Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is evidence that polymorphonuclear granulocytes release neutral proteinases such as elastase (E) and cathepsin G in the course of acute leukemia. These proteinases may inactivate clotting factors by unspecific degradation before they are eliminated via complex formation with endogenous inhibitors, e.g. the alpha 1-proteinase inhibitor (alpha 1-PI). In this study it was attempted to correlate plasma levels of the E-alpha 1-PI complex with factor XIII and antithrombin III in acute leukemia. Using a newly developed, sensitive enzyme-linked immunoassay the concentration of E-alpha 1-PI in patients with various types of leukemia, malignant lymphoma or multiple myeloma was determined. Only patients with acute myelocytic or promyelocytic leukemia (AML, APL) and chronic myelocytic leukemia with and without blastic transformation (CML) showed moderate to high levels of E-alpha 1-PI (2- to 20-fold of normal). However, coagulation factor concentration observed in the different types of leukemia seemed to be independent of elastase liberation. Most of the AML-patients with elevated E-alpha 1-PI levels showed peroxidase positive blood cell smears.
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PMID:Plasma levels of human granulocytic elastase alpha 1-proteinase inhibitor complex (E-alpha 1-PI) in leukemia. 637 1

Hematological malignancies including acute leukemia, and multiple myeloma are disorders characterized by the accumulation of neoplastic hematopoietic cells, resulting in aggressive clinical manifestations with poor prognosis. The therapeutic approach to these disorders is basically chemotherapy for achieving complete remission based on the concept of total cell kill. However, severe side effects and complications such as serious infection and bleeding due to anti-cancer drugs are major problems in the clinical setting. In addition, repeated episodes of relapse of the disease may lead to refractory or chemotherapy-resistant disorders. These problems are occurred because anti-cancer agents have effects on both cancer cells and normal hematopoietic cells. The clinical evidences thus suggest the limitations of the chemotherapy for hematological malignancies: novel effective therapeutic approaches with less toxicity are therefore actively being sought. Differentiation-inducing therapy employing a physiologically active derivative of vitamin A, all-trans retinoic acid (ATRA), brought remarkably advances in the therapeutic outcome of APL at the end of last century. More recently, the clinical success of imatinib mesylate (STI571), potent competitive inhibitor of the Bcr/Abl protein tyrosine kinase, in the treatment of CML has focused enthusiasm toward molecular targeted therapy for the hematological malignancies. The therapeutic activity of these agents can be explained by their abilities to modify cellular growth, differentiation, and apoptosis in cells by activating unknown gene programs that molecular cellular proliferation. We have actively sought out new agents among natural products and cytokines with the ability to induce cellular differentiation and apoptosis. In this symposium, I will present our recent data of these novel compounds and their molecular mechanisms for inducing differentiation and apoptosis of hematological malignant cells.
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PMID:A novel therapeutic approach for hematological malignancies based on cellular differentiation and apoptosis. 1243 Aug 59

The proven efficacy of ATO in the treatment of APL and the emerging importance of ATO in other diseases prompted extensive studies of the mechanisms of action of ATO in APL and in other types of cancers. In this review we will focus on downstream events in ATO-induced intrinsic and extrinsic apoptotic pathways with an emphasis on the role of pro-apoptotic and anti-apoptotic proteins and the role of p53 in ATO-induced apoptosis including its effect on cell cycle, its anti-mitotic effect and the role of apoptosis inducing factors (AIF) in ATO-induced apoptosis, chromatin condensation and nuclear fragmentation in myeloma cells as a model.
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PMID:Arsenic trioxide: an anti cancer missile with multiple warheads. 1601 69

In this study we investigated 3 domains of emotional functioning--emotion dysregulation, distress tolerance, and experiential avoidance--in young adult outpatients with borderline personality disorder (BPD) symptoms. Participants were 40 young adult outpatients at a university counseling center who reported current suicidal ideation and met diagnostic criteria for BPD or experienced subthreshold BPD symptoms (i.e., met diagnostic criteria for 3 or 4 symptoms). Participants completed 3 self-report measures of emotional functioning-experiential avoidance (Acceptance and Action Questionnaire-2; Bond et al., 2011; Hayes et al., 2004), emotion dysregulation (Difficulties in Emotion Regulation Scale; Gratz & Roemer, 2004), and distress tolerance (Distress Tolerance Scale; Simons & Gaher, 2005)-and a behavioral measure of distress tolerance (Paced Auditory Serial Addition Task-Computerized; Lejuez, Kahler, & Brown, 2003), in addition to self-report measures of depression and BPD symptom severity. Partial correlations demonstrated that both emotion dysregulation and experiential avoidance were significantly associated with BPD symptom severity after accounting for depression. However, neither the self-report nor behavioral measure of distress tolerance were related to BPD symptom severity. A regression analysis with emotion dysregulation and experiential avoidance as independent variables revealed that only experiential avoidance was significantly associated with BPD symptom severity after controlling for depression symptoms. The current findings suggest that experiential avoidance may be a central process in BPD symptom severity. Future research directions are discussed.
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PMID:An investigation of experiential avoidance, emotion dysregulation, and distress tolerance in young adult outpatients with borderline personality disorder symptoms. 2245 55