Christiane Werner-Favre

Quiescent memory B cells in human peripheral blood co‐express bcl‐2 and bcl‐xL anti‐apoptotic proteins at high levels

The anti‐apoptotic proteins bcl‐2 and bcl‐xL seem to exhibit strictly opposite expression patterns in normal lymphoid cell differentiation stages, with bcl‐2 low and bxl‐xL high in immature and mature proliferating cells, the reverse being the case in recirculating quiescent cells. However, it is in fact not known whether recirculating memory cells are bcl‐xL low or high. We analyzed memory (immunoglobulin isotype‐switched) B cells in human peripheral blood, which were small lymphocytes in the G0 phase of the cell cycle, but proliferated better than naive B cells in response to Staphylococcus aureus Cowan I. Ex vivo these cells co‐expressed bcl‐2 together with bcl‐xL mRNA and protein at high levels. The mcl‐1 mRNA level was low. The bcl‐xL mRNA level decreased during culture in medium containing fetal calf serum, which implies that it is maintained in vivo by continuous or frequent, non‐mitogenic signal(s). The high bcl‐xL expression of memory B cells may be relevant with regard to their longevity and/or their capacity to undergo an accelerated secondary type immune response.

Acute lymphoblastic leukemia in two children with a congenital chromosome anomaly: Familial inv(11)(p15q13) in one and ring chromosome No. 21 in the other

A congenital chromosome abnormality was found in two unrelated children with acute lymphoblastic leukemia (ALL). In the first case, a pericentric inversion of chromosome No. 11, inv(11)(p15q13), was observed and discovered to be familial, being present in five other members of the family over two generations. In the second case, the presence of a congenital ring chromosome No. 21, 46,XX,r(21), was considered to be the result of a de novo mutation. The possible relation between these congenital chromosome anomalies and a predisposition to neoplasia is discussed and could be explained by different mechanisms: (1) amplification of oncogenic determinants by gene duplication, and/or (2) alteration of the effects of wildtype alleles through deletion or changes in position.

Translocation 2;11 and other significant chromosome changes in acute monoblastic leukemia (M5) with clonal evolution: Sequential clinical and cytogenetic studies

An elderly woman presented with pancytopenia resulting from acute monoblastic leukemia (AMoL) type M5a. At the time of diagnosis, the marrow metaphase studies revealed a pseudodiploid idiogram: 46,XX,t(2;11)(q37;q23),(t(7;9;10)(q22;q22;p13). At relapse, 7 months later, a clonal derivative of the initial pseudodiploid pattern was identified. Though alterations of chromosome regions 7q22 and 9q22 are frequently seen in acute nonlymphocytic leukemia (ANLL), 11q structural anomalies are even more specific for this group of leukemias, and the involvement of band 11q23 is particularly striking in AMoL. Various chromosomes may take part in translocations with chromosome #11, but the participation of chromosome #2 as in this case is apparently rare.

Ring chromosomes and hematologic disorders

Based on 5 years of cytogenetic evaluation in hematology, we report our observations on various hematologic proliferative disorders with ring chromosomes. Comparing our data to those previously published in the literature we analyzed the occurrence of the ring in relation to the age of onset, previous history of therapeutic or professional exposure to mutagenic agents, and mean survival. It is concluded that the presence of ring chromosomes may be linked to a poor prognosis.