2020-12-13 亞太生醫矽谷精準醫療旗艦計畫成果展示暨學術硏討會

Genomic and transcriptomic study of head and neck cancer in Taiwan 楊慕華副校長  (YouTube)

• Ref in Slide 2: EMT 2016 (PubMed) (pdf5564)
• Genomic alterations
• Found in 37/39 samples (94.87%)
• Compared to that in targeted-req (HNSCC panel), and TCGA (tier 1)

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罹患口腔癌壽命少20年 台灣國健署：口內出現五徵兆應盡速就醫

 (From google Groups/sflinlab2020)

(台灣英文新聞/生活組 綜合報導)根據衛服部死因統計和國健署癌症登記資料，台灣每天有9名死於口腔癌，21人罹患口腔癌，尤其好發於中壯年族群，罹癌後平均壽命還整整少了一般人20年。國健署王英偉署長提醒，為預防口腔癌的發生，除拒絕使用檳榔、菸品外，還要定期口腔黏膜檢查，及注意口腔黏膜變化，可有效降低口腔癌發生及死亡風險，亦可以避免後續多重癌症之發生。

根據國健署所進行的國民健康訪問調查顯示，有嚼檳榔者7成有吸菸習慣，6成6長時間有喝酒，檳榔、菸、酒等習慣皆有者近5成。過去研究指出嚼檳榔造成口腔癌的機率為未嚼者的28倍。

嚼檳榔不僅會增加口腔癌發生機率，也會對上呼吸消化道(口腔、咽、喉、食道)造成傷害，近年研究指出嚼檳榔者罹患上呼吸消化道癌症風險，較不嚼檳榔者之風險高5倍，若檳榔、菸、酒三者皆有使用習慣，較無使用者罹患上呼吸消化道之風險更高達10.5倍!

國健署提醒「拒絕檳榔、定期檢查、及早就醫」才是預防口腔癌不二法門。早期發現口腔病灶是提升存活率與降低治療難度的關鍵，民眾若發現口內出現「破斑硬突腫」之一的情形，應盡速就醫：

破：口腔黏膜破皮超過兩週未癒合

斑：口腔黏膜出現不明的紅斑、白斑

硬：口腔黏膜逐漸變硬、緊，最終嘴巴張不開

突：口腔黏膜表面不規則突起(乳突狀或疣狀突起)

腫：臉或頸部出現腫塊或兩側不對稱

口腔癌是最容易預防的癌症！國民健康署呼籲國人要拒絕檳菸酒，定期篩檢、及早戒除。口腔黏膜檢查的目的，是要找出癌前病變，加以治療阻斷癌症發生的機會，提醒30歲以上有菸檳行為的民眾，每2年攜帶健保卡至健保特約牙科、耳鼻喉科醫療院所接受口腔黏膜檢查，若自己發現有「破、斑、硬、突、腫」其中一項症狀，要盡速就醫接受治療，就可預防口腔癌!

OSCC Cell Line STR information 20150312 更新版

OSCC Cell Line STR information 20150312 更新版
由 sufang 在 一, 03/30/2015 - 08:45 發表 Oral Cancer OSCC Cell Line STR analysis

Dear all,

更新oral cancer相關細胞株之STR資訊
共有16個細胞株, 其中DOK, FaDu, HOK, HSC-3, KB, OEC-M1, SCC-15, SCC-9, Tu-183(共9株)有送件STR的資訊(詳如附件)
須請大家注意的資訊如下:
1. HSC-3, 於Dr.郭靜娟's lab的新HSC-3為真, 請非此來源者把舊的細胞扔了吧! (p.s Dr. 李岳倫於2014年7月及9月分別定的STR結果同新HSC-3, 推測亦為可用細胞株)
2. KB, 於Dr.郭靜娟's lab定STR結果為HeLa細胞, ATCC/JCRB資料庫也證明KB為HeLa. 請勿使用此細胞株!
3. SCC-15, Dr.李岳倫's lab 於2014年9月及10月分別定的STR結果皆與SAS細胞株相符(90.9% match), 使用此細胞株請小心!
4. Tu-183, 於Dr.江士昇's lab於2014年12月所定STR結果未比對到現今資料庫中任何細胞株, 推測可能為可用細胞株. 但Dr. 江提供資訊:expression pattern與預期不同, 大家使用此細胞株請小心!

以上,
如有問題或錯誤的地方, 敬請不吝指正! 謝謝!

敬祝 研究順利

嬿如 敬上

原檔按我下載 (2015_0320_cell_lines_str_information20150312ding_gao.xlsx)

TCGA HNSCC Marker Paper

由 sufang 在 五, 02/27/2015 - 10:08 發表 Oral Cancer HNSCC TCGA

Comprehensive genomic characterization of head and neck squamous cell carcinomas (pdf 4292; PubMed Link)

The Cancer Genome Atlas profiled 279 head and neck squamous cell carcinomas (HNSCCs) to provide a comprehensive landscape of somatic genomic alterations. Here we show that human-papillomavirus-associated tumours are dominated by helical domain mutations of the oncogene PIK3CA, novel alterations involving loss of TRAF3, and amplification of the cell cycle gene E2F1. Smoking-related HNSCCs demonstrate near universal loss-of-function TP53 mutations and CDKN2A inactivation with frequent copy number alterations including amplification of 3q26/28 and 11q13/22. A subgroup of oral cavity tumours with favourable clinical outcomes displayed infrequent copy number alterations in conjunction with activating mutations of HRAS or PIK3CA, coupled with inactivating mutations of CASP8, NOTCH1 and TP53. Other distinct subgroups contained loss-of-function alterations of the chromatin modifier NSD1, WNT pathway genes AJUBA and FAT1, and activation of oxidative stress factor NFE2L2, mainly in laryngeal tumours. Therapeutic candidate alterations were identified in most HNSCCs.

Five Figures in the Main Text:

Figure 1 | DNA copy number alterations. a, Copy number alterations by anatomic site and HPV status for squamous cancers. Lung squamous cell carcinoma (LUSC, n = 358) and cervical squamous cell carcinoma (CESC, n = 114). b, Unsupervised analysis of copy number alteration of HNSCC (n = 279) with associated characteristics. The rectangle indicates chromosome 7 amplifications in the purple cluster. NA, not available. 

Figure 2 | Significantly mutated genes in HNSCC. Genes (rows) with significantly mutated genes (identified using the MutSigCV algorithm; q , 0.1) ordered by q value; additional genes with trends towards significance are also shown. Samples (columns, n = 279) are arranged to emphasize mutual exclusivity among mutations. Left, mutation percentage in TCGA. Right, mutation percentage in COSMIC (‘upper aerodigestive tract’ tissue). Top, overall number of mutations per megabase. Colour coding indicates mutation type.

Figure 3 | Candidate therapeutic targets and driver oncogenic events. Alteration events for key genes are displayed by sample (n = 279). TSG, tumour suppressor gene.

Figure 4 | Integrated analysis of genomic alterations. a,b,Samples (n=279) ared isplayed in columns and grouped by gene expression (a) or methylation (b) subtype (sub.). Unadjusted two-sided Fisher’s exact test P values assess the association of each genomic alteration. Methylation probe location of CpG islands, shores and shelves are shown on the left of b. Annotation shows HPV status and subtype (16, 33 and 35). CN, copy number.

Figure 5 | Deregulation of signalling pathways and transcription factors. Key affected pathways, components and inferred functions, are summarized in the main text and Supplementary Information section 7 for n = 279 samples. The frequency (%) of genetic alterations for HPV(–) and HPV(+) tumours are shown separately within sub-panels and highlighted. Also see Supplementary Fig. 7.15. Pathway alterations include homozygous deletions, focal amplifications and somatic mutations. Activated and inactivated pathways/genes, and activating or inhibitory symbols are based on predicted effects of genome alterations and/or pathway functions. 

---

Ten Parts of Supplementary Information: 

S1: Biospecimen collection and clinical data

S1.1. Biospecimen collection and clinical data  

S1.2. HPV detection methods  

S1.3. Survival analysis  **

Figure S1.1. HPV status as a function of clinical and molecular characteristics  

Figure  S1.2.  Receiver  operating  characteristic  (ROC)  curves  in  HPV-associated  miRNAs  in  oropharyngeal HNSCC  

Figure S1.3. DNA methylation signatures of HPV

Figure S1.4. Survival analysis for select clinical and genomic variables

Figure S1.5. Survival analysis for platform-specific subtypes 

Table S1.1. Summary of clinical data 

Data file S1.1. Data freeze clinical dataset (This file contains clinical and demographic information for all patients)

Data file S1.2. Summary of HPV detection results  (This file contains the results of molecular analyses used to determine the HPV status of all patients. These include data from in situ hybridization, p16 staining, RNA and DNA sequencing, and the MassArray assay.)

Data file S1.3 Mutation signatures by HPV status (This file contains counts of base changes seen in APOBEC and smoking mutation signatures for HPV(+) and HPV(-) subjects. Fisher’s exact test p-values are also shown.)

S2: Copy number analysis  

S2.1. SSNP array-based copy number analysis

S2.2. Structural alterations  

Figure S2.1. GISTIC 2.0  analysis  of  significantly  reoccurring  focal  alteration  in  279  HNSCC tumors  

Figure S2.2. GISTIC amplification and deletion peaks in lung squamous cell and cervical squamous cell  carcinoma  

Figure S2.3. Comparison of GISTIC 2.0 analyses of 243 HPV(–) and 36 HPV(+) head and neck tumors  

Figure S2.4. Number of copy number segments in HPV(+) and HPV(–) samples  

Data file S2.1. GISTIC amplification and deletion peak annotation in head and neck squamous cell (all  samples, by HPV

status, and by site), lung squamous cell carcinoma, cervical squamous cell carcinoma  (results from GISTIC analyses for head and neck (HNSC), lung, and cervical squamous cell carcinoma. Additional analyses for HNSC were conducted by HPV status and tumor site.)

Data  file  S2.2. Fisher’s  exact  test  p-values  for  frequency  comparisons  of  significantly  reoccurring  alterations by HPV

status and site (results of analyses of frequency comparisons of significantly reoccurring DNA copy number alterations by HPV status and tumor site. Fisher’s exact test p-values are also shown.)

S3: RNA sequencing  

S3.1. RNA sequencing and expression quantification  

S3.2. RNA-Seq for confirmation of somatic alterations reported in whole exome sequencing  

S3.3. Gene fusion detection  

S3.4. RNA-Seq for gene splicing and viral integration  

Figure S3.1. RNA-Seq for confirmation of somatic alterations reported in whole exome sequencing  

Figure S3.2.  FGFR3-TACC3 fusion event  

Figure S3.3. EGFR vIII mutant sample  

Figure S3.4. Exon 14 skipping in MET+ 

Figure S3.5. Alterations of CDKN2A gene structure, copy number, and expression of its protein coding  transcripts p16INK4A and p14ARF  

Figure S3.6. Integration of DNA mutation type, copy number, and gene expression for CDKN2A+ 

Figure S3.7. Alterations of FAT1 gene structure, copy number, and expression  

Figure S3.8. Integration of DNA mutation type, copy number, and gene expression for FAT1+ 

Figure S3.9. Integration of DNA mutation type, copy number, and gene expression for predicted driver  genes relevant to HNSCC  

Figure S3.10. Distribution of HPV integration breakpoints across the host genome

Figure S3.11. The KLK12 gene documents recurrent alternate transcription in HNSCC  Figure S3.12. Heterogeneous TP63 isoform usage in HNSCC+ 

Data file S3.1. RNA-Seq predicted fusions ( contains the results of fusion detection analyses performed with MapSplice. )

Data file S3.2. Viral integration sites (information about HPV viral integration sites based on the analysis of RNA and DNA sequencing 
data.)

Data file S3.3. SigFuge clustering results for alternatively spliced genes (the results of SigFuge analyses to detect differential expression of multiple gene isoforms. Uncorrected p-values are shown.)

Remarkable Role of Indoleamine 2,3-Dioxygenase and Tryptophan Metabolites

由 sufang 在 四, 11/20/2014 - 13:20 發表 Pre-published IDO1 KYN

Remarkable Role of Indoleamine 2,3-Dioxygenase and Tryptophan Metabolites in Infectious Diseases: Potential Role in Macrophage-Mediated Inflammatory Diseases (PubMed) (pdf 4235)

Figure 1. Schematic overview of the kynurenine pathway. It is estimated that only 1% of dietary tryptophan (TRP) can be converted into serotonin (5-HT). The remaining 99% of TRP is metabolized via the kynurenine (KYN) pathway. Tryptophan hydroxylase (TH), 5-hydroxy TRP (5-HTP), N-acetylserotonin (NAS), indoleamine 2,3-dioxygenase 1 and 2 (IDO1/2), tryptophan 2,3-dioxygenase (TDO), kynurenine 3-monooxygenase (KMO), kynurenine aminotransferase (KAT I, II, III), kynurenic acid (KA), anthranilic acid (AA), 3-hydroxykynurenine (3-HK), xanthurenic acid (XA), 3-hydroxyanthranilic acid (3-HAA), 3-hydroxyanthranilic acid oxidase (3-HAO), quinolinic acid (QUIN), quinolinic-acid phosphoribosyl transferase (QPRT), nicotinic acid mononucleotide (NaMN), nicotinamide mononucleotide adenylyltransferase (NMNAT), nicotinamide adenine dinucleotide (NAD).

Figure 2: T-cell immune regulation by IDO1. (a) IDO1 is induced by IFN-γ-dependent and/or -independent signal pathways, depending on the variety of immune stimuli by macrophages and dendritic cells (DCs) [28, 83]. IDO1 activity is suppressed by the formation of NO or the competitive enzyme inhibitor, 1MT. Marked increases in IDO1 suppress immune responses by locally depleting L-TRP and preventing T-cell proliferation [44]. Expression of IDO1 has been observed in certain types of activated macrophages and DCs. IDO1-expressing cells deplete TRP from the extracellular milieu and secrete TRP metabolites, including KYN, 3-HK, 3-HAA, and QUIN, which induce T-cell apoptosis and suppress immune responses in vitro. (b) CD19+ plasmacytoid DCs (pDCs) express high levels of IDO1, which can activate mature regulatory T (Treg) cells via activation of the protein kinase general control nonderepressing-2 (GCN2) pathway of protein synthesis inhibition [84]. pDC-produced IDO1 and activated Treg can convert naïve T cells into new Treg. IDO1 acts in an autocrine manner to suppress pDC production of IL-6, which prevents the conversion of Treg into IL-17-producing Th17 proinflammatory cells [79]. IDO1 also downregulates type I IFN (IFN-α) production by pDC [80].

Figure 3: IDO1 induction and proinflammatory cytokines. IFN-γ drives intense enzymatic IDO1 activity, resulting in TRP depletion and high-level production of immunoregulatory TRP metabolites, KYNs, which may foster Tregs expansion. Induced Tregs use TGF-β to maintain an IDO1-dependent regulatory environment, with IDO1 mostly functioning as a signaling molecule. Both mechanisms are interrupted by IL-6, which drives IDO1 degradation as potent inflammatory stimuli enter the local environment [85].

Figure 4: The mechanism of IDO1 regulation on viral infectious diseases. Innate defense occurs when pathogens contact or invade host cells and elicit the production of cytokines and chemokines, which in turn induce an influx of immune cells that affect pathogen clearance. Type I IFNs are critical mediators of innate immunity and limit disease caused by many viruses [73, 86]. The enhancement of TRP breakdown by IDO1 regulates the signal pathway for IFNs production, and TRP metabolites might contribute to the function of IFNs producing cells.

10/14 (二) 蕭醫師來訪建議.

由 sufang 在 日, 10/26/2014 - 09:14 發表 Pre-published IDO1

要找IHC能用的抗體，可以上 The human protein atlas網站．像以HNSC IDO1而言，就有三個選擇 HPA023072, HPA023149, HPA027772.

素芳提議染100例oral cancer檢體、或是補染40對T/N samples。

2014/10/28: TDO2也有抗體 Antibody HPA039611.   HNSC TDO2.    IDO2 則似乎沒有收錄．

食工所 Drs. 黃、謝 _ Skin Cell Talk Slides

由 sufang 在 四, 09/04/2014 - 11:26 發表 Pre-published A431 HaCaT Keratinocyte Knowledgebase

Cancer Epigenomics_Folate

由 sufang 在 日, 08/03/2014 - 09:28 發表 Pre-published Cancer epigenomics Folate MATHFR Methionine Methylation SAM

重要文獻 (Research Notes: Cacner epigenomics (folate))

1.    Kane, M. A. (2005) The role of folates in squamous cell carcinoma of the head and neck. Cancer detection and prevention 29, 46-53. (pdf 4099.)    The primary objective of this review is to explore the hypothesis that folate insufficiency may be important in the pathogenesis of squamous cell carcinomas of the head and neck (SCCHN) and that folate repletion may be an effective component of chemoprevention. The main results are that folate insufficiency disrupts DNA global and specific gene methylation patterns such that the activity of certain tumor suppressor genes such as p16 and possibly p53 may be lost. Folate pool imbalance and impaired repair mechanisms may contribute to DNA instability and strand breaks. Sensitive methods exist for identification of individuals with folate insufficiency in contrast to the relatively insensitive conventional serum or red cell folate assays with broad "normal" ranges. The impact of folate supplementation can thus be quantified. Folate imbalance may result from alterations in folate cellular uptake by the reduced folate carrier (RFC) and/or the folate receptor (FR) and polymorphisms in enzymes important in folate retention such as folylpolyglutamate synthetase and in folate modification such as methylene tetrahydrofolate reductase (MTHFR). Known predisposing factors for SCCHN such as alcohol and tobacco carcinogens may influence folate balance. Folate supplementation may reduce primary or secondary risk of cancer. Formal studies of folate sufficiency in persons at risk for or diagnosed and treated for SCCHN are needed to define the role of folate supplementation in the prevention of these cancers.

Field Effect

由 sufang 在 二, 07/29/2014 - 23:14 發表 Pre-published Field Effect NOTCH Oral Cancer

重要文獻:

1. Leemans CR, Braakhuis BJ, Brakenhoff RH (2011) The molecular biology of head and neck cancer. Nat Rev Cancer 11: 9-22. (pdf 2833)
2. Hu B, Castillo E, Harewood L, Ostano P, Reymond A, et al. (2012) Multifocal Epithelial Tumors and Field Cancerization from Loss of Mesenchymal CSL Signaling. Cell 149: 1207-1220. (PubMed) (pdf 3435)
3. Vanharanta S, Massague J (2012) Field cancerization: something new under the sun. Cell 149: 1179-1181. (PubMed) (pdf 3438)
4. Troester M (2012) Genomic Characterization of Cancer-Adjacent Tissue: Evidence of Field Effects and Expression Subtypes. TCGA Second Annual Scientific Symposium. (pdf 3938)
5. Alcolea MP, Greulich P, Wabik A, Frede J, Simons BD, et al. (2014) Differentiation imbalance in single oesophageal progenitor cells causes clonal immortalization and field change. Nat Cell Biol 10.1038/ncb2963. (Ingrid Journal Club Paper) (PubMed) (pdf 4024)
6. Frede J, Adams DJ, Jones PH (2014) Mutation, clonal fitness and field change in epithelial carcinogenesis. J Pathol 10.1002/path.4409. (pdf 4133)

J Pathol. 2014 Jul 21. doi: 10.1002/path.4409. [Epub ahead of print]

Mutation, clonal fitness and field change in epithelial carcinogenesis. (pdf 4133)

Frede J¹, Adams DJ, Jones PH.

Author information

Abstract

Developments in lineage tracing in mouse models have revealed how stem cells maintain normal squamous and glandular epithelia. Here we review recent quantitative studies tracing the fate of individual mutant stem cells which have uncovered how common oncogenic mutations alter cell behaviour, creating clones with a growth advantage that may persist long term. In the intestine this occurs by a mutant clone colonizing an entire crypt, whilst in the squamous oesophagus blocking differentiation creates clones that expand to colonize large areas of epithelium, a phenomenon known as field change. We consider the implications of these findings for early cancer evolution and the cancer stem cell hypothesis, and the prospects of targeted cancer prevention by purging mutant clones from normal appearing epithelia.

缺口計畫相關資訊

由 sufang 在 六, 07/05/2014 - 17:12 發表 Pre-published Arecoline COE (Cancer of Excellence) OPMD Potentially malignant disorder

10/05/2014 (SUN) PK大賽

第二期癌症研究缺口補強計畫評選會議議程

開會時間：103年10月5日（星期日）上午10時

開會地點：本部204會議室

壹、主席致詞

貳、報告

劉柯的4NQO老鼠與40T/N交叉比對部分

由 sufang 在 六, 06/28/2014 - 15:59 發表 Oral Cancer 4NQO Oral Cancer

說在前頭: 目前我拿的還是Illumina normalized的"group" data. 這和江博前次所提，做過SVA1的M0, M1, M2, M3稍稍不同。等江博轉好他的data給我，我會儘快送入Molas，到時就可reconfirm大家心目中有興趣的基因/pathway在兩組資料中有 沒有差很大。

所以，我再囉唆一次，因為看了下面兩個圖後，我把stage 2的資料先不加入分析，因此僅看 stage 0, stage1, stage 3, stage 4的基因變化趨勢，共篩出543個基因，也就是Pathway Book v1中的"mouse model"部份。

Janelle的部份

由 sufang 在 六, 06/28/2014 - 16:03 發表 Oral Cancer DOK NIC nicotine Oral Cancer

Nicotine (NIC) - treated DOK: 針對NIC4, NIC5, NIC6 vs DOK1的array data, 配合日前所提, NIC-treated DOK clones 有明顯增加cell proliferation及migration的現象, 可能參與的pathway/genes有:

1. DNA replication: MCM10 (3.37x), RECQL4 (2.32x), GINS2 (2.32x), CDC25A (3.01x), CDC7 (2.227x), NASP (2.19x), DTL (2.38x)。
2. Cell cycle: E2F2 (2.22x), CDC6 (2.75x), CDC7(2.27x), CDC25A (3.01x), PKMYT1 (2.31x), CDKN1A (=p21, 0.44x), SOX9 (0.31x), HBP1 (0.38x), STEAP3 (0.4x), RPS6KA2 (0.22x), RPS6KA3 (0.39x)
3. Transcriptional misregulation in cancers: SIN3A (0.52x), NUPR1 (0.39x)
4. Fibroblast growth factor binding: TGFBR3 (3.63x), FGFBP1 (2.51x), FGFR3 (2.83x, NIC獨有的)
5. TGF-beta signaling pathway: BMP4 (4.56x), BMP7 (8,98x)
6. Focal adhesion: COL5A1 (0.49x), LAMA3 (0.38x), THBS3 (0.53x), ITGA3 (0.5x) , ITGA5 (0.37x), MET (0.49x), ITGB5 (0.49x), VEGFA (0.37x), VEGFC (0.5x), SHC1 (0.52x), MAP2K1 (0.52x), CTNNB1 (0.42x) 細胞focal adhesion能力下降?
7. Cell adhesion: CLDN1 (0.46x), LPXN (0.34x), AMTN (0.21x) 細胞貼附能力下降?
8. Stress fiber: GAS2L1 (2.65x), ENAH (2.26x), NEBL (2.67x)
9. Epidermis development: KRT13 (75.39x, 可是不知為何去到40TN及4NQO mouse呈下降或不變趨勢)

小記一下:

–許多基因的上或下，AC和NNK較一致，但如果nicotine是由NNK來的，會期望看到nicotine與NNK較一致。先按下不表。

–KRT13被記載在下列這些GO中: tongue morphogenesis, keratin filament, intermediate filament, extracellular vesicular exosome, cellular response to retinoic acid, epidermis development, response to radiation

新書發表-Pathway Book v1

由 sufang 在 三, 06/25/2014 - 10:37 發表 Pre-published 40TN 4NQO DOK Molas Oral Cancer

親愛的大家：我心目中的pathway mapping結果終於做好了! (按我下載Pathway book v1)。這是由三項microarray 分析結果而得到的結果, including (1) 40對T/N病人檢體; (2) (娟與夏的)AC, NNK, NIC-treated DOK cells; (3) 劉柯的 4NQO/AC-mouse. (按我下載 40TN_DOK_4NQO_Combo v1)。

OrCa小組會議_DOK related

由 sufang 在 四, 03/27/2014 - 00:00 發表 Oral Cancer Arecoline DOK nicotine NNK

OrCa小組會議 (03/27/2014)

素芳的筆記本：

• nicotine: 500 uM
• NNK: 10 uM
• arecoline (AC): 50 uM or 100 uM
• treated for ~ 1 year, looking for carcinoge-tolerant cell clones, eg. NNK4, NNK5, NNK6, NIC4, NIC5, NIC6
• doubling time
• migration assay
• In vivo tumorigenesis
• Expression array  analysis ("Merged_Kuo_Shiah" from Jonhson on 4/18/2014)
  • from 靜娟 (第一次DOK1等七片arrray, 第二次DOK2等三片arrray)
    • DOK pool 1 (DOK1)
    • NIC4 (NIC4)
    • NIC5 (NIC5)
    • NIC6 (NIC6)
    • NNK4 (NNK4)
    • NNK5 (NNK5)
    • NNK6 (NNK6)
    • ------------------------------------------
    • DOK pool 2 (DOK2)
    • AC50 pool (AC50)
    • AC100 pool (AC100)
  • from 夏博 (5片arrray, S=Shiah, QN=quantile normalization):
    • Dok (DOK3)
    • Arecoline 50 uM 5-day (AC50_short)
    • Arecoline 50 uM 12-mo (來自靜娟;命名為 AC50_1)
    • NNK 10 uM 5-day (NNK_short)
    • NNK6 12-mo (來自靜娟;命名為 NNK6_1)
• ARE: anti-oxidant responsive element; Nrf2/ARE
• NRF2=NFE2L2
• KEAP1 (E3 ligase adaptor)
• AKR1C2, C3, C4
• SOD1, 2, 3
• nAchRa9

Primary and immortal oral keratinocyte cells

從paper翻到

Rheinwald JG 有建立Primary and immoral Oral keratinocyte (OKF)

然後逛他的網頁突然發現

他們有在販售

http://rheinwaldlab.bwh.harvard.edu/cell.html

cell list如下

http://rheinwaldlab.bwh.harvard.edu/Cell%20lines%20in%20Core%20collection.pdf

也有配送國外

或許這會是另外的OSCC control 來源

原始paper&culture condition
https://www.dropbox.com/s/9hutmyzp7jk77um/OKF6-paper.pdf

KegArray Results

由 sufang 在 一, 07/29/2013 - 20:10 發表 Pre-published 40 T/N ECM KEGG Microarray

Stiffer: Up in COL, LAM, FN, SPP1 (OPN), TNC, AGRN, IBSP (BSP), LOX, LOXL1, LOXL.

ITGA3/A5/A6/B3/B4/B6

長庚鄭教授系列文章

2009-04 Transriptome profiling and network pathway analysis of genes associated with invasive phenotype in oral cancer。
2010-兩篇和marker相關 One and Two。
2011-02 把OSCC細胞處理areca nut extract–Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract。
2011-07 Molecular chaperones as a common set of proteins that regulate the invasion phenotype of head and neck cancer。
2011-10 GP96 is over-expressed in oral cavity cancer and is a poor prognostic indicator for patients receiving radiotherapy。
2012-02 Oncogenic function and early detection potential of miRNA-10b in oral cancer as identified by microRNA profiling。

2/13/2012 OrCA Meeting

1. 下次開會: 6月
2. CA OrCA PIs + 王副院長、莊JL、陳YR、黃HG (RA:雪君)、江主秘。
3. BioSignature Program: Leader/Chang Gung 核醫科主任閻紫宸, looking for cause-effect marker. The third meeting will be held on March-8; focus on miRNA/epigenetics/DNAs; funding source, Academia Sinica.
4. 王副院長Lab學生報告 (Wei-Chieh Huang)—長庚閻醫師 has 53 OrCA T/N pairs; miR-491-5p is involved in cell migration and invasiveness, targeting GIT1 and RAB1; OC-3 and C9 were used。
5. Dr. 莊JL
Cellular prion is increased by alcohol consumption involved in tumorigenesis of OSCC
PrpSC/PRNP is significantly up-regulated in OSCC
以電腦判讀TMA result
Second primary tumor (what is the definition of second primary? second primary vs. recurrent)
Alcohol induced TGF-b1 elevaltion is modulated by PrpC
6. 雪君:
Small heat shock protein
HSP27, 60, 70, 90, 110 MW 10–30 are called as small HSP
HSPB1=HSP27
She uses HOK, Cai-27, OC3, OEC-M1, Ca9-22 as cell models
HSP27/HSPB1 enhances OSCC apoptosis via repression in response to oxidative stress
H2O2 (50 uM), ANE (10 ug/ml), ANE (30 ug/ml)
PKCdelta and PTP1B function as downstream of HSP27/HSPB1 in response to oxidative stress.