PubMed · 7787481
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A R Williams. 1995. Potential for abuse.. https://pubmed.ncbi.nlm.nih.gov/7787481/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Interferon consensus sequence binding protein (ICSBP) was first identified as a transcription factor of the interferon (IFN) regulatory factor family (IRF) which regulates expression of IFN-dependent genes by binding to DNA at specific sites, IFN-stimulated responsive elements. Analysis of ICSBP-deficient mice showed hematologic alterations similar to chronic myelogenous leukemia (CML) in humans and suggested a novel role for ICSBP in regulating proliferation and differentiation of hematopoietic progenitor cells. Here we show that ICSBP-mRNA expression is impaired in human myeloid leukemias: 27 of 34 CML patients (79%) and 21 of 32 patients with acute myeloid leukemia (AML) (66%) showed very low or absent transcript numbers of ICSBP. In contrast, only 2 of 33 normal volunteers (6%) showed low transcription of ICSBP (P < . 0001 both for CML and AML values). The lack of expression was not associated with lack of lymphatic cells, which normally have been shown to express ICSBP at the highest level. More detailed analysis showed an absence of ICSBP-mRNA also in sorted B cells derived from CML patients. To analyze whether ICSBP may be induced in leukemic cells, ex vivo experiments using a known inducer of ICSBP, IFN-gamma, were performed. Ex vivo treatment of primary CML cells using IFN-gamma resulted in induction of ICSBP transcripts. Furthermore, samples of CML patients during IFN-alpha treatment were analyzed. In 11 of 12 CML patients ICSBP-mRNA was inducible upon in vivo treatment with IFN-alpha, but decreased with progression of CML. Stable transfection of K-562 cell line with ICSBP led to no difference in bcr-abl expression in vitro, although two patients showed an inverse correlation between bcr-abl and ICSBP in vivo. These data suggest that lack of ICSBP may have an important role also in human myeloid leukemogenesis.
In chronic illness, day-to-day care responsibilities fall most heavily on patients and their families. Effective collaborative relationships with health care providers can help patients and families better handle self-care tasks. Collaborative management is care that strengthens and supports self-care in chronic illness while assuring that effective medical, preventive, and health maintenance interventions take place. In this paper, the following essential elements of collaborative management developed in light of behavioral principles and empirical evidence about effective care in chronic illness are discussed: 1) collaborative definition of problems, in which patient-defined problems are identified along with medical problems diagnosed by physicians; 2) targeting, goal setting, and planning, in which patients and providers focus on a specific problem, set realistic objectives, and develop an action plan for attaining those objectives in the context of patient preferences and readiness; 3) creation of a continuum of self-management training and support services, in which patients have access to services that teach skills needed to carry out medical regimens, guide health behavior changes, and provide emotional support; and 4) active and sustained follow-up, in which patients are contacted at specified intervals to monitor health status, identify potential complications, and check and reinforce progress in implementing the care plan. These elements make up a common core of services for chronic illness care that need not be reinvented for each disease.
Chronic graft-versus-host disease (GVHD) is likely caused by donor T lymphocytes. Because unmodified blood stem cell grafts contain one log more T lymphocytes than unmodified marrow grafts, we evaluated the incidence of chronic GVHD in previously reported 37 blood stem cell recipients and 37 computer-matched historical control marrow recipients (Bensinger et al, Blood 88:2794, 1996). All patients have been followed until death, relapse, or occurrence of chronic GVHD or for a minimum of 2 years. In a univariable proportional hazards regression model, the relative risk of developing clinical chronic GVHD (includes clinical limited and clinical extensive disease) by 2 years posttransplant among the peripheral blood stem cell recipients compared with the marrow recipients was 2.22 (95% confidence interval, 1.04 to 4.74; P = .039). For clinical extensive chronic GVHD, the relative risk was 2.37 (95% confidence interval, 1.07 to 5. 29; P = .035). In multivariable analyses, considering also the covariables of patient age, patient cytomegalovirus serostatus, and donor cytomegalovirus serostatus, the relative risks of clinical chronic GVHD and clinical extensive chronic GVHD were also greater than 2 (P < .05). We conclude that the transplantation of unmanipulated filgrastim-mobilized blood stem cells may result in a relatively high incidence of chronic GVHD.