Karl Munger

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Disruption of oncogene/tumor suppressor networks during human carcinogenesis
    Karl Munger
    Department of Pathology and Harvard Center for Cancer Biology, Harvard Medical School, Boston, MA 02115 5701, USA
    Cancer Invest 20:71-81. 2002
  2. ncbi request reprint Human papillomavirus immortalization and transformation functions
    Karl Munger
    Department of Pathology, Harvard Medical School, Armenise Building 544, 200 Longwood Avenue, Boston, MA 02115 5701, USA
    Virus Res 89:213-28. 2002
  3. pmc Clefts, grooves, and (small) pockets: the structure of the retinoblastoma tumor suppressor in complex with its cellular target E2F unveiled
    Karl Munger
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Armenise Research Building 544A, Boston, MA 02115 5701, USA
    Proc Natl Acad Sci U S A 100:2165-7. 2003
  4. pmc Mechanisms of human papillomavirus-induced oncogenesis
    Karl Munger
    Department of Pathology, Harvard Medical School, 77 Ave Louis Pasteur, NRB 0958C, Boston, MA 02115 5727, USA
    J Virol 78:11451-60. 2004
  5. ncbi request reprint The role of human papillomaviruses in human cancers
    Karl Munger
    Department of Pathology and Center for Cancer Biology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5701, USA
    Front Biosci 7:d641-9. 2002
  6. pmc Kinase requirements in human cells: II. Genetic interaction screens identify kinase requirements following HPV16 E7 expression in cancer cells
    Amy Baldwin
    The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115
    Proc Natl Acad Sci U S A 105:16478-83. 2008
  7. pmc Kinase requirements in human cells: V. Synthetic lethal interactions between p53 and the protein kinases SGK2 and PAK3
    Amy Baldwin
    Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:12463-8. 2010
  8. pmc Bovine papillomavirus E7 transformation function correlates with cellular p600 protein binding
    Joseph DeMasi
    Department of Pathology, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:11486-91. 2005
  9. ncbi request reprint Abrogation of the retinoblastoma tumor suppressor checkpoint during keratinocyte immortalization is not sufficient for induction of centrosome-mediated genomic instability
    Siribang On Piboonniyom
    Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA
    Cancer Res 63:476-83. 2003
  10. ncbi request reprint Molecular pathways executing the "trophic sentinel" response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation
    Alexandra Eichten
    Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Virology 319:81-93. 2004

Collaborators

Detail Information

Publications56

  1. ncbi request reprint Disruption of oncogene/tumor suppressor networks during human carcinogenesis
    Karl Munger
    Department of Pathology and Harvard Center for Cancer Biology, Harvard Medical School, Boston, MA 02115 5701, USA
    Cancer Invest 20:71-81. 2002
    ....
  2. ncbi request reprint Human papillomavirus immortalization and transformation functions
    Karl Munger
    Department of Pathology, Harvard Medical School, Armenise Building 544, 200 Longwood Avenue, Boston, MA 02115 5701, USA
    Virus Res 89:213-28. 2002
    ..This paper will review the state of the field at the time of the 19th International Papillomavirus Workshop in September 2001 with respect to the HPV encoded oncoproteins...
  3. pmc Clefts, grooves, and (small) pockets: the structure of the retinoblastoma tumor suppressor in complex with its cellular target E2F unveiled
    Karl Munger
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Armenise Research Building 544A, Boston, MA 02115 5701, USA
    Proc Natl Acad Sci U S A 100:2165-7. 2003
  4. pmc Mechanisms of human papillomavirus-induced oncogenesis
    Karl Munger
    Department of Pathology, Harvard Medical School, 77 Ave Louis Pasteur, NRB 0958C, Boston, MA 02115 5727, USA
    J Virol 78:11451-60. 2004
  5. ncbi request reprint The role of human papillomaviruses in human cancers
    Karl Munger
    Department of Pathology and Center for Cancer Biology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5701, USA
    Front Biosci 7:d641-9. 2002
    ..Taken together, there is compelling molecular and epidemiological evidence in support of an oncogenic function of certain HPVs...
  6. pmc Kinase requirements in human cells: II. Genetic interaction screens identify kinase requirements following HPV16 E7 expression in cancer cells
    Amy Baldwin
    The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115
    Proc Natl Acad Sci U S A 105:16478-83. 2008
    ....
  7. pmc Kinase requirements in human cells: V. Synthetic lethal interactions between p53 and the protein kinases SGK2 and PAK3
    Amy Baldwin
    Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:12463-8. 2010
    ..The kinases SGK2 and PAK3 may thus represent such targets for p53-specific drug development...
  8. pmc Bovine papillomavirus E7 transformation function correlates with cellular p600 protein binding
    Joseph DeMasi
    Department of Pathology, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:11486-91. 2005
    ..These studies thus identify p600 as a shared target of the E7 proteins of multiple papillomaviruses...
  9. ncbi request reprint Abrogation of the retinoblastoma tumor suppressor checkpoint during keratinocyte immortalization is not sufficient for induction of centrosome-mediated genomic instability
    Siribang On Piboonniyom
    Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA
    Cancer Res 63:476-83. 2003
    ..These results demonstrate that disruption of the p16INK4A/pRB checkpoint of epithelial cell immortalization does not necessarily lead to centrosome-associated genomic instability...
  10. ncbi request reprint Molecular pathways executing the "trophic sentinel" response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation
    Alexandra Eichten
    Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Virology 319:81-93. 2004
    ....
  11. ncbi request reprint Stabilization and functional impairment of the tumor suppressor p53 by the human papillomavirus type 16 E7 oncoprotein
    Alexandra Eichten
    Department of Pathology and Harvard Center for Cancer Biology, Harvard Medical School, Boston, Massachusetts, 02115 5701, USA
    Virology 295:74-85. 2002
    ..Taken together, these results suggest that E7 can interfere with the normal turnover of p53 but that the resulting increase of p53 has no detectable transcriptional consequences on the p53 targets that we investigated...
  12. pmc Human papillomavirus E7 oncoprotein dysregulates steroid receptor coactivator 1 localization and function
    Amy Baldwin
    The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, 181 Longwood Ave, Boston, MA 02115, USA
    J Virol 80:6669-77. 2006
    ..Dysregulation of SRC-1 localization and function by HPV E7 may provide insight into the molecular mechanisms by which steroid hormones act as cofactors in the induction and progression of cervical neoplasia...
  13. ncbi request reprint Make WARTS, not cancer!
    Kirsten M Edwards
    Department of Pathology, Harvard Medical School, Boston, MA 02115 5727, USA
    Oncogene 23:5263-5. 2004
    ....
  14. pmc The human papillomavirus E7 oncoprotein
    Margaret E McLaughlin-Drubin
    Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Virology 384:335-44. 2009
    ..This function is directly reflected in the transforming activities of E7, including tumor initiation and induction of genomic instability...
  15. pmc The human papillomavirus type 16 E6 oncoprotein activates mTORC1 signaling and increases protein synthesis
    Jennifer M Spangle
    Division of Infectious Diseases, Brigham and Women s Hospital and Committee on Virology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Virol 84:9398-407. 2010
    ..HPV16 E6-mediated activation of mTORC1 signaling and cap-dependent translation may be a mechanism to promote viral replication under conditions of limited nutrient supply in differentiated, HPV oncoprotein-expressing proliferating cells...
  16. ncbi request reprint Centrosome abnormalities and genomic instability induced by human papillomavirus oncoproteins
    Stefan Duensing
    Department of Pathology, Harvard Center for Cancer Biology, Harvard Medical School, Armenise Research Building, D2 537, 200 Longwood Avenue, Boston, MA 02115, USA
    Prog Cell Cycle Res 5:383-91. 2003
    ....
  17. pmc Human papillomavirus type 16 E7 oncoprotein associates with E2F6
    Margaret E McLaughlin-Drubin
    Department of Medicine, Infectious Diseases Division, The Channing Laboratory, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Virol 82:8695-705. 2008
    ..We show that E7-expressing cells show decreased staining for E2F6/polycomb complexes and that this is at least in part dependent on the association with E2F6...
  18. pmc Delocalization of the microtubule motor Dynein from mitotic spindles by the human papillomavirus E7 oncoprotein is not sufficient for induction of multipolar mitoses
    Christine L Nguyen
    Infectious Diseases Division, Channing Laboratories, Brigham and Women s Hospital and Committee on Virology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 68:8715-22. 2008
    ..However, contrary to previous reports, we provide evidence that dynein delocalization by HPV16 E7 is neither necessary nor sufficient to cause the formation of multipolar mitoses...
  19. pmc HPV16 E7 oncogene expression in normal human epithelial cells causes molecular changes indicative of an epithelial to mesenchymal transition
    Karin Hellner
    Infectious Diseases Division, The Channing Laboratories, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Virology 391:57-63. 2009
    ..Hence, HPV16 oncoproteins may contribute to malignant progression through EMT induction...
  20. pmc Viruses associated with human cancer
    Margaret E McLaughlin-Drubin
    The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, 8th Floor, 181 Longwood Avenue, Boston, MA 02115, USA
    Biochim Biophys Acta 1782:127-50. 2008
    ..These include the discovery of oncogenes and tumor suppressors, identification of regulatory networks that are critical for maintenance of genomic integrity, and processes that govern immune surveillance...
  21. pmc Human papillomavirus type 16 E7 oncoprotein associates with the cullin 2 ubiquitin ligase complex, which contributes to degradation of the retinoblastoma tumor suppressor
    Kyungwon Huh
    The Channing Laboratory 861, Brigham and Women s Hospital, 181 Longwood Avenue, Boston, MA 02115, USA
    J Virol 81:9737-47. 2007
    ..Hence, we propose that the HPV16 E7-associated cullin 2 ubiquitin ligase complex contributes to aberrant degradation of the pRB tumor suppressor in HPV16 E7-expressing cells...
  22. pmc Clld7, a candidate tumor suppressor on chromosome 13q14, regulates pathways of DNA damage/repair and apoptosis
    Xiaobo Zhou
    The Channing Laboratory, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 70:9434-43. 2010
    ..Furthermore, depletion of Clld7 in normal human epithelial cells conferred resistance to apoptosis triggered by DNA damage. Taken together, the biological actions of Clld7 are consistent with those of a tumor suppressor...
  23. pmc Association of the human papillomavirus type 16 E7 oncoprotein with the 600-kDa retinoblastoma protein-associated factor, p600
    Kyung Won Huh
    The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:11492-7. 2005
    ..Therefore, p600 is a cellular target of E7 that regulates cellular pathways that contribute to anchorage-independent growth and cellular transformation...
  24. ncbi request reprint The helix-loop-helix protein ID1 localizes to centrosomes and rapidly induces abnormal centrosome numbers
    Jens Hasskarl
    Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 23:1930-8. 2004
    ..Hence, ID1 may contribute to oncogenesis not only by inhibiting transcriptional activity of basic helix-loop-helix transcription factors and abrogate differentiation but also by subverting centrosome duplication...
  25. ncbi request reprint Aberrations in the MTS1 tumor suppressor locus in oral squamous cell carcinoma lines preferentially affect the INK4A gene and result in increased cdk6 activity
    Siribang On Piboonniyom
    Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, Boston, MA 02115, USA
    Oral Oncol 38:179-86. 2002
    ..These results suggest that hyperactivity of cdk6 represents a distinct mechanism for pRB inactivation in oral SCC...
  26. ncbi request reprint Human papillomaviruses and centrosome duplication errors: modeling the origins of genomic instability
    Stefan Duensing
    Department of Pathology, Harvard Medical School, Armenise Research Building, D2 537, 200 Longwood Avenue, Boston, Massachusetts, MA 02115, USA
    Oncogene 21:6241-8. 2002
    ..These findings suggest that HPV oncoprotein-induced chromosomal instability increases the risk for genetic changes that may ultimately facilitate carcinogenic progression...
  27. pmc Oncogenic activities of human papillomaviruses
    Margaret E McLaughlin-Drubin
    Infectious Diseases Division, Channing Laboratories, 181 Longwood Avenue, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Virus Res 143:195-208. 2009
    ....
  28. pmc Human papillomavirus type 16 E7 oncoprotein inhibits the anaphase promoting complex/cyclosome activity by dysregulating EMI1 expression in mitosis
    Yueyang Yu
    Division of Infectious Diseases, Brigham and Women s Hospital and Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA
    Virology 446:251-9. 2013
    ..The resulting abnormally high EMI1 levels in HPV16 E7-expressing mitotic cells may inhibit degradation of APC/C substrates and cause the prometaphase delay that we have previously observed in such cells. ..
  29. pmc Activation of cap-dependent translation by mucosal human papillomavirus E6 proteins is dependent on the integrity of the LXXLL binding motif
    Jennifer M Spangle
    Division of Infectious Diseases, Brigham and Women s Hospital, Boston, MA, USA
    J Virol 86:7466-72. 2012
    ....
  30. ncbi request reprint Selective suppression of monocyte chemoattractant protein-1 expression by human papillomavirus E6 and E7 oncoproteins in human cervical epithelial and epidermal cells
    Kerstin Kleine-Lowinski
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Int J Cancer 107:407-15. 2003
    ..These observations are consistent with a model in which MCP-1 expression by infected keratinocytes, which would stimulate an immune attack on HPV-transformed cells, is suppressed for invasive cervical cancer to appear...
  31. ncbi request reprint Id proteins--tumor markers or oncogenes?
    Jens Hasskarl
    Department of Pathology, Harvard Center for Cancer Biology, Harvard Medical School, 200 Longwood Avenue, Building D2, Room 544A, Boston, Massachusetts 02115 5701, USA
    Cancer Biol Ther 1:91-6. 2002
    ..Recent reports show that Id proteins are overexpressed in various cancer types implying a role of these regulatory proteins in carcinogenesis. This review focuses on the biology of the Id proteins and their role as potential oncogenes...
  32. pmc The human papillomavirus type 8 E6 protein interferes with NOTCH activation during keratinocyte differentiation
    Jordan M Meyers
    Division of Infectious Disease, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    J Virol 87:4762-7. 2013
    ..NOTCH inhibition impairs epithelial differentiation and may thus contribute to β-HPV replication and viral oncogenesis...
  33. pmc Human papillomavirus 16 E7 inactivator of retinoblastoma family proteins complements human cytomegalovirus lacking UL97 protein kinase
    Jeremy P Kamil
    Department of Biological Chemistry and Molecular Pharmacology, and Infectious Diseases Division, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:16823-8. 2009
    ..Our findings have implications for human cytomegalovirus disease and for drugs that target UL97...
  34. ncbi request reprint Expression of a viral oncoprotein in normal human epithelial cells triggers an autophagy-related process: is autophagy an "Achilles' heel" of human cancers?
    Xiaobo Zhou
    Department of Medicine, Infectious Diseases Division, Brigham and Women s Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA
    Autophagy 5:578-9. 2009
    ....
  35. pmc Human papillomavirus E7 protein deregulates mitosis via an association with nuclear mitotic apparatus protein 1
    Christine L Nguyen
    Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Virol 83:1700-7. 2009
    ....
  36. pmc Direct association of the HPV16 E7 oncoprotein with cyclin A/CDK2 and cyclin E/CDK2 complexes
    Christine L Nguyen
    Infectious Diseases Division, Channing Laboratories 861, Brigham and Women s Hospital, 181 Longwood Avenue, Boston, MA 02115, USA
    Virology 380:21-5. 2008
    ..These results suggest that cyclin/CDK2 complexes may be components of HPV E7-associated cellular complexes that do not contain retinoblastoma tumor suppressor family members...
  37. doi request reprint The human papillomavirus type 8 E2 gene encodes a transforming activity sufficient for skin tumor formation in transgenic mice
    Margaret McLaughlin-Drubin
    Infectious Diseases Division, The Channing Laboratory, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Invest Dermatol 128:2142-4. 2008
    ..2008, this issue)...
  38. ncbi request reprint Centrosomes, genomic instability, and cervical carcinogenesis
    Stefan Duensing
    Harvard Medical School, Department of Pathology, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
    Crit Rev Eukaryot Gene Expr 13:9-23. 2003
    ..Taken together, these findings support the general model in which chromosomal instability arises as a direct consequence of oncogenic insults and can develop at early stages of tumor progression...
  39. pmc Biochemical and functional interactions of human papillomavirus proteins with polycomb group proteins
    Margaret E McLaughlin-Drubin
    Division of Infectious Diseases, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, 181 Longwood Avenue, MCP 861, Boston, MA 02115, USA
    Viruses 5:1231-49. 2013
    ..Similar alterations are frequently observed in non-virus associated human cancers and may be harnessed for diagnosis and therapy...
  40. pmc Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins
    Orit Rozenblatt-Rosen
    Genomic Analysis of Network Perturbations Center of Excellence in Genomic Science, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Nature 487:491-5. 2012
    ..Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate the prioritization of cancer-causing driver genes to advance the understanding of the genetic basis of human cancer...
  41. pmc Systematic identification of interactions between host cell proteins and E7 oncoproteins from diverse human papillomaviruses
    Elizabeth A White
    Department of Microbiology and Immunobiology and Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:E260-7. 2012
    ..These studies refine the current understanding of HPV E7 functions and establish a platform for the rapid identification of virus-host interactions...
  42. pmc Human papillomavirus type 16 E7 oncoprotein can induce abnormal centrosome duplication through a mechanism independent of inactivation of retinoblastoma protein family members
    Stefan Duensing
    Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Virol 77:12331-5. 2003
    ..These results demonstrate that the molecular mechanism whereby HPV-16 E7 induces centrosome duplication errors is independent of its ability to inactivate pRB, p107, and p130 or to interact with the S4 proteasome subunit...
  43. pmc Expression of the human papillomavirus type 16 E7 oncoprotein induces an autophagy-related process and sensitizes normal human keratinocytes to cell death in response to growth factor deprivation
    Xiaobo Zhou
    Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, USA
    Virology 385:192-7. 2009
    ..These findings indicate that even under normal culture conditions, HPV16 E7 expression triggers metabolic stress that may result in autophagy, a pathway implicated in carcinogenesis...
  44. pmc Human papillomavirus type 16 E7 oncoprotein associates with the centrosomal component gamma-tubulin
    Christine L Nguyen
    Channing Laboratories, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Virol 81:13533-43. 2007
    ....
  45. pmc Excessive centrosome abnormalities without ongoing numerical chromosome instability in a Burkitt's lymphoma
    Stefan Duensing
    Department of Pathology, Harvard Medical School, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
    Mol Cancer 2:30. 2003
    ..Moreover, our results suggest a model in which additional cellular alterations may be required to promote centrosome-related mitotic defects in tumor cells...
  46. pmc Human papillomaviruses as therapeutic targets in human cancer
    Karin Hellner
    Brigham and Women s Hospital, The Channing Laboratories, 181 Longwood Ave, Boston, MA 02115, USA
    J Clin Oncol 29:1785-94. 2011
    ..Other HPV-associated anogenital and head and neck cancers are predicted to afflict another 700,000 men and women over this time period. Hence, therapeutic efforts to combat high-risk HPV-associated disease remain of critical importance...
  47. ncbi request reprint Depletion of physiological levels of the human TID1 protein renders cancer cell lines resistant to apoptosis mediated by multiple exogenous stimuli
    Kirsten M Edwards
    Department of Pathology, Harvard Medical School, NRB 0958, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Oncogene 23:8419-31. 2004
    ..These results suggest that hTID1 functions as an important cell death regulator and raise the interesting possibility that hTID1 could exert tumor suppressor activity...
  48. pmc The LKB1 tumor suppressor differentially affects anchorage independent growth of HPV positive cervical cancer cell lines
    Hildegard I D Mack
    Division of Infectious Diseases, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA, 02115, USA
    Virology 446:9-16. 2013
    ..Our studies revealed marked differences in the biological activities of two kinase defective LKB1 mutants in the various cell lines. Thus, our results suggest that LKB1 may be a cell-type specific tumor suppressor. ..
  49. pmc Cancer associated human papillomaviruses
    Margaret E McLaughlin-Drubin
    Division of Infectious Diseases, Brigham and Women s Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Curr Opin Virol 2:459-66. 2012
    ..This review emphasizes this interplay between virus and the infected host cells and points out biological similarities and differences between different groups of HPVs...
  50. ncbi request reprint The human papillomavirus type 16 E6 and E7 oncoproteins independently induce numerical and structural chromosome instability
    Stefan Duensing
    Department of Pathology and Harvard Center for Cancer Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 62:7075-82. 2002
    ..Our results therefore suggest that HPV oncoproteins are a source for both numerical and structural chromosome instability during HPV-associated carcinogenesis...
  51. pmc Human papillomavirus E7 oncoprotein induces KDM6A and KDM6B histone demethylase expression and causes epigenetic reprogramming
    Margaret E McLaughlin-Drubin
    Infectious Diseases Division, Department of Medicine, The Channing Laboratory, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 108:2130-5. 2011
    ..Most importantly, these effects are reversed when E7 expression is silenced, indicating that this pathway may have prognostic and/or therapeutic significance...
  52. pmc Kinase requirements in human cells: I. Comparing kinase requirements across various cell types
    Dorre A Grueneberg
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:16472-7. 2008
    ....
  53. pmc The HPV16 E6 oncoprotein causes prolonged receptor protein tyrosine kinase signaling and enhances internalization of phosphorylated receptor species
    Jennifer M Spangle
    Division of Infectious Diseases, Brigham and Women s Hospital, Department of Medicine and Committee on Virology, Harvard Medical School, Boston, MA, USA
    PLoS Pathog 9:e1003237. 2013
    ....
  54. pmc Human papillomavirus type 16 E7 oncoprotein engages but does not abrogate the mitotic spindle assembly checkpoint
    Yueyang Yu
    Division of Infectious Diseases, Brigham and Women s Hospital and Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA
    Virology 432:120-6. 2012
    ..Importantly, however, HPV16 E7 does not markedly compromise the SAC response to microtubule poisons...
  55. pmc A discrete population of squamocolumnar junction cells implicated in the pathogenesis of cervical cancer
    Michael Herfs
    Division of Women s and Perinatal Pathology, Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:10516-21. 2012
    ....
  56. ncbi request reprint NF-kappaB-mediated induction of p21(Cip1/Waf1) by tumor necrosis factor alpha induces growth arrest and cytoprotection in normal human keratinocytes
    John R Basile
    Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Mol Cancer Res 1:262-70. 2003
    ..In addition, TNFalpha-treated cell populations are markedly less susceptible to apoptosis by UV irradiation and this cytoprotective effect is at least in part mediated by p21(Cip1/Waf1) as well...