Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325647 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36
| PRJNA325477 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36 (I)
| PRJNA296106 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36 (II)
| PRJNA296105 | ENA
Project description:Targeting metastasis stem cells through the fatty acid receptor CD36
| PRJNA295964 | ENA
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE72938 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behavior. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE72935 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE83346 | GEO
Project description:Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behaviour. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours.
2016-12-16 | GSE83276 | GEO
Project description:Mesenchymal stem cells (MSCs) are present in the circulation of cancer patients, and are recruited to the stroma of both the primary tumor and metastasis. Recent preclinical research has shown that in response to platinum-based chemotherapy, MSCs secrete two specific platinum-induced fatty acids (PIFAs) which induce resistance to a broad spectrum of chemotherapies. The secreted PIFAs are the fatty acid oxo-heptadecatetraenoic acid (KHT) and the omega-3 fatty acid hexadecatetraenoic acid (16:4). These PIFAs are produced via the COX-1 pathway. COX inhibitors, including indomethacin. This phase 1 study explores the safety of combining indomethacin with platinum containing chemotherapy.
| 2134582 | ecrin-mdr-crc
Project description:Tyrosine kinase inhibitors (TKIs) are highly effective for treatment of chronic myeloid leukemia (CML), but very few patients are cured. Major drawbacks with TKIs are their low efficacy in eradicating the leukemic stem cells responsible for disease maintenance and relapse upon TKI cessation. Here, we performed RNA-sequencing of flow-sorted primitive (CD34+CD38low) and progenitor (CD34+CD38+) chronic phase CML cells and identified transcriptional upregulation of 32 cell surface molecules relative to corresponding normal bone marrow cells. Focusing on novel markers with increased expression on primitive CML cells, we confirmed upregulation of the scavenger receptor CD36 and the leptin receptor (LEPR) by flow cytometry. We also delineate a subpopulation of primitive CML cells expressing CD36 that is less sensitive to imatinib treatment. Using CD36 targeting antibodies, we show that the CD36 positive cells can be targeted and killed by antibody dependent cellular cytotoxicity (ADCC). In summary, CD36 defines a subpopulation of primitive CML cells with decreased imatinib sensitivity that can be effectively targeted by ADCC using an anti-CD36 antibody.
| EGAS00001002421 | EGA