ORCID Profile
0000-0002-1089-5325
Current Organisations
University of Hong Kong
,
University of Manchester
,
University of St Andrews
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Publisher: American Society of Hematology
Date: 23-12-2019
DOI: 10.1182/BLOODADVANCES.2019001062
Abstract: Children with PCNSL and no immunodeficiency have a good outcome when treated by a histological subtype–driven and radiation-free protocol. New treatment guidelines are needed for PCNSL in children and adolescents with an underlying immunodeficiency.
Publisher: Life Science Alliance, LLC
Date: 23-06-2020
Abstract: HIV and EBV are human pathogens that cause a considerable burden to worldwide health. In combination, these viruses are linked to AIDS-associated lymphomas. We found that EBV, which transforms B cells, renders them susceptible to HIV-1 infection in a CXCR4 and CD4-dependent manner in vitro and that CXCR4-tropic HIV-1 integrates into the genome of these B cells with the same molecular profile as in autologous CD4 + T cells. In addition, we established a humanized mouse model to investigate the in vivo interactions of EBV and HIV-1 upon coinfection. The respective mice that reconstitute human immune system components upon transplantation with CD34 + human hematopoietic progenitor cells could recapitulate aspects of EBV and HIV immunobiology observed in dual-infected patients. Upon coinfection of humanized mice, EBV/HIV dual-infected B cells could be detected, but were susceptible to CD8 + T-cell–mediated immune control.
Publisher: Proceedings of the National Academy of Sciences
Date: 07-03-2016
Abstract: Nasopharyngeal carcinoma (NPC) is a valuable cancer model to study the interaction of host genetics, viral infection, and environment in tumorigenesis. Little is known about the genetic basis for the remarkably distinct geographical distribution of NPC. We used a whole-exome sequencing approach to identify the genetic alterations associated with NPC susceptibility and revealed a strong link between macrophage-stimulating 1 receptor ( MST1R ) and NPC early-age onset (age of ≤20 y). MST1R is critical for innate immunity and plays an important role for host defense against viral infection. We further discovered that an interaction network involved in the MST1R/14-3-3 complex was frequently deregulated by genetic alterations in NPC. Our findings provide new insights in the pathogenesis of NPC by highlighting the involvement of the MST1R-mediated signaling pathways.
Publisher: Elsevier BV
Date: 07-1996
DOI: 10.1016/S0046-8177(96)90401-3
Abstract: Although nasal lymphomas showing midfacial destructive lesions had been classified as T-cell lymphomas, their exact cellular origin is still unclear. Although they usually express a restricted number of T-cell-related antigens, namely, CD2, CD43, and CD45RO, other pan-T or subset-T-lineage antigens, such as CD3 (membrane), CD5, CD4, CD8, and CD7, are frequently absent. Conversely, they often express a natural killer (NK) cell-associated antigen, CD56, but lack other mature NK markets. To study their cellular origin further, the authors analyzed T-cell receptor (TCR) gene transcription in three cases of nasal lymphomas and correlated the findings with the phenotype and gene rearrangement data. Two cases of nasal lymphomas with CD2+CD3(Leu4)-CD19-CD56+ phenotype were shown to express truncated 1.0-kb Tbeta and multiple unrearranged Tdelta transcripts with germline TCR beta, gamma, delta, and immunoglobulin heavy-chain joining region (JH) genes, consistent with NK cell lineage. In contrast, one case of nasal lymphoma with CD2+CD3(Leu4)+CD8+CD19-CD56+ phenotype expressed full-length Talpha, Tbeta, and Tgamma transcripts rearranged TCR beta, gamma, and deleted TCR delta genes, indicating T-lineage, These results support the view that nasal lymphomas can separated into NK-cell and T-cell neoplasms, based on differences genotypic characteristics. The possibility of these tumors being derived from a putative common precursor cell merits further investigation.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Alan Kwok Shing Chiang.