Hesize that this chromosomal rearrangement was arisen by one-step mechanism with at the least 4 simultaneous breaks and joints mainly because (i) atCase Reports in Geneticsder(12)chr 9 chr6 137 1481011X12 18 Yder(9)der(22)(a)(b)BCR (22q11)12q22q11 3 BCR5 BCR ABL9q34 ASS-ABL1 (9q34) Chr 9 chr 12 chr(c)der(9)der(12)der(22)Figure 1: (a) QFQ karyotype derived from bone marrow cells. The arrows indicate the derivative chromosomes involved in the rearrangement. (b) BCR/ABL1 FISH signal pattern on metaphase. The arrows indicate the rearranged chromosomes and also the standard chromosomes 9 and 22. (c) Ideogram of the rearrangement identified in our CML case using the schematic representation with the FISH probe signals.diagnosis we did not detect additional clonal abnormalities and (ii) on der(22) only 1 breakpoint occurred, which can be located within the BCR gene and that originated both the fusion gene and the t(12;22). Conversely other instances showed the coexistence of normal and complex translocation inside the exact same patient suggesting that two or additional consecutive translocations triggered the formation with the complex variant translocation [4]. Prognostic information on response to Imatinib in circumstances with complicated Philadelphia translocation are contradictory as well as the poor prognostic outcome in some patient of this group was explained by an improved frequency from the concomitant deletion on der(9) as opposed to for the type of chromosome rearrangement [5]. Our patient has been treated with Imatinib, and at 3 months of therapy she accomplished the hematological and cytogenetics responses regardless of the presence of the deletion on der(9), when at six months of therapy she developed a clone with trisomies eight and 9.1131614-65-7 Chemical name These trisomies have apparently no prognostic significance in CML.N-Fmoc-N’-methyl-L-asparagine uses In more detail trisomy eight might arise just after interferon and/or Imatinib therapy with unknown significance and trisomy 9 is assumed to represent a gain-of-function mechanism with respect towards the JAK2 gene on 9p24 coding for the JAK2 kinasewith no prognostic influence in line with follow-up research of limited sample sizes [17].PMID:23329650 Up to now our patient showed a superb response to Imatinib remedy, but further research are required to confirm this getting.Conflict of InterestsThe authors declare that there is no conflict of interests regarding the publication of this paper.
NIH Public AccessAuthor ManuscriptNanoscale. Author manuscript; offered in PMC 2014 April 21.Published in final edited form as: Nanoscale. 2013 April 21; 5(8): 3253?256. doi:ten.1039/c3nr00335c.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSynthesis of ligand-functionalized water-soluble [18F]YF3 nanoparticles for PET imagingLiqin Xionga,b,c, Bin Shena, Deepak Beheraa, Sanjiv S. Gambhira, Frederick T. China, and Jianghong RaoaLiqin Xiong: [email protected]; Jianghong Rao: [email protected] Imaging Program (MIPS), Departments of Radiology and Chemistry, Stanford University, Stanford, CA 94305-5484, USAbSchoolof Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200030, P. R.ChinacDepartmentof Nuclear Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, P. R. ChinaAbstractWe report a straightforward, efficient synthesis of novel 18F-labeled imaging agents determined by YF3 nanoparticles. Targeting ligands and antitumor drug molecules is usually introduced onto the YF3 nanoparticles within a one-pot synthesis. The 18F-labeling reaction proceeds in aqueous solutions at area tempe.
