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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 53 (2002), S. 369-381 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Notes: Abstract Chronic myelogenous leukemia (CML) is a clonal hematopoetic stem cell disorder characterized by the Philadelphia chromosome and resultant production of the constitutively activated Bcr-Abl tyrosine kinase. Characterized clinically by marked myeloid proliferation, it invariably terminates in an acute leukemia. Conventional therapeutic options include interferon-based regimens and stem cell transplantation, with stem cell transplantation being the only curative therapy. Through rational drug development, STI571, a Bcr-Abl tyrosine kinase inhibitor, has emerged as a paradigm for gene product targeted therapy, offering new hope for expanded treatment options for patients with CML.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The bcr–abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr–Abl fusion ...
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Heterozygous deletions within human chromosome 22q11 are the genetic basis of DiGeorge/velocardiofacial syndrome (DGS/VCFS), the most common deletion syndrome (1 in 4,000 live births) in humans. CRKL maps within the common deletion region for DGS/VCFS (ref. 2) and encodes an SH2-SH3-SH3 adapter ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature biotechnology 23 (2005), S. 1209-1210 
    ISSN: 1546-1696
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: [Auszug] To the editor: In the March issue (Nat. Biotechnol. 23, 329–336, 2005), Fabian et al. introduced an efficient method for quickly determining the kinase specificity profiles of small-molecule inhibitors targeted to the ATP site of kinases. In a data set profiling 20 kinase inhibitors against ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 10 (1981), S. 227-237 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro investigations were undertaken to determine the Con-A and mixed lymphocyte (MLR) blastogenic responses of spleen cells obtained from ACI rats inoculated intraperitoneally (IP) with BCG cell walls (BCGcw). Spleen cells from rats bearing the intramuscular (IM) Morris hepatoma 3924a and rats in which IP BCGcw immunization had caused an enhancement of tumor growth were also examined. Several time points were examined to determine the kinetics of the response. BCGcw-immunized animals showed a dose-related depression in Con-A blastogenesis, which was maximal 7–14 days after immunization. Removal of plastic-adherent cells resulted in near-complete restoration of normal Con-A responsiveness. The Con-A response of normal spleen cells could be depressed by the addition of an adherent population of spleen cells obtained from animals 7–14 days after IP immunization with 900 μg BCGcw. Animals which were immunized with 900 μg BCGcw showed a severe depression in MLR reactivity (〈10% of normal) throughout the experiment. Approximately 50% of the normal MLR response was restored by removal of plastic-adherent cells. Studies with animals inoculated with tumor only showed a depression of Con-A and MLR blastogenesis 28 days after tumor inoculation. BCGcw-preimmunized tumor-bearing animals showed a profound decrease in Con-A and MLR reactivity at all time points examined. A correlation is made relating the presence of BCGcw-induced suppressor cells with the observed in vivo enhancement of tumor growth by BCGcw immunization.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 10 (1981), S. 217-225 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present studies describe a systemic effect of BCGcw inoculated intraperitoneally by observing its influence on the development of Morris hepatomas inoculated intramuscularly. In none of our studies did we observe an inhibition of tumor growth. Instead, an enhancement of tumor growth was seen with four antigenically distinct Morris hepatomas (3924a, 9098, 7777, and 5123tc) in two strains of inbred rats (Buffalo and ACI). Extensive studies with Morris hepatoma 3924a showed consistent enhancement of intramuscular tumor growth in eight of eight experiments with a tumor cell dose of 1×105 and a BCGcw dose of 900 μg. In BCGcw-inoculated animals, palpable tumors (1–2 g) were detected approximately 1 week earlier than in controls, and significantly larger tumor masses were noted on the day of sacrifice. With the threshold dose of cells, 1×104, an increase in tumor incidence was observed. It was not necessary for the host to be immunized with BCGcw prior to tumor inoculation as enhancement of tumor growth occurred when the BCGcw were inoculated the same day or 7 days after tumor inoculation. Splenectomized animals also demonstrated BCGcw-mediated enhancement of tumor growth. BCGcw immunization blocks the induction of tumor-specific immunity. When 3924a ascites tumor cells were inoculated intradermally into normal animals, no tumor growth was observed and tumor-specific immunity resulted. When 3924a ascites tumor cells were inoculated intradermally into BCGcw-immunized animals, progressive intradermal tumors grew in all the animals, implying that tumor-specific immunity was not induced. The administration of BCGcw did not effect established tumor-specific immunity to line 3924a as assessed by tumor-specific rechallenge resistance. Studies with an allograft system showed that the ACI tumor 3924a would not grow in normal Buffalo rats, but transient tumor growth was observed when the Buffalo rats were immunized with BCGcw.
    Type of Medium: Electronic Resource
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