Search

Your search keyword '"Demircioglu, Fevzi"' showing total 10 results
Start Over Author "Demircioglu, Fevzi"
10 results on '"Demircioglu, Fevzi"'

1. Author Correction: Pericyte FAK negatively regulates Gas6/Axl signalling to suppress tumour angiogenesis and tumour growth

Author

Lechertier, Tanguy, Reynolds, Louise E., Kim, Hyojin, Pedrosa, Ana Rita, Gómez-Escudero, Jesús, Muñoz-Félix, José M., Batista, Silvia, Dukinfield, Matthew, Demircioglu, Fevzi, Wong, Ping Pui, Matchett, Kylie P., Henderson, Neil C., D’Amico, Gabriela, Parsons, Maddy, Harwood, Catherine, Meier, Pascal, and Hodivala-Dilke, Kairbaan M.

Published
2023
Full Text
View/download PDF

3. Cancer associated fibroblast FAK regulates malignant cell metabolism

Author

Demircioglu, Fevzi, Wang, Jun, Candido, Juliana, Costa, Ana S. H., Casado, Pedro, de Luxan Delgado, Beatriz, Reynolds, Louise E., Gomez-Escudero, Jesus, Newport, Emma, Rajeeve, Vinothini, Baker, Ann-Marie, Roy-Luzarraga, Marina, Graham, Trevor A., Foster, Julie, Wang, Yu, Campbell, James J., Singh, Rajinder, Zhang, Penglie, Schall, Thomas J., Balkwill, Frances R., Sosabowski, Jane, Cutillas, Pedro R., Frezza, Christian, Sancho, Patricia, and Hodivala-Dilke, Kairbaan

Published
2020
Full Text
View/download PDF

5. Endothelial-cell FAK targeting sensitizes tumours to DNA-damaging therapy

Author

Tavora, Bernardo, Reynolds, Louise E., Batista, Silvia, Demircioglu, Fevzi, Fernandez, Isabelle, Lechertier, Tanguy, Lees, Delphine M., Wong, Ping-Pui, Alexopoulou, Annika, Elia, George, Clear, Andrew, Ledoux, Adeline, Hunter, Jill, Perkins, Neil, Gribben, John G., and Hodivala-Dilke, Kairbaan M.

Subjects
Tyrosine -- Health aspects, Oncology, Experimental, Genetic research, Drug resistance -- Genetic aspects, Phosphotransferases -- Health aspects, Cancer -- Care and treatment -- Research, DNA damage -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Chemoresistance is a serious limitation of cancer treatment (1). Until recently, almost all the work done to study this limitation has been restricted to tumour cells (2). Here we identify a novel molecular mechanism by which endothelial cells regulate chemosensitivity. We establish that specific targeting of focal adhesion kinase (FAK; also known as PTK2) in endothelial cells is sufficient to induce tumour-cell sensitization to DNA-damaging therapies and thus inhibit tumour growth in mice. The clinical relevance of this work is supported by our observations that low blood vessel FAK expression is associated with complete remission in human lymphoma. Our study shows that deletion of FAK in endothelial cells has no apparent effect on blood vessel function perse, but induces increased apoptosis and decreased proliferation within perivascular tumour-cell compartments of doxorubicin- and radiotherapy-treated mice. Mechanistically, we demonstrate that endothelial-cell FAK is required for DNA-damage-induced NF-κB activation in vivo and in vitro, and the production of cytokines from endothelial cells. Moreover, loss of endothelial-cell FAK reduces DNA-damage-induced cytokine production, thus enhancing chemosensitization of tumour cells to DNA-damaging therapies in vitro and in vivo. Overall, our data identify endothelial-cell FAK as a regulator of tumour chemosensitivity. Furthermore, we anticipate that this proof-of-principle data will be a starting point for the development of new possible strategies to regulate chemosensitization by targeting endothelial-cell FAK specifically., Despite encouraging initial responses to DNA-damaging chemotherapies and radiotherapy, many tumours become resistant to treatment (1). Previous work has concentrated on understanding resistance by focusing on mechanisms within tumour cells [...]

Published
2014

7. Dual-Action Combination Therapy Enhances Angiogenesis while Reducing Tumor Growth and Spread

Author

Wong, Ping-Pui, primary, Demircioglu, Fevzi, additional, Ghazaly, Essam, additional, Alrawashdeh, Wasfi, additional, Stratford, Michael R.L., additional, Scudamore, Cheryl L., additional, Cereser, Biancastella, additional, Crnogorac-Jurcevic, Tatjana, additional, McDonald, Stuart, additional, Elia, George, additional, Hagemann, Thorsten, additional, Kocher, Hemant M., additional, and Hodivala-Dilke, Kairbaan M., additional

Published
2015
Full Text
View/download PDF

8. Cancer associated fibroblast FAK regulates malignant cell metabolism

Author

Demircioglu, Fevzi, Wang, Jun, Candido, Juliana, Costa, Ana S. H., Casado, Pedro, De Luxan Delgado, Beatriz, Reynolds, Louise E., Gomez-Escudero, Jesus, Newport, Emma, Rajeeve, Vinothini, Baker, Ann-Marie, Roy-Luzarraga, Marina, Graham, Trevor A., Foster, Julie, Wang, Yu, Campbell, James J., Singh, Rajinder, Zhang, Penglie, Schall, Thomas J., Balkwill, Frances R., Sosabowski, Jane, Cutillas, Pedro R., Frezza, Christian, Sancho, Patricia, and Hodivala-Dilke, Kairbaan

Subjects
13/31, 59/78, 59/57, article, 631/67/2327, 631/67/2328, 82/51, 59, 3. Good health, 631/67/327
Abstract

Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined. Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FAK. In breast and pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment, predicts reduced overall survival. In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant cell glycolysis and tumour growth. Proteomic and phosphoproteomic analysis in our mouse model identifies metabolic alterations which are reflected at the transcriptomic level in patients with low stromal FAK. Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2 on cancer cells, activate protein kinase A, leading to enhanced malignant cell glycolysis. Our data uncover mechanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in cancer cells.

9. Cancer associated fibroblast FAK regulates malignant cell metabolism

Author

Demircioglu, Fevzi, Wang, Jun, Candido, Juliana, Costa, Ana S H, Casado, Pedro, De Luxan Delgado, Beatriz, Reynolds, Louise E, Gomez-Escudero, Jesus, Newport, Emma, Rajeeve, Vinothini, Baker, Ann-Marie, Roy-Luzarraga, Marina, Graham, Trevor A, Foster, Julie, Wang, Yu, Campbell, James J, Singh, Rajinder, Zhang, Penglie, Schall, Thomas J, Balkwill, Frances R, Sosabowski, Jane, Cutillas, Pedro R, Frezza, Christian, Sancho, Patricia, and Hodivala-Dilke, Kairbaan

Subjects
3. Good health
Abstract

Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined. Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FAK. In breast and pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment, predicts reduced overall survival. In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant cell glycolysis and tumour growth. Proteomic and phosphoproteomic analysis in our mouse model identifies metabolic alterations which are reflected at the transcriptomic level in patients with low stromal FAK. Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2 on cancer cells, activate protein kinase A, leading to enhanced malignant cell glycolysis. Our data uncover mechanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in cancer cells.

10. Cancer associated fibroblast FAK regulates malignant cell metabolism

Author

Demircioglu, Fevzi, Wang, Jun, Candido, Juliana, Costa, Ana SH, Casado, Pedro, De Luxan Delgado, Beatriz, Reynolds, Louise E, Gomez-Escudero, Jesus, Newport, Emma, Rajeeve, Vinothini, Baker, Ann-Marie, Roy-Luzarraga, Marina, Graham, Trevor A, Foster, Julie, Wang, Yu, Campbell, James J, Singh, Rajinder, Zhang, Penglie, Schall, Thomas J, Balkwill, Frances R, Sosabowski, Jane, Cutillas, Pedro R, Frezza, Christian, Sancho, Patricia, and Hodivala-Dilke, Kairbaan

Subjects
Male, Breast Neoplasms, Phosphoproteins, Survival Analysis, Xenograft Model Antitumor Assays, 3. Good health, Mice, Inbred C57BL, Pancreatic Neoplasms, Cancer-Associated Fibroblasts, Cell Line, Tumor, Focal Adhesion Protein-Tyrosine Kinases, Neoplasms, Animals, Humans, Female, Chemokines, Stromal Cells, Glycolysis, Metabolic Networks and Pathways, Cell Proliferation
Abstract

Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined. Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FAK. In breast and pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment, predicts reduced overall survival. In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant cell glycolysis and tumour growth. Proteomic and phosphoproteomic analysis in our mouse model identifies metabolic alterations which are reflected at the transcriptomic level in patients with low stromal FAK. Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2 on cancer cells, activate protein kinase A, leading to enhanced malignant cell glycolysis. Our data uncover mechanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in cancer cells.

Catalog

Books, media, physical & digital resources
See catalog results