Dr. Serkan Kır received his PhD degree from the University of Texas Southwestern Medical Center at Dallas in 2011. After his postdoctoral fellowship at Dana-Farber Cancer Institute/Harvard Medical School, he joined Koç University in 2017 as an Assistant Professor in the Department of Molecular Biology and Genetics. Dr. Kir’s research interests include adverse effects of tumours on host metabolism. His ongoing studies address tumour-driven hypermetabolism and the loss of adipose and skeletal muscle tissues. Dr. Kir identified PTHrP, a tumour-derived hormonal factor, as an inducer of energy wasting and adipose tissue atrophy. His recent work demonstrated that the EDA2R/NIK signalling drives muscle atrophy in response to tumors. Kir laboratory continues to investigate molecular mechanisms underlying cancer-associated wasting. For more information please visit his laboratory website (https://sklab.ku.edu.tr/).

Selected Publications

EDA2R-NIK signalling promotes muscle atrophy linked to cancer cachexia. Bilgic SN, Domaniku A, Toledo B, Agca S, Weber BZC, Arabaci DH, Ozornek Z, Lause P, Thissen JP, Loumaye A, Kir S. Nature (2023) 617: 827-834.

Inhibition of epidermal growth factor receptor suppresses parathyroid hormone-related protein expression in tumours and ameliorates cancer-associated cachexia. Weber BZC, Agca S, Domaniku A, Bilgic SN, Arabaci DH, Kir S. J Cachexia Sarcopenia Muscle (2022) 13(3):1582-1594.

PTH/PTHrP receptor mediates cachexia in models of kidney failure and cancer. Kir S, Komaba H, Garcia AP, Konstantinos E, Suh H, Lanske B, Hodin RA, Spiegelman BM. Cell Metab (2016) 23: 315-323.

Tumour-derived PTH-related protein triggers adipose tissue browning and cancer cachexia. Kir S, White JP, Kleiner S, Kazak L, Cohen P, Baracos VE, Spiegelman BM. Nature (2014) 513: 100-104.

FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis. Kir S, Beddow SA, Samuel VT, Miller P, Previs SF, Suino-Powell K, Xu HE, Shulman GI, Kliewer SA, Mangelsdorf DJ. Science (2011) 331: 1621-24.