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    • Todd R Golub
    • Todd R Golub

      Todd R Golub

      Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA, USA. | Harvard Medical School, Boston, MA, USA. | Division of Pediatric Hematology/Oncology, Boston ...



      KOL Resume for Todd R Golub


      Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA, USA.

      Broad Institute of MIT and Harvard, Cambridge, MA, USA


      Dana Farber Cancer Institute, Boston, MA, USA

      Harvard Medical School, Boston, Massachusetts.


      Department of Experimental Oncology at IEO, European Institute of Oncology IRCCS, Milan, Italy

      Howard Hughes Medical Institute, Chevy Chase, Maryland.

      Harvard Medical School, Boston MA, USA

      Division of Pediatric Hematology/Oncology, Boston Children’s Hospital, Boston, MA, 02115


      Broad Institute, Cambridge, MA 02142, USA

      Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA


      Broad Institute of MIT and Harvard, Cambridge, 02142 MA USA

      Dana-Farber Cancer Institute, .



      Todd R Golub: Influence Statistics

      Sample of concepts for which Todd R Golub is among the top experts in the world.
      Concept World rank
      compacted layered canvases #1
      mllcbp fusion protein #1
      63 skin samples #1
      study ebpalpha deletion #1
      dipg lsd1 #1
      signatures cell types #1
      fkbp51 androgen #1
      subclass mapping submap #1
      p53inactivating mutations cas9 #1
      polygenic etiology swedish #1
      tel cases #1
      brd9876 #1
      mlbcls stat1 #1
      unstable lessfit karyotypes #1
      occurrence telaml1 fusion #1
      xpr1 copy amplifications #1
      ezh2 inhibitors patients #1
      expression dsamkl #1
      tel rearrangement deletion #1
      supratentorial inflammatory pathways #1
      retraction author xiaoyu #1
      lipoylated protein aggregation #1
      gehts humans leukemia #1
      amplification genes hpv31b #1
      dicer1 human cancer #1
      translation link #1
      primary tumors cnas #1
      inducible cell study #1
      cnas tumor evolution #1
      gene expression application #1
      bmyb cancer #1
      mep differentiation #1
      macrophages tel #1
      screen 1739 compounds #1
      micrornas heart disease #1
      cr8 acts #1
      prism drug resource #1
      dhfr inhibitors corticosteroids #1
      leukemic genes abl #1
      human leukemia tel #1
      simple phenotypic readouts #1
      expressionbased profiles #1
      syk aml target #1
      method maestro #1
      common geneexpression signatures #1
      gsea functional pathways #1
      escrtiii filament accumulation #1
      helixloophelix hlh domain #1
      transcriptomic signature bmp4 #1
      cancers harboring loss #1


      Prominent publications by Todd R Golub

      KOL-Index: 17713

      The TEL/PDGF beta R fusion protein is the product of the t(5;12) translocation in patients with chronic myelomonocytic leukemia. The TEL/PDGF beta R is an unusual fusion of a putative transcription factor, TEL, to a receptor tyrosine kinase. The translocation fuses the amino terminus of TEL, containing the helix-loop-helix (HLH) domain, to the transmembrane and cytoplasmic domain of the PDGF beta R. We hypothesized that TEL/PDGF beta R self-association, mediated by the HLH domain of TEL, ...

      Known for Growth Factor | Transforming Protein | Myelomonocytic Leukemia | Tel Pdgf Beta | Signaling Pathways
      KOL-Index: 16412

      BACKGROUND: The JAK2V617F allele has recently been identified in patients with polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis with myeloid metaplasia (MF). Subsequent analysis has shown that constitutive activation of the JAK-STAT signal transduction pathway is an important pathogenetic event in these patients, and that enzymatic inhibition of JAK2V617F may be of therapeutic benefit in this context. However, a significant proportion of patients with ET or MF are ...

      Known for Activating Mutation | Patients Mf | Extramedullary Hematopoiesis | Myeloid Metaplasia | Thrombopoietin Receptor Mpl
      KOL-Index: 16354

      Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas. Pre-clinical studies have demonstrated that the B-RAF(V600E) mutation predicts a dependency on the mitogen-activated protein kinase (MAPK) signalling cascade in melanoma-an observation that has been validated by the success of RAF and MEK inhibitors in clinical trials. However, clinical responses to targeted anticancer therapeutics are frequently confounded by de novo ...

      Known for Raf Inhibition | Kinase Pathway | Therapeutic Strategies | Drives Resistance | Tumor Clinical Trials
      KOL-Index: 16015

      All-trans-retinoic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, promyelocytic leukemia (PML)/RA receptor alpha (RARalpha). Microarray analyses previously revealed induction of UBE1L (ubiquitin-activating enzyme E1-like) after RA treatment of NB4 APL cells. We report here that this occurs within 3 h in RA-sensitive but not RA-resistant APL cells, implicating UBE1L as a direct retinoid target. A 1.3-kb fragment of the ...

      Known for Promyelocytic Leukemia | Retinoid Target | Pml Raralpha | Apl Cells | Oncogene Proteins
      KOL-Index: 15632

      TEL is a member of the Ets family of transcription factors which are frequently rearranged in human leukemia. The mechanism of TEL-mediated transformation, however, is unknown. We report the cloning and characterization of a chromosomal translocation associated with acute myeloid leukemia which fuses TEL to the ABL tyrosine kinase. The TEL-ABL fusion confers growth factor-independent growth to the marine hematopoietic cell line Ba/F3 and transforms Rat-1 fibroblasts and primary murine ...

      Known for Abl Tyrosine Kinase | Protein Tel | Messenger Rna | Human Leukemia | Cytoskeletal Localization
      KOL-Index: 15631

      Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. By using 3T3-L1 adipocytes and oligonucleotide microarrays, we identified 142 known genes reproducibly upregulated by at least threefold after 4 h and/or 24 h of TNF-alpha treatment, and 78 known genes downregulated by at least twofold after 24 h of TNF-alpha ...

      Known for Necrosis Factor | L1 Adipocytes | Tnf Alpha | Adipocyte Gene | Insulin Receptor
      KOL-Index: 15177

      The recurrent (12;21)(p13;q22) translocation fuses the two genes TEL and AML1 that have previously been cloned from translocation breakpoints in myeloid leukemias. Using mainly reverse transcriptase-polymerase chain reaction (RT-PCR), the TEL-AML1 chimeric transcript has been observed in 22–27% of pediatric patients with acute lymphoblastic leukemia (ALL), in particular in the early B-lineage ALL subtype, making it the most common genetic lesion in these patients. The vast majority of ...

      Known for Cell Lines | Aml1 Fusion | Human Pair | Genetic Translocation | Pediatric Patients
      KOL-Index: 14489

      ICSBP (IRF-8) is a transcription factor of the IRF family expressed only in the immune system. It is induced in macrophages by gamma interferon (IFN-gamma) and contributes to macrophage functions. By interacting with Ets family protein PU.1, ICSBP binds to the IRF/Ets composite element and stimulates transcription. ICSBP binds to another DNA element, the IFN-stimulated response element (ISRE), a common target of the IRF family. Limited knowledge as to how ICSBP and other IRF proteins ...

      Known for Icsbp Tel | Ifn Gamma | Binding Protein | Histone Deacetylase | Element Isre
      KOL-Index: 14064

      Drug resistance presents a challenge to the treatment of cancer patients. Many studies have focused on cell-autonomous mechanisms of drug resistance. By contrast, we proposed that the tumour micro-environment confers innate resistance to therapy. Here we developed a co-culture system to systematically assay the ability of 23 stromal cell types to influence the innate resistance of 45 cancer cell lines to 35 anticancer drugs. We found that stroma-mediated resistance is common, ...

      Known for Innate Resistance | Brafmutant Melanoma | Tumor Microenvironment | Stromal Cell | Targeted Agents
      KOL-Index: 13880

      Chromosomal rearrangements involving band 12p13 are found in a wide variety of human leukemias but are particularly common in childhood acute lymphoblastic leukemia. The genes involved in these rearrangements, however, have not been identified. We now report the cloning of a t(12;21) translocation breakpoint involving 12p13 and 21q22 in two cases of childhood pre-B acute lymphoblastic leukemia, in which t(12;21) rearrangements were not initially apparent. The consequence of the ...

      Known for Aml1 Gene | Lymphoblastic Leukemia | Pair Cloning | Fusion Transcription Factor | Binding Proteins
      KOL-Index: 13824

      We previously identified a region of recurrent amplification on chromosome 22q11.21 in a subset of primary lung adenocarcinomas. Here we show that CRKL, encoding for an adaptor protein, is amplified and overexpressed in non-small cell lung cancer (NSCLC) cells that harbor 22q11.21 amplifications. Overexpression of CRKL in immortalized human airway epithelial cells promoted anchorage-independent growth and tumorigenicity. Oncogenic CRKL activates the SOS1-RAS-RAF-ERK and SRC-C3G-RAP1 ...

      Known for Cell Lung | Growth Factor | Inhibitor Resistance | Crkl Amplifications | Proteins Signal
      KOL-Index: 13250

      The TEL/AML1 fusion associated with t(12;21)(p13;q22) is the most common gene rearrangement in childhood leukemia, occurring in approximately 25% of pediatric acute lymphoblastic leukemia (ALL), and is associated with a favorable prognosis. For example, a cohort of pediatric patients with ALL retrospectively analyzed for the TEL/AML1 fusion treated on Dana-Farber Cancer Institute (DFCI) ALL Consortium protocols between 1980 to 1991 demonstrated a 100% relapse-free survival in ...

      Known for Aml1 Fusion | Acute Lymphoblastic | Pediatric Patients | Leukemia Tel | Favorable Prognosis
      KOL-Index: 13200

      BACKGROUND: It is a challenge to identify patients who, after undergoing potentially curative treatment for hepatocellular carcinoma, are at greatest risk for recurrence. Such high-risk patients could receive novel interventional measures. An obstacle to the development of genome-based predictors of outcome in patients with hepatocellular carcinoma has been the lack of a means to carry out genomewide expression profiling of fixed, as opposed to frozen, tissue.

      METHODS: We aimed to ...

      Known for Hepatocellular Carcinoma | Gene Expression | Fixed Tissues | Survival Liver Tissue | Analysis Paraffin

      Key People For Gene Expression

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      Todd R Golub:Expert Impact

      Concepts for whichTodd R Golubhas direct influence:Gene expression,  Cancer cells,  Prostate cancer,  Tel gene,  Cell lines,  Multiple myeloma,  Breast cancer,  Genomic evolution.

      Todd R Golub:KOL impact

      Concepts related to the work of other authors for whichfor which Todd R Golub has influence:Gene expression,  Prostate cancer,  Hepatocellular carcinoma,  Stem cells,  Cell lines,  Transcription factors,  Multiple myeloma.



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      Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA, USA. | Harvard Medical School, Boston, MA, USA. | Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, MA, USA. | Departments of Pediatric and Medic

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