The patient journey in chronic myeloid leukemia patients on tyrosine kinase inhibitor therapies: qualitative insights using a global ethnographic approach.

Background: The advent and approval of tyrosine kinase inhibitors (TKIs) have dramatically improved the life expectancy of patients with chronic myeloid leukemia (CML), which has been transformed into a chronically manageable disease.

Objective: The objective was to qualitatively assess the effects of diagnosis and treatment on patients with CML to offer recommendations for health-care providers (HCPs) for the better support of patients.

Methods: By use of an ethnographic approach based on in-home interviews, photo journals, and an optional telephone debriefing interview, this study included 50 patients with CML from Brazil, France, Germany, Russia, and Spain, including patients within 18 months of diagnosis and receiving frontline TKI therapy (n = 20), patients between >18 months and 7 years from diagnosis and receiving ongoing frontline therapy (n = 20), and patients who switched to second- or third-line TKI therapy (n = 10).

Tumour necrosis factor-alpha- vs. growth factor deprivation-promoted cell death: distinct converging pathways.

Perturbations of neuronal physiological homeostasis are likely to underscore neuronal demise/impairments that are reportedly associated with aging of the central nervous system and age-related neurodegenerative diseases such as Alzheimer's disease (AD). A number of age- and/or disease-associated neurotoxic events has been described. These include abnormally modified proteins such as beta amyloid and hyper-phosphorylated Tau, cytokines such as tumour necrosis factor-alpha (TNFalpha), high levels of free radicals conducive to oxidative stress, and impaired/decreased neuronal trophic support by neurotrophic factors.

Tumour necrosis factor-alpha- vs. growth factor deprivation-promoted cell death: different receptor requirements for mediating nerve growth factor-promoted rescue.

Physiological and pathological aging of the central nervous system (CNS) is characterized by functional neuronal impairments which may lead to perturbed cell homeostasis and eventually to neuronal death. Many toxic events may underlie age-related neurodegeneration. These include the effects of beta amyloid, Tau and mutated presenilin proteins, free radicals and oxidative stress, pro-inflammatory cytokines and lack of growth factor support, which can be individually or collectively involved.