IL2-L

P1/2, N=12, Not yet recruiting, Twinpig Biolab, Inc.

Furthermore, IL2 expression was positively correlated with PD-1, PD-L1, and CTLA-4 expression. Our results indicate that down-regulation of IL2 predicts poor prognosis and is associated with immune escape in LUAD, and IL2 could serve as a potential novel prognostic biomarker of LUAD.

Taken together, GT201 demonstrated enhanced persistence and anti-tumor efficacy with low IL-2 dependency in vitro and in vivo. Currently, manufacturing process of GT201 TIL product has been successfully developed (StaViral®), and clinical assessment of GT201 as a next-generation TIL therapy is ongoing in an investigator-initiated trial in China.

Taken together, our data show that ascites fluids most favorable to the M2 phenotype were associated with high LIF, VEGF, IL6, CCL2, and CCL18 levels, and with elevated Kyn to Trp ratios - Kyn levels being strongly higher than in healthy plasmas. Our results thus highlight a peculiar altered environment of OC ascites where a mixture of suppressive cells and signaling factors mediate extracellular cues leading to immune cell activity dysfunction. Altogether, these translational findings highlight OC ascites as a valuable tool to understand the mechanisms of suppression and develop predictive profiles, and to provide new insights for the identification of new targets and development of targeted-therapies.

Mutation status was associated with improvements in PFS in FL pts with mutant BCL2 or mutant EZH2 treated with C+R. iNHL pts with low plasma levels of IL2 levels treated with C+R showed a significant improvement in OS.

Zolbetuximab mediates proficient ADCC in patients with pretreated advanced G/GEJ cancers. Co-treatment with ZA + IL-2 did not further improve this effect.

Conclusions CGC-601 with a unique βγ-only binding property, promotes moderate CD8 T and NK expansion and diminishes immunosuppressive Tregs in vivo, has a great potential in immune-stimulation indications. CGC-601’s safety evidence sets up a platform allowing multiple application scenarios (figure 9).

Correspondingly, we find that stroma-targeted stimulation of IL2 pathway in unresponsive tumors restores trastuzumab anti-cancer efficiency. Overall, our study underscores the therapeutic potential of exploiting the tumor microenvironment to identify and overcome mechanisms of resistance to anti-cancer treatment.

High expression of ILF2 is associated with a poorer prognosis independent of subtype in BC and our study warrants further investigation on ILF2 as a diagnostic and therapeutic target.

From the perspective of tumor immunobiology, we identify multiple inflammatory states (proposed as types I-III) and see that systemic chronic dysregulation, independent of tumor microenvironment, can be measured and is a possible tool for stratification. Thus, direct correlation of local cytokine levels to peripheral blood levels needs to be regarded with caution.

Tumor control of the combination treatment was accompanied by increased numbers of neoantigen-specific T cells and a T cell phenotype previously associated with successful cancer immunotherapy. An open-label, Phase I/II, first-in-human trial in patients with advanced solid tumors was recently initiated to further explore the clinical safety and efficacy of BNT151 as monotherapy or in combination with other anti-cancer agents (NCT04455620).

Our results indicate that the TME composition has relevant biological roles in MCL. In this setting, immunohistochemical detection of T-reg cells, IL17A and IL2, coupled with SNV genotyping in IL10, TGFBR2 and IL2, may represent novel prognostic factors in this disease, following future validations.

Our data suggested that baseline cytokine levels may predict patients' outcome and that the treatment may affect their kinetic even in end-stage patients. Cytokine profiling of end-stage patients might offer a tool for medical decisions (EUDRACT: 2016-000578-39).

Our proof-of-concept study proposes MSLN-retargeted herpesviruses as potential cancer immunotherapeutics for assessments in preclinical models of MSLN-positive tumors, complementing the available panel of oncolytic viruses to HER2-negative breast tumors.