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1 esulting from an underlying plasma cell (PC) dyscrasia.
2 a rare disease associated with a plasma cell dyscrasia.
3 n to multiple myeloma or another plasma cell dyscrasia.
4 ing patients with oligosecretory plasma cell dyscrasia.
5 fter relapse of their underlying plasma cell dyscrasia.
6 der resulting from an underlying plasma cell dyscrasia.
7 ng eradication of the underlying plasma cell dyscrasia.
8 L), which is the most aggressive plasma cell dyscrasia.
9 are untreated for the underlying plasma cell dyscrasia.
10 tween dormancy and disease progression in PC dyscrasias.
11 ying genetic determinants of inherited blood dyscrasias.
12 ent is a frequent consequence of plasma cell dyscrasias.
13  nontreatment-related factors in plasma cell dyscrasias.
14 bule epithelium, particularly in plasma cell dyscrasias.
15 at are seen in patients who have plasma cell dyscrasias.
16 into the molecular mechanisms of plasma-cell dyscrasias.
17 ence of an opportunistic infection and blood dyscrasias.
18 standing normal hematopoiesis and blood cell dyscrasias.
19 etting of comorbidities, such as plasma-cell dyscrasias.
20 e increase in the progression of plasma cell dyscrasias.
21 options for patients affected by plasma cell dyscrasias.
22 elodysplastic syndrome (MDS) and plasma cell dyscrasias.
23  as no evidence of an underlying plasma cell dyscrasia 1 year after treatment, was achieved in 40% of
24 nce of monoclonal gammopathy and plasma cell dyscrasias.2,3 The exact mechanism of monoclonal gammopa
25 ight chains produced by a clonal plasma cell dyscrasia accumulate in tissues and damage vital organs.
26 prove outcomes for patients with plasma cell dyscrasia and end-stage kidney disease.
27 ermined significance (MGUS) is a plasma cell dyscrasia and precursor to multiple myeloma.
28 re applied in a cohort of 46 samples with PC dyscrasias and 21 healthy donors (HDs).
29 lts also help elucidate the link between RBC dyscrasias and cardiovascular morbidity.
30 ategies in kidney transplant for plasma cell dyscrasias and end-stage kidney disease.
31 implicated in the pathogenesis of autoimmune dyscrasias and malignant diseases.
32 tant insights into the immunopathology of PC dyscrasias and MM immunotherapy.
33  healthy individuals at risk for plasma cell dyscrasias and that dominant inheritance of posttranslat
34 tution following rituximab leading to immune dyscrasias and the development of neutropenia.
35                                  Plasma cell dyscrasias appear to have a modestly increased incidence
36 s of gene methylated for L/L and plasma cell dyscrasias are different.
37                                  Plasma cell dyscrasias are frequently encountered malignancies often
38                                  Plasma cell dyscrasias are frequently encountered malignancies which
39 splanted for Hodgkin lymphoma or plasma cell dyscrasias, but was not observed among those transplante
40    Primary (AL) amyloidosis is a plasma cell dyscrasia characterized by clonal production of immunogl
41        Its underlying cause is a plasma cell dyscrasia characterized by misfolding of monoclonal immu
42       Multiple myeloma (MM) is a plasma cell dyscrasia characterized by the presence of multiple myel
43 patients with heavily pretreated plasma cell dyscrasias completing one cycle of therapy, there was on
44 %) at 12 months after treatment, plasma cell dyscrasias could not be detected.
45 y the activity of the underlying plasma cell dyscrasia (dFLC) and nephrotic-range albuminuria (ACR).
46 Cox regression analysis revealed plasma cell dyscrasia (difference between serum free light chains [d
47                                  Plasma cell dyscrasias encompass a spectrum from the precursors mono
48 r factor-kappaB may play a role in the blood dyscrasias encountered with the use of this drug.
49  routinely performed to diagnose plasma cell dyscrasia failed to detect lambda+ monoclonal PCs.
50 at genotypic sc identification of pPCs in PC dyscrasias has relevant pathogenic and clinical implicat
51 n, critical illness, thrombocytopenia, blood dyscrasias, hepatic disease, renal failure, antithrombot
52 sed for the initiation of drug-induced blood dyscrasias, hypersensitivity reactions, or lupus-like sy
53 ieve complete remission of their plasma cell dyscrasia, improvement in performance status, and clinic
54 ntation induces remission of the plasma cell dyscrasia in a substantial proportion of patients with A
55 sive treatment of the underlying plasma cell dyscrasia in AL amyloidosis can lead to the amelioration
56 associated amyloidosis (AL) is a plasma cell dyscrasia in which the secreted monoclonal immunoglobuli
57                    Patients with plasma cell dyscrasia, including multiple myeloma, AL amyloidosis, a
58         Conclusion: Pretreatment bone marrow dyscrasias, including an MCV greater than 95 fL, may pre
59 Cs is implicated throughout all stages of PC dyscrasias, including asymptomatic states called monoclo
60                                  Plasma cell dyscrasias, including monoclonal gammopathy of undetermi
61 determined significance or other plasma cell dyscrasias involving the bone marrow, express the Wnt-si
62 d not the result of a monoclonal plasma cell dyscrasia, may be misdiagnosed and lead to inappropriate
63 ases in malignancies such as the plasma cell dyscrasia multiple myeloma (MM) is not known.
64 differentiating POEMS from other plasma cell dyscrasias, neuropathic processes, and multisystem illne
65         POEMS syndrome is a rare plasma cell dyscrasia presenting with polyneuropathy and other syste
66 pathophysiology and diagnosis of plasma cell dyscrasia related kidney diseases.
67 to expand, but the cause of this plasma cell dyscrasia remains unclear.
68 y systemic amyloidosis (AL) is a plasma cell dyscrasia resulting in multisystem failure and death.
69              In the setting of a plasma cell dyscrasia, significant amounts of free light chains, now
70  largely present in premalignant plasma cell dyscrasia such as monoclonal gammopathy of undetermined
71 ficance (MGUS) is a premalignant plasma cell dyscrasia that consistently precedes multiple myeloma (M
72 the molecular defects underlying plasma cell dyscrasias that may explain their clinical heterogeneity
73                      Advances in plasma cell dyscrasia therapies are improving survival and expanding
74     We analyzed 81 patients with plasma cell dyscrasias using single-cell CNA sequencing.
75 rapy of the patient's underlying plasma-cell dyscrasia utilizing a daratumumab-based regimen showed d
76                               If plasma cell dyscrasia was present, histologic confirmation of ATTR a
77 arcinoma, malignant melanoma, or plasma cell dyscrasia, we related responses to questionnaires (admin
78                            Their plasma cell dyscrasias were evaluated with immunofixation electropho
79 ious liver toxic effects or white-blood-cell dyscrasias were noted.
80      Well-selected patients with plasma cell dyscrasias whose monoclonal Ig is well controlled may be
81 temic amyloidosis (AL) is a plasma cell (PC) dyscrasia with clinical similarities to multiple myeloma
82  symptoms, diuretic therapy, and plasma cell dyscrasia with evidence of myocardial uptake on bone sci
83 e myeloma (SMM) are asymptomatic plasma cell dyscrasias, with a propensity to progress to symptomatic
84 ies had two or more members with plasma cell dyscrasias, with or without a single case of MM.