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. Author manuscript; available in PMC: 2017 Feb 16.
Published in final edited form as: Immunity. 2016 Feb 9;44(2):343–354. doi: 10.1016/j.immuni.2015.11.024

Figure 1. Kras-Trp53-mutated lung adenocarcinomas are inadequately infiltrated by T cells and resist current treatment options.

Figure 1

A) Immunohistochemistry of CD3+ cells in KP lung tumor tissue on day 66 after tumor initiation. (B) Survival of KP mice treated or not with anti-PD-1 (αPD-1) mAbs (n=5-6 mice per group). Tumors were induced on day 0 by intratracheal intubation and inhalation (i.t.) of an adenovirus expressing Cre recombinase (AdCre). Mice were treated every third or fourth day with anti-PD-1 Abs intraperitoneally (i.p.) starting from day 60 to 86. (C) Lung weight as proxy for tumor burden (Cortez-Retamozo et al., 2012) measured on day 44 in mice bearing orthotopic KP1.9 tumors and treated or not with anti-PD-1 mAbs every third or forth day from day 25 to 42 after tumor cell injection (n=9-12 mice per group). (D) Micro-computed tomography of KP-OVA mice both pre- (day 122) and post-treatment (day 146) with no antibody (ø) or with anti-PD-1 and anti-CTLA-4 (αPD-1 + αCTLA-4) mAbs. Tumors were induced with a lentiviral vector containing OVA peptide sequences (LucOS) i.t. and mAb treatment was performed every second or third day from day 133 to 145. (E) Lung weight (n=4-5 mice per group) and (F) survival (n=11 mice per group) of KP mice treated or not with paclitaxel and carboplatin (Ptax-Carbo). Mice were treated once a week for three weeks starting on day 63 post i.t. tumor initiation and lungs analyzed three days after the last drug injection. For survival studies, Ptax-Carbo was injected i.p. once a week. ns, not significant. See also Figure S1.