Stage |
Criteria |
Median overall |
survival |
Source: Palumbo A et al 2015 8 |
and if not already performed, is per- |
1q21 amplifications are associated |
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formed on all patients with new diag- |
with high-risk disease. Myeloma is |
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noses. In selected cases, an MRI or PET |
not a curable disease, and prognosti- |
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scan may also be indicated to assess the |
cating can be difficult because there |
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patient’ s skeleton and soft tissues for |
is great disease heterogeneity. Treat- |
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myeloma damage or deposits. |
ment response is difficult to predict; |
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A 24-hour urine collection is per- |
however, the mostly widely accepted |
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formed on patients with a new diag- |
model is the Revised International |
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nosis to assess for the presence of a |
Staging System( R-ISS, see table 4). |
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|
Bence-Jones protein.
While not relevant to the initial diagnosis of MM, patients with certain chromosomal abnormalities are more likely to relapse or be resistant to therapy. Conventional cytogenetics is
|
Management
Treatment for myeloma varies and is individualised based on the patient’ s age, comorbidities and functional status. MM is incurable. While the
|
Figure 6. Multiple lytic lesions in the humerus, scapula and ribs. |
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a visual analysis of cells in metaphase |
disease course is varied, patients typ- |
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and can be used to identify macro- |
ically undergo a therapy regimen, |
performed in hospital and a patient’ s |
anti-myeloma therapy is based |
previously undetectable levels( mini- |
scopic karyotype abnormalities on |
which is( hopefully) followed by a |
own stem cells are collected and then |
around proteasome inhibitors and |
mum sensitivity in the most sensitive |
bone marrow samples. 17p deletions, |
period of remission and then an even- |
returned to them after high doses of |
lenalidomide. |
currently available flow cytometry |
hypodiploidy and chromosome 13 |
tual relapse that requires the consid- |
chemotherapy( that typically ablates |
As treatments for MM have |
techniques is 1 / 100,000 nucleated |
deletions are abnormalities associated |
eration of alternative therapies( see |
the bone marrow). Patients then usu- |
improved significantly over recent |
cells) and has been shown to correlate |
with high-risk disease. 8 |
figure 8). |
ally receive maintenance chemother- |
years, the importance of detecting |
with overall survival. 9 |
Fluorescent in situ hybridisa- |
Initial treatment usually includes |
apy, and their response to treatment |
deeper responses to treatment has |
There are two other modalities that |
tion( FISH), a cytogenetic technique, |
corticosteroids, a proteasome inhib- |
is graded based on bone marrow biop- |
emerged. Minimal residual disease |
are key to the overall management of |
uses fluorescent probes that bind |
itor( such as bortezomib) and if their |
sies, serum free light chain analysis, |
( MRD) and MRD-negative status can |
symptomatic myeloma: first, the man- |
to a specific sample of DNA. These |
renal function allows, lenalidomide or |
and SPE and immunofixation of the |
now be assessed via next-generation |
agement of bone disease and hyper- |
probes are able to identify translo- |
thalidomide. The standard of care for |
paraprotein on both serum and urine. |
flow cytometry or next-generation |
calcaemia; and second, anti-infective |
cations, amplifications and dele- |
younger and fitter patients is an autol- |
In‘ less fit’ patients in whom high- |
sequencing on bone marrow sam- |
prophylaxis. |
tions in plasma cells. Translocations |
ogous stem cell transplant follow- |
dose therapy and an autologous stem |
ples. These technologies can detect |
Myeloma cells produce osteo- |
t( 4; 14) and t( 14; 16), 17p deletion and |
ing initial induction therapy. This is |
cell transplant are inappropriate, |
the presence of the malignant clone at |
clast-activating factors while inhibiting |