Obesity reviews : an official journal of the International Association for the Study of Obesity
Authors: Lee CM, Woodward M, Batty GD, Beiser AS, Bell S, Berr C, Bjertness E, Chalmers J, Clarke R, Dartigues JF, Davis-Plourde K, Debette S, Di Angelantonio E, Feart C, Frikke-Schmidt R, Gregson J, Haan MN, Hassing LB, Hayden KM, Hoevenaar-Blom MP, Kaprio J, Kivimaki M, Lappas G, Larson EB, LeBlanc ES, Lee A, Lui LY, Moll van Charante EP, Ninomiya T, Nordestgaard LT, Ohara T, Ohkuma T, Palviainen T, Peres K, Peters R, Qizilbash N, Richard E, Rosengren A, Seshadri S, Shipley M, Singh-Manoux A, Strand BH, van Gool WA, Vuoksimaa E, Yaffe K, Huxley RR
Pacing and clinical electrophysiology : PACE
Authors: Hammami Bomholtz S, Refaat M, Buur Steffensen A, David JP, Espinosa K, Nussbaum R, Wojciak J, Hjorth Bentzen B, Scheinman M, Schmitt N
Journal of general internal medicine
Authors: Mehta S, Mehta N, Tang WH, Young J
Volume 130 of Issue 1 | The Journal of clinical investigation
Authors: Mahiddine K, Blaisdell A, Ma S, Créquer-Grandhomme A, Lowell CA, Erlebacher A
Polymorphonuclear neutrophils (PMNs) are increasingly recognized to influence solid tumor development, but why their effects are so context dependent and even frequently divergent remains poorly understood. Using an autochthonous mouse model of uterine cancer and the administration of respiratory hyperoxia as a means to improve tumor oxygenation, we provide in vivo evidence that hypoxia is a potent determinant of tumor-associated PMN phenotypes and direct PMN-tumor cell interactions. Upon relief of tumor hypoxia, PMNs were recruited less intensely to the tumor-bearing uterus, but the recruited cells much more effectively killed tumor cells, an activity our data moreover suggested was mediated via their production of NADPH oxidase-derived reactive oxygen species and MMP-9. Simultaneously, their ability to promote tumor cell proliferation, which appeared to be mediated via their production of neutrophil elastase, was rendered less effective. Relieving tumor hypoxia thus greatly improved net PMN-dependent tumor control, leading to a massive reduction in tumor burden. Remarkably, this outcome was T cell independent. Together, these findings identify key hypoxia-regulated molecular mechanisms through which PMNs directly induce tumor cell death and proliferation in vivo and suggest that the contrasting properties of PMNs in different tumor settings may in part reflect the effects of hypoxia on direct PMN-tumor cell interactions.
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Authors: Moslehi J, Rathmell WK
Clinical colorectal cancer
Authors: Snyder RA, Fournier K, Royal R, Venook AP, Chang GJ
JCI insight
Authors: Zhang WZ, Rice MC, Hoffman KL, Oromendia C, Barjaktarevic I, Wells JM, Hastie AT, Labaki WW, Cooper CB, Comellas AP, Criner GJ, Krishnan JA, Paine Iii R, Hansel NN, Bowler RP, Barr RG, Peters SP, Woodruff PG, Curtis JL, Han MK, Ballman KV, Martinez FJ, Choi AM, Nakahira K, Cloonan SM, Choi ME
Journal of general internal medicine
Authors: Glod SA, Alexandraki I, Jasti H, Lai CJ, Ratcliffe TA, Walsh K, Kisielewski M, LaRochelle J
Journal of palliative medicine
Authors: Nolley E, Fleck J, Kavalieratos D, Dew MA, Dilling D, Colman R, Crespo MM, Goldberg H, Hays S, Hachem R, Lease E, Lee J, Reynolds J, Morrell M, Schenker Y
Health services research
Authors: Bindman AB, Romano PS
