Citations 2
Sel1-like proteins and peptides are the major Oxalobacter formigenes-derived factors stimulating oxalate transport by human intestinal epithelial cells
Arvans, Donna L., Alshaikh, Altayeb, Tesar, C., Wolfgeher, Don, Antonopoulos, Dionysios A. , Bashir, Mohamed Elfatih H. , Cham, Candace M. , Musch, M., Chang, Eugene B. , Hassan, Hatim , Hassan, Hatim , Chang, Changsoo , Babnigg, G. , Kron, Stephen J. , Joachimiak, A.
American Journal of Physiology-Cell Physiology | May 1, 2023 | Volume: 325 | Issue: 1 | Pages: C344-C361
We previously identified Oxalobacter formigenes-derived secreted factors stimulating oxalate transport by human intestinal epithelial cells in vitro and reducing urinary oxalate excretion in hyperoxaluric mice by enhancing colonic oxalate secretion. We now identified Sel1-like proteins and small peptides as the major secreted factors and they have significant therapeutic potential for hyperoxalemia and hyperoxaluria, impacting the outcomes of patients suffering from kidney stones, primary and secondary hyperoxaluria, chronic kidney disease, kidney failure, and renal transplant recipients.
Therapy-Induced Senescence: Opportunities to Improve Anticancer Therapy
Prasanna, Pataje G.S. , Citrin, Deborah E. , Hildesheim, Jeffrey, Ahmed, Mansoor M. , Venkatachalam, Sundar, Riscuta, Gabriela , Xi, Dan , Zheng, Guangrong , Deursen, Jan van, Goronzy, Jörg J. , Kron, Stephen J. , Campisi, Judith , Brown, Stephen L. , Niedernhofer, Laura J. , Gius, David , Schmitt, Clemens A. , Abazeed, Mohamed E. , Kirkland, James L. , Lowe, Scott W. , Mendonca, Marc S. , Burma, Sandeep , Zhou, Daohong , Coleman, C. Norman , Prasanna, Pataje G , Goronzy, Jorg , Sharpless, Norman E , Campisi, Judith , Georgakilas, Alexandros G , Paris, Francois , Gewirtz, David A , Schmitt, Clemens A , Abazeed, Mohamed E , Kirkland, James L , Richmond, Ann , Romesser, Paul B , Gil, Jesus , Mendonca, Marc S , Niedernhofer, Laura J , Anscher, Mitchell S. , O’Loghlen, Ana , Georgakilas, Alexandros G. , Romesser, Paul B.
JNCI: Journal of the National Cancer Institute | March 31, 2021 | Volume: 113 | Issue: 10 | Pages: 1285-1298
Abstract Cellular senescence is an essential tumor suppressive mechanism that prevents the propagation of oncogenically activated, genetically unstable, and/or damaged cells. Induction of tumor cell senescence is also one of the underlying mechanisms by which cancer therapies exert antitumor activity. However, an increasing body of evidence from preclinical studies demonstrates that radiation and chemotherapy cause accumulation of senescent cells (SnCs) both in tumor and normal tissue. SnCs in tumors can, paradoxically, promote tumor relapse, metastasis, and resistance to therapy, in part, through expression of the senescence-associated secretory phenotype. In addition, SnCs in normal tissue can contribute to certain radiation- and chemotherapy-induced side effects. Because of its multiple roles, cellular senescence could serve as an important target in the fight against cancer. This commentary provides a summary of the discussion at the National Cancer Institute Workshop on Radiation, Senescence, and Cancer (August 10-11, 2020, National Cancer Institute, Bethesda, MD) regarding the current status of senescence research, heterogeneity of therapy-induced senescence, current status of senotherapeutics and molecular biomarkers, a concept of “one-two punch” cancer therapy (consisting of therapeutics to induce tumor cell senescence followed by selective clearance of SnCs), and its integration with personalized adaptive tumor therapy. It also identifies key knowledge gaps and outlines future directions in this emerging field to improve treatment outcomes for cancer patients.