Joan Massague

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. pmc Epigenetic expansion of VHL-HIF signal output drives multiorgan metastasis in renal cancer
    Sakari Vanharanta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Med 19:50-6. 2013
  2. doi request reprint Ubiquitin removal in the TGF-β pathway
    Kamna Aggarwal
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nat Cell Biol 14:656-7. 2012
  3. ncbi request reprint TGFβ signalling in context
    Joan Massague
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nat Rev Mol Cell Biol 13:616-30. 2012
  4. doi request reprint A very private TGF-beta receptor embrace
    Joan Massague
    Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Mol Cell 29:149-50. 2008
  5. ncbi request reprint Smad transcription factors
    Joan Massague
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 19:2783-810. 2005
  6. pmc Genome-wide impact of the BRG1 SWI/SNF chromatin remodeler on the transforming growth factor beta transcriptional program
    Qiaoran Xi
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Biol Chem 283:1146-55. 2008
  7. pmc Ubiquitin ligase Nedd4L targets activated Smad2/3 to limit TGF-beta signaling
    Sheng Gao
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Mol Cell 36:457-68. 2009
  8. pmc TGFbeta primes breast tumors for lung metastasis seeding through angiopoietin-like 4
    David Padua
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cell 133:66-77. 2008
  9. pmc Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors
    Andy J Minn
    Cancer Biology and Genetics Program, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Clin Invest 115:44-55. 2005
  10. ncbi request reprint Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation
    Joan Seoane
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, 1300 York Avenue, New York, NY 1002, USA
    Cell 117:211-23. 2004

Collaborators

Detail Information

Publications70

  1. pmc Epigenetic expansion of VHL-HIF signal output drives multiorgan metastasis in renal cancer
    Sakari Vanharanta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Med 19:50-6. 2013
    ..Thus, metastasis in ccRCC is based on an epigenetically expanded output of the tumor-initiating pathway...
  2. doi request reprint Ubiquitin removal in the TGF-β pathway
    Kamna Aggarwal
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nat Cell Biol 14:656-7. 2012
    ..Both ubiquitin-specific peptidase-4 (USP4) and -15 (USP15) extend the life of activated receptors against the negative pressure of receptor-ubiquitinating complexes, but through distinct modes of action...
  3. ncbi request reprint TGFβ signalling in context
    Joan Massague
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nat Rev Mol Cell Biol 13:616-30. 2012
    ..However, an old mystery has endured: how does the context determine the cellular response to TGFβ? Solving this question is key to understanding TGFβ biology and its many malfunctions. Recent progress is pointing at answers...
  4. doi request reprint A very private TGF-beta receptor embrace
    Joan Massague
    Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Mol Cell 29:149-50. 2008
    ..In this issue of Molecular Cell, Groppe et al. (2008) describe the crystal structure of a six-element TGF-beta:receptor complex, addressing long-standing questions about the restrictive nature of this vital receptor interaction...
  5. ncbi request reprint Smad transcription factors
    Joan Massague
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 19:2783-810. 2005
    ..Our growing understanding of TGFbeta signaling through the Smad pathway provides general principles for how animal cells translate complex inputs into concrete behavior...
  6. pmc Genome-wide impact of the BRG1 SWI/SNF chromatin remodeler on the transforming growth factor beta transcriptional program
    Qiaoran Xi
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Biol Chem 283:1146-55. 2008
    ..Our results provide a genome-wide scope of the participation of BRG1 in TGFbeta action and suggest a widespread yet differential involvement of BRG1 SWI/SNF remodeler in the transcriptional response of many genes to this cytokine...
  7. pmc Ubiquitin ligase Nedd4L targets activated Smad2/3 to limit TGF-beta signaling
    Sheng Gao
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Mol Cell 36:457-68. 2009
    ..Previously identified as a regulator of renal sodium channels, Nedd4L is shown here to play a broader role as a general modulator of Smad turnover during TGF-beta signal transduction...
  8. pmc TGFbeta primes breast tumors for lung metastasis seeding through angiopoietin-like 4
    David Padua
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cell 133:66-77. 2008
    ....
  9. pmc Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors
    Andy J Minn
    Cancer Biology and Genetics Program, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Clin Invest 115:44-55. 2005
    ..These results suggest that the bone-specific metastatic phenotypes and gene expression signature identified in a mouse model may be clinically relevant...
  10. ncbi request reprint Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation
    Joan Seoane
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, 1300 York Avenue, New York, NY 1002, USA
    Cell 117:211-23. 2004
    ..We suggest that the activity of this network confers resistance to TGF-beta-mediated cytostasis during the development of the telencephalic neuroepithelium and in glioblastoma brain tumor cells...
  11. ncbi request reprint Distinct domain utilization by Smad3 and Smad4 for nucleoporin interaction and nuclear import
    Lan Xu
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    J Biol Chem 278:42569-77. 2003
    ....
  12. pmc Genes that mediate breast cancer metastasis to the brain
    Paula D Bos
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nature 459:1005-9. 2009
    ..This co-option of a brain sialyltransferase highlights the role of cell-surface glycosylation in organ-specific metastatic interactions...
  13. pmc A FoxO-Smad synexpression group in human keratinocytes
    Roger R Gomis
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, and Bioinformatics Core Facility, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:12747-52. 2006
    ..The composition of the FoxO-Smad synexpression group suggests that stress reactions and adaptive functions accompany the cytostatic response of keratinocytes to TGF-beta...
  14. pmc Nuclear CDKs drive Smad transcriptional activation and turnover in BMP and TGF-beta pathways
    Claudio Alarcon
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 139:757-69. 2009
    ..Thus, nuclear CDK8/9 drive a cycle of Smad utilization and disposal that is an integral part of canonical BMP and TGF-beta pathways...
  15. ncbi request reprint Balancing BMP signaling through integrated inputs into the Smad1 linker
    Gopal Sapkota
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Mol Cell 25:441-54. 2007
    ..The interplay between linker phosphorylation, Smurf-dependent ubiquitination, and nucleoporin exclusion enables regulation of BMP action by diverse signals and biological contexts...
  16. pmc WNT/TCF signaling through LEF1 and HOXB9 mediates lung adenocarcinoma metastasis
    Don X Nguyen
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cell 138:51-62. 2009
    ..For a video summary of this article, see the PaperFlick file available with the online Supplemental Data...
  17. pmc Unique players in the BMP pathway: small C-terminal domain phosphatases dephosphorylate Smad1 to attenuate BMP signaling
    Marie Knockaert
    Molecular Vertebrate Embryology Laboratory, The Rockefeller University, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:11940-5. 2006
    ..The present identification of the SCP family as Smad C-terminal phosphatases sheds light on the events that attenuate Smad signaling and reveals unexpected links to the essential phosphatases that control RNA polymerase II in eukaryotes...
  18. pmc Transforming growth factor beta-induced cell cycle arrest of human hematopoietic cells requires p57KIP2 up-regulation
    Joseph M Scandura
    Molecular Pharmacology and Chemistry Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 101:15231-6. 2004
    ..Our studies identify a molecular pathway by which TGFbeta mediates its cytostatic effects on human hematopoietic cells and suggests an explanation for the frequent silencing of p57 expression...
  19. pmc Endogenous human microRNAs that suppress breast cancer metastasis
    Sohail F Tavazoie
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nature 451:147-52. 2008
    ..miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer...
  20. ncbi request reprint Myc suppression of the p21(Cip1) Cdk inhibitor influences the outcome of the p53 response to DNA damage
    Joan Seoane
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Nature 419:729-34. 2002
    ..By inhibiting p21(Cip1) expression Myc favours the initiation of apoptosis, thereby influencing the outcome of a p53 response in favour of cell death...
  21. ncbi request reprint Serpins promote cancer cell survival and vascular co-option in brain metastasis
    Manuel Valiente
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 156:1002-16. 2014
    ..By protecting cancer cells from death signals and fostering vascular co-option, anti-PA serpins provide a unifying mechanism for the initiation of brain metastasis in lung and breast cancers. ..
  22. pmc A poised chromatin platform for TGF-β access to master regulators
    Qiaoran Xi
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 147:1511-24. 2011
    ..In turn, Smad4 increases K18 acetylation to augment TRIM33-Smad2/3 binding. Thus, nodal effectors use the H3K9me3 mark as a platform to switch master regulators of stem cell differentiation from the poised to the active state...
  23. pmc Genes that mediate breast cancer metastasis to lung
    Andy J Minn
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nature 436:518-24. 2005
    ..Others contribute to aggressive growth selectively in the lung. Many encode extracellular proteins and are of previously unknown relevance to cancer metastasis...
  24. ncbi request reprint Breast cancer cells produce tenascin C as a metastatic niche component to colonize the lungs
    Thordur Oskarsson
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Med 17:867-74. 2011
    ..These findings link TNC to pathways that support the fitness of metastasis-initiating breast cancer cells and highlight the relevance of TNC as an extracellular matrix component of the metastatic niche...
  25. doi request reprint Selection of bone metastasis seeds by mesenchymal signals in the primary tumor stroma
    Xiang H F Zhang
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 154:1060-73. 2013
    ....
  26. ncbi request reprint A multigenic program mediating breast cancer metastasis to bone
    Yibin Kang
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Cell 3:537-49. 2003
    ....
  27. ncbi request reprint Hematopoiesis controlled by distinct TIF1gamma and Smad4 branches of the TGFbeta pathway
    Wei He
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 125:929-41. 2006
    ..Thus, Smad2/3-TIF1gamma and Smad2/3-Smad4 function as complementary effector arms in the control of hematopoietic cell fate by the TGFbeta/Smad pathway...
  28. pmc Breast cancer bone metastasis mediated by the Smad tumor suppressor pathway
    Yibin Kang
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Molecular Cytology Laboratory, Memorial Sloan Kettering Cancer Center, NY 10021, USA
    Proc Natl Acad Sci U S A 102:13909-14. 2005
    ..Our findings provide functional evidence for a switch of the Smad pathway, from tumor-suppressor to prometastatic, in the development of breast cancer bone metastasis...
  29. ncbi request reprint Mad upregulation and Id2 repression accompany transforming growth factor (TGF)-beta-mediated epithelial cell growth suppression
    Peter M Siegel
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021
    J Biol Chem 278:35444-50. 2003
    ..These results argue that induction of Mad expression and Id2 down-regulation are important events during the TGF-beta cytostatic program in epithelial cells...
  30. pmc A CXCL1 paracrine network links cancer chemoresistance and metastasis
    Swarnali Acharyya
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 150:165-78. 2012
    ..This network of endothelial-carcinoma-myeloid signaling interactions provides a mechanism linking chemoresistance and metastasis, with opportunities for intervention...
  31. pmc Multimodality imaging of TGFbeta signaling in breast cancer metastases
    Inna Serganova
    Department of Neurology, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    FASEB J 23:2662-72. 2009
    ....
  32. pmc Tumor self-seeding by circulating cancer cells
    Mi Young Kim
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 139:1315-26. 2009
    ..Tumor self-seeding could explain the relationships between anaplasia, tumor size, vascularity and prognosis, and local recurrence seeded by disseminated cells following ostensibly complete tumor excision...
  33. ncbi request reprint C/EBPbeta at the core of the TGFbeta cytostatic response and its evasion in metastatic breast cancer cells
    Roger R Gomis
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Cell 10:203-14. 2006
    ..We suggest that C/EBPbeta plays a key role in the coordination of TGFbeta cytostatic gene responses, and its malfunction may trigger evasion of these responses in breast cancer...
  34. ncbi request reprint Dephosphorylation of the linker regions of Smad1 and Smad2/3 by small C-terminal domain phosphatases has distinct outcomes for bone morphogenetic protein and transforming growth factor-beta pathways
    Gopal Sapkota
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Biol Chem 281:40412-9. 2006
    ....
  35. ncbi request reprint A self-enabling TGFbeta response coupled to stress signaling: Smad engages stress response factor ATF3 for Id1 repression in epithelial cells
    Yibin Kang
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Mol Cell 11:915-26. 2003
    ..As a common target of TGFbeta/Smad signals and stress signals via p38 kinase, ATF3 additionally serves to channel synergy between these pathways in the response of epithelial cells to stress and injury...
  36. pmc TGF-β control of stem cell differentiation genes
    Joan Massague
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    FEBS Lett 586:1953-8. 2012
    ..These findings provide exciting new insights into the global role of TGF-β signaling in the regulators of stem cell fate...
  37. ncbi request reprint Smad2 nucleocytoplasmic shuttling by nucleoporins CAN/Nup214 and Nup153 feeds TGFbeta signaling complexes in the cytoplasm and nucleus
    Lan Xu
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Mol Cell 10:271-82. 2002
    ..Thus, by directly contacting the nuclear pore complex, Smad2 undergoes constant shuttling, providing a dynamic pool that is competitively drawn by cytoplasmic and nuclear signal transduction partners...
  38. pmc Latent bone metastasis in breast cancer tied to Src-dependent survival signals
    Xiang H F Zhang
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cancer Cell 16:67-78. 2009
    ..Breast cancer cells that lodge in the bone marrow succumb in this environment when deprived of Src activity...
  39. ncbi request reprint Mediators of vascular remodelling co-opted for sequential steps in lung metastasis
    Gaorav P Gupta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nature 446:765-70. 2007
    ..These findings reveal how aggressive primary tumorigenic functions can be mechanistically coupled to greater lung metastatic potential, and how such biological activities may be therapeutically targeted with specific drug combinations...
  40. pmc MicroRNA-335 inhibits tumor reinitiation and is silenced through genetic and epigenetic mechanisms in human breast cancer
    Kim J Png
    Laboratory of Systems Cancer Biology, Rockefeller University, New York, NY 10065, USA
    Genes Dev 25:226-31. 2011
    ..We furthermore identify miR-335 as a robust inhibitor of tumor reinitiation. We thus implicate the miR-335 locus on 7q32.2 as the first selective metastasis suppressor and tumor initiation suppressor locus in human breast cancer...
  41. ncbi request reprint Opposite Smad and chicken ovalbumin upstream promoter transcription factor inputs in the regulation of the collagen VII gene promoter by transforming growth factor-beta
    María Julia Calonge
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Biol Chem 279:23759-65. 2004
    ..The results suggest that TGF-beta signaling may exert tight control over COL7A1 by offsetting the balance between opposing Smad and COUP-TFs...
  42. pmc ID genes mediate tumor reinitiation during breast cancer lung metastasis
    Gaorav P Gupta
    Cancer Biology and Genetics Program, Molecular Cytology Core Facility, Human Oncology and Pathogenesis Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 104:19506-11. 2007
    ..These results shed light on the proliferative mechanisms that initiate metastatic colonization, and they implicate Id1 and Id3 as mediators of this malignant function in the TN subgroup of breast cancers...
  43. ncbi request reprint Cyclin-dependent kinase inhibitors uncouple cell cycle progression from mitochondrial apoptotic functions in DNA-damaged cancer cells
    Hong Van Le
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Biol Chem 280:32018-25. 2005
    ..These observations suggest that by blocking dysregulated cell cycle progression, CDK inhibitors can influence the sensitivity of the mitochondria to proapoptotic signals in DNA damage-induced cancer cells...
  44. pmc Platelets and metastasis revisited: a novel fatty link
    Gaorav P Gupta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
    J Clin Invest 114:1691-3. 2004
    ..A study in this issue of the JCI suggests that platelet-derived lysophosphatidic acid is coopted by aggressive breast and ovarian cancer cells as a tumor cell mitogen and promoter of osteolysis during bone metastasis...
  45. pmc Diverted total synthesis leads to the generation of promising cell-migration inhibitors for treatment of tumor metastasis: in vivo and mechanistic studies on the migrastatin core ether analog
    Thordur Oskarsson
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA
    J Am Chem Soc 132:3224-8. 2010
    ..Both in vivo and in vitro studies indicate that ME exhibits a concentration-dependent inhibitory effect on migration of breast cancer cells...
  46. pmc Breast cancer methylomes establish an epigenomic foundation for metastasis
    Fang Fang
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Sci Transl Med 3:75ra25. 2011
    ..These findings significantly enhance our understanding of breast cancer oncogenesis and aid the development of new prognostic biomarkers for this common malignancy...
  47. ncbi request reprint Cytostatic and apoptotic actions of TGF-beta in homeostasis and cancer
    Peter M Siegel
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Nat Rev Cancer 3:807-21. 2003
  48. ncbi request reprint TGF-beta directly targets cytotoxic T cell functions during tumor evasion of immune surveillance
    Dori A Thomas
    Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Cell 8:369-80. 2005
    ..We suggest that TGF-beta suppresses CTL function in vivo through an anticytotoxic program of transcriptional repression...
  49. ncbi request reprint Genetic determinants of cancer metastasis
    Don X Nguyen
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Box 116, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York 10021, USA
    Nat Rev Genet 8:341-52. 2007
    ..With knowledge cemented in decades of research into tumour-initiating events, current experimental and conceptual models are beginning to address the genetic basis for cancer colonization of distant organs...
  50. doi request reprint Roles of TGFbeta in metastasis
    David Padua
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 116, New York, NY 10065, USA
    Cell Res 19:89-102. 2009
    ..The development of TGFbeta inhibitors for clinical use will require a deeper understanding of TGFbeta signaling, its consequences, and the contexts in which it acts...
  51. pmc Transforming growth factor beta signaling impairs Neu-induced mammary tumorigenesis while promoting pulmonary metastasis
    Peter M Siegel
    Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:8430-5. 2003
    ....
  52. doi request reprint Origins of metastatic traits
    Sakari Vanharanta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cancer Cell 24:410-21. 2013
    ..Recent experimental work and high-resolution sequencing of human tissues have started to reveal the molecular and tumor evolutionary principles that underlie the emergence of metastatic traits. ..
  53. pmc Molecular pathways: VCAM-1 as a potential therapeutic target in metastasis
    Qing Chen
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Clin Cancer Res 18:5520-5. 2012
    ..S. Food and Drug Administration approval or are undergoing clinical trials. Testing these drugs against tumor-stromal leukocyte interactions may provide a new strategy to suppress lung and bone relapse of breast cancer...
  54. pmc TGFbeta in Cancer
    Joan Massague
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 134:215-30. 2008
    ..The mechanistic basis and clinical relevance of TGFbeta's role in cancer is becoming increasingly clear, paving the way for a better understanding of the complexity and therapeutic potential of this pathway...
  55. ncbi request reprint Is cancer a disease of self-seeding?
    Larry Norton
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nat Med 12:875-8. 2006
  56. ncbi request reprint Cancer metastasis: building a framework
    Gaorav P Gupta
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 127:679-95. 2006
    ..Recent conceptual and technological advances promote our understanding of the origins and nature of cancer metastasis...
  57. pmc TGF-β-Id1 signaling opposes Twist1 and promotes metastatic colonization via a mesenchymal-to-epithelial transition
    Marko Stankic
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 415 East 68 th Street, New York, NY 10065, USA Department of Molecular Biology, Weill Cornell Medical College, 445 East 69 th Street, New York, NY 10021, USA
    Cell Rep 5:1228-42. 2013
    ..Collectively, these studies underscore the importance of Id-mediated phenotypic switching during distinct stages of breast cancer metastasis. ..
  58. ncbi request reprint Integration of Smad and MAPK pathways: a link and a linker revisited
    Joan Massague
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genes Dev 17:2993-7. 2003
  59. ncbi request reprint Selective compounds define Hsp90 as a major inhibitor of apoptosis in small-cell lung cancer
    Anna Rodina
    Program in Molecular Pharmacology and Chemistry, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
    Nat Chem Biol 3:498-507. 2007
    ..These results provide important evidence for a transformation-specific interplay between chaperones in regulating apoptosis in malignant cells...
  60. pmc Modeling metastasis in the mouse
    Paula D Bos
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Curr Opin Pharmacol 10:571-7. 2010
    ..By integrating the information obtained with these complementary approaches the field is currently obtaining an unprecedented level of understanding of the biology, molecular basis, and therapeutic vulnerabilities of metastasis...
  61. doi request reprint Metastasis: from dissemination to organ-specific colonization
    Don X Nguyen
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nat Rev Cancer 9:274-84. 2009
    ....
  62. doi request reprint Clinical implications of cancer self-seeding
    Elizabeth Comen
    Department of Medicine, Memorial Sloan Kettering Cancer Center and the Weill College of Medicine of Cornell University, New York, NY 10021, USA
    Nat Rev Clin Oncol 8:369-77. 2011
    ..Indeed, reframing our understanding of metastasis within the self-seeding model offers new opportunities for prevention and cure of metastatic cancer...
  63. pmc Off-target effects dominate a large-scale RNAi screen for modulators of the TGF-β pathway and reveal microRNA regulation of TGFBR2
    Nikolaus Schultz
    Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Silence 2:3. 2011
    ..The TGF-β pathway is integral to mammalian cell proliferation and survival, and aberrant TGF-β responses have been strongly implicated in cancer...
  64. ncbi request reprint G1 cell-cycle control and cancer
    Joan Massague
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Box 116, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York 10021, USA
    Nature 432:298-306. 2004
    ....
  65. ncbi request reprint New concepts in tissue-specific metastases
    Joan Massague
    Memorial Sloan Kettering Cancer Center, USA
    Clin Adv Hematol Oncol 1:576-7. 2003
  66. pmc Macrophage binding to receptor VCAM-1 transmits survival signals in breast cancer cells that invade the lungs
    Qing Chen
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cancer Cell 20:538-49. 2011
    ..Thus, newly disseminated cancer cells expressing VCAM-1 can thrive in leukocyte-rich microenvironments through juxtacrine activation of a VCAM-1-Ezrin-PI3K/Akt survival pathway...
  67. ncbi request reprint E2F4/5 and p107 as Smad cofactors linking the TGFbeta receptor to c-myc repression
    Chang Rung Chen
    Cell Biology Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 110:19-32. 2002
    ..Smad proteins therefore mediate transcriptional activation or repression depending on their associated partners...
  68. pmc Phase II trial of saracatinib (AZD0530), an oral SRC-inhibitor for the treatment of patients with hormone receptor-negative metastatic breast cancer
    Ayca Gucalp
    Breast Cancer Medicine Service, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Clin Breast Cancer 11:306-11. 2011
    ..We performed this trial to evaluate the efficacy and safety of saracatinib monotherapy in patients with estrogen receptor (ER)(-) and progesterone receptor (PR)(-) metastatic breast cancer (MBC)...
  69. ncbi request reprint The logic of TGFbeta signaling
    Joan Massague
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, P O Box 116, 1275 York Avenue, New York, NY 10021, USA
    FEBS Lett 580:2811-20. 2006
    ..The deconstruction of one of these responses - the cell cycle arrest response - into its elemental molecular parts has shed light into the mechanisms used by tumors to evade surveillance and cause metastasis...
  70. ncbi request reprint Field cancerization: something new under the sun
    Sakari Vanharanta
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 149:1179-81. 2012
    ..Now Hu et al. provide evidence that the sun's harmful rays may also cause tumor-promoting epigenetic modifications in dermal fibroblasts, highlighting further the importance of tumor-stroma interactions in cancer...