Research Topics
Genomes and Genes | L ChinSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Comprehensive genomic characterization defines human glioblastoma genes and core pathwaysRoger McLendon
Nature 455:1061-8. 2008..Together, these findings establish the feasibility and power of TCGA, demonstrating that it can rapidly expand knowledge of the molecular basis of cancer...
Malignant melanoma: genetics and therapeutics in the genomic eraLynda 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...- A comparison of DNA copy number profiling platformsJoel 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... - Feedback circuit among INK4 tumor suppressors constrains human glioblastoma developmentRuprecht Wiedemeyer
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 13:355-64. 2008.... - Essential role for oncogenic Ras in tumour maintenanceL 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... - The genetics of malignant melanoma: lessons from mouse and manLynda Chin
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Rev Cancer 3:559-70. 2003.... - Flipping the oncogene switch: illumination of tumor maintenance and regressionL 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.... - Making sense of cancer genomic dataLynda Chin
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Genes Dev 25:534-55. 2011.... 
Cancer genomics: from discovery science to personalized medicineLynda 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...- Translating insights from the cancer genome into clinical practiceLynda Chin
Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Nature 452:553-63. 2008.... - Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiationK 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... - Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in miceS 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... - Excessive tumor-elaborated VEGF and its neutralization define a lethal paraneoplastic syndromeA 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... - Dual inactivation of RB and p53 pathways in RAS-induced melanomasN 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... - Pten and p53 converge on c-Myc to control differentiation, self-renewal, and transformation of normal and neoplastic stem cells in glioblastomaH 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.... - Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasisC 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... - Telomere dysfunction alters the chemotherapeutic profile of transformed cellsK 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... - Integrative genome comparison of primary and metastatic melanomasOmar Kabbarah
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
PLoS ONE 5:e10770. 2010.... - Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletionsN 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... - p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesisL Chin
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cell 97:527-38. 1999.... - Modeling malignant melanoma in mice: pathogenesis and maintenanceL 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 - A dosimetric comparison of two multileaf collimator designsJ 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... - Virtual light field projection for CT-simulationH 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... - A technique for optimization of digitally reconstructed radiographs of the chest in virtual simulationJ 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... - Reduction of cardiac volume in left-breast treatment fields by respiratory maneuvers: a CT studyH 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... - Advances in malignant melanoma: genetic insights from mouse and manOmar 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... - What drives intense apoptosis resistance and propensity for necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional cell death regulatorAlexander H Stegh
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cell Cycle 7:2833-9. 2008.... - Oncogenic B-RAF negatively regulates the tumor suppressor LKB1 to promote melanoma cell proliferationBin 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... - Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastomaAlexander 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... - Genetic dissection of melanoma pathways in the mouseF 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... - Common and contrasting genomic profiles among the major human lung cancer subtypesG 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... - Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entitiesElizabeth 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... - Genomic alterations link Rho family of GTPases to the highly invasive phenotype of pancreas cancerAlec 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... - Comparative oncogenomics identifies NEDD9 as a melanoma metastasis geneMinjung 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... - Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastomaAlexander 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... - High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patientsDaniel R Carrasco
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Cell 9:313-25. 2006.... - High-resolution genomic profiles of human lung cancerGiovanni 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... - Pattern of retinoblastoma pathway inactivation dictates response to CDK4/6 inhibition in GBMW 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... - Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in miceMingjian 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... - BRAF activation initiates but does not maintain invasive prostate adenocarcinomaJoseph H Jeong
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, United States of America
PLoS ONE 3:e3949. 2008.... - Role of epidermal growth factor receptor signaling in RAS-driven melanomaNabeel 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... - 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 - p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiationHongwu Zheng
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 455:1129-33. 2008.... - A genome-wide screen reveals functional gene clusters in the cancer genome and identifies EphA2 as a mitogen in glioblastomaFenghua 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... - Mig-6 controls EGFR trafficking and suppresses gliomagenesisHaoqiang 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... - PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomasHongwu 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... - Targeting EGFR induced oxidative stress by PARP1 inhibition in glioblastoma therapyMasayuki 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... - The brothers RAFLawrence 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... - Balanced-PCR amplification allows unbiased identification of genomic copy changes in minute cell and tissue samplesGang 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... - Telomere dysfunction provokes regional amplification and deletion in cancer genomesSandy Chang
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... - Expression of high in normal-1 (HIN-1) and uteroglobin related protein-1 (UGRP-1) in adult and developing tissuesDale 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... - FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasisJi 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... - Both products of the mouse Ink4a/Arf locus suppress melanoma formation in vivoNorman 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... - A genetic screen for candidate tumor suppressors identifies RESTThomas 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... - FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasisJi 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... - GOLPH3 modulates mTOR signalling and rapamycin sensitivity in cancerKenneth L Scott
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Nature 459:1085-90. 2009.... - Molecular characterization of the tumor microenvironment in breast cancerMinna 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... - mTORC1-dependent and -independent regulation of stem cell renewal, differentiation, and mobilizationBoyi 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... - High-resolution global profiling of genomic alterations with long oligonucleotide microarrayCameron Brennan
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Res 64:4744-8. 2004.... - The metastasis problem gets stickierLawrence 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... - In vivo assessment of RAS-dependent maintenance of tumor angiogenesis by real-time magnetic resonance imagingYi Tang
Center for Molecular Imaging Research, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
Cancer Res 65:8324-30. 2005.... - Components of the Rb pathway are critical targets of UV mutagenesis in a murine melanoma modelKaruppiah 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... - 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... - Mutations in BRAF and KRAS converge on activation of the mitogen-activated protein kinase pathway in lung cancer mouse modelsHongbin 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... - Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapiesJayne 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... - Glioma oncoprotein Bcl2L12 inhibits the p53 tumor suppressorAlexander 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... - Lineage-specific transcriptional regulation of DICER by MITF in melanocytesCarmit 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... - Common and distinct genomic events in sporadic colorectal cancer and diverse cancer typesEric 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.... - Frequent met oncogene amplification in a Brca1/Trp53 mouse model of mammary tumorigenesisGromoslaw A Smolen
Massachusetts General Hospital Cancer Center, Harvard Medical School, 13th Street, Charlestown, MA 02129, USA
Cancer Res 66:3452-5. 2006.... - Revealing the genomic heterogeneity of melanomaOmar Kabbarah
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 8:439-41. 2005.... - Telomere dysfunction promotes genome instability and metastatic potential in a K-ras p53 mouse model of lung cancerSamanthi 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... - Characterization of melanocyte-specific inducible Cre recombinase transgenic miceMarcus Bosenberg
Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
Genesis 44:262-7. 2006.... - p16(Ink4a) in melanocyte senescence and differentiationElena 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..Mutations of the INK4A-ARF locus may favor tumorigenesis from melanocytes by impairing senescence, cell differentiation, and (where ARF is disrupted) cell death... - Array comparative genome hybridization for tumor classification and gene discovery in mouse models of malignant melanomaRónán 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... - Reprogramming of a melanoma genome by nuclear transplantationKonrad 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... - Epigenetic transdifferentiation of normal melanocytes by a metastatic melanoma microenvironmentElisabeth 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... - Spontaneous uveal amelanotic melanoma in transgenic Tyr-RAS+ Ink4a/Arf-/- miceWilliam H Tolleson
Division of Biochemical Toxicology, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079, USA
Arch Ophthalmol 123:1088-94. 2005.... - The INK4a/ARF locus and melanomaE 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... - Inhibitor of differentiation 4 drives brain tumor-initiating cell genesis through cyclin E and notch signalingHye 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... - Nuclear cloning of embryonal carcinoma cellsRobert 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... - Direct transcriptional activation of promyelocytic leukemia protein by IFN regulatory factor 3 induces the p53-dependent growth inhibition of cancer cellsTae 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.... - Malignant astrocytic glioma: genetics, biology, and paths to treatmentFrank 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... - Amplification of CDK4 and MDM2 in malignant melanomaViswanathan 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... - Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouseNabeel 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.... - New approaches to the biology of melanoma: a workshop of the National Institutes of Health Pathology B Study SectionMeenhard Herlyn
Wistar Institute, Philadelphia, Pennsylvania, USA
Am J Pathol 161:1949-57. 2002
Research Grants
- The genetic Basis of Melanoma MetastasisLynda 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 ..
- Genomic & Genetic Characterization of Amplicons in GBMsLynda Chin; Fiscal Year: 2007..The highest potential candidate glioma oncogene will be further validated by rigorous in vivo transgenesis study. ..
- The genetic Basis of Melanoma MetastasisLynda Chin; Fiscal Year: 2007....
- MET Activation in Melanoma Genesis and ProgressionLynda 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 ..
- MOLECULAR PATHOGENESIS OF MALIGNANT MELANOMALynda Chin; Fiscal Year: 2002....