-b inhibits EGF-receptor-induced apoptosis by enhancing ubiquitination and degradation of activated receptors.
- cbl-3: a new mammalian cbl family protein.
- The 100-kDa proteolytic fragment of RB is retained predominantly within the nuclear compartment of apoptotic cells.
- cbl-b inhibits epidermal growth factor receptor signaling.
- Tyrosine phosphorylation and complex formation of Cbl-b upon T cell receptor stimulation.
- Chemotherapy augments TRAIL-induced apoptosis in breast cell lines.
- Serine phosphorylation of Cbl induced by phorbol ester enhances its association with 14-3-3 proteins in T cells via a novel serine-rich 14-3-3-binding motif.
- Apoptosis is associated with cleavage of a 5 kDa fragment from RB which mimics dephosphorylation and modulates E2F binding.
- Fas expression and function in normal and malignant breast cell lines.
- The protein tyrosine phosphatase DEP-1 is induced during differentiation and inhibits growth of breast cancer cells.
- Cloning and characterization of cbl-b: a SH3 binding protein with homology to the c-cbl proto-oncogene.
- Lymphocyte-specific genetic instability and cancer.
- Two new Drosophila genes related to human hematopoietic and neurogenic transcription factors.
- A comparative structural characterization of the human NSCL-1 and NSCL-2 genes. Two basic helix-loop-helix genes expressed in the developing nervous system.
- A measure of genomic instability and its relevance to lymphomagenesis.
- Interlocus V-J recombination measures genomic instability in agriculture workers at risk for lymphoid malignancies.
- NSCL-2: a basic domain helix-loop-helix gene expressed in early neurogenesis.
- Molecular characterization of NSCL, a gene encoding a helix-loop-helix protein expressed in the developing nervous system.
- Localization of murine HLH gene NSCL to chromosome 1 by use of recombinant inbred strains.
- Hybrid T cell receptor genes formed by interlocus recombination in normal and ataxia-telangiectasis lymphocytes.
- Inversion of chromosome 7 in ataxia telangiectasia is generated by a rearrangement between T-cell receptor beta and T-cell receptor gamma genes.
- Human B lymphoblastoid cell lines provide an interleukin 1-like signal for mitogen-treated T lymphocytes via direct cell contact.
- Expression of receptors for interleukin 2: Role in the commitment of T lymphocytes to proliferate.
- Cellular and growth factor requirements for activation of human T lymphocytes by neuraminidase and galactose oxidase-treated lymphoid cells.
- ONC201: Stressing tumors to death.
- Recruitment of Cbl-b to B Cell Antigen Receptor Couples Antigen Recognition to Toll-Like Receptor 9 Activation in Late Endosomes.
Schools
Weill Cornell Medical College
New York Hospital
Nci
Doctors Specialties
- Medical Oncology
- Oncology
Accepted Insurances
Education
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National Institutes of Health Clinical Center -
New York Presbyterian Hospital - Cornell Campus -
Weill Cornell Medical College of Cornell University
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