ObjectivesTo investigate the skeletal and dental changes during chincup versus facemask treatment, to compare the long-term effects of the two appliances, and to document the impact of each on treatment success.MethodsIn all, 61 patients with Class III syndrome were retrospectively analyzed at three examination times: 7.8 ± 1.7 years of age (T0, pretreatment), 9.6 ± 2.4 years of age (T1, posttreatment), and around 15–20 years later (T2, long-term follow-up).ResultsSignificant changes of specific cephalometric parameters for all treatment times: T0–T1 (SNA, interbase and gonial angle, Björk’s sum angle, maxillomandibular differential, and distance of upper lip to esthetic line), T1–T2 (NL-NSL, SNB, mandibular-body length, effective mandibular length, and effective maxillary length), and T0–T2 (mandibular-body length, effective mandibular length, effective maxillary length, maxillomandibular differential, SNB, ANB, gonial angle, Björk’s sum angle, and Wits appraisal). The T1–T2 results illustrate that in both treatment groups the typical Class III growth pattern often reappeared after treatment, including gains in SNB angle, condylion-gnathion length, and gonion-menton distance.ConclusionsEither a facemask or a chincup may be effectively used to treat Class III malocclusion. There were differences in long-term stability. Maxillary development was similarly favorable in both groups of patients with successful outcome. The subgroup in whom chincup treatment had failed were mainly characterized by excessive mandibular growth, or lack of maxillary catch-up growth, with deterioration of the maxillomandibular relationship notably in the initial phase of treatment. Early chincup treatment did not have an adverse impact on the temporomandibular joints.

This is the first study to report the follow up of DTC in BM in colorectal cancer using the A45-B/B3 antibody. The presence of tumour cells in the preoperative BM had no impact on outcome. The BM status had changed after 12 months in a quarter of patients.

SummaryChronic myelomonocytic leukaemia is a rare disease and data on the treatment are often extrapolated from myelodysplastic syndrome studies. Although several scores exist for the prognosis of overall survival in chronic myelomonocytic leukaemia, so far there is no designated score for the prediction of the time to first treatment. We tested clinical parameters and cytogenetic information for their ability to predict the time to first treatment in our single center cohort of 55 unselected consecutive chronic myelomonocytic leukaemia patients. In multivariate analysis we identified elevated lactate dehydrogenase (≥223 U/l), higher bone marrow blast percentage (≥7.5%) and thrombocytopenia (<55 G/l) at initial diagnosis as the most relevant parameters for the time to first treatment. Using these three parameters we developed a risk score that efficiently estimates the time to treatment initiation with azacitidine or hydroxyurea (p < 0.001; log-rank). In the high-risk group (≥2 risk factors) 85% of patients required treatment within 1 year, whereas this was the case in 48% in the intermediate-risk (1 risk factor) and in 0% in the low-risk group (0 risk factors). Our risk model was validated in an external test cohort of 65 patients and may serve as a simplified and easily applicable tool for identifying patients who may not require early treatment initiation.

Introduction: Lenalidomide (Revlimid®) plus dexamethasone therapy and single-agent bortezomib therapy are approved for the treatment of relapsed/refractory multiple myeloma (MM) patients. A recent phase II trial has shown activity of lenalidomide/bortezomib/dexamethasone in patients with relapsed/refractory MM (Richardson, IMW 2007). Here, we present a case report on the efficacy of combination therapy with lenalidomide, bortezomib, liposomal doxorubicin, and dexamethasone in a patient who was refractory to prior treatments with bortezomib, lenalidomide, and doxorubicin. Methods and Results: A male patient (58 years) presented with IgG-lambda MM in June 2006. Laboratory tests at diagnosis showed total protein of 123g/L (normal value, 66–87 g/L) and a serum IgG of 87.3g/l (normal value, 7–16 g/L). The patient had t(11;14)(q13;q32) translocation and a del13q14, and bone marrow aspirate showed >90% plasma cells. From July 2006 to March 2007, the patient received 3 different chemotherapy treatment regimens (VAD: vincristine, Adriamycin® [doxorubicin], dexamethasone; VDD: Velcade® [bortezomib], doxorubicin, dexamethasone; and LD: lenalidomide, dexamethasone). He showed primary resistance to VAD treatment and developed resistance after 3 and 5 cycles of VDD and LD, respectively. At that point, the patient’s free light chain (fLCh) concentration was 2,320 mg/L (normal value, 5.7–26.3 mg/L). We changed the patient’s treatment regimen to the 4-fold combination of lenalidomide plus bortezomib plus liposomal doxorubicin (lipD) plus dexamethasone (LBlipDD), (lenalidomide 25 mg day 1–21, bortezomib 1mg/m2 day 1+4+8+11, lipD 50 mg/m2 day 4, dexamethasone 40 mg day 1+2+4+5+8+9+11+12; q28 days). The patient received 3 cycles of LBlipDD from May 2007 to July 2007. This treatment combination was well tolerated with no WHO grade 3 or 4 adverse events. The patient was reassessed after 3 treatment cycles. FISH showed a complete eradication of the former cytogenetic abnormalities, bone marrow aspirate showed <5% plasma cells and serum analysis demonstrated a normalized serum IgG value, and a decrease in the fLCh from 2,320 to 173 mg/L. The patient is for the first time transfusion independent and in very good clinical condition. High-dose melphalan with autologous stem cell support is currently planned. Conclusion: Treatment with LBlipDD leads to a good remission in a VAD-, VDD- and LD-resistant patient. The present observation suggests that the use of 4-fold combination of lenalidomide, bortezomib, liposomal doxorubicin, and dexamethasone can be effective in high-risk MM patients and warrants further investigation.