Dataset: Gene Expression Profiles of human primary alveolar type II (ATII) cells and macrophages (AMs) after influenza virus infection
Abnormal function of genes is at the root of most cancers, but heritable cancer syndromes account for a very small minority of all tumors...
Abnormal function of genes is at the root of most cancers, but heritable cancer syndromes account for a very small minority of all tumors in humans and domestic animals. The majority of cancers are “sporadic,” that is, they are not heritable in the strictest sense. Instead, sporadic cancers occur due to interactions of unknown intrinsic (heritable) and environmental factors that lead to malignant transformation and uncontrolled growth. Identification of heritable risk factors in sporadic human cancers is difficult because individual genetic backgrounds are very heterogeneous. To this end, individual genetic backgrounds of purebred dogs are more homogeneous, and dog breeds show different predilection to develop specific cancers. Here, we used genomic screens based on gene expression profiling to identify sets of genes that may contribute to the development of canine hemangiosarcoma, a relatively common endothelial sarcoma. Specific genes in a single breed (Golden Retrievers) are modulated by (or with) heritable risk traits, showing functional features that appear to modulate tumor behavior. Our results suggest these methods are suitable to identify genes that will enhance our understanding of how these cancers happen, as well as possible treatment targets that will improve outcomes of both human and canine cancer patients. 24 samples were analysed. 12 samples with ATII cells with without influenza virus infection at 4h and 24h; 12 samples with AMs with without influenza virus infection at 4h and 24h primary cultured cells were infected with or without influenza virus PR/8 at moi of 0.5. At 4h and 24h, total RNA were isolated for microarray experiments
- Species:
- human
- Samples:
- 24
- Source:
- E-GEOD-30723
- Updated:
- Dec.12, 2014
- Registered:
- Sep.16, 2014
Sample | INDIVIDUAL | CELL TYPE | INFECTION | TIME |
---|---|---|---|---|
GSM762682 | donor 39 | primary alveolar epithelial cells | control | 24h |
GSM762683 | donor 39 | primary alveolar epithelial cells | control | 4h |
GSM762684 | donor 39 | primary alveolar epithelial cells | PR8 | 24h |
GSM762685 | donor 39 | primary alveolar epithelial cells | PR8 | 4h |
GSM762686 | donor 39 | primary alveolar macrophages | control | 24h |
GSM762687 | donor 39 | primary alveolar macrophages | control | 4h |
GSM762688 | donor 39 | primary alveolar macrophages | PR8 | 24h |
GSM762689 | donor 39 | primary alveolar macrophages | PR8 | 4h |
GSM762690 | donor 40 | primary alveolar epithelial cells | control | 24h |
GSM76269 | donor 40 | primary alveolar epithelial cells | control | 4h |
GSM762692 | donor 40 | primary alveolar epithelial cells | PR8 | 24h |
GSM762693 | donor 40 | primary alveolar epithelial cells | PR8 | 4h |
GSM762694 | donor 40 | primary alveolar macrophages | control | 24h |
GSM762695 | donor 40 | primary alveolar macrophages | control | 4h |
GSM762696 | donor 40 | primary alveolar macrophages | PR8 | 24h |
GSM762697 | donor 40 | primary alveolar macrophages | PR8 | 4h |
GSM762698 | donor 46 | primary alveolar epithelial cells | control | 24h |
GSM762699 | donor 46 | primary alveolar epithelial cells | control | 4h |
GSM762700 | donor 46 | primary alveolar epithelial cells | PR8 | 24h |
GSM76270 | donor 46 | primary alveolar epithelial cells | PR8 | 4h |
GSM762702 | donor 46 | primary alveolar macrophages | control | 24h |
GSM762703 | donor 46 | primary alveolar macrophages | control | 4h |
GSM762704 | donor 46 | primary alveolar macrophages | PR8 | 24h |
GSM762705 | donor 46 | primary alveolar macrophages | PR8 | 4h |