Joseph Bertino

Summary

Affiliation: New Jersey
Country: USA

Publications

  1. pmc MiR-24 tumor suppressor activity is regulated independent of p53 and through a target site polymorphism
    Prasun J Mishra
    Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 4:e8445. 2009
  2. doi Lack of expression of MTAP in uncommon T-cell lymphomas
    Joseph R Bertino
    Department of Medicine, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 18901, USA
    Clin Lymphoma Myeloma Leuk 12:306-9. 2012
  3. pmc Quantitative correlation between promoter methylation and messenger RNA levels of the reduced folate carrier
    Rui Yang
    Department of Pediatrics and Molecular Pharmacology R, Y, R, G, The Albert Einstein College of Medicine, The Children s Hospital at Montefiore, Bronx, NY 10461, USA
    BMC Cancer 8:124. 2008
  4. ncbi Is the measurement of thymidylate synthase to determine suitability for treatment with 5-fluoropyrimidines ready for prime time?
    Joseph R Bertino
    The Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA
    Clin Cancer Res 9:1235-9. 2003
  5. ncbi Cancer research: from folate antagonism to molecular targets
    Joseph R Bertino
    Department of Molecular Therapeutics, The Cancer Institute of New Jersey, New Brunswick, NJ 08901, USA
    Best Pract Res Clin Haematol 22:577-82. 2009
  6. ncbi Thymidylate synthase as an oncogene?
    J R Bertino
    Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA
    Cancer Cell 5:301-2. 2004
  7. pmc Targeting tumors that lack methylthioadenosine phosphorylase (MTAP) activity: current strategies
    Joseph R Bertino
    Departments of Medicine and Pharmacology, The Cancer Institute of NJ, Robert Wood Johnson Medical School, New Brunswick, USA
    Cancer Biol Ther 11:627-32. 2011
  8. ncbi Thymidylate synthase expression in hepatic tumors is a predictor of survival and progression in patients with resectable metastatic colorectal cancer
    Mithat Gonen
    Departments of Epidemiology and Biostatistics, Medicine, Surgery, and Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Clin Oncol 21:406-12. 2003
  9. ncbi Methotrexate and cytarabine inhibit progression of human lymphoma in NOD/SCID mice carrying a mutant dihydrofolate reductase and cytidine deaminase fusion gene
    Tulin Budak-Alpdogan
    Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Mol Ther 10:574-84. 2004
  10. doi Retinoblastoma tumor suppressor gene expression determines the response to sequential flavopiridol and doxorubicin treatment in small-cell lung carcinoma
    Tulin Budak-Alpdogan
    Department of Medicine, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Cancer Institute of New Jersey, New Brunswick, NJ 08903, USA
    Clin Cancer Res 15:1232-40. 2009

Research Grants

  1. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 1999
  2. CANCER CENTER SUPPORT GRANT
    Joseph Bertino; Fiscal Year: 2007
  3. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2007
  4. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2007
  5. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2006
  6. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2005
  7. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2004
  8. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2003
  9. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2002
  10. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2001

Collaborators

Detail Information

Publications41

  1. pmc MiR-24 tumor suppressor activity is regulated independent of p53 and through a target site polymorphism
    Prasun J Mishra
    Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 4:e8445. 2009
    ..A novel function for miR-24 as a p53-independent cell cycle inhibitory miRNA is proposed...
  2. doi Lack of expression of MTAP in uncommon T-cell lymphomas
    Joseph R Bertino
    Department of Medicine, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 18901, USA
    Clin Lymphoma Myeloma Leuk 12:306-9. 2012
    ..Importantly, tumors that lack this enzyme have been shown to be more sensitive to inhibitors of de novo purine synthesis (6-thioguanine, methotrexate)...
  3. pmc Quantitative correlation between promoter methylation and messenger RNA levels of the reduced folate carrier
    Rui Yang
    Department of Pediatrics and Molecular Pharmacology R, Y, R, G, The Albert Einstein College of Medicine, The Children s Hospital at Montefiore, Bronx, NY 10461, USA
    BMC Cancer 8:124. 2008
    ..Heavy promoter methylation was previously identified as a basis for the complete silencing of RFC in MDA-MB-231 breast cancer cells, its role and prevalence in RFC transcription regulation are, however, not widely studied...
  4. ncbi Is the measurement of thymidylate synthase to determine suitability for treatment with 5-fluoropyrimidines ready for prime time?
    Joseph R Bertino
    The Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA
    Clin Cancer Res 9:1235-9. 2003
  5. ncbi Cancer research: from folate antagonism to molecular targets
    Joseph R Bertino
    Department of Molecular Therapeutics, The Cancer Institute of New Jersey, New Brunswick, NJ 08901, USA
    Best Pract Res Clin Haematol 22:577-82. 2009
    ..MTX remains a potent and widely used agent...
  6. ncbi Thymidylate synthase as an oncogene?
    J R Bertino
    Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA
    Cancer Cell 5:301-2. 2004
    ..We discuss the possibility that elevated levels of thymidylate synthase noted in some human malignancies may contribute to tumor progression and may also reflect increased levels of its transcriptional activator E2F-1...
  7. pmc Targeting tumors that lack methylthioadenosine phosphorylase (MTAP) activity: current strategies
    Joseph R Bertino
    Departments of Medicine and Pharmacology, The Cancer Institute of NJ, Robert Wood Johnson Medical School, New Brunswick, USA
    Cancer Biol Ther 11:627-32. 2011
    ..In MTAP-deficient tumor cells, conversion proceeds and the tumor cells are selectively killed. Successful mouse studies using this novel strategy were recently reported...
  8. ncbi Thymidylate synthase expression in hepatic tumors is a predictor of survival and progression in patients with resectable metastatic colorectal cancer
    Mithat Gonen
    Departments of Epidemiology and Biostatistics, Medicine, Surgery, and Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Clin Oncol 21:406-12. 2003
    ....
  9. ncbi Methotrexate and cytarabine inhibit progression of human lymphoma in NOD/SCID mice carrying a mutant dihydrofolate reductase and cytidine deaminase fusion gene
    Tulin Budak-Alpdogan
    Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Mol Ther 10:574-84. 2004
    ..05), suggesting that early treatment allowed for enrichment of transduced marrow progenitors. These results encourage clinical studies using this retroviral fusion gene construct...
  10. doi Retinoblastoma tumor suppressor gene expression determines the response to sequential flavopiridol and doxorubicin treatment in small-cell lung carcinoma
    Tulin Budak-Alpdogan
    Department of Medicine, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Cancer Institute of New Jersey, New Brunswick, NJ 08903, USA
    Clin Cancer Res 15:1232-40. 2009
    ..Flavopiridol inhibits proliferation and induces apoptosis in SCLC cell lines. We hypothesized that the sequence flavopiridol followed by doxorubicin would be synergistic in pRb-deficient SCLC cells...
  11. ncbi Novel aspects of resistance to drugs targeted to dihydrofolate reductase and thymidylate synthase
    Debabrata Banerjee
    Program of Molecular Pharmacology and Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Biochim Biophys Acta 1587:164-73. 2002
    ....
  12. ncbi Hematopoietic stem cell gene therapy with drug resistance genes: an update
    Tulin Budak-Alpdogan
    Department of Medicine, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, 195 Little Albany Street, New Brunswick, New Jersey 08903, USA
    Cancer Gene Ther 12:849-63. 2005
    ..In this review, we describe ongoing experimental approaches, observations from clinical trials, and safety concerns related to the drug resistance gene transfer...
  13. ncbi Myeloprotection with drug-resistance genes
    Debabrata Banerjee
    Molecular Pharmacology and Experimental Therapeutics Program, Sloan Kettering Institute for Cancer Research, New York, USA
    Lancet Oncol 3:154-8. 2002
    ..Clinical trials, which have established that the approach is safe, are now being designed to address more therapeutically relevant issues...
  14. pmc Translational modulation of proteins expressed from bicistronic vectors
    Prasun J Mishra
    Department of Pharmacology, Robert Wood Johnson Medical School, Cancer Institute of New Jersey, USA
    Mol Imaging 8:305-18. 2009
    ..To our knowledge, this is the first report demonstrating that levels of proteins in DHFR-based bicistronic constructs can be induced and modulated using MTX and rapamycin treatment...
  15. ncbi Chemoprotection by transfer of resistance genes
    Tulin Budak-Alpdogan
    Department of Medicine, The Cancer Institute of New Jersey, Robert Wood Johson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ, USA
    Methods Mol Biol 542:661-704. 2009
    ....
  16. ncbi Functional assessment of the engraftment potential of gammaretrovirus-modified CD34+ cells, using a short serum-free transduction protocol
    Tulin Budak-Alpdogan
    Department of Medicine, Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, 08903, USA
    Hum Gene Ther 17:780-94. 2006
    ..We have thus developed a short and efficient human MBP CD34(+) transduction protocol under serum-free conditions that is suitable and broadly applicable for phase I clinical trials...
  17. ncbi Role of pemetrexed in non-small cell lung cancer
    Giuseppe S A Longo-Sorbello
    Departments of Medicine and Pharmacology, Cancer Institute of New Jersey Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA
    Cancer Invest 25:59-66. 2007
    ..Further increases in drug dose may be possible using transfer of drug resistance genes in hematopoietic stem cells...
  18. ncbi MiRSNPs or MiR-polymorphisms, new players in microRNA mediated regulation of the cell: Introducing microRNA pharmacogenomics
    Prasun J Mishra
    Department of Pharmacology and Medicine, Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Jersey, USA
    Cell Cycle 7:853-8. 2008
    ....
  19. ncbi Implantable pump for long-term chemotherapy administration via the hepatic artery: has it fulfilled its promise?
    Joseph R Bertino
    University of Medicine and Dentistry of New Jersey, USA
    J Clin Oncol 26:4528-9. 2008
  20. pmc Species-specific differences in translational regulation of dihydrofolate reductase
    Yi Ching Hsieh
    Department of Medicine and Pharmacology, Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey 08903, USA
    Mol Pharmacol 76:723-33. 2009
    ..We also present evidence to suggest that the translational up-regulation of dihydrofolate reductase by methotrexate in tumor cells is an adaptive mechanism that decreases sensitivity to this drug...
  21. pmc A miR-24 microRNA binding-site polymorphism in dihydrofolate reductase gene leads to methotrexate resistance
    Prasun J Mishra
    Department of Pharmacology, Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA
    Proc Natl Acad Sci U S A 104:13513-8. 2007
    ..We demonstrate that a naturally occurring miRSNP (a SNP located at or near a microRNA binding site in 3' UTR of the target gene or in a microRNA) is associated with enzyme overproduction and drug resistance...
  22. ncbi E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents
    Angelo J Russo
    The Cancer Institute of New Jersey, Robert Wood Johnson School of Medicine, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey 08903, USA
    Cancer Res 66:7253-60. 2006
    ..These studies add support to recent reports that show E2F regulates genes involved in mitotic entry and exit and allow the suggestion that mitotic inhibitors may have selective effects in tumors that overexpress E2F-1...
  23. ncbi Pharmacogenomics of microRNA: a miRSNP towards individualized therapy
    Joseph R Bertino
    Pharmacogenomics 8:1625-7. 2007
  24. ncbi EGFP fluorescence as an indicator of cancer cells response to methotrexate
    Magdalena Dabrowska
    Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur St, 02 093 Warsaw, Poland
    Eur J Pharmacol 555:93-9. 2007
    ..As the increase in EGFP fluorescence could also be visualized by fluorescence microscopy, this reporter system may be employed to image methotrexate action in cancer cells in living models...
  25. pmc Cells exposed to antifolates show increased cellular levels of proteins fused to dihydrofolate reductase: a method to modulate gene expression
    Philipp Mayer-Kuckuk
    Molecular Pharmacology and Therapeutics Program, Department of Surgery, Nuclear Medicine Service, Radiochemistry Cyclotron, and Preparative Synthesis Chemistry Core Facilities, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 99:3400-5. 2002
    ..Drug-mediated elevation of cellular DHFR-fused proteins is a very useful method to modulate gene expression in vivo for imaging as well as therapeutic purposes...
  26. ncbi Identification of amino acids required for the functional up-regulation of human dihydrofolate reductase protein in response to antifolate Treatment
    Nancy Skacel
    Weill Cornell Graduate School of Medical Sciences, New York, New York, USA
    J Biol Chem 280:22721-31. 2005
    ..The mutants that are not up-regulated by methotrexate are unable to bind their cognate mRNA...
  27. ncbi Methotrexate selection of long-term culture initiating cells following transduction of CD34(+) cells with a retrovirus containing a mutated human dihydrofolate reductase gene
    Naoko Takebe
    Program of Molecular Pharmacology and Experimental Therapeutics, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Gene Ther 9:308-20. 2002
    ..These are the first investigations to demonstrate selection for transduced long-term culture initiating cells using MTX. The DHFR/MTX system holds promise for improving selection of gene-transduced hematopoietic progenitor cells in vivo...
  28. ncbi Molecular therapies for colorectal cancer metastatic to the liver
    Philipp Mayer-Kuckuk
    Program of Molecular Pharmacology and Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Mol Ther 5:492-500. 2002
    ..Here we review molecular therapies for colorectal cancer metastatic to the liver...
  29. ncbi Characterization of potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases
    David Wisniewski
    Molecular Pharmacology and Chemistry Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 62:4244-55. 2002
    ..These compounds are potent inhibitors of both the Bcr-Abl and c-kit receptor tyrosine kinases and deserve further study as potential treatments for both CML and for diseases in which c-kit has a role...
  30. ncbi Imaging of dihydrofolate reductase fusion gene expression in xenografts of human liver metastases of colorectal cancer in living rats
    Philipp Mayer-Kuckuk
    Molecular Pharmacology and Therapeutics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Eur J Nucl Med Mol Imaging 30:1281-91. 2003
    ..It is concluded that the two examined nucleotide imaging methods are feasible techniques for monitoring of DHFR-HSV TK fusion protein expression in hepatic colorectal tumor tissue in living animals...
  31. ncbi Retroviral transduction of a mutant dihydrofolate reductase-thymidylate synthase fusion gene into murine marrow cells confers resistance to both methotrexate and 5-fluorouracil
    Gina M Capiaux
    Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Hum Gene Ther 14:435-46. 2003
    ..As MTX and 5-FU are used in combination therapy for diseases such as breast and colon cancer, this fusion gene may be useful in the clinic to reduce myelosuppressive toxicity associated with this drug combination...
  32. ncbi mRNA expression levels of E2F transcription factors correlate with dihydrofolate reductase, reduced folate carrier, and thymidylate synthase mRNA expression in osteosarcoma
    Rebecca Sowers
    Department of Pediatrics, Orthopaedic Surgery Service, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Mol Cancer Ther 2:535-41. 2003
    ....
  33. ncbi Reduced folate carrier and dihydrofolate reductase expression in acute lymphocytic leukemia may predict outcome: a Children's Cancer Group Study
    Adam S Levy
    Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    J Pediatr Hematol Oncol 25:688-95. 2003
    ..The purpose of this study was to assess whether reduced folate carrier (RFC) and DHFR expression in untreated leukemic blasts correlated with outcome...
  34. ncbi Overexpression of E2F-1 in lung and liver metastases of human colon cancer is associated with gene amplification
    Marian Iwamoto
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Cancer Biol Ther 3:395-9. 2004
    ..In as much as TS is transcriptionally regulated by E2F-1, these results provide an explanation for the high levels of TS mRNA noted in some tumor samples...
  35. ncbi p14ARF expression increases dihydrofolate reductase degradation and paradoxically results in resistance to folate antagonists in cells with nonfunctional p53
    Pellegrino G Magro
    Joan and Sanford I Weill Graduate School of Medical Sciences of Cornell University, and Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Res 64:4338-45. 2004
    ..Depletion of thymidine in the medium reversed this resistance, indicating that p14(ARF) induction increases the reliance of these cells on thymidine salvage...
  36. ncbi Protection of hematopoietic stem cells from pemetrexed toxicity by retroviral gene transfer with a mutant dihydrofolate reductase-mutant thymidylate synthase fusion gene
    Gina M Capiaux
    Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Cancer Gene Ther 11:767-73. 2004
    ..Co-expression of mutant DHFR and TS enzymes has additive effects in conferring resistance to pemetrexed-induced toxicity. This construct may be useful for conferring myeloprotection to patients receiving this drug...
  37. ncbi Fas-mediated signaling enhances sensitivity of human soft tissue sarcoma cells to anticancer drugs by activation of p38 kinase
    Weiwei Li
    Program of Molecular Pharmacology and Chemistry, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Mol Cancer Ther 1:1343-8. 2002
    ..These results demonstrate that stimulation of the Fas pathway by a subtoxic dose of a Fas agonist can selectively enhance sensitivity of STS cells to certain chemotherapeutic agents through activation of p38...
  38. ncbi Sequence-dependent synergistic cytotoxicity of ecteinascidin-743 and paclitaxel in human breast cancer cell lines in vitro and in vivo
    Naoto Takahashi
    Program of Molecular Pharmacology and Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 62:6909-15. 2002
    ..These results suggest that the combination of ET-743 and paclitaxel should be assessed in clinical trials for the treatment of breast cancer...
  39. ncbi Specific tumour localisation of a huA33 antibody--carboxypeptidase A conjugate and activation of methotrexate-phenylalanine
    P Markus Deckert
    Medizinische Klinik III Haematology, Oncology and Transfusion Medicine, Charite Campus Benjamin Franklin, D 12200 Berlin, Germany
    Int J Oncol 24:1289-95. 2004
    ..In summary, our results demonstrate in principle the feasibility of A33-based enzyme targeting, but they call for small recombinant antibody-enzyme constructs to facilitate tumour penetration and clearance from the bloodstream...
  40. ncbi Methylthioadenosine phosphorylase gene deletions are common in osteosarcoma
    José M García-Castellano
    Orthopaedic Surgery Service, affiliated with Weil Medical College of Cornell University, New York, NY 10021, USA
    Clin Cancer Res 8:782-7. 2002
    ..The aim of this study was to investigate the frequency of molecular alterations in MTAP in osteosarcoma...
  41. ncbi Potential regional differences for the tolerability profiles of fluoropyrimidines
    Daniel G Haller
    Abramson Cancer Center at the University of Pennsylvania, Philadelphia, PA, USA
    J Clin Oncol 26:2118-23. 2008
    ....

Research Grants17

  1. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 1999
    ....
  2. CANCER CENTER SUPPORT GRANT
    Joseph Bertino; Fiscal Year: 2007
    ..abstract_text> ..
  3. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2007
    ..The use of MEF cells null for p53, p19 ARF and both will be utilized to test in a more well defined system the function of these proteins on DHFR levels. ..
  4. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2007
    ..The use of MEF cells null for p53, p19 ARF and both will be utilized to test in a more well defined system the function of these proteins on DHFR levels. ..
  5. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2006
    ..The use of MEF cells null for p53, p19 ARF and both will be utilized to test in a more well defined system the function of these proteins on DHFR levels. ..
  6. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2005
    ..The use of MEF cells null for p53, p19 ARF and both will be utilized to test in a more well defined system the function of these proteins on DHFR levels. ..
  7. Mechanism of Action of Folate Antagonist
    Joseph Bertino; Fiscal Year: 2004
    ..The use of MEF cells null for p53, p19 ARF and both will be utilized to test in a more well defined system the function of these proteins on DHFR levels. ..
  8. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2003
    ....
  9. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2002
    ....
  10. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2001
    ....
  11. MECHANISM OF ACTION OF FOLATE ANTAGONISTS
    Joseph Bertino; Fiscal Year: 2000
    ....