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Martin's Conjecture is a proposed classification of the definable functions on the Turing degrees. It is usually divided into two parts, the first classifies functions which are not above the identity and the second of classifies functions which are above the identity. Slaman and Steel proved the second part of the conjecture for Borel functions which are order-preserving (i.e. which preserve Turing reducibility). We prove the first part of the conjecture for all order-preserving functions. We do this by introducing a class of functions on the Turing degrees which we call "measure-preserving" and proving that part 1 of Martin's Conjecture holds for all measure-preserving functions and also that all non-trivial order-preserving functions are measure-preserving. Our result on measure-preserving functions has several other consequences for Martin's Conjecture, including an equivalence between part 1 of the conjecture and a statement about the structure of the Rudin-Keisler order on ultrafilters on the Turing degrees., Comment: 44 pages

SCOPUS: le.j, info:eu-repo/semantics/published

International audience; Acute lymphoblastic leukemia of T cell lineage (T-ALL) is an aggressive ă malignant disease which accounts for 15 % of childhood ALL. T(11;14) is ă the more frequent chromosomal abnormality in childhood T-ALL, but its ă prognostic value remained controversial. Our aim was to analyze the ă outcome of childhood T-ALL with t(11;14) to know if the presence of this ă translocation is associated with a poor prognosis. We conducted a ă retrospective study from a series of 20 patients with t(11;14), treated ă in two consecutive trials from the European Organization for Research ă and Treatment of Cancer Children Leukemia Group over a 19-year period ă from 1989 to 2008. There were no significant differences between the 2 ă consecutive groups of patients with t(11;14) regarding the clinical and ă biological features at diagnosis. Among 19 patients who reached complete ă remission, 9 patients relapsed. We noticed 7 deaths all relapse- or ă failure-related. In the 58881 study, a presence of t(11;14) was ă associated with a poor outcome with an event-free survival at 5 years at ă 22.2 % versus 65.1 % for the non-t(11;14) T-ALL (p = 0.0004). In the ă more recent protocol, the outcome of T-ALL with t(11;14) reached that of ă non-t(11;14) T-ALL with an event-free survival at 5 years at 65.5 versus ă 74.9 % (p = 0.93). The presence of t(11;14) appeared as a poor ă prognostic feature in the 58881 trial whereas this abnormality no longer ă affected the outcome in the 58951 study. This difference is probably ă explained by the more intensive chemotherapy in the latest trial.

Abstract 863 Aims: In order to investigate the efficacy and the safety of imatinib in children and adolescents with untreated Philadelphia-positive CML, the CML working party of the Société Française des Cancers de l'enfant (SFCE) conducted an open label, multicentric phase IV study trial (Clinical Trials.gov.NCT00845221). Patients and methods. Patients less than 18 yrs of age with newly diagnosed CP CML were eligible. Imatinib was administered orally at a dose of 260 mg/m2 which is equivalent in terms of drug exposure to the total dose of 400 mg in adults. Forty four children (64% boys) with a median age of 11.5 yrs (range 10 months-17 yrs) have been enrolled from 15 French pediatric centres between July 2004 and December 2008. Side effects were reported prospectively using the NIH CTCv2.0 criteria. Results. Median follow up is currently 17 months (range:1-67). The complete hematologic response rate was 86% and 98% (ITT) at 3 months and 6 months, respectively. The rate of complete cytogenetic response (CCyR) was 62% (ITT) at 12 months. The rate of major molecular response (MMR) defined as a BCR-ABL/ABL ratio ≤ 0.1% according to the International Scale was 34% (ITT) at 12 months. The median daily dose of imatinib was close to the intended doses, 250 mg/m2 (range 176-405) with a median treatment duration of 16 months (2 w to 67 mo). Three pts (7%) had a dose reduction of more than 25% of the theoretic dose. Nine pts (20%) interrupted imatinib temporarily at least once for a median duration of dose interruption of 12 days (range 2-70). Ten pts (23%) discontinued imatinib. The reasons for discontinuation were the following: allogeneic HSCT in CCyR or MMR (2 pts) according to the investigator choice, adverse event (2 pts: muscle pain 1 pt, liver enzyme elevation 1 pt), disease progression or failure (6 pts: loss of CHR [L248V mutation] 1pt, loss of CCyR [L384M mutation] 1pt, no cytogenetic response 1 pt, no molecular response 1 pt, loss of MMR 2 pts). One of them (loss of hematologic response) transformed to blastic phase shortly after coming off study and died. Grade III or IV toxicity was recorded in 14 pts (32%). GradeIII-IV hematologic toxicity was recorded in 8 pts (18%) including neutropenia in 18% and thrombocytopenia in 5%. Nine pts (21%) developed grade III or IV non-hematologic toxicity: muscle pain (2.5%), arthralgia (5%), weight gain (13%), liver enzyme (GOT/GPT) increase (6.5%). Change of body height was observed during the first year of treatment with imatinib in the 22 pts with a sufficient follow-up: a significant decrease of height standard deviation scores (SDS) was observed with a median of the difference of -0.37 (range, -1.09 to +0.14)(p Conclusion. Imatinib is efficient in children and adolescent with previously untreated CML in early chronic phase. However, we report for the first time, a negative impact of imatinib on the growth in a cohort of children and adolescents treated with imatinib. Disclosures: No relevant conflicts of interest to declare.