Veach DR, Namavari M, Pillarsetty N, Santos EB, Beresten T, Lambek C, Punzalan BJ, Antczak C, Smith-Jones P, Djaballah H, Clarkson B, Larson SM. Synthesis and Biological evaluation of a Fluorine-18 derivative of Dasatinib.- Journal of Medicinal Chemistry, 50, (23), 5853-5857, 2007.
Wendel H G, de Stanchina E, Cepero E, Ray S, Emig M, Fridman JS, Veach DR, Bornmann WG, Clarkson B, McCombie WR, Kogan SC, Hochhaus A, and Lowe SW: Loss of p53 impedes the antileukemic response to BCR ABL inhibition. PNAS 103:7444 7449, 2006.
Azam M, Nardi V, Shakespeare WC, Metcalf III CA, Bohacek RS, Wang Y, Sundaramoorthi R, Sliz P, Veach DR, Bornmann WG, Clarkson B, Dalgarno DC, Sawyer TK, and Daley GQ: Activity of dual SRC ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance. PNAS 103:9244 9249, 2006.
Liang X, Hajivandi M, Veach D, Wisniewski D, Clarkson B, Resh, MD, and Pope MR: Quantification of change in phosphorylation of BCR ABL kinase and its substrates in response to Imatinib treatment in human chronic myelogenous leukemia cells. Proteomics August; 6 (16): 4554-64, 2006.
Wolff NC, Veach DR, Tong WP, Bornmann WG, Clarkson B, and Ilaria, RL Jr.: PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia. Blood 105:3995 4003, 2005.
von Bubnoff N, Veach DR, van der Kuip H, Aulitsky WE, Sanger J, Seipel P, Bornmann WG, Peschel C, Clarkson B, and Duyster J: A cell based screen for resistance of Bcr Abl positive leukemia identifies the mutation pattern for a PD166326, an alternative Abl kinase inhibitor. Blood 105:1652 1659, 2005.
Veach DR, Namavari M, Beresten T, Balatoni J, Minchenko M, Djaballah H, Finn RD, Clarkson B, Gelovani JG, Bornmann WG, and Larson SM: Synthesis and in vitro examination of [124I] , [125I] and [131I] 2 (4 iodophenylamino) pyrido [2,3 d] pyrimidin 7 one radiolabeled Abl kinase inhibitors. Nuclear Medicine and Biology 32:313 321, 2005.
Tipping AJ, Baluch S, Barnes DJ, Veach DR, Clarkson BM(sic), Bornmann WG, Mahon FX, Goldman JM, and Melo JV: Molecular Targets For Therapy (MTT): Efficacy of dual specific Bcr Abl and Src family kinase inhibitors in cells sensitive and resistant to imatinib mesylate. Leukemia 18 (8)1352 1356. 2004.
von Bubnoff N, Veach DR, Miller WT, Li W, Sänger J, Peschel C, Bornmann WG, Clarkson B, Duyster J. Inhibition of wild-type and mutant Bcr-Abl by pyrido- pyrimidine-type small molecule kinase inhibitors. Cancer Res. 2003;63:6395-6404.
Strife A, Wisniewski D, Liu C, Lambek CL, Darzynkiewicz Z, Silver RT, and Clarkson B. Direct evidence that Bcr-Abl tyrosine kinase activity disrupts normal synergistic interactions between kit ligand and cytokines in primary primitive progenitor cells. Mol Cancer Res. 2003;1:176-185.
Netzer WJ, Dou F, Cai D, Veach D, Jean S, Li Y, Bornmann WG, Clarkson B, Xu H, Greengard P. Gleevec inhibits beta-amyloid production but not Notch cleavage. Proc Natl Acad Sci USA. 2003;100:12444-12449.
Nagar B, Hantschel O, Young MA, Scheffzek K, Veach D, Bornmann W, Clarkson B, Superti-Furga G, Kuriyan J. Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell. 2003;112:859-871.
Clarkson B, Strife A, Wisniewski D, Lambek CL, Liu C. Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies. Leukemia. 2003;17:1211-1262.
Wisniewski D, Lambek C, Liu C, Strife A, Veach D, Nagar B, Young MA, Schindler T, Bornmann W, Bertino JR, Kuriyan J, Clarkson B. Characterization of potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases. Cancer Res. 2002;62:4244-4255.
Nagar B, Bornmann W, Pellicena P, Schindler T, Veach D, Miller TW, Clarkson B, Kuriyan J. Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571). Cancer Res. 2002;62:4236-4243.
Liang X, Wisniewski D, Strife A, Shivakrupa, Clarkson B and Resh MD. Phosphatidylinositol 3-kinase and Src family kinases are required for phosphorylation and membrane recruitment of Dok-1 in c-kit signaling. J Biol Chem. 277:13732-13738, 2002.
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cancer (KAN-ser)
A term for diseases in which abnormal cells divide without control and can invade nearby tissues. Cancer cells can also spread to other parts of the body through the blood and lymph systems. There are several main types of cancer. Carcinoma is a cancer that begins in the skin or in tissues that line or cover internal organs. Sarcoma is a cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. Leukemia is a cancer that starts in blood-forming tissue such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the blood. Lymphoma and multiple myeloma are cancers that begin in the cells of the immune system. Central nervous system cancers are cancers that begin in the tissues of the brain and spinal cord. Also called malignancy.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)chronic (KRAH-nik)
A disease or condition that persists or progresses over a long period of time.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)clinical (KLIH-nih-kul)
Having to do with the examination and treatment of patients.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)etiology (EE-tee-AH-loh-jee)
The cause or origin of disease.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)incidence (IN-sih-dents)
The number of new cases of a disease diagnosed each year.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)kinase (KY-nays)
A type of enzyme that causes other molecules in the cell to become active. Some kinases work by adding chemicals called phosphates to other molecules, such as sugars or proteins. Kinases are a part of many cell processes. Some cancer treatments target certain kinases that are linked to cancer.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)medicine (MEH-dih-sin)
Refers to the practices and procedures used for the prevention, treatment, or relief of symptoms of a diseases or abnormal conditions. This term may also refer to a legal drug used for the same purpose.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)myelogenous (MY-eh-LAH-jeh-nus)
Having to do with, produced by, or resembling the bone marrow. Sometimes used as a synonym for myeloid; for example, acute myeloid leukemia and acute myelogenous leukemia are the same disease.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)National Institutes of Health (NA-shuh-nul IN-stih-TOOTS … helth)
A federal agency in the U.S. that conducts biomedical research in its own laboratories; supports the research of non-Federal scientists in universities, medical schools, hospitals, and research institutions throughout the country and abroad; helps in the training of research investigators; and fosters communication of medical information. Access the National Institutes of Health Web site at . Also called NIH.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)prognosis (prog-NO-sis)
The likely outcome or course of a disease; the chance of recovery or recurrence.
Source: The National Cancer Institute's Dictionary of Cancer Terms
(http://www.cancer.gov/dictionary)
