Body mass index does not impact on molecular response rate of chronic myeloid leukaemia patients treated frontline with second generation tyrosine kinase inhibitors.

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Aberrations of chromosome No. 1 in blastic phase of chronic myeloid leukemia

Aberrations of chromosome No. 1 were detected at the time of blastic crisis in 7 patients with Ph1-positive chronic myeloid leukemia (CML). Two patients had trisomy 1; trisomy for a long arm segment of chromosome No. 1 was present in 2 patients; trisomy for a short arm segment occurred in 2 patients; and one patient had an apparently balanced translocation affecting chromosome No. 1. All patients with extra material of chromosome No. 1 were trisomic for the region 1p22–1pter or 1q21–1qter. A survey of abnormalities of chromosome No. 1 in this series and in other patients with CML previously reported show, in all patients, a relative increase or decrease of genetic material of two specific regions: 1q32–1q42 and 1p36–1pter

Quality controls for cell cultures: identification of interspecies cross-contamination by PCR-RFLP analysis of the cytochrome b gene

Cross-contaminations of a cell line with cells of different species represent a potential risk in laboratories handling human and animal cells. Therefore, it is necessary to control such contaminations. Tests based on mitochondrial DNA (mtDNA) are used in forensic analysis, phylogenetic studies and in food authentication. However, the use of mtDNA in quality controls of cell cultures is recent. Mitochondrial sequence differences of closely related animal species are five- to tenfold higher than those of nuclear genes. On the contrary, intraspecies variation in mitochondrial sequences is low in most animal species. Moreover, each cell contains 100–10.000 mitochondrial genomes. The amount of mtDNA is greater than nuclear DNA, so that mtDNA can be analyzed also from small or partially degraded samples. In the present study, a method based on a PCR-Restriction Fragment Length Polymorphism (RFLP) analysis of the mitochondrial cytochrome b gene was used (2). This gene has some stable sequences which are recognized from universal primers and some variable sequences used for animal species identification by PCR-RFLP method

Search for Charged Massive Long-Lived Particles

This is the publisher's version, also available electronically from http://journals.aps.org/prl/abstract/10.1103/PhysRevLett.108.121802.We report on a search for charged massive long-lived particles (CMLLPs), based on 5.2  fb^(−1) of integrated luminosity collected with the D0 detector at the Fermilab Tevatron ppbar collider. We search for events in which one or more particles are reconstructed as muons but have speed and ionization energy loss (dE/dx) inconsistent with muons produced in beam collisions. CMLLPs are predicted in several theories of physics beyond the standard model. We exclude pair-produced long-lived gauginolike charginos below 267 GeV and Higgsino-like charginos below 217 GeV at 95% C.L., as well as long-lived scalar top quarks with mass below 285 GeV

Imatinib mesylate therapy in chronic myeloid leukemia patients in stable complete cytogenetic response after interferon-alpha results in any high complete molecular response.

To determine the impact on minimal residual disease by switching to imatinib chronic phase chronic myeloid leukaemia (CP-CML) patients responsive to interferon-alpha (IFNα), in stable complete cytogenetic response (CCR) but with persistent PCR positivity. Twenty-six Philadelphia positive (Ph+) CML patients in stable CCR after IFNα but persistently positive at PCR analysis during this treatment, were given imatinib mesylate at standard dose. At enrolment into the study, median IFN treatment and CCR duration were 88 months (range 15–202) and 73 months (range 10–148), respectively. Imatinib treatment resulted in a progressive and consistent decline of the residual disease as measured by quantitative PCR (RQ-PCR) in all but one of the 26 patients; at the end of follow-up, after a median of 32 months (range 21–49) of treatment, a major molecular response (BCR/ABL levels <0.1) was reached in 20 patients (77%), and BCR/ABL transcripts were undetectable in 13 (50%). The achievement of molecular response was significantly correlated with post-IFN baseline transcript level (mean 1.194 for patients achieving complete molecular response versus 18.97 for those who did not; p < 0.001), but not with other clinical/biological disease characteristics. These results indicate that patients induced into CCR by IFN treatment represent a subset with very favourable prognosis, which can significantly improve molecular response with imatinib and further support investigative treatment schedules combining these two drugs