High incidence of meningeal leukemia in lymphoid blast crisis of chronic myelogenous leukemia

Abstract

Fifteen patients with lymphoid blast crisis of chronic myelogenous leukemia (LyBC-CML) and five patients with acute lymphoblastic leukemia converting to Philadelphia-positive (Ph+) chronic myeloid leukemia (ALL Ph + CML) were followed. Seven of 15 (46.7%) LyBC-CML patients developed meningeal leukemia within a median period of 6 months (range 2-11 months), while there was no medullary relapse. Five of these responded well to triple intrathecal therapy. In the ALL Ph + CML patients, in spite of central nervous system (CNS) prophylaxis with IT MTX and 18 Gy cranial radiation, two of five patients (40%) experienced meningeal leukemia, one isolated and the other with medullary relapse. The data confirm that LyBC-CML patients experience a high incidence of meningeal leukemia. The role of CNS prophylaxis is not very clear, but its use may delay development and reduce morbidity due to CNS disease.

Isolated Ocular Manifestation of Relapsed Chronic Myelogenous Leukemia Presenting as Myeloid Blast Crisis in a Patient on Imatinib Therapy: A Case Report and Review of the Literature

“…The central nervous system is relatively prone to disease involvement while on imatinib therapy and this is attributed mainly to poor permeability of imatinib through the blood brain barrier [ 11 , 13 ]. The most common sites of CNS involvement are the lateral ventricular walls [ 14 ], meninges [ 15 ], and the optic nerve [ 16 ], causing symptoms such as headache, cognitive changes, raised intracranial pressure, and visual disturbances. Intraocular optic nerve involvement has been associated with poor prognosis and impermeability to intrathecal chemotherapeutic agents [ 17 ].…”

Emerging stem cell concepts for imatinib‐resistant chronic myeloid leukaemia: implications for the biology, management, and therapy of the disease

“…Clinically, the poor uptake into the CNS is reflected by CNS relapses that may occur in imatinib‐treated patients (Abruzzese et al , 2003; Bornhäuser et al , 2004; Leis et al , 2004; Rajappa et al , 2004; Rytting & Wierda, 2004; Matsuda et al , 2005; Pavlu et al , 2005; Kim et al , 2006), indicating that CML stem cells can migrate into the CNS. However, compared with a relatively high incidence of CNS relapses in lymphoid or mixed blast crisis (up to 47%; Saikia et al , 1993), the incidence of CNS relapses in pure myeloid BP of CML is very low (estimated <3%).…”

Involvement of BCR::ABL1 in laminin adhesion of Philadelphia chromosome‐positive acute lymphoblastic leukemia through upregulation of integrin α6

“…In this scenario, a higher level of CD49f expression might be associated with a higher incidence of CNS invasion in ALL patients. Of note, a high incidence of meningeal leukemia was reported in the lymphoid blast crisis of CML patients 39 . Moreover, high incidence of CNS leukemia at diagnosis was reported in childhood Ph‐positive ALL 40 and a trend toward higher frequency of initial CNS involvement was reported in adult Ph‐positive ALL 41 .…”

“…Of note, a high incidence of meningeal leukemia was reported in the lymphoid blast crisis of CML patients. 39 Moreover, high incidence of CNS leukemia at diagnosis was reported in childhood Ph-positive ALL 40 and a trend toward higher frequency of initial CNS involvement was reported in adult Ph-positive ALL. 41 Since we confirmed that laminin binding of Ph-positive ALL cell lines is mediated through the heterodimer composed of CD49f and CD29, higher levels of CD49f expression in Ph-positive ALL might, at least partly, be involved in higher incidence of CNS invasion.…”