Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR33186508_1.fastq.gz | Fastqsanger.gz | |||
| SRR33186509_1.fastq.gz | Fastqsanger.gz | |||
| SRR33529054_1.fastq.gz | Fastqsanger.gz | |||
| SRR33529054_2.fastq.gz | Fastqsanger.gz |
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Project description:Resistance and virulence analysis of hv-CRKP
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Project description:The identification of changes in transcriptional regulation during priming and differentiation of embryonic stem (ES) cells towards the endoderm lineage. Specific populations of ES cells, either primed or committed to endoderm, were isolated and subjected to global nuclear run on sequencing (GRO-Seq). The hHex-Venus (HV) reporter ES cell line, HVJu5.1 (Canham et al., 2010) was used to isolate HV- and HV+ ES cells. Primed ES cells were identified based on the expression of the HV marker in addition to the cell surface marker of undifferentiated ES cells, SSEA-1, (the lower and upper 25% of SSEA-1+, HV expressing cells). When challenged to differentiate, HV- ES cells are primed towards an epiblast fate, while HV+ ES cells are primed towards primitive endoderm. However, these populations are considered primed, rather than committed, as they will readily interconvert when re-introduced into standard ES cell culture conditions. ES cells were grown in self-renewing conditions (GMEM, LIF, 10% FCS, plated on gelatin coated dishes). Endoderm was obtained by differentiating ES cells in medium without the cytokine LIF for 5 days. The HV+, SSEA-1- differentiated fraction was then sorted and represents an early stage in endoderm differentiation.
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Project description:Since the first reports of hepatitis of unknown aetiology occurring in UK children, over 1000 cases have been reported worldwide, including 268 cases in the UK, with the majority younger than 6 years old. Using genomic, proteomic and immunohistochemical methods, we undertook extensive investigation of 28 cases and 136 control subjects. In five cases who underwent liver transplantation, we detected high levels of adeno-associated virus 2 (AAV2) in the explanted livers. AAV2 was also detected at high levels in blood from 10/11 non-transplanted cases. Low levels of Adenovirus (HAdV) and Human Herpesvirus 6B (HHV-6B), both of which enable AAV2 lytic replication, were also found in the five explanted livers and blood from 15/17 and 6/9 respectively, of the 23 non-transplant cases tested. In contrast, AAV2 was detected at low titre in 6/100 whole bloods from child controls from cohorts with presence or absence of hepatitis and/or adenovirus infection. Our data show an association of AAV2 at high titre in blood or liver tissue, with unexplained hepatitis in children infected in the recent HAdV-F41 outbreak. We were unable to find evidence by electron microscopy, immunohistochemistry or proteomics of HAdV or AAV2 viral particles or proteins in explanted livers, suggesting that hepatic pathology is not due to direct lytic infection by either virus. The potential that AAV2, although not previously associated with disease, may, together with HAdV-F41 and/or HHV-6, be causally implicated in the outbreak of unexplained hepatitis, requires further investigation.
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Project description:Histologic variant (HV) subtypes of bladder cancer are clinically aggressive tumors that are more resistant to standard therapy compared to conventional urothelial carcinoma (UC). Little is known about the transcriptional programs that account for the morphological and biological differences in HV tumors. To investigate the tumor biology of HV bladder cancers, we generated a single cell RNA sequencing (scRNA-seq) atlas of nine HV tumors and three UC tumors. Our analyses revealed a tumor cell state specific to HVs that is characterized by expression of MUC16 (CA125), KRT24, and WISP2. This CA125+ cell state bears transcriptional hallmarks of epithelial-mesenchymal transition, is enriched in metastases, is predicted to be highly chemotherapy resistant, and is linked with poor survival, suggesting that this cell state plays an important role in the aggressive biology of HV tumors. Our analyses also provide evidence of transcriptional “mimicry” between HVs and histologically similar non-urothelial cell types. Lastly, we identified higher expression of TM4SF1, a cell surface protein associated with cancer metastasis, in HV tumor cells compared to UC tumor cells. Chimeric antigen receptor (CAR) T cells engineered against TM4SF1 protein demonstrated in vitro and in vivo activity against bladder cancer cell lines in a TM4SF1 expression-dependent manner, highlighting its potential as a therapeutic target in bladder cancer.
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