Pier Paolo Pandolfi

Pier Paolo Pandolfi
Born (1963-05-14) May 14, 1963
Rome, Italy
Residence Boston, Massachusetts
Citizenship United States
Italy
Nationality Italian
Fields Cancer Genetics
Biochemistry
Cell Biology
Institutions Harvard Medical School
Beth Israel Deaconess Medical Center
Alma mater University of Rome
University of Perugia, Italy
Website
http://www.pandolfilab.org

Pier Paolo Pandolfi, MD, PhD (born May 14, 1963) is an Italian-American geneticist and molecular biologist. His research focuses on the molecular mechanisms and genetics underlying the pathogenesis of leukemias and solid tumors. Pandolfi’s elucidation of fusion oncoproteins and genes involved in the chromosomal translocations of acute promyelocytic leukemia (APL) led to the development of effective therapies.[1] APL is now considered curable. His research also yielded novel conceptual insights into the role of tumor suppressor genes in the development of human cancer with important therapeutic implications.[1][2][3] Pandolfi’s extensive modeling of cancer in the mouse resulted in new discovery platforms that are used to evaluate drugs and predict the course of disease, treatment and resistance. Recently, he presented a theory describing how RNAs exert biological functions with profound implications for cancer biology and human health.[4][5]

Pandolfi is Director of the Cancer Center and the Cancer Research Institute at Beth Israel Deaconess Medical Center[6] and George C. Reisman Professor of Medicine at Harvard Medical School. Previously, he was a faculty member at Memorial Sloan-Kettering Cancer Center and professor of at the Weill Graduate School of Medical Sciences at Cornell University. He is a recipient of the Weizmann Institute Lombroso Prize [7] for Cancer Research and the Pezcoller-AACR International Award [8] for cancer research. A citizen of both Italy and the United States, he was “knighted” by the Republic of Italy.[9]

Biography

Pier Paolo Pandolfi was born May 14, 1963 in Rome, Italy. His parents were both humanities professors and both died of cancer.[10] Pandolfi studied philosophy as an undergraduate at the University of Rome and went on to study medicine at the University of Perugia, where he received his MD in 1989. In 1995, he received a PhD in molecular and cellular biology from the same institution. He completed post-graduate training at the National Institute for Medical Research and the University of London in the United Kingdom. He married fellow scientist Letizia Longo, PhD, in 1991. They have two daughters.

Pandolfi continued his career in New York, where from 1994 to 2007, he received appointments in molecular biology and genetics. He served as Director of the Molecular and Developmental Biology Laboratory at Memorial-Sloan-Kettering Cancer Center and professor of biology, genetics and pathology at the Weill Graduate School of Medical Sciences at Cornell University.

In 2007, Pandolfi joined the faculty of Harvard Medical School and accepted an appointment as Scientific Director of the Cancer Center at Beth Israel Deaconess Medical Center. He currently holds the George C. Reisman Endowed Chair of Medicine at Harvard Medical School, where he is professor of medicine and pathology. In 2013, he was appointed Director of the Cancer Center and the Cancer Research Institute at BIDMC.[11] He is an associate member of the Broad Institute of MIT and Harvard University.[12] His laboratory is located at Beth Israel Deaconess Medical Center.

Research

Research carried out in Pandolfi’s laboratory has clarified the molecular mechanisms and genetics underlying the pathogenesis of leukemias, lymphomas and solid tumors, and modeled these cancers in the mouse.[1][13] His basic and translational research has led to the development of many experimental trials. He has also presented a new theory describing how messenger RNAs and non-coding RNAs exert their biological functions with profound implications for human genetics, cell biology and cancer biology.[4][5]

Acute promyelocytic leukemia (APL)

While a medical student, Pandolfi cloned and characterized PML-RARa (retinoic acid receptor alpha), the product of the long-sought after t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL) and its normal counterpart promyelocytic leukemia protein (PML).[14][15] Later, Pandolfi's lab deconstructed the genetics and complex molecular mechanisms underlying APL, studying other molecular subtypes that respond differentially to treatment.[16][17][18][19] The lab identified optimal APL treatment strategies by modeling these APL subtypes in mice.[16][17][18][20][21][22] As a result, combinatorial treatments are now available for each APL subtype, and APL is considered a curable disease.[1] The lab further discovered that APL genes (e.g. PML, PLZF, NPM) are implicated in the pathogenesis of human cancer at large, beyond their involvement in APL, by acting as tumor suppressor genes (TSGs).[23][24][25][26][27][28]

Cancer and developmental pathways

The role of developmental pathways and genes in tumorigenesis is a major focus of the lab. By analyzing APL genes and associated proteins, Pandolfi and colleagues tested the hypothesis that fundamental developmental processes are deregulated in cancer. Examples are PLZF and LRF/POKEMON, members of the POZ and Kruppel (POK) family of transcriptional repressors.[26][27][28][29][30][31][32] PLZF is the second most frequent RARa partner in APL associated chromosomal translocations.[26][28][29] More recently the lab identified POKEMON (for POK, Erythroid, Myeloid ONtogenic factor), also a member of the POK family, as a key player in tumorigenesis.[30][31][32] Pandolfi showed that both proteins play critical and essential roles in both developmental processes and cancer pathogenesis.[27][31][33][34] Other example are Pandolfi’s identification of NPM1 and PTEN as essential developmental genes.[24][35]

Co-clinical trials

Based on his experience modeling APL in the mouse, Pandolfi developed the “Co-Clinical Trial Project,” a paradigm for conducting clinical trials concurrently in humans and in mice.[1][36] This platform utilizes a variety of mouse models, with a focus on genetically engineered mouse models, generated to mimic the spontaneous incidence observed for human cancer. By mirroring human clinical studies in these genetically engineered mouse models (i.e. a Co-Clinical approach) scientists can stratify patients and identify optimal therapies based on molecular determinants.[36][37] Pandolfi and colleagues have proposed a “Mouse Hospital” model to standardize infrastructure and practices for these co-clinical trials.[38][39]

New paradigms in the function of tumor suppressor genes

The Pandolfi Lab extensively characterized the function of major tumor suppressors including PML[23][40][41][42], p53[43][44][45], INPP4B[35][46][47][48] and PTEN, in vivo in the mouse.[35][49][50][51] This in turn led to the new conceptual advances with important implications for cancer prevention and therapy.[2] For example, the demonstration that even a subtle downregulation in the dose of PTEN can lead to tumorigensis lead to the notion of tumor suppressor qausi-insufficiency, and prompted therapeuticc efforts towards PTEN activation.[50][52][53] Conversely, the Pandolfi Lab discovered that complete abrogation of tumor suppressor genes can elicit failsafe mechanisms such as cellular senescence and cancer stem cell exhaustion that can be hijacked for therapy.[45][54]

RNA research

In recent years, non-coding RNAs have emerged as a new area of investigation within the mammalian transcriptome. Micro RNAs, long non-coding RNAs, pseudogenes and circular RNAs vastly outnumber the protein coding mRNA dimension.[55] The Pandolfi Lab recently contributed to determine the importance of this non-coding RNAs dimension in tumorigenesis, through in vivo modeling efforts in the mouse.[56][57][58][59][60] Pandolfi has also presented a theory describing how non-coding RNAs as well as protein coding messenger RNAs can cross-talk through a new RNA language by acting as “competing endogenous RNAs” (ceRNAs).[4][5][57][60][61][62] This in turn attributes a “non-coding” function to mRNAs,[4][5][57] and makes it possible to bioinformatically predict and experimentally validate how RNA communicate in both physiology and disease.

Awards and honors

Pandolfi has received more than 30 awards for his research, including consecutive NCI Merit Awards and, more recently, the NCI Outstanding Investigator Award. A few selected recognitions are as follows:

References

  1. 1 2 3 4 5 C. Nardella, A. Lunardi, A. Patnaik. L.C Cantley and P.P. Pandolfi. "The APL paradigm and the 'Co-Clinical Trial' Project." Cancer Discovery AACR, 2011; 1(2); 108–16.
  2. 1 2 A.H. Berger, A.G. Knudson and P.P. Pandolfi. "A continuum model for tumour suppression." Nature, 2011 Aug 10; 476(7359):163-9.
  3. ↑ A.H. Berger and P.P. Pandolfi. "Etiology of Cancer: Cancer Susceptibility Syndromes." In: DeVita, Lawrence and Rosenberg, eds. Cancer: Principles and Practice of Oncology, 9th edition, Philadelphia: Lippincott Williams and Williams, 2011.
  4. 1 2 3 4 L. Salmena, L. Poliseno, Y. Tay, L. Kats and P.P. Pandolfi. "The ceRNA hypothesis: the new Rosetta stone of a hidden RNA language." Cell, 2011 Aug 5; 146(3): 353-8.
  5. 1 2 3 4 Y. Tay, J. Rinn, P.P. Pandolfi. "The multilayered complexity of ceRNA crosstalk and competition." Nature, 2014 Jan 16; 505(7483): 344-52.
  6. ↑ http://www.bidmc.org/Research/Research-Centers/CancerResearchInstitute.aspx “Cancer Research Institute”. Beth Israel Deaconness Medical Center. 10 March, 2017.
  7. 1 2 https://www.weizmann.ac.il/acadaff/awards-and-honors/institute-honors-and-prizes/lombroso “Sergio Lombroso Award in Cancer Research”. Academic Affairs Office. Weizmann Institute of Science. 10 March, 2017.
  8. 1 2 http://www.aacr.org/Research/Awards/PAGES/PEZCOLLER-FOUNDATION-AACR-AWARD___8470D6.ASPX#.WMHELFXyu70 “Pezcoller Foundation-AACR International Award for Cancer Research Recipients”. American Association for Cancer Research. 10 March, 2017
  9. 1 2 http://bostoniano.info/community/local-scientists-fava-loda-pandolfi-knighted-republic-italy/ Orchuia, Nicola. “Local scientists Fava, Loda, Pandolfi knighted by Republic of Italy”. Bostoniano. 5 June, 2015. 10 March, 2017.
  10. ↑ V. Gewin. “Movers: Pier Paolo Pandolfi, Director, Cancer Genetics Programme, Beth Israel Deaconess Medical Center, Harvard University.” Nature 447, 2007 May 9: 228.
  11. ↑ http://www.bidmc.org/News/PRLandingPage/2013/October/PandolfiCancerCenter.aspx Prescott, Bonnie. “Pier Paolo Pandolfi MD, PHD, to Head Cancer Center at Beth Israel Deaconess Medical Center”. Best Israel Deaconess Medical Center. 8 October, 2013. 10 March, 2017.
  12. ↑ https://www.broadinstitute.org/what-broad/history-leadership/founders/our-faculty-associate-members “Our Faculty: Associate Members”. Broad Institute. 10 March, 2017.
  13. ↑ A. Lunardi, C. Nardella, J.G. Clohessy, P.P. Pandolfi. “Of Model Pets and Cancer Models.” Mouse Models of Cancer: A Laboratory Manual. Cold Spring Harbor Laboratory Press, Jan 1, 2014.
  14. ↑ P.P. Pandolfi, F. Grignani, M. Alcalay, A. Mencarelli, A. Biondi, F. LoCoco, F. Grignani and P.G. Pelicci. "Structure and origin of the acute promyelocytic leukemia myl/RAR cDNA and characterization of its retinoid-binding and transactivation properties." Oncogene, 6:1285-1292, 1991.
  15. ↑ P.P. Pandolfi, M. Alcalay, M. Fagioli, D. Zangrilli, A. Mencarelli, D. Diverio, A. Biondi, F. Lo Coco, A. Rambaldi, F. Grignani, C. Rochette-Egly, M.-P. Gaub, P. Chambon and P.G. Pelicci. "Genomic variability and alternative splicings generate multiple PML/RAR transcripts that encode aberrant PML proteins and PML/RAR isoforms in acute promyelocytic leukemias." EMBO J., 11:1397-1407, 1992.
  16. 1 2 L.-Z. He, F. Guidez, C. Tribioli, D. Peruzzi, M. Ruthardt, A. Zelent and P.P. Pandolfi. Distinct interactions of PML-RAR and PLZF-RAR with co-repressors determine differential responses to RA in APL. Nature Genetics, 18:126-135, 1998.
  17. 1 2 E.M. Rego, L.-Z. He, R.P. Warrell Jr., Z.-G. Wang and P.P. Pandolfi. "RA and As2O3 treatment in transgenic models of APL unravel the distinct nature of the leukemogenic process induced by the PML-RAR and PLZF-RAR oncoproteins." Proc. Natl. Acad. Sci. USA, 97:10173-10178, 2000.
  18. 1 2 L.-Z. He, T. Tolentino, P. Grayson, S. Zhong, R.P. Warrell, Jr., R.A. Rifkind, P.A. Marks, V.M. Richon and P.P. Pandolfi. "Histone deacetylase inhibitors induce remission in transgenic models of therapy resistant acute promyelocytic leukemia." J. Clin. Invest., 108:1321–1330, 2001.
  19. ↑ E.M. Rego, D. Ruggero, C. Tribioli, G. Cattoretti, S. Kogan, R.L. Redner and P.P. Pandolfi. "Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR, PLZF/RAR or NPM/RAR." Oncogene, 25:1974-1979, 2006.
  20. ↑ S.S. Soignet, P. Maslak, Z.-G. Wang, S. Jhanwar, E. Calleja, L.J. Dardashanti, D. Corso, A. DeBlasio, J. Gabrilove, D.A. Scheinberg, P.P. Pandolfi and R.P. Warrell, Jr. "Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide." N. Engl. J. Med., 339:1341-1348, 1998.
  21. ↑ M.A. Sukhai, X. Wu, Y. Xuan, T. Zhang, P.P. Reis, K. Dube, E.M. Rego, M. Bhaumik, D.J. Bailey, R.A. Wells, S. Kamel-Reid and P.P. Pandolfi. "Myeloid leukemia with promyelocytic features in transgenic mice expressing hCG-NuMA-RAR." Oncogene, 23:665-78, 2004.
  22. ↑ R.P. Warrell, Jr., L.-Z. He, V. Richon, E. Calleja and P.P. Pandolfi. "Therapeutic targeting of transcription in acute promyelocytic leukemia by use of an inhibitor of histone deacetylase." J. Natl. Can. Inst., 90:1621-1625, 1998.
  23. 1 2 Z. Wang, L. Delva, M. Gaboli, H. Zhang, R. Rivi, C. Cordon-Cardo, F. Grosveld and P.P. Pandolfi. "Role of PML in cell growth and the retinoic acid pathway." Science, 279:1547-1551, 1998.
  24. 1 2 {{Cite S. Grisendi, R. Bernardi, M. Rossi, K. Cheng, L. Khandker, K. Manova and P.P. Pandolfi. "Role of Npm in embryonic development and tumourigenesis." Nature, 437:147-53, 2005.
  25. ↑ S. Grisendi, C. Mecucci, B. Falini and P.P. Pandolfi. "Nucleophosmin and cancer." Nature Reviews Cancer, 6:493-505, 2006.
  26. 1 2 3 R.M. Hobbs, M. Seandel, I. Falciatori, S. Rafii, P.P. Pandolfi. "Plzf Regulates Germline Progenitor Self-Renewal by Opposing mTORC1." Cell. 142:468-479, 2010, E-published 2010 Aug 6.
  27. 1 2 3 Hobbs RM, Pandolfi PP. "Shape-shifting and tumor suppression by PLZF." Oncotarget, 2010 May;1(1):3-5.
  28. 1 2 3 L.C. Trotman, A. Alimonti, P.P. Scaglioni, J.A. Koutcher, C. Cordon-Cardo and P.P. Pandolfi. "Identification of a tumour suppressor network opposing nuclear Akt function." Nature, 441:523-7 2006.
  29. 1 2 J.A. Costoya, R. Hobbs, M. Barna, G. Cattoretti, K. Manova, M. Sukhwani, K.E. Orwig, D.J. Wolgemuth and P.P. Pandolfi. "Essential role of Plzf in maintenance of spermatogonial stem cells." Nature Genetics, 36:653-659, 2004.
  30. 1 2 T. Maeda, R. Hobbs, T. Merghoub, I. Guernah, A. Zelent, C. Cordon-Cardo, J. Teruya-Feldstein and P.P. Pandolfi. "Role of the proto-oncogene POKEMON in cellular transformation and ARF repression." Nature, 433:278-285, 2005.
  31. 1 2 3 A. Lunardi, J. Guarnerio, G. Wang, T. Maeda, P.P. Pandolfi. "Role of LRF/Pokemon in lineage fate decisions." Blood, 2013 Apr 11; 121(15):2845-53. E-published Feb 8.
  32. 1 2 T. Maeda, T. Merghoub, R.M. Hobbs, L. Dong, M. Maeda, J. Zakrzewski, M.R.M. van den Brink, A. Zelent, H. Shigematsu, K. Akashi, J. Teruya-Feldstein, G. Cattoretti and P.P. Pandolfi. "Regulation of B versus T lymphoid lineage fate decision by the proto-oncogene LRF." Science, 316: 860-866, 2007.
  33. ↑ L.-Z. He, M. Bhaumik, C. Tribioli, E. M. Rego, S. Ivins, A. Zelent and P.P. Pandolfi. "Two critical hits for promyelocytic leukemia." Molecular Cell, 6:1131-1141, 2000.
  34. ↑ G. Wang, A. Lunardi, J. Zhang, Z. Chen, U. Ala, K.A. Webster, Y. Tay, E. Gonzalez-Billalabeitia, A. Egia, D.R. Shaffer, B. Carver, X.S. Liu, R. Taulli, W. P. Kuo, C. Nardella, S. Signoretti, C. Cordon-Cardo, W.L. Gerald, P.P. Pandolfi. "Zbtb7a suppresses prostate cancer through repression of a Sox9-dependent pathway for cellular senescence bypass and tumor invasion." Nature Genetics, 2013 Jun 2; 45(7):739-746. E-published June 2.
  35. 1 2 3 A. Di Cristofano, B. Pesce, C. Cordon-Cardo and P.P. Pandolfi. "PTEN is essential for embryonic development and tumor suppression." Nature Genetics, 19:348-355, 1998.
  36. 1 2 A. Lunardi, U. Ala, M.T. Epping, L. Salmena, J.G. Clohessy, K.A. Webster, G. Wang, R. Mazzucchelli, M. Bianconi, E.C. Stack, R. Lis, A. Patnaik, L.C. Cantley, G. Bubley, C. Cordon-Cardo, W.L. Gerald, R. Montironi, S. Signoretti, M. Loda, C. Nardella, P.P. Pandolfi. "A co-clinical approach identifies mechanisms and potential therapies for androgen deprivation resistance in prostate cancer." Nature Genetics, 2013 July; 45(7): 747-55. E-published June 2.
  37. ↑ Z. Chen, K. Cheng, Z. Walton, Y. Wang, H. Ebi, T. Shimamura, Y. Liu, T. Tupper, J. Ouyang, J. Li, P. Gao, M.S. Woo, C. Xu, M. Yanagita, A. Altabef, S. Wang, C. Lee, Y. Nakada, C.G. Peña, Y. Sun, Y. Franchetti, C. Yao, A. Saur, M.D. Cameron, M. Nishino, D.N. Hayes, M.D. Wilkerson, P.J. Roberts, C.B. Lee, N. Bardeesy, M. Butaney, L.R. Chirieac, D.B. Costa, D. Jackman, N.E. Sharpless, D.H. Castrillon, G.D. Demetri, P.A. Jänne. P.P. Pandolfi, L.C. Cantley, A.L. Kung, J.A. Engelman, K.K. Wong. "A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response." Nature, 2012 Mar 18; 483(7391): 613-7.
  38. ↑ J. Clohessy, P.P. Pandolfi. “Mouse hospital and co-clinical trial project-from bench to bedside.” Nature Reviews Clinical Oncology, 2015 Aug; 12(8):491-8.
  39. ↑ C. Abate-Shen, P.P. Pandolfi. “Effective Utilization and Appropriate Selection of GEMMs for Translational Integration of Mouse and Human Trials.” Mouse Models of Cancer: A Laboratory Manual. Cold Spring Harbor Laboratory Press, Nov 2013.
  40. ↑ H.-K. Lin, S. Bergmann and P.P. Pandolfi. "Cytoplasmic PML function in TGF- signaling." Nature, 431:205-11, 2004.
  41. ↑ R. Bernardi, I. Guernah, D. Jin, C. Cordon-Cardo, M. Celeste Simon, S. Rafii and P.P. Pandolfi. "PML inhibits Hif-1 translation and neoangiogenesis through repression of mTOR." Nature, 442:779-785, 2006.
  42. ↑ C. Giorgi, K. Ito, H-K. Lin, C. Santangelo, M. R. Wieckowski, M. Lebiedzinska, A. Bononi, M. Bonora, J. Duszynski, R. Bernardi, R. Rizzuto, C. Tacchetti, P. Pinton, P. P. Pandolfi. "PML Regulates Apoptosis at Endoplasmic Reticulum Modulating Calcium Release." Science, 2010 Nov 26; 330(6008): 1247-51. E-published 2010 Oct 28.
  43. ↑ A. Guo, P. Salomoni, J. Luo, A. Shih, S. Zhong, W. Gu and P.P. Pandolfi. "Role of PML in p53-dependent apoptosis." Nature Cell Biology, 2:730-736, 2000.
  44. ↑ R. Bernardi, P.P. Scaglioni. S. Bergmann, H.F. Horn, K.H. Vousden and P.P. Pandolfi. "PML regulates p53 stability through nucleolar sequestration of Mdm2." Nature Cell Biology, 7:665-672, 2004.
  45. 1 2 Z.chen, L.C. Trotman, D. Shaffer, H.-K. Lin, Z.A. Dotan, M. Niki, J.A. Koutcher, H.I. Scher, T. Ludwig, W. Gerald, C. Cordon-Cardo and P.P. Pandolfi. "Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis." Nature, 436:725-730, 2005.
  46. ↑ C.L. Chew, A. Lunardi, F. Gulluni, D.T. Ruan, M. Chen, L. Salmena, M. Nishino, A. Papa, C. Ng, J. Fung, J.G. Clohessy, J. Sasaki, T. Sasaki, R.T. Bronson, E. Hirsch, P.P. Pandolfi. "In vivo role of INPP4B in tumor and metastasis suppression through regulation of PI3K/AKT signaling at endosomes." Cancer Discover, 2015 Jul; 5(7):740-51
  47. ↑ C. Gewinner, Z. C. Wang, A. Richardson, J. Teruya-Feldstein, W. Lin, L. Rameh, L. Salmena, P.P. Pandolfi, and L. C. Cantley. "Evidence that Inositol Polyphosphate 4-Phosphatate Type II is a Tumor Suppressor that Inhibits PI3K signaling." Cancer Cell, 16:115-25, 2009.
  48. ↑ C.L. Chew, M. Chen, P.P. Pandolfi. “Endosome and INPP4B.” Oncotarget. 2016 Jan 5;7(1):5-6.
  49. ↑ M.S. Song, L. Salmena, A. Carracedo-Perez, A. Egia, F. Lo Coco, J. Teruya-Feldstein and P.P. Pandolfi. "The deubiquitinylation and localization of PTEN are regulated by a HAUSP-PML network." Nature, 455:813-7, 2008, Epublished 2008 20 August.
  50. 1 2 I. Garcia-Cao, M.S. Song, R.M. Hobbs, G. Laurent, C. Giorgi, V.C.J. de Boer, D. Anastasiou, K. Ito, A. Sasaki, L. Rameh, A. Carracedo, M.G.Vander Heiden, L.C. Cantley, P. Pinton, M.C Haigis, P.P. Pandolfi. "Systemic elevation of PTEN induces a tumor-suppressive metabolic state." Cell, 2012 Mar 30; 149(1):49-62.
  51. ↑ A.Papa, L. Wan, M. Bonora, L. Salmena, M.S. Song, R.M. Hobbs, A. Lunardi, K. Webster, C. Ng, R.H. Newton, N. Knoblauch, J. Guarnerio, K. Ito, L.A. Turka, A.H. Beck, P. Pinton, R.T. Bronson, W. wei, P.P.Pandolfi. "Cancer-associated PTEN mutants act in dominant-negative manner to supress PTEN protein function." Cell, 2014 Apr 24; 157(3): 595-610
  52. ↑ L. Trotman, M. Niki, Z. Dotan, J. Koutcher, A. Di Cristofano, A. Xiao, A. Khoo, P. Roy-Burman, N. Greenberg, T. Van Dyke, C. Cordon-Cardo and P.P. Pandolfi. "Pten dose dictates cancer progression in the prostate." PLoS, Biology, 1:385-396, 2003.
  53. ↑ A. Alimonti, A. Carracedo, J.G. Clohessy, L.C. Trotman, C. Nardella, L. Salmena, K. Sampieri, E. Brogi, J. Zhang, and P.P. Pandolfi. "Subtle variations in Pten dose determine cancer susceptibility." Nature Genetics, 42:454-8, 2010. E-published 2010 Apr 18.
  54. ↑ A. Alimonti C. Nardella, Z. Chen, J.G. Clohessy, A. Carracedo, L.C. Trotman, K. Cheng, S. Varmeh, S.C. Kozma, G. Thomas, E. Rosivatz, R. Woscholski, F. Cognetti, H.I. Scher, P.P. Pandolfi. "A novel type of cellular senescence that can be enhanced in mouse models and human tumor xenografts to suppress prostate tumorigenesis." J Clin Invest.120:681-93, 2010, E-published 2010 February 8.
  55. ↑ A. Pasut, A. Matsumoto, J.G. Clohessy, P.P. Pandolfi. “The pleiotropic role of non-coding genes in development and cancer.” Curr Opin Cell Biol. 2016 Dec;43:104-113.
  56. ↑ L. Poliseno, L. Salmena, L. Riccardi, A. Fornari, M. S. Song, R. M. Hobbs, P. Sportoletti, S. Varmeh, A. Egia, G. Fedele, L. Rameh, M. Loda and P.P. Pandolfi. "Identification of the miR-106b~25 microRNA Cluster as a Proto-Oncogenic PTEN-Targeting Intron that Cooperates with its Host Gene MCM7 in Transformation." Science Signalling, 2010 April 13; 3(117): ra29. Erratum in: Science Signalling, 3:er6, 2010.
  57. 1 2 3 L. Poliseno, L. Salmena, J. Zhang, B. Carver, W. J. Haveman , P.P. Pandolfi. "A coding-independent function of gene and pseudogene mRNAs regulates tumour biology." Nature, 465:1033-8, 2010.
  58. ↑ S.J. Song, K. Ito, U. Ala, L. Kats, K. Webster, S.M. Sun, M. Jongen-Lavrencic, K. Manova-Todorva, J. Teruya-Feldstein, D.E. Avigan, R. Delwel, P.P. Pandolfi. "The Oncogenic microRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation." Cell Stem Cell, 2013 July 3; 13(1): 87-101.
  59. ↑ S. J. Song, L. Poliseno, M.S. Song, U. Ala, L. Kats, G. Beringer, K. Webster, X. Yuan, J.E. Brock, A. L. Richardson, L. C. Cantley, P.P. Pandolfi. "MicroRNA-antagonism Regulates Breast Cancer Stemness and Metastasis via TET-Family-Dependent Chromatin Remodeling." Cell, 2013 Jul 18; 154(2):311-24. E-published July 2.
  60. 1 2 F.A. Karreth, M. Reschke, A. Ruocco, C. Ng, B. Chapuy, V. Léopold, M. Sjoberg, T.M. Keane, A. Verma, U. Ala, Y. Tay, N. Seitzer, A. Bothmer, J. Fung, F. Langellotto, S.J. Rodig, O. Elemento, M.A. Shipp, D.J. Adams, R. Chiarle, P.P. Pandolfi. 2015. “The BRAF pseudogene functions as a competitive endogenous RNA and induces lymphoma in vivo.” Cell, 2015 Apr 9; 161(2):319-32.
  61. ↑ Y. Tay, L. Kats, L. Salmena, D. Weiss, S.M. Tan, U. Ala, F. Karreth, L. Poliseno, P. Provero, F. Di Cunto, J. Lieberman, I. Rigoutsos and P.P. Pandolfi. "Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs." Cell, 2011 Oct 14; 147 (2): 344-357. Highlighted on cover.
  62. ↑ F.A. Karreth, Y. Tay, D. Perna, U. Ala, A.G. Rust, K.A. Webster, D. Weiss, P.A. Perez-Mancera, M. Krauthammer, R. Halaban, P. Provero, D.J. Adams, D.A. Tuveson and P.P. Pandolfi. "In vivo identification of tumor suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma." Cell, 2011 Oct 14; 147(2): 382-395. Erratum: Nov 11; 147 (4): 948.
  63. ↑ http://www.hmaward.org.ae/profile.php?id=284 “Internation Awards: Hamdan Award for Medical Research Excellence-Therapy in Leukemia 1999-2000”. Sheikh Hamdan Bin Rashid Al Maktoum Award for Medical Sciences. 284. 10 March, 2017.

Selected recent publications

Recent publications from a total of 456:

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