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Note: A path to efficient gene editing Doi: 10.1038/s41591-018-0110-y Gene editing in human pluripotent stem cells (hPSCs) and iPSC -- the efficiency is very low compared to the other cell types. Kaykas and colleagues and Taipale and colleagues finding p53 antagonizing efficient genome editing using Cas9 in hPSC and immortalized human retinal pigment epithelial cells Editing gene that is silent in hPSCs -- > same result as editing one that active Single DSB induced by Cas9 in the genome of hPSC -- > reduces their survival Cas9 screens in transformed cells Copy number of gene target (rather than nature of individual genes) -- > drive phenotype of edited cells Thus -- clinical applications -- this could cause undesired side effects Kaykas and colleagues  Study transcriptional response of hPSC using gene editing with Cas9 Even one single strand break -- > increases expression of genes involved in programmed cell death Cas9-induced toxicity is mediated by p53 Reduced the le...

Note: Innovative Precision Gene-Editing Tools in Personalized Cancer Medicine doi: 10.1002/advs.201902552 Overview of gene editing applications Application; Discovery of Cancer Driver Genes Using Gene-Editing Tools -- library screening Targeted Delivery Systems for Genome and Epigenome-Editing Establishment of Animal Models for Cancer Target Validation Using Gene-Editing Tools EpiGenome Engineering in Cancer Cells -- using gRNA+genetic engineered CAS9+fused epigenome manipulated enzyme Clinical Applications of Gene-Editing Tools -- immunotherapy Applications of Gene-Editing Tools in Cancer Treatment Generation of Universal T Cells for Cancer Immunotherapy Enhancement of T Cells’ Functionalities in Cancer Immunotherapy Editing of Cancer Driver Genes in Cancer Therapy Applications of Gene-Editing Tools in Cancer Prevention Challenges: Technical issues Restricted genomic target sites by sgRNA Require improvement on sgRNA design to improve target efficiency Structural characteristic of sgR...

MCC เป็นค่าที่บ่งบอกถึง performance ของ machine learning เป็นค่าที่คิดโดยนักชีวเคมี ชื่อ Brain W. Matthews  ใช้สำหรับ categorical data CV -- normally not more than 10 MCC > 0.5 is good After we receive the model we determine MCC between Training vs testing Training vs CV If the difference is less than 0.2 is good Ref: https://en.wikipedia.org/wiki/Matthews_correlation_coefficient

Ethics related to traditional medicine. It is very important for grant proposals, scientific integrity and patients' safety. Link relates to this topic:  https://t-lerksuthirat.blogspot.com/2021/05/note-musc-research-forum-new-normal.html

Install anaconda https://www.youtube.com/watch?v=5mDYijMfSzs Dealing with virtual environment python https://www.youtube.com/watch?v=mIB7IZFCE_k https://www.youtube.com/watch?v=rFCBiP9Gkoo ttps://www.youtube.com/watch?v=Uz4dadzu5i0 https://www.youtube.com/watch?v=Ro9l0eapoJU Python packages list https://pypi.org/ Downloading the building tool C++ https://docs.microsoft.com/en-us/answers/questions/136595/error-microsoft-visual-c-140-or-greater-is-require.html Some packages were developed from particular version of python.

Note: The DNA damage response and cancer therapy_2012 Doi: 10.1038/nature10760 Future issues; Pharmacological targeting  Biochemical and genetic interactions between the various DNA repair pws -- not clearly understood Having small potent inhibitors which specifically inhibits particular pw facilitating the interplay between DNA repair pws. Cancer stem cells and tumor micro-environment Systemic knowledge in DNA damage and DDR in stem cells need to be explored Genomic scar Cancer being classified according to their underlying pattern of pathogenic mutations Sequence scare -- reflects bot mutagens which tumor has been exposed to and repair processes that have to operated to mitigate their impact Example; HRD Microsatellite instability Mismatch repair is defective Matching molecular signatures of DNA mutation and repair -- require functional biomarkers -- which identify DDR defect and facilitate in the selection of therapy Example -- RAD51 foci formation Requiring genotoxic stress fol...

Note: Mechanisms of DNA double-strand break repair and their potential to induce chromosomal aberrations_2000 Doi: 10.1093/mutage/15.4.289 Theory of cancer formation Breakage and reunion theory Exchange theory Molecular theory Initial lesion -- chemical and physical-DNA damaging agents Artificially induced DSB IR Endonuclease Cellular (spontaneous) sources of DSB Can occur in any stage of cell cycle Briefly summarize the main causes of spontaneous DSB Topoisomerases Topo-I -- generates SSB Topo-II -- generate DSB Replication Prevalent source of DSB -- DNA replication Cell estimates to suffer ~ 10 DSB/cell cycle (estimate from spontaneous sister chromatid exchange) Meiosis V(D)J recombination Other recombinant process Transposable elements Fragile sites Extended micro- and minisatellite sequences -- potential source of DSB in mammalian genome At this time of writing (2000) -- the instability of this fragile site is not well-understood DSB as a results of excision repair Considering on t...