2018 GRC NPC [NPC tumorigenesis model] WES-seq of 111 NPC patient Nat Commun 18: 14121, 2017 LCM enrichment of tumor cells. -> higher somatic mutation than the Singapore study (because of LCM?) LMP1 activates both canonical and non-canonical NFKB pathways Homozygous deletion f BIRC2(cIAP) and BIRC3(cIAP2) in primary NPC Identification of a novel 12p13.3 amplicon […]
Fei-Fei Liu (Princess Margaret Hospital, Canada)“Prognostic Significance of miRNA Signatures for Detection of Metastatic NPC” metastatic NPC, metastamirs let-7 miR9 Nanostring 654 miRNA + 34 EBV mi RNA + mi RNA from other viruses on 124 patients Bruce Oncotarget , 2015 miRNAS 154 + miRNA 449 – MENA 140 – MIRNA 34c (Bruce
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Xin Lu (Ludwig Institute for Cancer Research, United Kingdom) “p53, a Key Regulator of Genomic Stability in Cancer” Discovery of p53: 1979 about the same time “tumor antigen” by Lloyd and Old, PNAS. Binding partner of large T antigen of SV40 (A Larid and David Lane) p53 mutation in 30–40% BL, why only 9 % in
Andrew Futreal (University of Texas MD Anderson Cancer Center, USA) “Cancer Genomics and Evolution” tumors heterogeneous from one patient to another intratumor heterogeneity—a state where subclonal subpopulations within the same tumor accumulate different kinds of mutations over time (65% heterogeneity in RCC) 1 mutation/wk, 40 mutations / year APOLLO platform https://goo.gl/uRmjHX Moon shot platform 40% subclonal
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Allan Hildesheim (National Cancer Institute, NIH, USA) “Use of Viral and Genetic Markers for Risk Stratification for Development of Screening Programs for the Early Detection of NPC” 1987 Use of viral and genetic markers for NPC risk stratification. 16% cancers are caused by infectious agents (Lancet Oncol 2012, de Martel) EBV vaccination: EBV gp350 (Coghill et
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Harald zur Hausen (German Cancer Research Center, Germany) “Discovery and Early Studies of EBV in Burkitt’s Lymphoma and NPC” EBV provides a step in the malignization of pre-malignant NPC lesion (methylation of p16) Endemic multiple sclerosis TGFb is an inducing agent for EBV lytic replication Vit D deficiency -> TGFb increase -> EBV reactivation EBV enhances
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Wed Poster #5 Dr. Timothy Wai Ho Shuen 孫傳豪 Singapore TESSA therapeutics (http://goo.gl/zdbYpA) NPC stage IVb patients → 抽300-400 ml blood → 一部分加B95-8 養成LCL → 養成的LCL與病人自己PBL aliquot co-culture → mapping 出effective CTL → expand → 打回去病人身上 (response rate還蠻不錯的! 整個時程約1-2個月) Wed Poster #9 University of Malaya Velapasamy, Sharmila … LF Yap SB-431542 10 uM, a TGFBRI
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LogID Title Initial Date AF001 Codebook for GA341 (= YJC AE538 = YMU RNA-seq on OKB2/S1F/THP1) SFL 10/21/15 AF002 Experimental sheme for AE592 (YMU RNA-seq GA416 and GA417) SFL 10/23/15 AF003 Codebook for GA417 SFL 11/3/15 AF004 Codebook for GA416 SFL 11/4/15 AF005 Codebook for Po-Ting SFL 11/5/15 AF006 Codebook for tidy 40T/N raw data
2006/10 Molecular and cytogenetic changes involved in the immortalization of nasopharyngeal epithelial cells by telomerase (the link to NCBI) 2008/10/10 根據這一篇, 那送EBV進入NP460h-hTERT不就等同於把EBV關禁閉? 另外Dr.George Miller有篇在J.Virol.Methods(2006)的文章,看起來像是一位MD/PhD的學生做的。他以兩位IM病人血清(富含各種anti-EBV抗體)去分離經NaB處理過的P3HR1(HH514)細胞。分什麼呢?分那些在走lytic cycle和不被NaB活化的HH514。分下來後的細胞再送回去petri-dish養。結果發現走lytic cycle的細胞無一存活、而沒有induce的細胞可以再被養回來,而且induction rate隨著時間增加而增加。很有意思的一篇文章。George大學是學歷史的,非常會寫文章,邏輯性很強而且要言不贅,讀他的paper總覺得能做science真好。 2010/02 MTA_Signed_LinSF_NP460hTERT 2010/08 Epstein-Barr virus infection in immortalized nasopharyngeal epithelial cells: regulation of infection and phenotypic characterization (the link to NCBI) 2010/11 (YJC)AC301 To test the infectivity of Akata-p2089
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-台中清新會館-陳老師述說從前 NCI與衛生署歷史: 第一次三年20多篇paper, 第二次、第三次…-台北美兆健檢中心 -wondering thought: BEX1/LDOC1; miR-329 and miR410
20150902–09033 PI Retreat Read More »