Fig. 7: Associations of human CD8+ T cell clusters and gene signatures with clinical response to tiragolumab plus atezolizumab. | Nature Cancer

Fig. 7: Associations of human CD8+ T cell clusters and gene signatures with clinical response to tiragolumab plus atezolizumab.

From: TIGIT and PD-L1 co-blockade promotes clonal expansion of multipotent, non-exhausted antitumor T cells by facilitating co-stimulation

Fig. 7

a, Human gene signature scores in baseline tumor bulk RNA-seq samples from the phase 2 CITYSCAPE NSCLC trial. Patients, irrespective of treatment arm, were separated on the basis of clinical response (CR/PR, n = 37 patients; SD/PD, n = 67 patients). Boxplots are centered at the median, with the box boundaries set at the 25th and 75th percentiles; whiskers extend 1.5 × the interquartile range. P values are indicated for statistically significant differences by two-tailed t-test without correction for multiple comparisons. b, Individual human gene expression in baseline tumor bulk RNA-seq samples from CITYSCAPE patients who were treated with T + A or P + A separated on the basis of clinical response as described in a. Statistics were performed as described in a. c, Forest plot comparing high or low expression of indicated gene associated with OS HR in T + A (n = 53 patients) or P + A (n = 51 patients) treatment groups. Mean HR with 95% CIs, determined using a univariate Cox model and P values from a two-sided Wald test, are shown. d, KM curves showing the probability of OS in P + A or T + A treatment groups dichotomized on the basis of high or low expression of indicated gene. Number of patients in each subgroup were as follows: CD8A: P + A high, n = 26; P + A low, n = 25; T + A high, n = 26; T + A low, n = 27; CXCR6: P + A high, n = 27; P + A low, n = 24; T + A high, n = 25; T + A low, n = 28; CXCR3: P + A high, n = 29; P + A low, n = 22; T + A high, n = 23; T + A low, n = 30; CCL5: P + A high, n = 29; P + A low, n = 22; T + A high, n = 23; T + A low, n = 30. For KM plots, the P value is from a log-rank test with a null hypothesis that there is no difference between the groups. e, Gene score calculated using the average expression of the CD8 gene panel consisting of CXCR3, CXCR6 and CCL5 in tumor bulk RNA-seq samples from patients treated with T + A separated on the basis of clinical response. f, Forest plot comparing high or low expression of composite gene score associated with OS HR in T + A (n = 53 patients) or P + A (n = 51 patients) treatment groups. Mean HR with 95% CIs, determined using a univariate Cox model and P values from a two-sided Wald test, are shown. g, KM curves showing the probability of OS in P + A or T + A treatment groups dichotomized on the basis of high or low composite gene score. Number of patients in each subgroup were as follows: P + A high, n = 26; P + A low, n = 25; T + A high, n = 26; T + A low, n = 27. For KM plots, the P value is from a log-rank test with a null hypothesis that there is no difference between the groups.

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