world cancer report - iarc

A B
Fig. 5.113 Acute myeloid leukaemia; agranular myeloblasts (A) and granulated myeloblasts (B).
bone marrow and lymph nodes, admixed
with prolymphocytes and paraimmunoblasts,
usually expressing CD5 and
CD23 surface antigen [5]. Chronic lymphocytic
leukaemia [10] is a heterogeneous
disease which can occur in an indolent
form with very little progression, whilst at
the other extreme it may present with
severe bone marrow failure and a poor
prognosis.
Management
Remarkable progress in the understanding
and treatment of leukaemia has been
made in the past century [11]. In the first
instance, this generalization refers specifically
to paediatric disease. Prior to 1960,
leukaemia was the leading cause of death
Fig. 5.115 Spectral karyotyping of a chronic myeloid leukaemia case reveals
a variant Philadelphia chromosome involving translocations between chromosomes
3, 9, 12 and 22. Secondary changes involving chromosomes 1, 5,
8, 18 and X are also seen, indicating advanced disease.
from malignancy in children under 15; currently,
more than 80% of children with
acute lymphoblastic leukaemia can be
cured with chemotherapy [12]. Treatment
involves induction of remission with combinations
of agents (such as vincristine,
daunorubicin, cytarabine [cytosine arabinoside],
L-asparaginase, 6-thioguanine,
and steroids) followed by consolidation,
maintenance and post-remission intensification
therapy to eradicate residual
leukaemic blast cells, aiming at cure.
Intensive supportive care throughout treatment
is of major importance. Prophylactic
treatment with intrathecal methotrexate
injections, with or without craniospinal
irradiation, is mandatory in the management
of acute lymphoblastic leukaemia to
Fig. 5.114 A bone marrow biopsy of acute promyelocytic
leukaemia. Abnormal promyelocytes have
abundant hypergranulated cytoplasm. The nuclei
are generally round to oval, several being irregular
and invaginated.
prevent possible involvement of or relapse
in the central nervous system. The use of
radiotherapy is limited because of the
potential long-term side-effects, particularly
effects on the growth of the young child
and the risk of second malignancies. The
adult form of acute lymphoblastic
leukaemia is also susceptible to therapy
and can be cured, (although not as readily
as childhood leukaemia), with intensive
combination therapy [13].
For acute leukaemia in adults, the initial
aim of management is to stabilize the
patient with supportive measures to counteract
bone marrow failure which leads to
anaemia, neutropenia and thrombocytopenia.
Most patients with leukaemia
who die in the first three weeks of diagno-
Fig. 5.116 Acute promyelocytic leukaemia cells with t(15;17)(q22;q12)
translocation. Fluorescence in situ hybridization with probes for PML (red)
and RARα (green) demonstrates the presence of a PML/RARα fusion protein
(overlapping of red and green = yellow signal) resulting from the breakage
and fusion of these chromosome bands.
Leukaemia
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