Project description:SCLC transformation is one of the mechanisms of TKI resistance in lung cancer. To clarify its epigenetic changes, we used Chip-seq to detect the changes of H3K9me2 in pre-LUAD and post-SCLC transformation cells.
Project description:SCLC transformation is one of the mechanisms of TKI resistance in lung cancer. To clarify its epigenetic changes, we used RNA-seq to detect the changes of genes in pre-LUAD and post-SCLC transformation cells.
Project description:The histological transformation of lung adenocarcinoma (LUAD) to an aggressive neuroendocrine (NE) derivative resembling SCLC is a signature example of lineage plasticity in cancer.But the changes of gene expression need to be studied. We used microarrays to detail the global programme of gene expression under transformation and reversed transformation cells and identified distinct classes of up-regulated genes during this process.
Project description:We hypothesized that functional polymorphisms in NEUROD1 target genes may also affect the clinical outcomes of patients with SCLC, as NEUROD1 plays a crucial role in SCLC carcinogenesis. To test this hypothesis, we performed ChIP-seq of NeuroD1 and H3K4me3 in SCLC cells. Then we evaluated the association between putative functional polymorphisms in NEUROD1 target genes and the chemotherapy response and survival outcomes of patients with SCLC.
Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.
