L Chin

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Malignant melanoma: genetics and therapeutics in the genomic era
    Lynda Chin
    Melanoma Program, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 20:2149-82. 2006
  2. ncbi request reprint A comparison of DNA copy number profiling platforms
    Joel Greshock
    Translational Medicine, GlaxoSmithKline, King of Prussia, Pennsylvania, USA
    Cancer Res 67:10173-80. 2007
  3. pmc Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis
    C Nogueira
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA
    Oncogene 29:6222-32. 2010
  4. pmc Melanoma genome sequencing reveals frequent PREX2 mutations
    Michael F Berger
    The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA
    Nature 485:502-6. 2012
  5. pmc Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development
    Ruprecht Wiedemeyer
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 13:355-64. 2008
  6. pmc Making sense of cancer genomic data
    Lynda Chin
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 25:534-55. 2011
  7. doi request reprint Cancer genomics: from discovery science to personalized medicine
    Lynda Chin
    Belfer Institute for Applied Cancer Science, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Nat Med 17:297-303. 2011
  8. ncbi request reprint The genetics of malignant melanoma: lessons from mouse and man
    Lynda Chin
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Rev Cancer 3:559-70. 2003
  9. ncbi request reprint Flipping the oncogene switch: illumination of tumor maintenance and regression
    L Chin
    Departments of Adult Oncology, Dana Farber Cancer Institute, Department of Dermatology, Harvard Medical School, Boston, MA 02115, USA
    Trends Genet 16:147-50. 2000
  10. ncbi request reprint Essential role for oncogenic Ras in tumour maintenance
    L Chin
    Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 400:468-72. 1999

Detail Information

Publications86

  1. ncbi request reprint Malignant melanoma: genetics and therapeutics in the genomic era
    Lynda Chin
    Melanoma Program, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 20:2149-82. 2006
    ..In addition, we look forward toward how these new insights will impact on therapeutic options for metastatic melanoma in the near future...
  2. ncbi request reprint A comparison of DNA copy number profiling platforms
    Joel Greshock
    Translational Medicine, GlaxoSmithKline, King of Prussia, Pennsylvania, USA
    Cancer Res 67:10173-80. 2007
    ..Availability of these comparison results should guide study design decisions and facilitate further computational development...
  3. pmc Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis
    C Nogueira
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA
    Oncogene 29:6222-32. 2010
    ..Thus, Pten inactivation can drive the genesis and promote the metastatic progression of RAS activated Ink4a/Arf deficient melanomas...
  4. pmc Melanoma genome sequencing reveals frequent PREX2 mutations
    Michael F Berger
    The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA
    Nature 485:502-6. 2012
    ..Thus, whole-genome sequencing of human melanoma tumours revealed genomic evidence of ultraviolet pathogenesis and discovered a new recurrently mutated gene in melanoma...
  5. pmc Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development
    Ruprecht Wiedemeyer
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 13:355-64. 2008
    ....
  6. pmc Making sense of cancer genomic data
    Lynda Chin
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 25:534-55. 2011
    ....
  7. doi request reprint Cancer genomics: from discovery science to personalized medicine
    Lynda Chin
    Belfer Institute for Applied Cancer Science, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Nat Med 17:297-303. 2011
    ..In this Perspective, we emphasize the importance of establishing the biological relevance of a cancer genomic discovery in realizing its clinical potential and discuss some of the major obstacles to moving from the bench to the bedside...
  8. ncbi request reprint The genetics of malignant melanoma: lessons from mouse and man
    Lynda Chin
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Rev Cancer 3:559-70. 2003
    ....
  9. ncbi request reprint Flipping the oncogene switch: illumination of tumor maintenance and regression
    L Chin
    Departments of Adult Oncology, Dana Farber Cancer Institute, Department of Dermatology, Harvard Medical School, Boston, MA 02115, USA
    Trends Genet 16:147-50. 2000
    ....
  10. ncbi request reprint Essential role for oncogenic Ras in tumour maintenance
    L Chin
    Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 400:468-72. 1999
    ..Our results provide genetic evidence that H-RasV12G is important in both the genesis and maintenance of solid tumours...
  11. pmc Translating insights from the cancer genome into clinical practice
    Lynda Chin
    Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nature 452:553-63. 2008
    ....
  12. ncbi request reprint Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation
    K K Wong
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Nat Genet 26:85-8. 2000
    ..Our findings establish a intimate relationship between functionally intact telomeres and the genomic, cellular and organismal response to ionizing radiation...
  13. ncbi request reprint Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
    S E Artandi
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 406:641-5. 2000
    ..Our data suggest a model in which telomere dysfunction brought about by continual epithelial renewal during life generates the massive ploidy changes associated with the development of epithelial cancers...
  14. pmc Excessive tumor-elaborated VEGF and its neutralization define a lethal paraneoplastic syndrome
    A K Wong
    Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:7481-6. 2001
    ..Thus, our findings in the mouse have suggested an etiologic role for VEGF in this disease and may lead to diagnostic and therapeutic options for this debilitating condition in humans...
  15. ncbi request reprint Pten and p53 converge on c-Myc to control differentiation, self-renewal, and transformation of normal and neoplastic stem cells in glioblastoma
    H Zheng
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard MedicalSchool, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Cold Spring Harb Symp Quant Biol 73:427-37. 2008
    ....
  16. ncbi request reprint Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions
    N E Sharpless
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 8:1187-96. 2001
    ..Together, these findings support the view that loss of a single lig4 allele results in NHEJ activity being sufficiently reduced to engender chromosomal aberrations that drive non-lymphoid tumorigenesis...
  17. pmc Dual inactivation of RB and p53 pathways in RAS-induced melanomas
    N Bardeesy
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 21:2144-53. 2001
    ..Together, these data validate a role for p53 inactivation in melanomagenesis and suggest that both the RB and p53 pathways function to suppress melanocyte transformation in vivo in the mouse...
  18. pmc Telomere dysfunction alters the chemotherapeutic profile of transformed cells
    K H Lee
    Department of Adult Oncology, Dana-Farber Cancer Institute, Departments of Medicine and Genetics, and Dermatology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:3381-6. 2001
    ..Together, these results point to the combined use of DSB-inducing agents and telomere maintenance inhibition as an effective anticancer therapeutic approach particularly in cells with intact p53-dependent checkpoint responses...
  19. pmc Integrative genome comparison of primary and metastatic melanomas
    Omar Kabbarah
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 5:e10770. 2010
    ....
  20. ncbi request reprint Genetic dissection of melanoma pathways in the mouse
    F C Yang
    Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Mayer 448, Boston, MA 02115, USA
    Semin Cancer Biol 11:261-8. 2001
    ..These experimental findings suggest that both RB and p53 pathways function to suppress melanocyte transformation in vivo in the mouse...
  21. ncbi request reprint Modeling malignant melanoma in mice: pathogenesis and maintenance
    L Chin
    Department of Dermatology, Harvard Medical School, Department of Adult Oncology, Dana Farber Cancer Institute, 44 Binney Street, M413 Boston, Massachusetts, MA 02115, USA
    Oncogene 18:5304-10. 1999
  22. ncbi request reprint p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis
    L Chin
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell 97:527-38. 1999
    ....
  23. ncbi request reprint Reduction of cardiac volume in left-breast treatment fields by respiratory maneuvers: a CT study
    H M Lu
    Joint Center for Radiation Therapy, Harvard Medical School, Boston, MA 02215, USA
    Int J Radiat Oncol Biol Phys 47:895-904. 2000
    ..In the present study, we evaluated the heart volume in the fields and, thus, the true benefit of this respiratory maneuver in breast cancer patients undergoing CT simulation...
  24. ncbi request reprint A dosimetric comparison of two multileaf collimator designs
    J H Killoran
    Department of Radiation Oncology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA
    Med Phys 29:1752-8. 2002
    ..However, the SF-MLC has a noticeably sharper penumbra, which we attribute to its position further from the source. We conclude that these results are relevant for accurate dosimetric modeling of these devices...
  25. ncbi request reprint Virtual light field projection for CT-simulation
    H M Lu
    Joint Center for Radiation Therapy, Harvard Medical School, Boston, Massachusetts 02215, USA
    Med Phys 26:1222-9. 1999
    ..Based on the measured data, the overall accuracy of the portal localization system is estimated to be +/-2 mm. The system has been in clinical use for our CT simulator...
  26. ncbi request reprint A technique for optimization of digitally reconstructed radiographs of the chest in virtual simulation
    J H Killoran
    Longwood Radiation Oncology Center, Department of Radiation Oncology, Harvard Medical School, Boston, MA, USA
    Int J Radiat Oncol Biol Phys 49:231-9. 2001
    ..We present techniques to improve DRR quality for clinical purposes. The results of two approaches to DRR optimization are presented...
  27. pmc Oncogenic B-RAF negatively regulates the tumor suppressor LKB1 to promote melanoma cell proliferation
    Bin Zheng
    Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Mol Cell 33:237-47. 2009
    ..Our findings provide a molecular linkage between the LKB1-AMPK and the RAF-MEK-ERK pathways and suggest that suppression of LKB1 function by B-RAF V600E plays an important role in B-RAF V600E-driven tumorigenesis...
  28. pmc Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastoma
    Alexander H Stegh
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 21:98-111. 2007
    ..Thus, Bcl2L12 contributes to the classical tumor biological features of GBM such as intense apoptosis resistance and florid necrosis, and may provide a target for enhanced therapeutic responsiveness of this lethal cancer...
  29. ncbi request reprint Advances in malignant melanoma: genetic insights from mouse and man
    Omar Kabbarah
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Front Biosci 11:928-42. 2006
    ..With the rapid improvements in drug design, these recent advances are generating optimism for the development of better therapeutic options for melanoma patients...
  30. ncbi request reprint What drives intense apoptosis resistance and propensity for necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional cell death regulator
    Alexander H Stegh
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cell Cycle 7:2833-9. 2008
    ....
  31. ncbi request reprint Comparative oncogenomics identifies NEDD9 as a melanoma metastasis gene
    Minjung Kim
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cell 125:1269-81. 2006
    ..Thus, comparative oncogenomics has enabled the identification and facilitated the validation of a highly relevant cancer gene governing metastatic potential in human melanoma...
  32. pmc Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastoma
    Alexander H Stegh
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:10703-8. 2008
    ..Thus, alphaB-crystallin is a Bcl2L12-induced oncoprotein that enables Bcl2L12 to block the activation of both effector caspases via distinct mechanisms, thereby contributing to GBM pathogenesis and its hallmark biological properties...
  33. pmc Genomic alterations link Rho family of GTPases to the highly invasive phenotype of pancreas cancer
    Alec C Kimmelman
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:19372-7. 2008
    ..Like RIOK3, PAK4 promotes pancreas ductal cell motility and invasion. Together, the genomic and functional profiles establish the Rho family GTP-binding proteins as integral to the hallmark invasive nature of this lethal disease...
  34. ncbi request reprint Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entities
    Elizabeth A Maher
    Center for Neuro Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 66:11502-13. 2006
    ..We conclude that glioblastoma is composed of at least three distinct molecular subtypes, including novel subgroups of secondary glioblastoma, which may benefit from different therapeutic strategies...
  35. ncbi request reprint Common and contrasting genomic profiles among the major human lung cancer subtypes
    G Tonon
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cold Spring Harb Symp Quant Biol 70:11-24. 2005
    ..These findings suggest that the AC and SCC subtypes may arise from a common cell of origin and they are driven to their distinct phenotypic end points by altered expression of a limited number of key genes such as p63...
  36. ncbi request reprint High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patients
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:313-25. 2006
    ....
  37. pmc High-resolution genomic profiles of human lung cancer
    Giovanni Tonon
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:9625-30. 2005
    ..Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer...
  38. pmc Pattern of retinoblastoma pathway inactivation dictates response to CDK4/6 inhibition in GBM
    W Ruprecht Wiedemeyer
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:11501-6. 2010
    ..More generally, these observations demonstrate that the integration of genomic, functional and pharmacologic data can be exploited to inform the development of targeted therapy directed against specific cancer pathways...
  39. pmc Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice
    Mingjian James You
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:1455-60. 2002
    ..This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo...
  40. pmc BRAF activation initiates but does not maintain invasive prostate adenocarcinoma
    Joseph H Jeong
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 3:e3949. 2008
    ....
  41. pmc Role of epidermal growth factor receptor signaling in RAS-driven melanoma
    Nabeel Bardeesy
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Mol Cell Biol 25:4176-88. 2005
    ..Thus, this inducible tumor model system permits the identification and validation of alternative points of therapeutic intervention without neutralization of the primary genetic lesion...
  42. doi request reprint The brothers RAF
    Lawrence N Kwong
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cell 140:180-2. 2010
    ..In this issue, Heidorn et al. (2010) find that a class of targeted molecular therapies with clinical effectiveness against one melanoma subtype may have adverse clinical effects in another...
  43. pmc PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomas
    Hongwu Zheng
    Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Cell 17:497-509. 2010
    ..The identification of PLAGL2 as a glioma oncogene highlights the importance of a growing class of cancer genes functioning to impart stem cell-like characteristics in malignant cells...
  44. pmc p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation
    Hongwu Zheng
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 455:1129-33. 2008
    ....
  45. pmc Targeting EGFR induced oxidative stress by PARP1 inhibition in glioblastoma therapy
    Masayuki Nitta
    Department of Radiation Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS ONE 5:e10767. 2010
    ..These observations suggest that oxidative stress secondary to EGFR hyper-activation necessitates increased cellular reliance on PARP1 mediated BER, and offer critical insights into clinical trial design...
  46. pmc Growth factors and oncogenes as targets in melanoma: lost in translation?
    Lawrence Kwong
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Adv Dermatol 23:99-129. 2007
  47. ncbi request reprint A genome-wide screen reveals functional gene clusters in the cancer genome and identifies EphA2 as a mitogen in glioblastoma
    Fenghua Liu
    Department of Neurological Surgery, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Cancer Res 66:10815-23. 2006
    ..This novel genome-wide approach greatly expanded the list of target genes in glioblastoma and represents a powerful new strategy to identify the upstream determinants of tumor phenotype in a range of human cancers...
  48. pmc Mig-6 controls EGFR trafficking and suppresses gliomagenesis
    Haoqiang Ying
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:6912-7. 2010
    ..In GBM, the highly frequent loss of Mig-6 would therefore serve to sustain aberrant EGFR-mediated oncogenic signaling. Together, these data uncover a unique tumor suppression mechanism involving the regulation of receptor trafficking...
  49. ncbi request reprint Expression of high in normal-1 (HIN-1) and uteroglobin related protein-1 (UGRP-1) in adult and developing tissues
    Dale Porter
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Mech Dev 114:201-4. 2002
    ..The expression of HIN-1 is restricted to terminally differentiated airway epithelial cells in vivo and in vitro implicating HIN-1 in the acquisition or maintenance of terminally differentiated epithelial phenotype...
  50. ncbi request reprint Telomere dysfunction provokes regional amplification and deletion in cancer genomes
    Rónán C O'Hagan
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 2:149-55. 2002
    ..This model provides a platform for discovery of genes responsible for the major cancers affecting aged humans...
  51. pmc Balanced-PCR amplification allows unbiased identification of genomic copy changes in minute cell and tissue samples
    Gang Wang
    Department of Radiation Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Nucleic Acids Res 32:e76. 2004
    ..Balanced-PCR allows amplification and recovery of modestly degraded genomic DNA for subsequent retrospective analysis of human tumors with known outcomes...
  52. ncbi request reprint Revealing the genomic heterogeneity of melanoma
    Omar Kabbarah
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell 8:439-41. 2005
    ....
  53. ncbi request reprint In vivo assessment of RAS-dependent maintenance of tumor angiogenesis by real-time magnetic resonance imaging
    Yi Tang
    Center for Molecular Imaging Research, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Cancer Res 65:8324-30. 2005
    ....
  54. ncbi request reprint A genetic screen for candidate tumor suppressors identifies REST
    Thomas F Westbrook
    Howard Hughes Medical Institute, Department of Genetics, Harvard Partners Center for Genetics and Genomics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
    Cell 121:837-48. 2005
    ..These results implicate REST as a human tumor suppressor and provide a novel approach to identifying candidate genes that suppress the development of human cancer...
  55. pmc mTORC1-dependent and -independent regulation of stem cell renewal, differentiation, and mobilization
    Boyi Gan
    Department of Medical Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:19384-9. 2008
    ..Thus, TSC1 is a critical regulator of HSC self-renewal, mobilization, and multilineage development and executes these actions via both mTORC1-dependent and -independent pathways...
  56. pmc FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis
    Ji Hye Paik
    Department of Medical Oncology, Belfer Institute for Applied Cancer Science, Harvard Medical School, Boston, MA 02115, USA
    Cell Stem Cell 5:540-53. 2009
    ..Thus, the FoxO family coordinately regulates diverse genes and pathways to govern key aspects of NSC homeostasis in the mammalian brain...
  57. doi request reprint The metastasis problem gets stickier
    Lawrence N Kwong
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Cell 15:1-2. 2009
    ..evaluate candidate oncogenes in a recurrent amplification in poor-prognosis breast cancers. They identify and validate the prometastatic gene metadherin (MTDH) as a key modulator of endothelial adhesion and chemoresistance...
  58. ncbi request reprint Molecular characterization of the tumor microenvironment in breast cancer
    Minna Allinen
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 6:17-32. 2004
    ..Thus, chemokines may play a role in breast tumorigenesis by acting as paracrine factors...
  59. ncbi request reprint High-resolution global profiling of genomic alterations with long oligonucleotide microarray
    Cameron Brennan
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 64:4744-8. 2004
    ....
  60. ncbi request reprint Both products of the mouse Ink4a/Arf locus suppress melanoma formation in vivo
    Norman Edward Sharpless
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street M413, Boston, MA 02115, USA
    Oncogene 22:5055-9. 2003
    ..These genetic studies provide definitive proof that p16INK4a and p19ARF cooperate to suppress the development of melanoma in vivo...
  61. ncbi request reprint Frequent met oncogene amplification in a Brca1/Trp53 mouse model of mammary tumorigenesis
    Gromoslaw A Smolen
    Massachusetts General Hospital Cancer Center, Harvard Medical School, 13th Street, Charlestown, MA 02129, USA
    Cancer Res 66:3452-5. 2006
    ....
  62. pmc FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis
    Ji Hye Paik
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    Cell 128:309-23. 2007
    ..Functional studies validated Sprouty2 and PBX1, among others, as FoxO-regulated mediators of endothelial cell morphogenesis and vascular homeostasis...
  63. ncbi request reprint Mutations in BRAF and KRAS converge on activation of the mitogen-activated protein kinase pathway in lung cancer mouse models
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 67:4933-9. 2007
    ..These results unveil a potential common vulnerability of BRAF and KRas mutant lung tumors that potentially affects rational deployment of MEK targeted therapies to non-small-cell lung cancer patients...
  64. ncbi request reprint Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies
    Jayne M Stommel
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Science 318:287-90. 2007
    ..Thus, effective GBM therapy may require combined regimens targeting multiple RTKs...
  65. pmc Glioma oncoprotein Bcl2L12 inhibits the p53 tumor suppressor
    Alexander H Stegh
    Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 24:2194-204. 2010
    ..Thus, Bcl2L12 is a multifunctional protein that contributes to intense therapeutic resistance of GBM through its ability to operate on two key nodes of cytoplasmic and nuclear signaling cascades...
  66. ncbi request reprint Common and distinct genomic events in sporadic colorectal cancer and diverse cancer types
    Eric S Martin
    Department of Medical Oncology, Belfer Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 67:10736-43. 2007
    ....
  67. pmc Lineage-specific transcriptional regulation of DICER by MITF in melanocytes
    Carmit Levy
    Department of Dermatology, Cutaneous Biology Research Center, Mass General Hospital, Harvard Medical School, MA 02115, USA
    Cell 141:994-1005. 2010
    ..These observations highlight a central mechanism underlying lineage-specific miRNA regulation which could exist for other cell types during development...
  68. pmc Components of the Rb pathway are critical targets of UV mutagenesis in a murine melanoma model
    Karuppiah Kannan
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:1221-5. 2003
    ..Together, these molecular and genetic data identify components of the Rb pathway as critical biological targets of UV-induced mutagenesis in the development of murine melanoma in vivo...
  69. doi request reprint Telomere dysfunction promotes genome instability and metastatic potential in a K-ras p53 mouse model of lung cancer
    Samanthi A Perera
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Carcinogenesis 29:747-53. 2008
    ..Furthermore, these findings clearly demonstrate (in an in vivo model system) the dual nature of telomere shortening as both a tumor-suppressive and tumor-promoting mechanism in lung cancer, dependent on p53 status...
  70. doi request reprint Full complexity genomic hybridization on 60-mer oligonucleotide microarrays for array comparative genomic hybridization (aCGH)
    Alexei Protopopov
    Center for Applied Cancer Science, Belfer Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Methods Mol Biol 439:87-100. 2008
    ..Here, we describe the optimized technical protocol for comparative genomic hybridization with full-complexity genomic DNA on 60-mer oligonucleotide microarrays...
  71. pmc GOLPH3 modulates mTOR signalling and rapamycin sensitivity in cancer
    Kenneth L Scott
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Nature 459:1085-90. 2009
    ....
  72. ncbi request reprint Spontaneous uveal amelanotic melanoma in transgenic Tyr-RAS+ Ink4a/Arf-/- mice
    William H Tolleson
    Division of Biochemical Toxicology, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079, USA
    Arch Ophthalmol 123:1088-94. 2005
    ....
  73. ncbi request reprint Array comparative genome hybridization for tumor classification and gene discovery in mouse models of malignant melanoma
    Rónán C O'Hagan
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 63:5352-6. 2003
    ..Kannan, et al., Proc. Natl. Acad. Sci. USA, 21: 2003). These results are the first to establish the utility of array-CGH as a means of etiology-based tumor classification in genetically defined cancer-prone models...
  74. pmc Reprogramming of a melanoma genome by nuclear transplantation
    Konrad Hochedlinger
    Whitehead Institute for Biomedical Research, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
    Genes Dev 18:1875-85. 2004
    ..Our findings serve as a paradigm for studying the tumorigenic effect of a given cancer genome in the context of a whole animal...
  75. ncbi request reprint p16(Ink4a) in melanocyte senescence and differentiation
    Elena V Sviderskaya
    Department of Anatomy and Developmental Biology, St George s Hospital Medical School, Cranmer Terrace, London SW17 0RE, U K
    J Natl Cancer Inst 94:446-54. 2002
    ..Because senescence is believed to be an anticancer mechanism, we investigated the role of Ink4a-Arf and its individual components in melanocyte senescence...
  76. ncbi request reprint Epigenetic transdifferentiation of normal melanocytes by a metastatic melanoma microenvironment
    Elisabeth A Seftor
    Children s Memorial Research Center and Robert H Lurie Comprehensive Cancer Center at Northwestern University, Chicago, IL 60614, USA
    Cancer Res 65:10164-9. 2005
    ..This novel approach identifies specific genes involved in the transdifferentiation of melanocytes to a more aggressive phenotype, which may offer significant therapeutic value...
  77. ncbi request reprint Characterization of melanocyte-specific inducible Cre recombinase transgenic mice
    Marcus Bosenberg
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Genesis 44:262-7. 2006
    ....
  78. ncbi request reprint Malignant astrocytic glioma: genetics, biology, and paths to treatment
    Frank B Furnari
    Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, California 92093, USA
    Genes Dev 21:2683-710. 2007
    ..This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses...
  79. pmc New approaches to the biology of melanoma: a workshop of the National Institutes of Health Pathology B Study Section
    Meenhard Herlyn
    Wistar Institute, Philadelphia, Pennsylvania, USA
    Am J Pathol 161:1949-57. 2002
  80. ncbi request reprint Direct transcriptional activation of promyelocytic leukemia protein by IFN regulatory factor 3 induces the p53-dependent growth inhibition of cancer cells
    Tae Kyung Kim
    The Laboratory of Cell Growth and Function Regulation, Division of Biotechnology, College of Life Sciences and Biotechnology, School of Medicine, Korea University, Anam Dong, Seongbuk gu, Seoul 136 713, South Korea
    Cancer Res 67:11133-40. 2007
    ....
  81. pmc Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse
    Nabeel Bardeesy
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 103:5947-52. 2006
    ....
  82. ncbi request reprint The INK4a/ARF locus and melanoma
    E Sharpless
    Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Oncogene 22:3092-8. 2003
    ..In addition, the potential importance of these two pathways in mediating UV-induced melanoma genesis will be addressed via genetic and molecular evidence in the mouse...
  83. ncbi request reprint Amplification of CDK4 and MDM2 in malignant melanoma
    Viswanathan Muthusamy
    Department of Pathology, University of Vermont, Burlington, Vermont 05495, USA
    Genes Chromosomes Cancer 45:447-54. 2006
    ..These results suggest that coamplification of CDK4 and MDM2 may substitute for loss of P16INK4A and P14ARF function in a subset of melanomas...
  84. pmc Inhibitor of differentiation 4 drives brain tumor-initiating cell genesis through cyclin E and notch signaling
    Hye Min Jeon
    School of Life Sciences and Biotechnology, Korea University, Seoul 136 713, Republic of Korea
    Genes Dev 22:2028-33. 2008
    ..Thus, Id4 plays an integral role in the transformation of astrocytes via its combined actions on two-key cell cycle and differentiation regulatory molecules...
  85. pmc Nuclear cloning of embryonal carcinoma cells
    Robert H Blelloch
    Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 101:13985-90. 2004
    ..Our findings support the notion that cancer results from the deregulation of stem cells and further suggest that the genetics of ECs will reveal genes involved in stem cell self-renewal and pluripotency...

Research Grants15

  1. The genetic Basis of Melanoma Metastasis
    Lynda Chin; Fiscal Year: 2010
    ..pursue the validation of new metastasis candidates through low-complexity in vivo genetic screens followed by rigorous functional and clinical validation in human melanoma cells and melanoma specimen on TMA, respectively ..
  2. MET Activation in Melanoma Genesis and Progression
    Lynda Chin; Fiscal Year: 2002
    ..will be examined on phenotypic, molecular/genetic and genomic levels to validate a role for MET in progression, and ultimately to delineate genes and pathways critically important for tumor progression, and possibly metastasis ..
  3. The genetic Basis of Melanoma Metastasis
    Lynda Chin; Fiscal Year: 2009
    ..pursue the validation of new metastasis candidates through low-complexity in vivo genetic screens followed by rigorous functional and clinical validation in human melanoma cells and melanoma specimen on TMA, respectively ..
  4. Genomic & Genetic Characterization of Amplicons in GBMs
    Lynda Chin; Fiscal Year: 2007
    ..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
  5. The genetic Basis of Melanoma Metastasis
    Lynda Chin; Fiscal Year: 2007
    ....
  6. Genomic & Genetic Characterization of Amplicons in GBMs
    Lynda Chin; Fiscal Year: 2006
    ..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
  7. MET Activation in Melanoma Genesis and Progression
    Lynda Chin; Fiscal Year: 2006
    ..will be examined on phenotypic, molecular/genetic and genomic levels to validate a role for MET in progression, and ultimately to delineate genes and pathways critically important for tumor progression, and possibly metastasis ..
  8. Genomic & Genetic Characterization of Amplicons in GBMs
    Lynda Chin; Fiscal Year: 2005
    ..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
  9. MET Activation in Melanoma Genesis and Progression
    Lynda Chin; Fiscal Year: 2005
    ..will be examined on phenotypic, molecular/genetic and genomic levels to validate a role for MET in progression, and ultimately to delineate genes and pathways critically important for tumor progression, and possibly metastasis ..
  10. Genomic & Genetic Characterization of Amplicons in GBMs
    Lynda Chin; Fiscal Year: 2004
    ..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
  11. MET Activation in Melanoma Genesis and Progression
    Lynda Chin; Fiscal Year: 2004
    ..will be examined on phenotypic, molecular/genetic and genomic levels to validate a role for MET in progression, and ultimately to delineate genes and pathways critically important for tumor progression, and possibly metastasis ..
  12. Genomic & Genetic Characterization of Amplicons in GBMs
    Lynda Chin; Fiscal Year: 2003
    ..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
  13. MET Activation in Melanoma Genesis and Progression
    Lynda Chin; Fiscal Year: 2003
    ..will be examined on phenotypic, molecular/genetic and genomic levels to validate a role for MET in progression, and ultimately to delineate genes and pathways critically important for tumor progression, and possibly metastasis ..
  14. MOLECULAR PATHOGENESIS OF MALIGNANT MELANOMA
    Lynda Chin; Fiscal Year: 2002
    ....