Nabeel Bardeesy

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. 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
  2. pmc Obligate roles for p16(Ink4a) and p19(Arf)-p53 in the suppression of murine pancreatic neoplasia
    Nabeel Bardeesy
    Department of Adult Oncology, Dana Farber Cancer Institute, National Cancer Institute, Bethesda, Maryland, USA
    Mol Cell Biol 22:635-43. 2002
  3. ncbi request reprint Genetics and biology of pancreatic ductal adenocarcinoma
    Aram F Hezel
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Genes Dev 20:1218-49. 2006
  4. ncbi request reprint Modeling INK4/ARF tumor suppression in the mouse
    Justin H Berger
    Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Boston, MA 02114, USA
    Curr Mol Med 7:63-75. 2007
  5. pmc A mouse plasma peptide atlas as a resource for disease proteomics
    Qing Zhang
    Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
    Genome Biol 9:R93. 2008
  6. ncbi request reprint RAS unplugged: negative feedback and oncogene-induced senescence
    Nabeel Bardeesy
    Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Cell 10:451-3. 2006
  7. pmc Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer
    Nabeel Bardeesy
    Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 20:3130-46. 2006
  8. 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
  9. pmc Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms
    Aram F Hezel
    MGH Cancer Center, Simches Research Building, CPZN 4216, 185 Cambridge St, Boston, MA 02114, USA
    Mol Cell Biol 28:2414-25. 2008
  10. ncbi request reprint The LKB1 tumor suppressor negatively regulates mTOR signaling
    Reuben J Shaw
    Department of Systems Biology, Harvard Medical School and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    Cancer Cell 6:91-9. 2004

Research Grants

Detail Information

Publications59

  1. 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
    ....
  2. pmc Obligate roles for p16(Ink4a) and p19(Arf)-p53 in the suppression of murine pancreatic neoplasia
    Nabeel Bardeesy
    Department of Adult Oncology, Dana Farber Cancer Institute, National Cancer Institute, Bethesda, Maryland, USA
    Mol Cell Biol 22:635-43. 2002
    ..This genetically defined model provides insights into the molecular pathogenesis of SCA and serves as a platform for dissection of cell-specific programs of epithelial tumor suppression...
  3. ncbi request reprint Genetics and biology of pancreatic ductal adenocarcinoma
    Aram F Hezel
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Genes Dev 20:1218-49. 2006
    ..This confluence of developments offers the opportunity for accelerated discovery and the future promise of improved treatment...
  4. ncbi request reprint Modeling INK4/ARF tumor suppression in the mouse
    Justin H Berger
    Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Boston, MA 02114, USA
    Curr Mol Med 7:63-75. 2007
    ....
  5. pmc A mouse plasma peptide atlas as a resource for disease proteomics
    Qing Zhang
    Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
    Genome Biol 9:R93. 2008
    ..A major finding from this study is the identification of novel isoforms and transcript variants not previously predicted from genome analysis...
  6. ncbi request reprint RAS unplugged: negative feedback and oncogene-induced senescence
    Nabeel Bardeesy
    Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Cell 10:451-3. 2006
    ....
  7. pmc Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer
    Nabeel Bardeesy
    Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 20:3130-46. 2006
    ....
  8. 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...
  9. pmc Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms
    Aram F Hezel
    MGH Cancer Center, Simches Research Building, CPZN 4216, 185 Cambridge St, Boston, MA 02114, USA
    Mol Cell Biol 28:2414-25. 2008
    ..These genetic studies provide in vivo evidence of a key role for LKB1 in the establishment of epithelial cell polarity that is vital for pancreatic acinar cell function and viability and for the suppression of neoplasia...
  10. ncbi request reprint The LKB1 tumor suppressor negatively regulates mTOR signaling
    Reuben J Shaw
    Department of Systems Biology, Harvard Medical School and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    Cancer Cell 6:91-9. 2004
    ..These findings position aberrant mTOR activation at the nexus of these germline neoplastic conditions and suggest the use of mTOR inhibitors in the treatment of Peutz-Jeghers syndrome...
  11. ncbi request reprint LKB1 modulates lung cancer differentiation and metastasis
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 448:807-10. 2007
    ..These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis...
  12. pmc Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma
    Andrew J Aguirre
    Department of Medical Oncology, Dana Farber Cancer Institute and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Genes Dev 17:3112-26. 2003
    ..This faithful mouse model may permit the systematic analysis of genetic lesions implicated in the human disease and serve as a platform for the identification of early disease markers and for the efficient testing of novel therapies...
  13. 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...
  14. pmc Integrative genomic and proteomic analyses identify targets for Lkb1-deficient metastatic lung tumors
    Julian Carretero
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115 USA
    Cancer Cell 17:547-59. 2010
    ..These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathways that may be targeted for treatment...
  15. ncbi request reprint Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation
    Nabeel Bardeesy
    Department of Adult Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 419:162-7. 2002
    ..Together, our data rationalize several features of PJS polyposis--notably its peculiar histopathological presentation and limited malignant potential--and place Lkb1 in a distinct class of tumour suppressors...
  16. pmc The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin
    Reuben J Shaw
    Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA
    Science 310:1642-6. 2005
    ..Finally, we show that metformin, one of the most widely prescribed type 2 diabetes therapeutics, requires LKB1 in the liver to lower blood glucose levels...
  17. pmc Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway
    Jaekyoung Son
    Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Nature 496:101-5. 2013
    ..The essentiality of this pathway in PDAC and the fact that it is dispensable in normal cells may provide novel therapeutic approaches to treat these refractory tumours...
  18. pmc STAT3 plays a critical role in KRAS-induced pancreatic tumorigenesis
    Ryan B Corcoran
    Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA
    Cancer Res 71:5020-9. 2011
    ..Moreover, our work suggests that gp130 and phospho-STAT3 expression may be effective biomarkers for predicting response to JAK2 inhibitors...
  19. pmc Hippo signaling regulates differentiation and maintenance in the exocrine pancreas
    Tao Gao
    Gastroenterology Division, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Gastroenterology 144:1543-53, 1553.e1. 2013
    ..In this study, we investigated the role of the core Hippo kinases-Mst1 and Mst2-in pancreatic development and homeostasis...
  20. pmc Monitoring tumorigenesis and senescence in vivo with a p16(INK4a)-luciferase model
    Christin E Burd
    Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7264, USA
    Cell 152:340-51. 2013
    ..This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation...
  21. pmc KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs
    Alexandros Tzatsos
    Massachusetts General Hospital Cancer Center, Boston, Massachusetts, USA
    J Clin Invest 123:727-39. 2013
    ..These results defined epigenetic programs through which KDM2B subverts cellular differentiation and drives the pathogenesis of an aggressive subset of PDAC...
  22. pmc TGF-β and αvβ6 integrin act in a common pathway to suppress pancreatic cancer progression
    Aram F Hezel
    Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Res 72:4840-5. 2012
    ..Therefore, our findings indicate that αvβ6 and TGF-β act in a common tumor suppressor pathway whose pharmacologic inactivation promotes pancreatic cancer progression...
  23. pmc Mst1 and Mst2 maintain hepatocyte quiescence and suppress hepatocellular carcinoma development through inactivation of the Yap1 oncogene
    Dawang Zhou
    Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA
    Cancer Cell 16:425-38. 2009
    ..Approximately 30% of human HCCs show low Yap1(Ser127) phosphorylation and a majority exhibit loss of cleaved, activated Mst1. Mst1/2 inhibition of Yap1 is an important pathway for tumor suppression in liver relevant to human HCC...
  24. pmc The Lkb1 metabolic sensor maintains haematopoietic stem cell survival
    Sushma Gurumurthy
    Cancer Center and Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA
    Nature 468:659-63. 2010
    ..Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint...
  25. pmc Metabolic and functional genomic studies identify deoxythymidylate kinase as a target in LKB1-mutant lung cancer
    Yan Liu
    Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
    Cancer Discov 3:870-9. 2013
    ..Thus, LKB1-mutant lung cancers have deficits in nucleotide metabolism that confer hypersensitivity to DTYMK inhibition, suggesting that DTYMK is a potential therapeutic target in this aggressive subset of tumors. ..
  26. pmc LKB1 deficiency sensitizes mice to carcinogen-induced tumorigenesis
    Sushma Gurumurthy
    Massachusetts General Hospital, Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Res 68:55-63. 2008
    ..Our data indicate that Lkb1 is a potent suppressor of carcinogen-induced skin and lung cancers and that downstream targets beyond the AMPK-mTOR pathway are likely mediators of Lkb1-dependent tumor suppression...
  27. pmc SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression
    Zhihu Ding
    Belfer Institute for Applied Cancer Science, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 470:269-73. 2011
    ..This model-informed progression analysis, together with genetic, functional and translational studies, establishes SMAD4 as a key regulator of PCA progression in mice and humans...
  28. pmc Lysine-specific demethylase 2B (KDM2B)-let-7-enhancer of zester homolog 2 (EZH2) pathway regulates cell cycle progression and senescence in primary cells
    Alexandros Tzatsos
    Cancer Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA
    J Biol Chem 286:33061-9. 2011
    ....
  29. pmc YAP oncogene overexpression supercharges colon cancer proliferation
    Joseph Avruch
    Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA
    Cell Cycle 11:1090-6. 2012
    ..This interplay between overexpressed YAP and β-catenin also drives proliferation of colon cancer cells. The dispensability of YAP in normal intestine makes YAP's expression or outputs attractive targets for cancer therapy...
  30. pmc A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response
    Zhao Chen
    Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 483:613-7. 2012
    ....
  31. pmc The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stress
    Reuben J Shaw
    Department of Systems Biology, Harvard Medical School, and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 101:3329-35. 2004
    ..The role of LKB1/AMPK in the survival of a subset of genetically defined tumor cells may provide opportunities for cancer therapeutics...
  32. pmc Aberrant overexpression of satellite repeats in pancreatic and other epithelial cancers
    David T Ting
    Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA
    Science 331:593-6. 2011
    ..The overexpression of satellite transcripts in cancer may reflect global alterations in heterochromatin silencing and could potentially be useful as a biomarker for cancer detection...
  33. pmc Protein kinases of the Hippo pathway: regulation and substrates
    Joseph Avruch
    Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA
    Semin Cell Dev Biol 23:770-84. 2012
    ....
  34. pmc Inhibition of gamma-secretase activity inhibits tumor progression in a mouse model of pancreatic ductal adenocarcinoma
    Ruben Plentz
    Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA
    Gastroenterology 136:1741-9.e6. 2009
    ..We investigated the role of this pathway in PDAC progression...
  35. pmc High-resolution characterization of the pancreatic adenocarcinoma genome
    Andrew J Aguirre
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:9067-72. 2004
    ..Thus, the integration of DNA and RNA profiles provides a highly productive entry point for the discovery of genes involved in the pathogenesis of pancreatic adenocarcinoma...
  36. pmc Causes, consequences, and remedies for growth-induced solid stress in murine and human tumors
    Triantafyllos Stylianopoulos
    Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
    Proc Natl Acad Sci U S A 109:15101-8. 2012
    ..In addition to providing insights into the mechanopathology of tumors, our approach can serve as a rapid screen for stress-reducing and perfusion-enhancing drugs...
  37. pmc PTEN is a major tumor suppressor in pancreatic ductal adenocarcinoma and regulates an NF-κB-cytokine network
    Haoqiang Ying
    Belfer Institute for Applied Cancer Science, Dana Farber Cancer Institute, Boston, MA 02215, USA
    Cancer Discov 1:158-69. 2011
    ..Thus, PTEN/phosphoinositide 3-kinase (PI3K) pathway alteration is a common event in PDAC development and functions in part to strongly activate the NF-κB network, which may serve to shape the PDAC tumor microenvironment...
  38. pmc RNA sequencing of pancreatic circulating tumour cells implicates WNT signalling in metastasis
    Min Yu
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA
    Nature 487:510-3. 2012
    ..Thus, molecular analysis of CTCs may identify candidate therapeutic targets to prevent the distal spread of cancer...
  39. ncbi request reprint Pancreatic cancer biology and genetics
    Nabeel Bardeesy
    Department of Adult Oncology, Dana Farber Cancer Institute and Departments of Medicine and Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Rev Cancer 2:897-909. 2002
    ....
  40. pmc Somatic inactivation of the PHD2 prolyl hydroxylase causes polycythemia and congestive heart failure
    Yoji Andrew Minamishima
    Department of Medical Oncology, Brigham and Women s Hospital and Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 111:3236-44. 2008
    ..The latter is likely the result of hyperviscosity syndrome and volume overload, although a direct effect of chronic, high-level HIF stimulation on cardiac myocytes cannot be excluded...
  41. doi request reprint Ink4a/Arf regulation by let-7b and Hmga2: a genetic pathway governing stem cell aging
    Alexandros Tzatsos
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA
    Cell Stem Cell 3:469-70. 2008
    ....
  42. pmc Targeting cathepsin E in pancreatic cancer by a small molecule allows in vivo detection
    Edmund J Keliher
    Center for Systems Biology, Massachusetts General Hospital, Boston, MA 02114, USA
    Neoplasia 15:684-93. 2013
    ..This approach should be useful for more refined surgical staging, planning, and resection with curative intent. ..
  43. pmc Rassf family of tumor suppressor polypeptides
    Joseph Avruch
    Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA
    J Biol Chem 284:11001-5. 2009
    ..Herein, we review the binding of the Rassf polypeptides to Ras-like GTPases and the Mst1/2 kinases and their role in Rassf function...
  44. ncbi request reprint LKB1 (XEEK1) regulates Wnt signalling in vertebrate development
    Olga Ossipova
    Department of Cancer Biology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Nat Cell Biol 5:889-94. 2003
    ..These studies show that LKB1/XEEK1 is required for Wnt-beta-catenin signalling in frogs and mammals and provides novel insights into its role in vertebrate developmental patterning and carcinogenesis...
  45. pmc The WTX tumor suppressor regulates mesenchymal progenitor cell fate specification
    Annie Moisan
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA
    Dev Cell 20:583-96. 2011
    ..Furthermore, the constellation of anomalies in Wtx null mice suggests that this tumor suppressor broadly regulates MPCs in multiple tissues...
  46. pmc Pancreatic cancers require autophagy for tumor growth
    Shenghong Yang
    Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 25:717-29. 2011
    ....
  47. pmc Mutational profiling reveals PIK3CA mutations in gallbladder carcinoma
    Vikram Deshpande
    Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA
    BMC Cancer 11:60. 2011
    ..The genetics of advanced biliary tract cancers (BTC), which encompass intra- and extra-hepatic cholangiocarcinomas as well as gallbladder carcinomas, are heterogeneous and remain to be fully defined...
  48. pmc Deletion of Smad4 in fibroblasts leads to defective chondrocyte maturation and cartilage production in a TGFβ type II receptor independent manner
    Yingqi Teng
    Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Biochem Biophys Res Commun 407:633-9. 2011
    ..Our results emphasize the importance of BMP signaling pathways in the maturation and function of certain lineages of chondrocytes and offer an insight into the heterogeneity of the chondrocyte population in the body...
  49. pmc Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma
    Kimberly A Kelly
    Center for Molecular Imaging Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, United States of America
    PLoS Med 5:e85. 2008
    ..Here we sought to identify novel molecular markers and to test their potential as targeted imaging agents...
  50. pmc D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice
    Esra A Akbay
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Genes Dev 28:479-90. 2014
    ..Together, these findings indicate that inhibitors of mutant IDH2 may be beneficial in the treatment of D2HGA and suggest that 2HG produced by IDH mutant tumors has the potential to provoke a paraneoplastic condition. ..
  51. pmc Macrophages in pancreatic cancer: starting things off on the wrong track
    Xavier Deschênes-Simard
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA
    J Cell Biol 202:403-5. 2013
    ....
  52. pmc In vivo quantitative microvasculature phenotype imaging of healthy and malignant tissues using a fiber-optic confocal laser microprobe
    Ken Young Lin
    Center for Molecular Imaging Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
    Transl Oncol 1:84-94. 2008
    ..This clinically approved fiber-optic system, together with the fractal-based image analysis, can potentially be applied to characterize other tumors in vivo and may be a valuable tool to facilitate their clinical evaluation...
  53. pmc Kras(G12D) and p53 mutation cause primary intrahepatic cholangiocarcinoma
    Michael R O'Dell
    James P Wilmot Cancer Center, University of Rochester School of Medicine, Rochester, New York 14642, USA
    Cancer Res 72:1557-67. 2012
    ..These findings establish a new genetically and histopathologically faithful model of IHCC and lend experimental support to the hypothesis that IPBN and VMC are precursors to invasive cancers...
  54. pmc LKB1-AMPK axis revisited
    Filippos Kottakis
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA
    Cell Res 22:1617-20. 2012
    ..demonstrates that the LKB1-AMPK pathway can also have an unexpected positive role in tumorigenesis, acting to maintain metabolic homeostasis and attenuate oxidative stress thereby supporting the survival of cancer cells...
  55. ncbi request reprint Telomere induced senescence: end game signaling
    Aram F Hezel
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Curr Mol Med 5:145-52. 2005
    ..In addition, we discuss how the telomere-induced pathways intersect with the DNA damage response and document how the failure in either process results in unrestrained chromosomal instability...
  56. doi request reprint Loss of Lkb1 provokes highly invasive endometrial adenocarcinomas
    Cristina M Contreras
    Department of Pathology, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390 9072, USA
    Cancer Res 68:759-66. 2008
    ..This study shows that Lkb1 plays an important role in the malignant transformation of endometrium and that Lkb1 loss promotes a highly invasive phenotype...
  57. ncbi request reprint Pten constrains centroacinar cell expansion and malignant transformation in the pancreas
    Ben Z Stanger
    Howard Hughes Medical Institute and the Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA
    Cancer Cell 8:185-95. 2005
    ....
  58. doi request reprint LKB1 signaling in mesenchymal cells required for suppression of gastrointestinal polyposis
    Pekka Katajisto
    Genome Scale Biology Program and Institute of Biomedicine, Biomedicum Helsinki, 00014 University of Helsinki, Finland
    Nat Genet 40:455-9. 2008
    ..We also noted TGFbeta signaling defects in polyps of individuals with PJS, suggesting that the identified stromal-derived mechanism of tumor suppression is also relevant in PJS...
  59. pmc A mouse to human search for plasma proteome changes associated with pancreatic tumor development
    Vitor M Faca
    Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
    PLoS Med 5:e123. 2008
    ....

Research Grants1

  1. Mouse Model of Pancreatic Cancer Progression-Maintenance
    Nabeel Bardeesy; Fiscal Year: 2007
    ..An important component of my program will be my continued participation in a multidisciplinary consortium of pancreatic cancer researchers currently in the process of addressing a series of programmatic initiatives. ..