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  • Erythematous Rash Following Hematopoietic Stem Cell Transplantation

    Abstract Full Text
    JAMA. 2017; 318(18):1822-1823. doi: 10.1001/jama.2017.14949

    A 66-year-old man developed noninfectious fever and rash after autologous HSCT. Chest computed tomography showed ground-glass and consolidative lung opacities; skin punch biopsy showed vacuolar change and superficial perivascular mononuclear cell infiltrate. What would you do next?

  • Acute Anuric Renal Failure in an 80-Year-Old Man

    Abstract Full Text
    JAMA. 2017; 317(14):1471-1472. doi: 10.1001/jama.2017.0704

    An 80-year-old man with stage 4 chronic kidney disease, 2 days of anuria, and an elevated serum κ to λ free light chain ratio had a bone marrow biopsy that stained positive for the plasma cell marker CD138. What would you do next?

  • Trends and Patterns of Disparities in Cancer Mortality Among US Counties, 1980-2014

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    JAMA. 2017; 317(4):388-406. doi: 10.1001/jama.2016.20324

    This cancer epidemiology study uses National Center for Health Statistics population data to estimate trends in age-standardized cancer mortality rates by US county between 1980 and 2014.

  • Effect of Longer-Interval vs Standard Dosing of Zoledronic Acid on Skeletal Events in Patients With Bone Metastases: A Randomized Clinical Trial

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    JAMA. 2017; 317(1):48-58. doi: 10.1001/jama.2016.19425

    This noninferiority trial compares the effects of zoledronic acid administered every 12 weeks vs every 4 weeks over 2 years on prevention of skeletal events in patients with bone metastases due to breast cancer, prostate cancer, or multiple myeloma.

  • The Ethical Challenges of Compassionate Use

    Abstract Full Text
    JAMA. 2016; 315(10):979-980. doi: 10.1001/jama.2016.0416

    This Viewpoint discusses ethical issues related to rapid access to investigational agents (compassionate use) and outlines a patient-focused approach to responding to compassionate use requests.

  • Association Between World Trade Center Exposure and Excess Cancer Risk

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    JAMA. 2012; 308(23):2479-2488. doi: 10.1001/jama.2012.110980
    Li and coauthors report on the association between exposure to the destruction of the World Trade Center and excess cancer risk from 2003 through 2008.
  • JAMA September 5, 2012

    Figure: Effect of BRMs on Occurrence of Specific Types of Cancer in Patients With Rheumatoid Arthritis

    BRM indicates biologic response modifier; OR, odds ratio; TNF, tumor necrosis factor. Numbers of patients included in each comparison are reported in eTable 5. Diamonds represent pooled effect estimates with 95% CIs for all TNF inhibitors. aFor infliximab, 1 patient reported both squamous cell carcinoma and melanoma. bAdrenal, bladder, breast, cholangiocarcinoma, fibrosarcoma, gastrointestinal, hepatic, leiomyosarcoma, liposarcoma, lung, ovarian, pancreatic, prostate, renal, testicular, thyroid, tongue, and uterine. cMultiple myeloma and leukemia.
  • Multiple Myeloma Precursor Disease

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    JAMA. 2010; 304(21):2397-2404. doi: 10.1001/jama.2010.1713
  • Multiple Myeloma

    Abstract Full Text
    JAMA. 2010; 304(21):2430-2430. doi: 10.1001/jama.304.21.2430
  • Phase 3 Trials Suggest Ways to Improve Current Hematologic Cancer Therapies

    Abstract Full Text
    JAMA. 2008; 299(5):510-512. doi: 10.1001/jama.299.5.510
  • William R. Barclay, MD, 1919-2006

    Abstract Full Text
    JAMA. 2006; 295(21):2465-2465. doi: 10.1001/jama.295.21.2465
  • Multiple Myeloma Discovery

    Abstract Full Text
    JAMA. 2004; 291(12):1434-1434. doi: 10.1001/jama.291.12.1434-d
  • Thalidomide Battles Myeloma

    Abstract Full Text
    JAMA. 2001; 286(8):909-909. doi: 10.1001/jama.286.8.909-JQU10007-2-1
  • Diagnostic Criteria For Electrophoretic Patterns of Serum and Urinary Proteins in Multiple Myeloma: Study of One Hundred and Sixty-five Multiple Myeloma Patients and of Seventy-seven Nonmyeloma Patients with Similar Electrophoretic Patterns

    Abstract Full Text
    JAMA. 1960; 174(3):245-251. doi: 10.1001/jama.1960.03030030025005
  • JAMA December 1, 2010

    Figure 5: Biological Events Related to Progression From Precursor Disease to Multiple Myeloma

    The biological transition from normal plasma cells to multiple myeloma precursor disease (monoclonal gammopathy of undetermined significance [MGUS] and smoldering myeloma) to multiple myeloma consists of many overlapping oncogenic events. These events do not all occur in each affected individual, eg, hyperdiploidy is present in approximately 50% of precursor and multiple myeloma tumors. In this illustration, solid lines approximate the period during which the oncogenic event is likely to occur; dashed lines indicate less certainty in the timing. Once an oncogenic event occurs, it almost always persists. The 2 major types of early events include IgH translocations [most commonly: t(4;14), t(14;16), t(6;14), t(11;14), and t(14;20)] and hyperdiploidy, although most tumor cells have only 1 of these 2 events. Either of these can coexist with deletion of chromosome 13, although this abnormality most commonly (>80% to 90% of patients) occurs with the t(4;14), t(14;16), and t(14;20) IgH translocations. A unifying early event in most, perhaps all, precursor and multiple myeloma tumors is the dysregulation of a cyclin D gene. Secondary translocations, sometimes involving an Ig locus, can occur at any stage of myelomagenesis. Activating mutations of NRAS and KRAS are each present in about 15% of multiple myeloma tumors; NRAS mutations are present in MGUS tumors while KRAS mutations are absent from MGUS tumors. Constitutive activation of the nuclear factor κB (NFκB) pathway is mediated by mutations in some tumors during progression. Other events, such as Rb gene inactivation or deletion of p53 or p18 genes, are mostly seen at the level of advanced intramedullary or extramedullary multiple myeloma. Through the stage of intramedullary multiple myeloma the tumor cells are strongly dependent on the bone marrow microenvironment. The reciprocal interaction of the bone marrow microenvironment and the tumor cells results in changes in the bone marrow microenvironment, which are responsible for the lytic lesions that are characteristic of multiple myeloma. Extramedullary tumor cells have developed features that make them independent of the bone marrow microenvironment.
  • JAMA December 1, 2010

    Figure: Multiple Myeloma

  • Progression From Precursor Disease to Multiple Myeloma

    Abstract Full Text
    JAMA. 2011; 305(11):1094-1094. doi: 10.1001/jama.2011.301
  • Progression From Precursor Disease to Multiple Myeloma—Reply

    Abstract Full Text
    JAMA. 2011; 305(11):1094-1094. doi: 10.1001/jama.2011.302

    Abstract Full Text
    JAMA. 1940; 115(1):36-38. doi: 10.1001/jama.1940.72810270001008