Growth of V79 Cells as Xenograft Tumors Promotes Multicellular Resistance but does not Increase Spontaneous or Radiation-Induced Mutant Frequency

2005 ◽  
Vol 164 (6) ◽  
pp. 733-744 ◽  
Author(s):  
J. P. Banáth ◽  
L. Sinnott ◽  
B. Larrivée ◽  
S. H. MacPhail ◽  
P. L. Olive
1990 ◽  
Vol 122 (3) ◽  
pp. 316 ◽  
Author(s):  
Helen H. Evans ◽  
Mark Nielsen ◽  
Jaroslav Mencl ◽  
Min-Fen Horng ◽  
Marlene Ricanati

2006 ◽  
Vol 113 (1) ◽  
pp. 343-359 ◽  
Author(s):  
Arthur W. Jones ◽  
J. A. Dvorak ◽  
M. M. Hossain ◽  
J. L. Huffman ◽  
C. P. Hutchins ◽  
...  

1997 ◽  
Vol 148 (3) ◽  
pp. 203 ◽  
Author(s):  
Silvia Ogheri ◽  
Valeria Bruna ◽  
Franco Cera ◽  
Silvia Favaretto ◽  
Roberto Cherubini ◽  
...  

Author(s):  
Guogang Xu ◽  
Gabriel W. Intano ◽  
John R. McCarrey ◽  
Ronald B. Walter ◽  
C. Alex McMahan ◽  
...  

1998 ◽  
Vol 41 (3) ◽  
pp. 286-292
Author(s):  
Huaixing Li ◽  
Hua Yang ◽  
Jianxiu Li ◽  
Yiping Hu ◽  
Xiaopeng Wang ◽  
...  

2021 ◽  
Vol 118 (37) ◽  
pp. e2016963118
Author(s):  
Julia M. Lewis ◽  
Patrick F. Monico ◽  
Fatima N. Mirza ◽  
Suzanne Xu ◽  
Sara Yumeen ◽  
...  

Chronic ultraviolet (UV) radiation exposure is the greatest risk factor for cutaneous squamous cell carcinoma (cSCC) development, and compromised immunity accelerates this risk. Having previously identified that epidermal Langerhans cells (LC) facilitate the expansion of UV-induced mutant keratinocytes (KC), we sought to more fully elucidate the immune pathways critical to cutaneous carcinogenesis and to identify potential targets of intervention. Herein, we reveal that chronic UV induces and LC enhance a local immune shift toward RORγt+ interleukin (IL)-22/IL-17A–producing cells that occurs in the presence or absence of T cells while identifying a distinct RORγt+ Sca-1+ CD103+ ICOS+ CD2+/− CCR6+ intracellular CD3+ cutaneous innate lymphoid cell type-3 (ILC3) population (uvILC3) that is associated with UV-induced mutant KC growth. We further show that mutant KC clone size is markedly reduced in the absence of RORγt+ lymphocytes or IL-22, both observed in association with expanding KC clones, and find that topical application of a RORγ/γt inhibitor during chronic UV exposure reduces local expression of IL-22 and IL-17A while markedly limiting mutant p53 KC clonal expansion. We implicate upstream Toll-like receptor signaling in driving this immune response to chronic UV exposure, as MyD88/Trif double-deficient mice also show substantially reduced p53 island number and size. These data elucidate key immune components of chronic UV–induced cutaneous carcinogenesis that might represent targets for skin cancer prevention.


1973 ◽  
Vol 42 (5-6) ◽  
pp. 491-501 ◽  
Author(s):  
T.D. Allen ◽  
M.V. Haigh ◽  
A. Howard

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