DASL: cDNA mediated Annealing Selection, extension and Ligation (Illumina)
expression array of 40 N/T OSCC samples from Dr.蕭.
ShSSAT: growth inhibition escape. Illumina’s miRNA and methylation array for 40 N/T OSCC samples from Dr.蕭. ※Prof. Cheng has a natural compound for regulating the miRNA concentratin as fast as in 30 min.
SFL: Prof Cheng sugggested me to do the protien chip or pay more attention to the original material collection/ Prof Yan asked me if we have siRNA library for PTKs.
ENO1: 甲型烯醇酶 alphaEnolase. (Chimei 251 oral cancer patients. 106/251 with lymphonode metastasis)※ENO1/uPA/PA1 → MMP → galectin-3 cleavage → BrCA metastasis. ※ PAI promoter SNP polymorphism → higher incidence..? ※ Additional signals CXCL12, CCL2, STAT3※ENO1/Nrf2 and radiation resistance (IL6 by macrophage) → protect from chemotherapy and radiation therapy. Professor comments: inflammation is very close to hypoxia condition. VEGFR is closely related to metastasis. Question is: what is the resaronthat causese ENO1 to go up? is it totally the consequence of Hypoxia ? HIF1alpha?※the use of second ATG of ENO1 (48 kDa) produced MBP (37 kDa)
OVTA1/KIAAxxx/a Ser/Thr kinase: Ab from lung patient (turned out was a ovarian meta from lung) → serological screening of OVTA1 on ovarian cancer samples by using phage displaying system → N-terminus/Pro-rich/Ser/Thr Kinase domain/Ubi docking domain/regularatory domain (TPHGYAH motif identified by the Ab/phage displaying system) → expression level fo OVTA1 is associated with cell growth → si OVTA1, cell growth shut down/over-express OVTA1, cell growth increases → OVTA1 faciltates G1 progression※p21KO mouse 比同期的wild type 不易(or更容易)罹癌. OVTA1 may exert functions via Src. → OVTA1 gene-KO mouse with Dr.林SW at NTU. ※ENO1/inflammatory response and NF-KB
Nrf2/Keap1/ARF forms ubiquitination complex →IHC of Nrf2 expession level is high in oral cancer sample, but is heterogenesis (the use of wrong antibody?)※hypoxia and reoxygeneration※cisplatin/IR-resistant cells
B292 causes the increament of acetylated alpha tubulin, but inhibits tubulin polymerization ※a hybrid of J30 (taxol) and HDAC275※B292: for a series of cell line IC50 is about 50-100 nM but HUVEC is 42 uM, SAHA is 15.5 uM, 可是tube formation及 angiogenesis 又有被抑制. [me: alpha tubulin/HDAC6 expression in HUVEC, possibly be different from that of in other cell type??] low neuro toxicity in SH-SY5Y 250 nM no calcium influx.
PI3K/mTOR signaling pathways and H&N cancer: 90% EGFR is over-expressed in Euro/USA but no mutations was found; In Taiwan, EGFR amplicfication was found in 24~58% patients, EGFRVIII 42%. ※Dual mTOR and PI3K inhibitor:BGT226 Norvatis) (※No mutations was found in the PI3K or ?? regions of Taiwan HNSCC samples. Growth inhibition 12.5±5.1 nm. (Here comes a quiestion, Dr. Chang’s 2 cell lines whose BGT226 sensitivity were not correlated with AKT phosphporylation) 覺得這部份的pathway 和 feed-back事件要搞清楚.
Secretome paper註載NPC and HNSCC and Chang-Gung Dr. Yu’s Mac-2 in OEC-M1 and SCC-4.
3D culture and tumor micro-environment的模型建立. Valerie M Weaver的Webpage.
Dr.常DOH got funded, VEGF and SDF1/CXCR4 and signaling pathway biomarker with pancreatic cancer; desmoplastic (?) reactionin PDAC (=high fibrosis) → blood flow 差, 藥物無法到達tumor. ※ Tumor interstitial fluid pressure increases , vascular normalization by anti anti-angiogenesis. ※ Tumor blood flow interruption after radiation therapy strongly inhibts tumor regression. ※ radiation 造成細胞最嚴重傷害是在G2/M ※ shear stress/G2/M arrest/FAK activation/T84 cells/醫工組2008 PNAS paper/ ※ Prof Cheng’s comment 搞清楚並模擬collagen I or IV/相對ITGs/ECM與coronial invasion system之關連.
Aldo-keto rectase (AKR) and redox GADD45-alpha ※ Nrf2 increases 則AKR increases, why? (because Nrf2 is related to ubiquitination system?) ※ c-Kit TK1 versus HSP90: AUY922 is a HSP90 inhibitor, AUY922 can efficiently suppress c-Kit and phosphorylated form of c-Kit, why?
Gemcitabine resistant cell lines ※ 2% O2 is a physiological hypoxia condition ※ HIF-alpha Yale 查一查..??
Treg and TAM in PDAC (a form of highly inflammatory disease)※ADM (acinar to ductal)→PanIN → PDA: K-Ras mutation (90%) → p16 loss (90%) → p53 inactivation (50-75%) → Smad4 loss (55%) ※Tumor associated macrophage (TAM) in BrCA and lung CA, the more infiltration of TAMs, the worse prognosis ※ conditional media from PBMCor THP-1 could stimulate the secretion of IL10, TGFb by TAM, to inhibits cancer cell proliferation. ※ Conditional media from cancer cells could stimulate TAM to secrete CCL22 ※ Lox-Stop-Lox (LSL)_Kras G12D x Pdx1-Cre
RT-PCR sequencing instead of genetic mutation check-u
TIEG1/KLF10: TGFbeta inducible early gene [Rev]. 與Sp1/Smad有關. Binding sites CCCTC??, could this be involved in DNA boundary process? HPRD shows the full-length one interacts with Sp1. ※Pim1 binds to a consensus motif pS/TP. ※Promoter of TIEG1 is highly methylated in oral cancer samples.
Kallikrein: KLK13/Cx 19/clustered gene family (proteases) [GeneID]: potential good biomarkers.
AXL inhibitor: 10-20 nM (IC50) Rigel Pharm… (CA, USA)
Combine Gencitabine and target thearpy (ex TKI, NFKB..) ※Aspirin is a IKKbeta inhibitor ※SAHA可contact夏醫師 ※first in man traial made in house: SCB01Q (BPRoL075)/CA4P tubulin polymerization and VDA (vascular disruption agent) ※CPT11在亞洲用藥要先genotype UGTA1*x6 nad UG1A1*28, Prof Yan suggested GenMED Chip {?} to analyze the genotype ※ Prof Cheng mentioned about Japan’s CYP2D6.
Walter: MAGE A (CT1) gene family ※ 12 related gene members in the A family/located at Xq28, expressed during spermatogenesis. functions: binds to Skip, MAGE A11 can stablize ligand-free androgen, MAGE A and C-termunus can induces p53 dependent and independent apoptosis ※ MAGE A3: GSK 已將此分子列為tumor vaccine therapy, is a potential tumor marker present in 35-50% lung CA, 35% bladder CA, 74% in melanoma and HCC, 49% in Head and Neck cancers.