Pg 239 first aid 2017 error tca treatment

PG 239 FIRST AID 2017 ERROR TCA TREATMENT DRIVER

Furthermore, MM are highly secretory cells, characterized by staggering rate of synthesis of clonal immunoglobulins which further contributes to baseline ER stress. This deregulation of gene expression results in the accumulation of toxic misfolded proteins that exerts additional stress on MM cells. The high frequency of genomic mutations may confer a survival advantage by enabling MM cells to quickly adapt to stresses in the environment.

PG 239 FIRST AID 2017 ERROR TCA TREATMENT DRIVER

While single driver mutations have not been identified in MM, marked genomic instability is a hallmark of the disease and contributes to elevated proteotoxic stress. Patients with MGUS and SMM progress to active MM at a rate of 1% and 10% per year, respectively. Evidence of end organ damage related to the plasma cell disorder is an exclusion criteria for MGUS/SMM diagnosis. MGUS is characterized by low levels of monoclonal protein ( 3 g/dL of monoclonal protein with BM plasmacytosis exceeding 10% but less than 60%. MM is generally preceded by the asymptomatic precursor conditions MGUS and/or SMM. uninvolved light chain equal or greater than 100 or the presence of more than 1 focal lesion on magnetic resonance imaging). A diagnosis of active MM requires the presence of greater than 10% clonal bone marrow (BM) plasma cells in association with either one or more of the CRAB features or a biomarker of malignancy (BM plasmacytosis equal or greater than 60%, ratio of involved vs. Clinical suspicion for active MM is often based on the presence of one or more laboratory/imaging abnormalities, termed the CRAB criteria, particularly if occurring in a patient with a precursor plasma cell disorder such as monoclonal gammopathy of undetermined significance (MGUS) or smoldering MM (SMM). Multiple myeloma (MM) is a neoplastic disorder characterized by the dysregulated proliferation of a plasma cell clone that typically produces a monoclonal immunoglobulin, ultimately resulting in end-organ damage. We highlight the potential utility of therapeutically targeting autophagy in MM, focusing on preclinical data of autophagic modulators in combination with alkylators, anthracyclines, PI, and immunomodulatory drugs. This review provides an overview of the role that autophagy plays in MM pathogenesis, survival, and drug-resistance. However, excessive induction of autophagy in MM cells leads to autophagic cell death, highlighting the double-edged nature of autophagy modulation in MM. Unsurprisingly then, basal levels of autophagy were recently found to confer a survival and drug-resistance benefit to MM cells. Autophagy is an intracellular self-digestion mechanism that plays a role in the ER protein quality control process. Consequently, MM cells rely heavily on protein quality control pathways for survival as evidenced by the clinical efficacy of proteasome inhibitors (PI). Multiple myeloma (MM) is a plasma cell cancer characterized by sustained endoplasmic reticulum (ER) stress and unfolded protein response activation in the setting of high rates of immunoglobulin synthesis.

Pg 239 first aid 2017 error tca treatment