TEST:

Oncomine™ Immune Response Research Assay

Utilization of a multi-modal CGIP testing strategy resulted in a high rate of test success and detection of clinically relevant biomarkers and optimizing tissue usage.

In the future, these biological alterations are the first step to provide new treatment modalities with different classes of drugs currently in use in a systemic or local approach, including classical chemotherapy drugs such as cisplatin and fluorouracile, older drugs like fenretinide, and new checkpoint inhibitor drugs such as nivolumab and pembrolizumab, as well as newer options like T cell therapy (CAR-T). Following these observed alterations, it is possible to differentiate which dysplasias progress or not or relapse quickly. This information could, in the future, be the basis for determining a close follow-up, minimizing surgical interventions, planning a correct and personalized treatment protocol for each patient and, after specific clinical trials, tailoring new drug treatments.

These findings suggest that bronchoscopic thermal injury of NSCLC results in an increase in antigen presentation within the TME with some features to suggest activation of a T cell-mediated immune response. The increase of CD4+ T cells and Macrophages seen within the tumour only suggests that this is a tumour-specific response. Further work is needed to elucidate these findings.

These findings highlight the heterogeneity and distinct molecular characteristics of PrBC and EOBC. The upregulation of specific immune-related gene families, such as CT and Chemokines, in different PrBC subtypes may suggest their potential role as actionable biomarkers (e.g. MAGEA, a well-known oncogene and potential immunotherapy target).

Downregulation of CXCL13, which acts as a B lymphocyte chemoattractant, has previously been shown in both WM and chronic lymphocytic leukaemia after Ibrutinib treatment, minimising the migration of tumour cells and disrupting the TME. This pilot study has shown regions of the WM immune microenvironment with significant changes in gene expression after BTKi therapy, namely in pathways involving NK cells and type 2 interferon signalling. A larger cohort with paired samples pre and post BTKi treatment is under investigation.

A better understanding of the complex interplay between cancer cells and host immunity is essential for the choice of personalized treatment in Luminal A BC. The DEGs here identified in metastatic SLNs of Luminal A BC may improve prognosis accuracy and increase the efficacy and safety of targeted therapies. Particularly, VTCN1, CD44, NECTIN2, LRG1, CD276 and FOXM1 seems extremely promising biomarkers and potentially useful for target immunotherapy.

High CXCL9 expression correlated with increased infiltration levels of immune cells in the TME, including CD8+ T lymphocytes and M1 macrophages. These findings suggest that high PD-L1 expression is a prognostic factor of early-stage CRC, and CXCL9 may play a key role in regulating PD-L1 expression.

Herein we interrogated the molecular and phenotypic profiles of the T cell compartment in 1 treatment-naïve and 15 relapsed/refractory CLL patients who received ven either as monotherapy (n=12) or in combination with an anti-CD20 antibody (obinutuzumab, n=1; rituximab, n=3). In conclusion, ven treatment led to increased numbers of CD8+ effector subpopulations along with prominent clonal expansions and transcriptional rewiring that could conceivably contribute to clinical response. Downregulation of immune-related genes implicated in core regulatory/activation pathways supports immune recovery by ven, offering a rationale for future combination strategies aiming to increase the depth of clinical response.

We identified eight immune genes which were associated with better prognosis and drug responses. The 8-gene score may serve as a prognostic marker for breast cancer patients who receiving neoadjuvant chemotherapy.

Conclusions The greatest changes in the immune expression profile during neoadjuvant treatment were observed in CPR tumors reflecting an active immune response. There were little differences between paired samples of non-CPR tumors that denotes ineffective immune stimulation after treatment.

By DSP, we confirm that LUAD patients with high expression levels of IL-11 express lower levels of some immune markers. Conclusion Collectively, our data demonstrate that IL-11 dysregulates tumor immunity towards an immunosuppressive microenvironment favoring cancer progression.

The upregulated pathways in surgical samples of CPR patients suggested that an effective immune response to PD-1 blockade was done. Additionally, we have identified an immune expression signature in surgical specimens associated to disease progression for non-CPR patients which could help in the follow-up and therapeutic management of these high-risk patients.

Overexpression of LAG3 in large neoplastic B-cells of RT, specifically in cases clonally-related to CLL is an important finding that may serve as a diagnostic marker. Checkpoint molecules LAG3 and TIM3 can serve as new immune-therapy targets for the treatment of RT. IL-10 blockade has been shown to enhance T-cell immunity, and may be a potential therapeutic target.

The AUC ROC for response prediction based on IFNG, GZMB expression or M1 macrophages proportion was 1.000 (p=0.0027), 0.911 (p=0.0136) and 0.9778 (p=0.004), respectively. Conclusions In our study, a pro-inflammatory profile measured in the pre-treatment tissue by RNA-sequencing is associated with CPR following neoadjuvant CI in patients with stage IIIA NSCLC.

PrBC TME is characterized by specific patterns of TILs subpopulations due to the possible activation of type I IFNs and its assessment might help in identifying women at high risk of death and recurrence.

The activation of immune-related pathways might play a part in the development of IBE in patients with a diagnosis of DCIS. The evaluation of immune-related gene expression profiles might improve risk stratification in patients with DCIS.