| Cancer name | Colon Cancer |
| Cancer Type | COCA |
| Immunotherapy type | Immune Checkpoint Therapy |
| Treatment | SP142 |
| Drugstatus | NA |
| Drugbank ID | NA |
| Checkpoints | PD-L1 |
| Signature Type | Cell |
| Signature | CD8+ T cells |
| Official Symbol | NA |
| Mode of action | CE_D_UP |
| Description for ‘mode of action’：the ‘mode of action’ for signature is composed of three parts: A_B_C. A describes the level at which the corresponding signature changes, it may contain the following values: TRAN(translation), PROT(protein), CE(cell), METH(methylation), AC(acetylation), PHOS(phosphorylation), MU(mutation), SNP(single nucleotide polymorphism), GLYC(glycosylation) and PATH(pathway). B describes the corresponding signature in which cancer immunotherapy condition group has changed, it may contain the following values: R (immunotherapy response group), NR(immunotherapy non-response group), D (Immunotherapy group), ND (No immunotherapy group). C describes the change detail (specific direction) of the corresponding signature, it may contain the following values: UP (High gene/protein expression or increased cellular abundance or enhanced epigenetic modification), DN (Low gene/protein expression or reduced cellular abundance or attenuated epigenetic modifications), LOSS (deletion mutation), GAIN (gain mutation)，Other. For example, the search/browse detail result for CD274 was “PROT_R_UP”, it can be interpreted that the protein level of CD274 was upregulated in immunotherapy response individuals. | |
| Experimental | mouse model |
| Description | 1.These data indicate that the tumor inflammatory microenviron-mentinduced by RFA plays adirect rolein the upregulation of PD-L1 expression. 2. To test the hypothesis, CT26-bearingmice were treated with RFA plus an isotype control antibody, RFA plus anti–PD-1 monoclonal antibodies (mAbs; RFA?a-PD-1),anti–PD-1 mAbs alone (a-PD-1), or left without treatment. Because CD8+ TIL were significantly increased in tumors after RFA treatment, we also sought to determine whether CD8+ T cells mediate theeffect of RFAand PD-1blockade using CD8-depletingmAbs. No recurrence occurred in the ablation zone. RFA had amodest inhibitory effect on contralateral tumor progression.Anti–PD-1 itself also led to a modest inhibition of tumor growth,consistent with a previous observation. In contrast, we observed significant tumor regression, much longer duration ofinhibition of tumor growth and prolonged survival in the RFA/anti–PD-1–treated mice, as compared with mice in the no-treat-ment or single treatment groups. Depletion ofCD8+ T cells completely eliminated the inhibition of tumor growth of mice with the combined treatment (Fig. 5B and C).These data indicate that RFA and PD-1 blockade further enhanceCD8?T-cell–mediated antitumor immunity. |
| PMID | 26933175 |
| Title | PD-1 Blockade Boosts Radiofrequency Ablation-Elicited Adaptive Immune Responses against Tumor. |