Ghost wanna share a good video illustrating how immunotherapy works. Immunoediting Battle between tumor and immune system is a equilibrium phrase that can last years. This dynamic process consists of immunosurveillance and tumor progression. During immunosurveillance, immune system recognizes tumor cells through neoantigens presented by MHC (HLA) on the surface of the cell. Those neoantigens include tumor associated antigen: Proteins expressed in some normal tissues at low le

First, a figure shows why targeted therapy is, in certain circumstance, slightly better than chemo. Of course still less competitive than immunotherapy which will be discussed in the another topic. In terms of toxicity: Chemo targets all the fast growing cells and therefore bring non-minor damages to normal cells. Some of the side effects are: Immunosuppression and myelosuppression: paralyzing the bone marrow and leading to a decrease of white blood cells, red blood cells, a

Figure below summarizes sources of some duplicate types: Here Ghost gonna focus on the most common type: PCR duplicates and talk about how to treat them in several sequencing type data. Where PCR duplicates come from and why do we care? They are introduced when the multiple PCR amplified reads of same origin lay to the different spot on the flowcell. The reason we care about them is because that they mess up the allele frequency of variant and make our variant calling biased

Roughly, RNA-Seq may have the following bias sources: Random priming PolyA selection (3’ bias) and ribosomal depletion PCR duplicates Normal cell contamination (when evaluating tumor) Tumor purity Batch effect Random priming Appears at first 12 base of per base sequence content. It is caused by primer preference during PCR amplification. Although it is normal, be cautious for adapter contamination if it is too much. This bias will not cause variant detection bias since the al