Generation of repetitive sequence-depleted microdissected chromosome arm painting probe

Program no. 897postprin

Highly stable fiber Bragg gratings written in hydrogen-loaded fiber

Author name used in this publication: Xiao-Ming Tao2000-2001 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Simultaneous strain and temperature measurement using a superstructure fiber Bragg grating

Author name used in this publication: Xiao-Ming Tao2000-2001 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Study of chromosomal abnormalities in esophageal squamous cell carcinoma by comparative genomic hybridization

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Annexin A3 is a therapeutic target for CD133+ liver cancer stem cells

This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CAFrequent tumor relapse in hepatocellular carcinoma (HCC) has been commonly attributed to the failure to completely eradicate cancer stem cells (CSCs) in the tumor residues by conventional treatments. We have previously reported that the tumor growth of HCC is fuelled, at least in part, by a small subset of CSCs marked by the CD133 surface phenotype. Our present study aims 1) to delineate the molecular mechanism by which CD133+ liver CSCs mediate HCC tumor formation and progression; and 2) to develop a novel diagnostic / prognostic biomarker and targeted therapy for HCC detection and treatment. RNA-Seq profiling was employed to compare the gene expression profiles between sorted CD133+ and CD133- subsets isolated from HCC cell lines ...postprin

Pericentromeric Regions Are Refractory To Prompt Repair after Replication Stress-Induced Breakage in HPV16 E6E7-Expressing Epithelial Cells

Chromosomal instability is the major form of genomic instability in cancer cells. Amongst various forms of chromosomal instability, pericentromeric or centromeric instability remains particularly poorly understood. In the present study, we found that pericentromeric instability, evidenced by dynamic formation of pericentromeric or centromeric rearrangements, breaks, deletions or iso-chromosomes, was a general phenomenon in human cells immortalized by expression of human papillomavirus type 16 E6 and E7 (HPV16 E6E7). In particular, for the first time, we surprisingly found a dramatic increase in the proportion of pericentromeric chromosomal aberrations relative to total aberrations in HPV16 E6E7-expressing cells 72 h after release from aphidicolin (APH)-induced replication stress, with pericentromeric chromosomal aberrations becoming the predominant type of structural aberrations (~70% of total aberrations). In contrast, pericentromeric aberrations accounted for only about 20% of total aberrations in cells at the end of APH treatment. This increase in relative proportion of pericentromeric aberrations after release from APH treatment revealed that pericentromeric breaks induced by replication stress are refractory to prompt repair in HPV16 E6E7-expressing epithelial cells. Telomerase-immortalized epithelial cells without HPV16 E6E7 expression did not exhibit such preferential pericentromeric instability after release from APH treatment. Cancer development is often associated with replication stress. Since HPV16 E6 and E7 inactivate p53 and Rb, and p53 and Rb pathway defects are common in cancer, our finding that pericentromeric regions are refractory to prompt repair after replication stress-induced breakage in HPV16 E6E7-expressing cells may shed light on mechanism of general pericentromeric instability in cancer. © 2012 Deng et al.published_or_final_versio

Fast-FISH using repeat sequence-depleted painting probes from microdissected DNA

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Growth of long-period gratings in H₂-loaded fiber after 193-nm UV inscription

2000-2001 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma

Aim: To investigate the mechanism and significance of NF-κB activation regulated by hepatitis B virus X protein (HBx) in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Methods: The expression levels of HBx, p65, IκB-α and ubiquitin were detected by immunohistochemistry in HCC tissue microarrays (TMA) respectively, and IκB-α was detected by Western blot in HCC and corresponding liver tissues. Results: The percentage of informative TMA samples was 98.8% in 186 cases with a total of 367 samples. Compared with corresponding liver tissues (60.0%), the HBx expression was obviously decreased in HBV-associated HCC (47.9%, u=2.24, P<0.05). On the contrary, the expressions of p65 (20.6% vs 45.3%, u=4.85, P<0.01) and ubiquitin (8.9% vs 59.0%, u=9.68, P<0.01 ) were notably elevated in HCC. In addition, IκB-α had a tendency to go up. Importantly, positive relativity was observed between HBx and p65 (χ2=10.26, P<0.01), p65 and IκB-α (χ2=16.86, P<0.01), IκB-α and ubiquitin (χ2=8.90, P<0.01) in HCC, respectively. Conclusion: Both active and non-active forms of NF-κB are increased in HBV-associated HCC. Variant HBx is the major cause of the enhancement of NF-κB activity. The activation always proceeds in nucleus and the proteasome complexes play an important role in the activation.published_or_final_versio

Characterization of a complex chromosome rearrangement involving 6q in a melanoma cell line: isolation of a candidate tumor suppressor gene interrupted by the breakpoint at 6q16

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