about
Inhibition of p38 MAPK suppresses inflammatory cytokine induction by etoposide, 5-fluorouracil, and doxorubicin without affecting tumoricidal activityAtypical depression is more common than melancholic in fibromyalgia: an observational cohort study.CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasmsProduction of IL-1β by bone marrow-derived macrophages in response to chemotherapeutic drugs: synergistic effects of doxorubicin and vincristine.The HMG-I oncogene causes highly penetrant, aggressive lymphoid malignancy in transgenic mice and is overexpressed in human leukemia.Proinflammatory cytokines and DHEA-S in women with fibromyalgia: impact of psychological distress and menopausal status.An epidermotypic model of interface dermatitis reveals individual functions of fas ligand and gamma interferon in hypergranulosis, cytoid body formation, and gene expression.Preliminary evidence of a blunted anti-inflammatory response to exhaustive exercise in fibromyalgia.Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Doxorubicin and daunorubicin induce processing and release of interleukin-1β through activation of the NLRP3 inflammasome.Cancer chemotherapy-related symptoms: evidence to suggest a role for proinflammatory cytokines.Small molecule kinase inhibitors block the ZAK-dependent inflammatory effects of doxorubicin.A role for orexin in cytotoxic chemotherapy-induced fatigue.The role of IL-1β and TNF-α signaling in the genesis of cancer treatment related symptoms (CTRS): a study using cytokine receptor-deficient mice.Preliminary differences in peripheral immune markers and brain metabolites between fatigued and non-fatigued breast cancer survivors: a pilot study.Upregulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large-cell lung cancer.Characterization of murine JAK2V617F-positive myeloproliferative disease.A specific need for CRKL in p210BCR-ABL-induced transformation of mouse hematopoietic progenitors.c-CBL is not required for leukemia induction by Bcr-Abl in mice.The cancer chemotherapy drug etoposide (VP-16) induces proinflammatory cytokine production and sickness behavior-like symptoms in a mouse model of cancer chemotherapy-related symptoms.
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description
hulumtuese
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onderzoeker
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researcher
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հետազոտող
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name
Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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Lisa J. Wood
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P496
0000-0003-1145-3649