Search Results - "BEDI, Atul"

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    Targeted sequencing reveals clonal genetic changes in the progression of early lung neoplasms and paired circulating DNA by Izumchenko, Evgeny, Chang, Xiaofei, Brait, Mariana, Fertig, Elana, Kagohara, Luciane T., Bedi, Atul, Marchionni, Luigi, Agrawal, Nishant, Ravi, Rajani, Jones, Sian, Hoque, Mohammad O., Westra, William H., Sidransky, David

    Published in Nature communications (16-09-2015)
    “…Lungs resected for adenocarcinomas often harbour minute discrete foci of cytologically atypical pneumocyte proliferations designated as atypical adenomatous…”
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    The relative expression of Mig6 and EGFR is associated with resistance to EGFR kinase inhibitors by Chang, Xiaofei, Izumchenko, Eugene, Solis, Luisa M, Kim, Myoung Sook, Chatterjee, Aditi, Ling, Shizhang, Monitto, Constance L, Harari, Paul M, Hidalgo, Manuel, Goodman, Steve N, Wistuba, Ignacio I, Bedi, Atul, Sidransky, David

    Published in PloS one (31-07-2013)
    “…The sensitivity of only a few tumors to anti-epidermal growth factor receptor EGFR tyrosine kinase inhibitors (TKIs) can be explained by the presence of EGFR…”
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    Conversion of Bcl-2 to a bax-like death effector by caspases by CHENG, E. H.-Y, KIRSCH, D. G, CLEM, R. J, RAVI, R, KASTAN, M. B, BEDI, A, UENO, K, HARDWICK, J. M

    “…Caspases are a family of cysteine proteases implicated in the biochemical and morphological changes that occur during apoptosis (programmed cell death). The…”
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    Adenylate kinase 3 sensitizes cells to cigarette smoke condensate vapor induced cisplatin resistance by Chang, Xiaofei, Ravi, Rajani, Pham, Vui, Bedi, Atul, Chatterjee, Aditi, Sidransky, David

    Published in PloS one (15-06-2011)
    “…The major established etiologic risk factor for bladder cancer is cigarette smoking and one of the major antineoplastic agents used for the treatment of…”
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    Elimination of hepatic metastases of colon cancer cells via p53-independent cross-talk between irinotecan and Apo2 ligand/TRAIL by RAVI, Rajani, JAIN, Ajay J, BEDI, Atul, SCHULICK, Richard D, PHAM, Vui, PROUSER, Traci S, ALLEN, Heather, MAYER, Elizabeth Garrett, HUA YU, PARDOLL, Drew M, ASHKENAZI, Avi

    Published in Cancer research (Chicago, Ill.) (15-12-2004)
    “…The majority of colorectal cancers have lost/inactivated the p53 tumor suppressor gene. Using isogenic human colon cancer cells that differ only in their p53…”
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    Inhibition of apoptosis during development of colorectal cancer by ATUL BEDI, PASRICHA, P. J, AKHTAR, A. J, BARBER, J. P, BEDI, G. C, GIARDIELLO, F. M, ZEHNBAUER, B. A, HAMILTON, S. R, JONES, R. J

    Published in Cancer research (Chicago, Ill.) (01-05-1995)
    “…Colorectal tumorigenesis proceeds through an accumulation of specific genetic alterations. Studies of the mechanism by which these genetic changes effect…”
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    BCR-ABL-Mediated Inhibition of Apoptosis With Delay of G2/M Transition After DNA Damage: A Mechanism of Resistance to Multiple Anticancer Agents by Bedi, Atul, Barber, James P., Bedi, Gauri C., El-Deiry, Wafik S., Sidransky, David, Vaia, Milada S., Akhtar, Adil J., Hilton, John, Jones, Richard J.

    Published in Blood (01-08-1995)
    “…A critical determinant of the efficacy of antineoplastic therapy is the response of malignant cells to DNA damage induced by anticancer agents. The p53…”
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    The effects of sulindac on colorectal proliferation and apoptosis in familial adenomatous polyposis by Pasricha, P J, Bedi, A, O'Connor, K, Rashid, A, Akhtar, A J, Zahurak, M L, Piantadosi, S, Hamilton, S R, Giardiello, F M

    Published in Gastroenterology (New York, N.Y. 1943) (01-09-1995)
    “…The mechanism by which sulindac causes regression of adenomas in patients with familial adenomatous polyposis (FAP) is unclear. Conflicting data on the drug's…”
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    Potential methods to circumvent blocks in apoptosis in lymphomas by Ravi, Rajani, Bedi, Atul

    Published in Current opinion in oncology (01-09-2002)
    “…We review our current understanding of the molecular determinants and mechanisms of lymphocyte apoptosis and identify the key regulators of these…”
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    The TGFβ―miR200―MIG6 Pathway Orchestrates the EMT-Associated Kinase Switch That Induces Resistance to EGFR Inhibitors by IZUMCHENKO, Evgeny, XIAOFEI CHANG, SIDRANSKY, David, MICHAILIDI, Christina, KAGOHARA, Luciane, RAVI, Rajani, PAZ, Keren, BRAIT, Mariana, HOQUE, Mohammad, SHIZHANG LING, BEDI, Atul

    Published in Cancer research (Chicago, Ill.) (15-07-2014)
    “…Although specific mutations in the tyrosine kinase domain of epidermal growth factor receptor (EGFR) identify tumors that are responsive to EGFR tyrosine…”
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    BCR-ABL gene rearrangement and expression of primitive hematopoietic progenitors in chronic myeloid leukemia by ATUL BEDI, ZEHNBAUER, B. A, COLLECTOR, M. I, BARBER, J. P, ZICHA, M. S, SHARKIS, S. J, JONES, R. J

    Published in Blood (01-06-1993)
    “…Chronic myeloid leukemia (CML) is characterized by an initial chronic phase of expanded yet orderly clonal hematopoiesis that is distinguished by the BCR-ABL…”
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    Inhibition of TGF-β enhances the in vivo antitumor efficacy of EGF receptor-targeted therapy by Bedi, Atul, Chang, Xiaofei, Noonan, Kimberly, Pham, Vui, Bedi, Rishi, Fertig, Elana J, Considine, Michael, Califano, Joseph A, Borrello, Ivan, Chung, Christine H, Sidransky, David, Ravi, Rajani

    Published in Molecular cancer therapeutics (01-11-2012)
    “…EGF receptor (EGFR)-targeted monoclonal antibodies (mAb), such as cetuximab, execute their antitumor effect in vivo via blockade of receptor-ligand…”
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    Cytotoxic T cells overcome BCR-ABL-mediated resistance to apoptosis by FUCHS, E. J, ATUL BEDI, JONES, R. J, HESS, A. D

    Published in Cancer research (Chicago, Ill.) (01-02-1995)
    “…Chronic myeloid leukemia is a disease marked by expanded clonal hematopoiesis; it is incurable by chemotherapy or radiation but is cured in a majority of…”
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    NF-κB in cancer—a friend turned foe by Ravi, Rajani, Bedi, Atul

    Published in Drug resistance updates (01-02-2004)
    “…The nuclear factor of κB (NF-κB) family of heterodimeric transcription factors plays an instrumental role in immune, inflammatory, and stress responses. NF-κB…”
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    Regulation of p53 Family Member Isoform ΔNp63α by the Nuclear Factor-κB Targeting Kinase IκB Kinase β by Chatterjee, Aditi, Chang, Xiaofei, Sen, Tanusree, Ravi, Rajani, Bedi, Atul, Sidransky, David

    Published in Cancer research (Chicago, Ill.) (15-02-2010)
    “…The p53 family gene p63 plays an instrumental role in cellular stress responses including responses to DNA damage. In addition to encoding a full-length…”
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