R Halaban

Summary

Affiliation: Yale University
Country: USA

Publications

  1. pmc Future perspectives in melanoma research. Meeting report from the "Melanoma Research: a bridge Naples-USA. Naples, December 6th-7th 2010"
    Paolo A Ascierto
    Department of Melanoma, Sarcoma, and Head and Neck Disease, Istituto Nazionale Tumori Fondazione Pascale, Naples, Italy
    J Transl Med 9:32. 2011
  2. pmc Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032
    Jill C Rubinstein
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Transl Med 8:67. 2010
  3. pmc Genome-wide methylation and expression profiling identifies promoter characteristics affecting demethylation-induced gene up-regulation in melanoma
    Jill C Rubinstein
    Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA
    BMC Med Genomics 3:4. 2010
  4. pmc Detecting copy number status and uncovering subclonal markers in heterogeneous tumor biopsies
    Fabio Parisi
    Department of Pathology and Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut, USA
    BMC Genomics 12:230. 2011
  5. pmc Integrative analysis of epigenetic modulation in melanoma cell response to decitabine: clinical implications
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut, United States of America
    PLoS ONE 4:e4563. 2009
  6. ncbi request reprint Pigmentation in melanomas: changes manifesting underlying oncogenic and metabolic activities
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520 8059, USA
    Oncol Res 13:3-8. 2002
  7. ncbi request reprint Coexpression of wild-type tyrosinase enhances maturation of temperature-sensitive tyrosinase mutants
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520 8059, USA
    J Invest Dermatol 119:481-8. 2002
  8. ncbi request reprint Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 277:14821-8. 2002
  9. ncbi request reprint Proper folding and endoplasmic reticulum to golgi transport of tyrosinase are induced by its substrates, DOPA and tyrosine
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 276:11933-8. 2001
  10. pmc Endoplasmic reticulum retention is a common defect associated with tyrosinase-negative albinism
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 97:5889-94. 2000

Research Grants

Collaborators

Detail Information

Publications35

  1. pmc Future perspectives in melanoma research. Meeting report from the "Melanoma Research: a bridge Naples-USA. Naples, December 6th-7th 2010"
    Paolo A Ascierto
    Department of Melanoma, Sarcoma, and Head and Neck Disease, Istituto Nazionale Tumori Fondazione Pascale, Naples, Italy
    J Transl Med 9:32. 2011
    ..Four topics of discussion were identified: New pathways in Melanoma, Biomarkers, Clinical Trials and New Molecules and Strategies...
  2. pmc Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032
    Jill C Rubinstein
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Transl Med 8:67. 2010
    ..Here we present evidence that a patient bearing the BRAF V600K mutation responded remarkably to PLX4032, suggesting that clinical trials should include all patients with activating BRAF V600E/K mutations...
  3. pmc Genome-wide methylation and expression profiling identifies promoter characteristics affecting demethylation-induced gene up-regulation in melanoma
    Jill C Rubinstein
    Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA
    BMC Med Genomics 3:4. 2010
    ..The cytosine analog 5-aza-2'-deoxycytidine (decitabine) induces genomic hypomethylation by inhibiting DNA methyltransferase, and is an example of an epigenetic agent that is thought to act by up-regulating silenced genes...
  4. pmc Detecting copy number status and uncovering subclonal markers in heterogeneous tumor biopsies
    Fabio Parisi
    Department of Pathology and Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut, USA
    BMC Genomics 12:230. 2011
    ..However, heterogeneity of tumor subclones dramatically complicates the task of detecting aberrations...
  5. pmc Integrative analysis of epigenetic modulation in melanoma cell response to decitabine: clinical implications
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut, United States of America
    PLoS ONE 4:e4563. 2009
    ..Our integrative analysis show that improved therapy can be achieved by comprehensive analysis of cancer cells, identified biomarkers for patient's selection and monitoring response, as well as targets for improved combination therapy...
  6. ncbi request reprint Pigmentation in melanomas: changes manifesting underlying oncogenic and metabolic activities
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520 8059, USA
    Oncol Res 13:3-8. 2002
    ..These lesions might have encountered anaerobic conditions, and have adapted to the reduced oxygen by enhanced glycolysis, leading to extracellular acidification and activation of V-ATPase...
  7. ncbi request reprint Coexpression of wild-type tyrosinase enhances maturation of temperature-sensitive tyrosinase mutants
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520 8059, USA
    J Invest Dermatol 119:481-8. 2002
    ..The results may explain the variation in pigmentation and the development of pigment later in life in patients carrying different mutant alleles of oculocutaneous albinism 1B...
  8. ncbi request reprint Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 277:14821-8. 2002
    ....
  9. ncbi request reprint Proper folding and endoplasmic reticulum to golgi transport of tyrosinase are induced by its substrates, DOPA and tyrosine
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 276:11933-8. 2001
    ..Loss of pigmentation, therefore, in tyrosinase-positive melanoma cells is a consequence of tumor-induced metabolic changes that suppress tyrosinase activity and DOPA production within these cells...
  10. pmc Endoplasmic reticulum retention is a common defect associated with tyrosinase-negative albinism
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 97:5889-94. 2000
    ..From these results we concluded that albinism, at least in part, is an ER retention disease...
  11. ncbi request reprint The regulation of normal melanocyte proliferation
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520 8059, USA
    Pigment Cell Res 13:4-14. 2000
    ..Molecular events that disrupt this tight control of pocket proteins and cause their inactivation, increase E2F transcriptional activity and confer autonomous growth on melanocytes...
  12. pmc Deregulated E2F transcriptional activity in autonomously growing melanoma cells
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520 8059, USA
    J Exp Med 191:1005-16. 2000
    ....
  13. ncbi request reprint Melanoma cell autonomous growth: the Rb/E2F pathway
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT, USA
    Cancer Metastasis Rev 18:333-43. 1999
    ..Since all pocket proteins are regulated by CDKs activity, it is likely that agents that inhibit this class of enzymes will be effective in treating melanoma patients...
  14. pmc PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT, USA
    Pigment Cell Melanoma Res 23:190-200. 2010
    ..The results suggest that the drug can confer an advantage to BRAF(WT) primary and metastatic tumor cells in vivo and provide markers for monitoring clinical responses...
  15. pmc Aberrant retention of tyrosinase in the endoplasmic reticulum mediates accelerated degradation of the enzyme and contributes to the dedifferentiated phenotype of amelanotic melanoma cells
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 94:6210-5. 1997
    ..Proteolysis of tyrosinase by proteasomes is consistent with the production of antigenic tyrosinase peptides that are presented to the immune system by major histocompatibility complex class I molecules...
  16. ncbi request reprint Rb/E2F: a two-edged sword in the melanocytic system
    Ruth Halaban
    Department of Dermatology, Yale University School of Medicine, 15 York Street, P O Box 208059, New Haven, CT, 06520 8059, USA
    Cancer Metastasis Rev 24:339-56. 2005
    ..In addition, the high E2F transcriptional activity in melanoma cells can be exploited to deliver cytotoxic molecules specifically to tumors, sparing the normal tissues...
  17. ncbi request reprint Release of cell cycle constraints in mouse melanocytes by overexpressed mutant E2F1E132, but not by deletion of p16INK4A or p21WAF1/CIP1
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Oncogene 16:2489-501. 1998
    ..Thus, mechanisms other than the loss of p16INK4A or p21WAF1/CIP1 that activate E2F may play an important role in melanomas...
  18. pmc Murine and human b locus pigmentation genes encode a glycoprotein (gp75) with catalase activity
    R Halaban
    Department of Dermatology, Yale University School of Medicine, New Haven, CT 06510
    Proc Natl Acad Sci U S A 87:4809-13. 1990
    ....
  19. pmc UV-induced ubiquitination of RNA polymerase II: a novel modification deficient in Cockayne syndrome cells
    D B Bregman
    Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 93:11586-90. 1996
    ..Alternatively, these findings may reflect a role played by the CSA and CSB gene products in transcription...
  20. ncbi request reprint Regulation of fibroblast growth factor 2 expression in melanoma cells by the c-MYB proto-oncoprotein
    M R Miglarese
    Department of Cancer, Immunology and Infectious Diseases, Pfizer Central Research, Groton, Connecticut 06340, USA
    Cell Growth Differ 8:1199-210. 1997
    ..We suggest that c-MYB contributes to FGF-2-mediated autocrine growth of melanomas by indirectly regulating the FGF-2 promoter...
  21. ncbi request reprint Recognition of activated CSF-1 receptor in breast carcinomas by a tyrosine 723 phosphospecific antibody
    M B Flick
    Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut 06520 8040, USA
    Oncogene 14:2553-61. 1997
    ..This data represents the first direct evidence of in vivo phosphorylation of CSF-1R in human breast carcinomas...
  22. pmc A Variant in a MicroRNA complementary site in the 3' UTR of the KIT oncogene increases risk of acral melanoma
    S E Godshalk
    Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT, USA
    Oncogene 30:1542-50. 2011
    ..This work identifies a novel genetic marker for increased heritable risk of melanoma...
  23. ncbi request reprint Her2/neu is not a commonly expressed therapeutic target in melanoma -- a large cohort tissue microarray study
    Harriet M Kluger
    Department of Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Melanoma Res 14:207-10. 2004
    ..Our findings suggest that drugs that specifically target Her2/neu are not likely to be useful for the treatment of metastatic melanoma or as adjuvant therapy for melanoma patients at high risk for recurrence...
  24. ncbi request reprint The tyrphostin AG1024 accelerates the degradation of phosphorylated forms of retinoblastoma protein (pRb) and restores pRb tumor suppressive function in melanoma cells
    Maria von Willebrand
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Cancer Res 63:1420-9. 2003
    ..Thus, inhibition of melanoma cell proliferation by AG1024 is mediated by inhibition of mitogen-activated protein kinase/extracellular signal-regulated kinase 2 signaling and activation of pRb by a mechanism involving protein degradation...
  25. ncbi request reprint Tyrosinase maturation and oligomerization in the endoplasmic reticulum require a melanocyte-specific factor
    Edwin Francis
    Department of Biochemistry and Molecular Biology, Program in Molecular and Cellular Biology, University of Massachusetts, Amherst, Massachusetts 01003, USA
    J Biol Chem 278:25607-17. 2003
    ..These findings suggested that oligomerization is a step in proper TYR maturation within the ER that requires melanocyte-specific factors...
  26. ncbi request reprint Carbohydrates act as sorting determinants in ER-associated degradation of tyrosinase
    Sherri Svedine
    Department of Biochemistry and Molecular Biology, Program in Molecular and Cellular Biology, University of Massachusetts, 710 North Pleasant Street, Amherst, MA 01003, USA
    J Cell Sci 117:2937-49. 2004
    ....
  27. pmc Expression of tumor necrosis factor--related apoptosis-inducing ligand receptors 1 and 2 in melanoma
    Mary M McCarthy
    Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Clin Cancer Res 12:3856-63. 2006
    ..We assessed TRAIL-R1 and TRAIL-R2 expression patterns in a large cohort of melanomas and benign nevi...
  28. ncbi request reprint Melanocyte and keratinocyte carcinogenesis: p53 family protein activities and intersecting mRNA expression profiles
    Molly Kulesz-Martin
    Department of Dermatology, Oregon Health and Science University, Portland, Oregon 97239, USA
    J Investig Dermatol Symp Proc 10:142-52. 2005
    ..Thus, clonal lineage mouse models representing early through late cancer progression stages may inform the focus on early, potentially causal events from microarray studies of human cancers, facilitating prognosis and molecular therapy...
  29. ncbi request reprint Subcellular localization of activating transcription factor 2 in melanoma specimens predicts patient survival
    Aaron J Berger
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cancer Res 63:8103-7. 2003
    ..Moreover, our findings suggest that ATF2 might be a useful prognostic marker in early-stage melanoma...
  30. ncbi request reprint Automated quantitative analysis of HDM2 expression in malignant melanoma shows association with early-stage disease and improved outcome
    Aaron J Berger
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Cancer Res 64:8767-72. 2004
    ....
  31. ncbi request reprint Expression profiling reveals novel pathways in the transformation of melanocytes to melanomas
    Keith Hoek
    Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, 15 York Street, New Haven, CT 06520 8059, USA
    Cancer Res 64:5270-82. 2004
    ..These results provide a comprehensive view of changes in advanced melanoma relative to normal melanocytes and reveal new targets that can be used in assessing prognosis, staging, and therapy of melanoma patients...
  32. ncbi request reprint Novel tyramide-based tyrosinase assay for the detection of melanoma cells in cytological preparations
    Cesar Angeletti
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Diagn Cytopathol 31:33-7. 2004
    ..This method may be a useful ancillary procedure for the resolution of challenging melanoma cases...
  33. ncbi request reprint Rab33A: characterization, expression, and suppression by epigenetic modification
    Elaine Cheng
    Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520 8059, USA
    J Invest Dermatol 126:2257-71. 2006
    ..This information is important for understanding carcinogenesis as well as other aberrant processes because Rab33A may have an important role in disorders involving X-chromosome-linked genes associated with vesicular transport...
  34. pmc Nuclear to non-nuclear Pmel17/gp100 expression (HMB45 staining) as a discriminator between benign and malignant melanocytic lesions
    Bonnie E Gould Rothberg
    Department of Pathology, Yale University School of Medicine, New Haven, CT 06520 8023, USA
    Mod Pathol 21:1121-9. 2008
    ..80 for distinguishing benign nevi from malignant melanomas. On the basis of this preliminary study, we propose that the ratio of nuclear to non-nuclear HMB45 staining may be useful for diagnostic challenges in melanocytic lesions...
  35. ncbi request reprint Roadmap for new opportunities in melanoma research
    Meenhard Herlyn
    Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA 19104, USA
    Semin Oncol 34:566-76. 2007
    ..This group provides recommendations for both short- and long-term strategies that build on research strengths and opportunities established by the many members of the research community...

Research Grants14

  1. Epigenetic Chromatin Changes as Melanoma Markers
    Ruth Halaban; Fiscal Year: 2006
    ..Altogether, the results are likely to generate a novel marker(s) that can be used to assess propensity for malignant transformation, tumor progression and/or sensitivity to chemotherapeutic drugs that target chromatin conformation. ..
  2. PROLIFERATION & MALIGNANT TRANSFORMATION OF MELANOCYTES
    Ruth Halaban; Fiscal Year: 2004
    ..Our functional studies may provide a basis for the design of new therapeutical agents for the treatment of patients with metastatic melanomas. ..
  3. 2003 Conference Pan-American Society Pigment Cell Resea
    Ruth Halaban; Fiscal Year: 2003
    ..3. To provide partial support to students and junior faculty to attend the meeting. They request funds for the 2003 meeting as well as for the 2 subsequent PASPCR annual meetings in years 2004 and 2006. ..