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  • Balancing Access and Innovation: India’s Supreme Court Rules on Imatinib

    Abstract Full Text
    JAMA. 2013; 310(3):263-264. doi: 10.1001/jama.2013.7336
  • One vs Three Years of Adjuvant Imatinib for Operable Gastrointestinal Stromal Tumor: A Randomized Trial

    Abstract Full Text
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    JAMA. 2012; 307(12):1265-1272. doi: 10.1001/jama.2012.347
  • JAMA March 28, 2012

    Figure 1: Flow of Patients in Study

    ITT indicates intention-to-treat. aThe numbers of individuals screened for eligibility and the reasons for exclusion were not available. b1 patient assigned to 12 months of imatinib was mistakenly treated with 36 months of imatinib.
  • JAMA March 28, 2012

    Figure 2: Comparison of Recurrence-Free Survival and Overall Survival Between Groups

    Comparison of recurrence-free survival in the modified intention-to-treat population (A) and the efficacy population (B). Comparison of overall survival in the modified intention-to-treat population (C) and the efficacy population (D). The 3-year survival rates of patients assigned to 36 months of imatinib and those assigned to 12 months of imatinib are 86.6% vs 60.1% (A), 88.1% vs 62.1% (B), 96.3% vs 94.0% (C), and 97.6% vs 95.8% (D), respectively, and the 5-year survival rates, 65.6% vs 47.9% (A), 67.4% vs 50.3% (B), 92.0% vs 81.7% (C), and 93.9% vs 81.7% (D).
  • Optimal Duration of Adjuvant Therapy for Patients With Resected Gastrointestinal Stromal Tumors

    Abstract Full Text
    JAMA. 2012; 307(12):1312-1314. doi: 10.1001/jama.2012.368
  • JAMA June 8, 2011

    Figure 2: Radiographic Responses to Imatinib Mesylate

    MRI indicates magnetic resonance imaging; PET, positron emission tomography. MRI and PET scans from a representative patient with vulvovaginal mucosal melanoma harboring both an exon 11 L576P mutation and amplification of KIT are shown at baseline (yellow arrows, A and C) and after 6 weeks of therapy with imatinib mesylate (yellow arrows, B and D). The arrowhead in A indicates a heterogeneous multilobulated mass distending the entire vagina and extending inferiorly to the introitus. This lesion demonstrates intense fluorodeoxyglucose uptake on PET imaging (arrowhead in C). After 6 weeks of therapy with imatinib mesylate, there was significant shrinkage in the size of this mass with interval resolution of hypermetabolic activity (arrowheads in B and D indicate baseline locations of tumor). This patient ultimately achieved a complete radiographic response to therapy at her week 12 scan. Baseline and posttreatment PET images of a second representative patient with an acral melanoma harboring an exon 11 576P mutation and amplification are shown in E and F. This patient ultimately achieved a complete radiographic and pathological response to therapy at his week 12 scan.
  • KIT as a Therapeutic Target in Metastatic Melanoma

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    JAMA. 2011; 305(22):2327-2334. doi: 10.1001/jama.2011.746
  • JAMA June 8, 2011

    Figure 1: Treatment Response Over Time by Melanoma Subtype and Genetic Alteration of KIT

    CSD indicates melanoma arising from chronically sun-damaged skin; NA, not applicable. The melanoma subtype, KIT mutational and amplification status, the ratio of mutant to wild-type alleles as determined by their respective electropherogram peak heights, and the RECIST (Response Evaluation Criteria in Solid Tumors) response achieved for each patient treated with imatinib mesylate is shown. Amplification was defined as a KIT -to-centromere ratio of 2.5 or more, with the pattern of amplification described as uniform (homogeneous) or mixed (heterogeneous) across the tumor specimen. The best response as determined by RECIST is identified by the color of the bar. The length of the bar represents the duration of time in weeks that each patient remained receiving therapy. aMutations previously identified in melanoma and gastrointestinal stroma tumors.bTumors with mutant to wild-type allelic ratios of more than 1:1, which are those hypothesized most likely to respond to therapy with KIT inhibition. cPatients receiving treatment at the time of this report.
  • Looking Beyond Imatinib

    Abstract Full Text
    JAMA. 2006; 295(4):369-370. doi: 10.1001/jama.295.4.369
  • JAMA September 17, 2003

    Figure: Scientists Probe Cancer Cell Resistance

    The BCR-ABL fusion protein binds adenosine triphosphate (ATP) and transfers phosphate to tyrosine residues on its substrate, leading to transmission of intracellular signals that promote unregulated cell proliferation and anti-apoptotic effects and alter cell adhesion. Imatinib blocks the ATP binding site and thereby inhibits protein kinase activity. Mutations in the BCR-ABL gene that affect the tyrosine kinase region of the BCR-ABL fusion protein impair the ability of imatinib to bind to the protein, resulting in resistance to the drug.
  • Scientists Probe Cancer Cell Resistance

    Abstract Full Text
    JAMA. 2003; 290(11):1435-1437. doi: 10.1001/jama.290.11.1435
  • JAMA August 27, 2003

    Figure 2: Putative Effect of Therapy on Chronic Myelogenous Leukemia (CML) Burden

    Hydroxyurea rarely results in hematologic remissions but controls most manifestations of stable-phase disease. A minority of patients enter hematologic and cytogenetic remission with interferon, but most people still have detectable disease by reverse transcriptase polymerase chain reaction (RT-PCR). Imatinib is more likely to induce remission than interferon or hydroxyurea, but 95% of patients have detectable BCR-ABL by polymerase chain reaction. Stem cell transplantation is known to cure the disease. The conditioning regimen (chemotherapy or chemoradiotherapy administered prior to stem cell infusion) contributes modest cytoreduction, but the bulk of the benefit derives from immunologic control of the disease through a graft-vs-leukemia effect. The number of residual cells that are tantamount to cure of the disease cannot be determined. The arrows indicate that for each therapy, a proportion of patients may have a smaller burden of CML cells. FISH indicates fluorescence in situ hybridization; HSCT, hematopoietic stem cell transplantation.
  • A 41-Year-Old Woman With Chronic Myelogenous Leukemia

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    JAMA. 2003; 290(8):1083-1090. doi: 10.1001/jama.290.8.1083
  • New Indication for Gleevec

    Abstract Full Text
    JAMA. 2002; 287(9):1103-1103. doi: 10.1001/jama.287.9.1103-JFD20003-2-1
  • Precision Medicine: The Future or Simply Politics?

    Abstract Full Text
    JAMA. 2015; 313(11):1089-1091. doi: 10.1001/jama.2015.0957
  • Sunitinib in Patients With Metastatic Renal Cell Carcinoma

    Abstract Full Text
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    JAMA. 2006; 295(21):2516-2524. doi: 10.1001/jama.295.21.2516
  • Fostering Innovation and Discovery in Biomedical Research

    Abstract Full Text
    JAMA. 2005; 294(11):1390-1393. doi: 10.1001/jama.294.11.1390
  • Cancer Drug

    Abstract Full Text
    JAMA. 2003; 290(16):2194-2195. doi: 10.1001/jama.290.16.2194
  • Trends in the Risks and Benefits to Patients With Cancer Participating in Phase 1 Clinical Trials

    Abstract Full Text
    JAMA. 2004; 292(17):2130-2140. doi: 10.1001/jama.292.17.2130
  • Ethics of Phase 1 Oncology Studies: Reexamining the Arguments and Data

    Abstract Full Text
    JAMA. 2003; 290(8):1075-1082. doi: 10.1001/jama.290.8.1075